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  • Q1:Blood Glucose Data Analysis hhmi BioInteractive Activity Student Handout INTRODUCTION Although we can easily digest milk as babies, most of us lose this ability as adults. This is because we usually stop producing lactase, an enzyme that breaks down the main sugar in milk. However, about one-third of people worldwide still produce lactase as adults. In this activity, you will learn about a test for whether someone is likely to produce lactase. This test is based on the amount of a sugar called glucose in a person's blood. BACKGROUND Milk is packed with proteins, fats, and carbohydrates that support the growth, development, and survival of baby mammals. The main carbohydrate in milk is a sugar called lactose. To digest milk, lactose must be cleaved, or broken down, by lactase, an enzyme produced in the small intestine. Lactase cleaves lactose into two smaller sugars, glucose and galactose, which are easily absorbed through the walls of the small intestine. Once these sugars are absorbed into the bloodstream, they can be delivered to the cells of the body and used for energy. arr Lactase enzyme + & HO Lactose H2O Glucose Galactose Figure 1. A diagram showing how the lactase enzyme cleaves the sugar lactose. As baby mammals grow up and stop drinking their mother's milk, their bodies usually stop producing the lactase enzyme (presumably because it is no longer needed). Individuals that do not produce lactase as adults are called lactase nonpersistent. Most mammals are lactase nonpersistent and do not drink milk as adults. Humans are unusual in that some adults continue to drink milk from other mammals, such as cows. When an individual who is lactase nonpersistent drinks milk, they cannot easily break down the lactose in the milk. The lactose passes from their small intestine to their large intestine, where it is fermented by bacteria. Fermentation produces various gases in the large intestine, which can cause abdominal pain, bloating, flatulence, and diarrhea - all symptoms of lactose intolerance, the inability to digest lactose. Most adults are lactase nonpersistent and thus typically lactose intolerant (although some may not know it because their symptoms are mild). However, about 35% of the global human population continues to produce lactase into adulthood. These individuals are called lactase persistent and are typically lactose tolerant, meaning that they can digest lactose easily and drink milk without problems. Enzymes & Reactions www.BioInteractive.org Updated January 2020 Page 1 of 5 hhmi BioInteractive Blood Glucose Data Analysis Activity Student Handout PROCEDURE There are several ways to test whether someone is lactase persistent or nonpersistent. One method, the blood glucose test, is shown in the short film Got Lactase? The Co-evolution of Genes and Culture. Table 1 shows the blood glucose levels of the film's narrator, Spencer Wells, and six other individuals over time. The glucose levels were measured using glucose strips and a glucose reader similar to the one in the film. After baseline levels (i.e., the ones at "0 minutes") were measured, each person drank a liter of milk. Their blood glucose levels were measured again at 15, 30, 45, and 60 minutes after drinking the milk. Table 1. Blood glucose test results for seven adults tested in Sarah Tishkoff's laboratory. Blood Glucose (mg/dL) Individual 0 minutes 15 minutes 30 minutes 45 minutes 60 minutes Spencer Wells 117 128 146 160 152 Peter 97 111 135 154 143 Rachel 96 99 105 101 98 Katherine 95 97 99 101 102 Sarah 108 116 129 141 139 Michael 94 109 128 143 140 Arthur 97 96 94 83 88 1. Plot the data in Table 1 on the graph below, which already includes the results for Spencer Wells. Add more entries to the legend as needed. Blood Glucose Test Results 160 150- 140- Spencer Wells Blood Glucose (mg/dl) 130- 120- 110 100 90 80 0 10 20 30 40 50 60 Time (minutes) Enzymes & Reactions www.BioInteractive.org Updated January 2020 Page 2 of 5 hhmi BioInteractive Blood Glucose Data Analysis Activity Student Handout After graphing the data, answer the following questions. 2. For someone that is lactase persistent, explain why their blood glucose concentrations rise after drinking milk despite milk containing no glucose. 3. Divide the individuals in Table 1 into two groups (A and B) based on their blood glucose test results. Write the names of the individuals in each group, including Spencer Wells, below. Group A: Group B: 4. Explain your rationale for dividing the individuals into these two groups. Use data from your graph to support your answer. 5. Based on the data in the graph and table, do you think the individuals in Group A are lactase persistent or nonpersistent? Describe the evidence that supports your answer. 6. Based on these data, do you think the individuals in Group B are lactase persistent or nonpersistent? Describe the evidence that supports your answer. 7. If the blood glucose test was performed on people from the Maasai population in Kenya, would their results be more like those of the individuals in Group A or Group B? Explain your prediction. (Hint: As discussed in the film Got Lactase? The Co-evolution of Genes and Culture, the Maasai traditionally raise cows for food.) 8. Explain why it is possible for lactose intolerant individuals to digest the proteins in milk even though they lack the lactase enzyme. Enzymes & Reactions www.BioInteractive.org Updated January 2020 Page 3 of 5 Activity hhmi Biointeractive Blood Glucose Data Analysis Activity Student Handout 9. A milk allergy is the result of a reaction to one or more of the components of milk, such as the protein casein. Explain how an allergy to milk is different from lactose intolerance. EXTENSION: THE HYDROGEN BREATH TEST Another common way to test whether a person is lactase persistent or nonpersistent is the hydrogen breath test. This test uses the amount of hydrogen in a person's breath to check for lactose fermentation. As described in the "Background" section, undigested lactose is fermented by bacteria in the large intestine. Fermentation produces several gases, including hydrogen, that can exit the body through the anus. These gases can also be absorbed into the blood, circulated to the lungs, and eliminated through the breath. With lactase Lactase Lactose Glucose + Galactose Small intestine Without lactase Gas (H2, CH2) + Lactose Lactose Fermentation Acids Small intestine Large intestine Figure 2. A diagram comparing what happens to lactose in the intestines of individuals with and without the lactase enzyme. Table 2 shows the levels of hydrogen in the breath of four adults tested for lactase persistence. As in Table 1, the measurements at "0 minutes" represent baseline levels before drinking milk. The other measurements were taken at various times after drinking milk. Table 2. Hydrogen test results for four adults. Hydrogen Breath Levels (ppm) Individual 0 minutes 30 minutes 60 minutes 90 minutes 120 minutes 5 6 9 8 5 Lisa 4 9 8 29 35 Dan 6 8 10 31 32 Cindy 4 7 6 9 6 Brian Updated January 2020 Page 4 of 5 Enzymes & Reactions www.BioInteractive.org hhmi BioInteractive Blood Glucose Data Analysis Activity Student Handout 1. Create your own graph of the data in Table 2. Your graph should include a title, labels for the x- and y-axes, and a legend. Hydrogen Breath Levels (ppm) 2. Which individuals in Table 2 are likely to be lactase persistent? Use data from your graph to support your answer. 3. Which individuals in Table 2 are likely to be lactase non-persistent? Use data from your graph to support your answer. 4. Think of another type of test to determine whether a person is lactase persistent or nonpersistent. Describe your idea in one or two sentences. Enzymes & Reactions www.BioInteractive.org Updated January 2020 Page 5 of 5/nANSWER ALL THE QUESTIONS MENTIONED IN ASSIGNMENT FILE AND DO THE GRAPHS Instructions: Word requirement – min 500 words Plagiarism free Solutions generated from any AI platform is strictly Prohibited Referencing and formatting Style APA Need Typed Solutions only.See Answer
  • Q2:LAB REPORT The practical report involves performing a Bradford protein assay to calculate the total concentration of an unknown sample extracted by protein extraction, ‘method A’. The expected target yield for method A is 750 μg/mL. Results • It is recommended that you allocate 200 words to the results section. • In the results section, you should provide a summary of the main results and present your main results in a logical order. Data analysis should be performed using Excel or SPSS. You should present the following data in the results section: • BSA standard curve with appropriate figure legend - You should only plot data where the relationship is linear. Table and table title to present the concentration of sample A/ the target value/ key statistical results. - Remember to refer to the figure and table within the text and do not attempt to interpret the data in this section. Discussion • It is recommended that you allocate 300 words to the discussion • You may use further subheadings to structure the discussion • This is the section where you should interpret the data - What have the results found in relation to the overall aim of the report stated in the introduction? Would you accept/reject the alternative/null hypotheses? Did the protein assay work? Is the quality of the data good? Critically assess the methods used - discuss potential sources of error in your laboratory work. What improvements could you make if this experiment were to be repeated in the future? What are the implications of the findings? Reference list • You should provide a reference list for all sources cited within the report • Reference list should be provided as per APA 7th style. Language/writing style • Use a formal academic writing style and use scientific language throughout (APA formatting mandatory) • The report should be written in the third person • Write terms in full before using abbreviations • Proofread your report before submission to avoid spelling, grammatical and punctuation errors. You should submit a single file which is structured as follows: • Results • Discussion • References Strictly refrain from providing AI-generated and plagiarised solutions/nMethod Preparation of 2 mg/mL BSA stock solution In this first part, you will need to prepare 2mg/mL stock of BSA in DPBS (diluent) - you will need to prepare 10 mL of this stock solution. How much BSA will you need to weigh out using the analytical balance? Write any calculations in the space provided here: 1) Using the spatula and small weighing boat, weigh out the required volume of BSA powder 2) Transfer the BSA powder to a 15mL centrifuge tube. Label the tube '2mg/mL BSA solution' and label with your initials and the date 3) Pipette 10 mL DPBS into the 15mL centrifuge tube containing the BSA powder which you have weighed out 4) Mix by vortexing until all of the BSA powder has dissolved into solution 55 Preparation of standards (non-serial dilution) Non-serial dilutions (V1C1=V2C2) In this practical, the standards will be produced by performing non-serial dilutions. In non-serial dilutions, each standard is diluted from the stock solution. You will need to use the V1C1 = V2C2 equation to calculate how you are going to prepare the standards: V x C = V. x C 2 V = volume of stock C = concentration of stock V2 = volume of dilution (standard required) C = concentration of dilution (standard required) 2 ** Remember the units must be consistent on each side ** 5) Prepare the following standards by diluting the BSA stock solution (2mg/mL) in DPBS: · 2000 µg/mL 1500 µg/mL · 1000 µg/mL . 750 µg/mL . 500 µg/mL · 250 µg/mL · 125 µg/mL · 0 µg/mL You will need to prepare a total volume of 500uL of each standard. Prepare the standards in 1.5 mL microcentrifuge tubes which you should clearly label with the relevant BSA concentration. Record your calculations on the following pages. 56 Adding standards to a 96-welll plate 6) Add 5uL of each standard (0 - 2000 µg/mL) in triplicate to the 96-well plate as shown: Note: ensure each standard is mixed before pipetting onto the plate Note: 5uL is a small volume and accurate pipetting is required, pipette the standard into the bottom of the well and make sure you keep track of which standards you have added. 1 2 3 4 5 6 7 8 9 10 11 12 A 2000 2000 2000 X X X X X X X X X B 1500 1500 1500 X X X X X X X X X C 1000 1000 1000 X X X X X X D 750 750 750 X X X X X E 500 500 500 X X X X X X X X F 250 250 250 X X X X X X G 125 125 125 X X X X X X X X H 0 0 0 X X X X X X X X X Adding the unknown sample 'A' to a 96-well plate 7) Add 5uL of the unknown sample 'A' in triplicate to the 96-well plate as shown: Note: ensure the sample is mixed before pipetting onto the plate 1 2 3 4 5 6 7 8 9 10 11 12 A X X X A A A X X X X X X B X X X X X X X X X X X X C X X X X X X X X X X X X D X X X X X X X X X X X X E X X X X X X X X X X X X F X X X X X X X X X X X X G X X X X X X X X X X X X H X X X X X X X X X X X X 8) Using a single-channel pipette, pipette 200uL of the Coomassie protein assay reagent to each well containing standard or sample 9) Mix on the plate shaker for around 1 minute 10) Incubate the plate at room temperature for around 15 minutes 59 Measuring the absorbance values 11) Measure the absorbance of the plate at 620 nm using the plate reader Stick your results onto this page. 1 2 3 4 5 6 A 1.2111 1.1195 1.1158 0.7756 0.7212 0.7444 B 1.1132 1.1056 1.1009 C 0.9843 0.8255 0.9666 D 0.7821 0.7777 0.7644 E 0.6592 0.6543 0.5273 F 0.4563 0.4422 0.4816 G 0.3981 0.3991 0.4022 H 0.3172 0.3224 0.3116 60See Answer
  • Q3:Unit Essay Assignments Information about Unit Essay Questions Write an essay about the function of that element (Calcium) in human biochemistry. Remember we are seeking biochemical information at a molecular level, not just nutritional requirements. Cite at least three references that you used to answer this question. Compare the element’s abundance in the environment vs its concentration in human cells. How is the element assimilated/transported into human cells? What is the element’s biological function in human physiology? Is the element bound to proteins or other biopolymers and if so how? If the element serves as a cofactor in enzyme reactions describe its catalytic role. If the element not permanently bound to an organic molecule is it bound transiently and how? What happens if there is a nutritional deficiency of the element? Instructions: Submit essays of at least 500 words in length on or before the deadline. The writing must be ENTIRELY in your own words. Plagiarism and AI content won't be accepted. Your sources should be cited in the text, not just at the end. Those sources should be from published reports or articles. The reference list does not contribute to your word count. For these essays, please use complete sentences, acceptable grammar, appropriate punctuation, and normal paragraph structure. Your grade will be based on content, clarity, accuracy and fluency, acceptable writing style, and grammar. Referencing and formatting style : APASee Answer
  • Q4:Question The nervous system sends electrical impulses that travel very rapidly and tend to result in short term effects, such as muscle contraction. The endocrine system is responsible for much slower signals that tend to have a much longer lasting effect on the body. a) Discuss how the endocrine system sends signals around the body, where the signals originate from, where they are targeted, and explain why these signals take much longer than nerve impulses. The major glands, hormones and target tissues can be included in a table which needs to be accompanied by a brief discussion of how the endocrine system works. b) Explain how the activity of these endocrine glands is regulated. Total word count: 450-500 words Instructions: Answer all the questions following the instructions. Strictly do not use AI for solving questions. The solution should be free of Plagiarism. Solution to be formatted in APA and use appropriate references with in-text citations in APA.See Answer
  • Q5:Question Journal Article Perspective Papers Do the summary statement of the paper attached in not more than one page For your summary statement, address the following questions: - What specific question/hypothesis were the researchers attempting to address? - What are the most important experiments in the paper that addressed this question? (DO NOT try to discuss all the experiments—choose the ones that you feel are most important) - What methods/techniques did the researchers use in these experiments? - What conclusions did the authors draw based on these results? - How did the conclusions address the researchers’ original question/hypothesis? Instructions: Answer all the questions following the instructions. Strictly do not use AI for solving questions. The solution should be free of Plagiarism. Solution to be formatted in APA and use appropriate references with in-text citations in APA./nRESEARCH | REPORTS 2. B. Bosworth, K. Zhang, "Evidence of Increasing Differential Mortality: A Comparison of the HRS and SIPP," Center for Retirement Research at Boston College Working Paper 2015-13 (2015). 3. R. Chetty et al., JAMA 10.1001/jama.2016.4226 (2016). 4. National Research Council, Committee on the Long-Run Macroeconomic Effects of the Aging U.S. Population, "The Growing Gap in Life Expectancy by Income: Implications for Federal Programs and Policy Responses" (2015). 5. J. Pijoan-Mas, J. V. Ríos-Rull, Demography 51, 2075-2102 (2014). 6. H. Waldron, Soc. Secur. Bull. 67, 1-28 (2007). 7. H. Waldron, Soc. Secur. Bull. 73, 1-37 (2013). 8. J. Wilmoth, C. Boe, M. Barbieri, in International Differences in Mortality at Older Ages: Dimensions and Sources, E. M. Crimmins, S. H. Preston, B. Cohen, Eds. (National Academies Press, Washington, DC, 2011), pp. 337-372. 9. G. K. Singh, M. Siahpush, Int. J. Epidemiol. 35, 969-979 (2006). 10. M. Ezzati, A. B. Friedman, S. C. Kulkarni, C. J. Murray, PLOS Med. 5, e66 (2008). 11. C. J. Murray et al., PLOS Med. 3, e260 (2006). 12. H. Wang, A. E. Schumacher, C. E. Levitz, A. H. Mokdad, C. J. Murray, Popul. Health Metr. 11, 8 (2013). 13. J. S. Olshansky et al., Health Aff. 31, 1803-1813 (2011). 14. E. R. Meara, S. Richards, D. M. Cutler, Health Aff. 27, 350-360 (2008). 15. D. M. Cutler, F. Lange, E. Meara, S. Richards-Shubik, C. J. Ruhm, J. Health Econ. 30, 1174-1187 (2011). 16. J. K. Montez, L. F. Berkman, Am. J. Public Health 104, e82-e90 (2014). 17. Human Mortality Database; www.mortality.org. 18. D. D. Reidpath, P. Allotey, J. Epidemiol. Community Health 57, 344-346 (2003). 19. A. Case, A. Deaton, Proc. Natl. Acad. Sci. U.S.A. 112, 15078-15083 (2015). 20. J. Bound, A. Geronimus, J. Rodriguez, T. Waidman, "The Implications of Differential Trends in Mortality for Social Security Policy," University of Michigan Retirement Research Center Working Paper 2014-314 (2014). 21. J. B. Dowd, A. Hamoudi, Int. J. Epidemiol. 43, 983-988 (2014). 22. T. Goldring, F. Lange, S. Richards-Shubik, "Testing for Changes in the SES-Mortality Gradient When the Distribution of Education Changes Too," National Bureau of Economic Research Working Paper 20993 (2015). 23. A. S. Hendi, Int. J. Epidemiol. 44, 946-955 (2015). 24. A. Aizer, J. Currie, Science 344, 856-861 (2014). 25. D. Brown, A. Kowalski, I. Lurie, "Medicaid as an Investment in Children: What Is the Long-Term Impact on Tax Receipts?" National Bureau of Economic Research Working Paper 20835 (2015). 26. S. Cahodes, S. Kleiner, M. F. Lovenhem, M. Grossman, "Effect of Child Health Insurance Access on Schooling." National Bureau of Economic Research Working Paper 20178 (2014). 27. S. Miller, L. R. Wherry, "The Long-Term Health Effects of Early Life Medicaid Coverage," Social Science Research Network Working Paper 2466691 (2015). 28. L. R. Wherry, B. Meyer, "Saving Teens: Using and Eligibility Discontinuity to Estimate the Effects of Medicaid Eligibility." National Bureau of Economic Research Working Paper 18309 (2013). 29. L. R. Wherry, S. Miller, R. Kaestner, B. D. Meyer, "Childhood Medicaid Coverage and Later Life Health Care Utilization," National Bureau of Economic Research Working Paper 20929 (2015). 30. J. Ludwig, D. L. Miller, Q. J. Econ. 122, 159-208 (2007). 31. H. Hoynes, D. Whitmore-Schanzanbach, D. Almond, "Long Run Impacts of Childhood Access to the Safety Net," National Bureau of Economic Research Working Paper 18535 (2012). 32. A. Isen, M. Rossin-Slater, R. Walker, "Every Breath You Take Every Dollar You'll Make: The Long-Term Consequences of the Clean Air Act of 1970," National Bureau of Economic Research Working Paper 19858 (2014). 33. A. Fenelon, S. H. Preston, Demography 49, 797-818 (2012). 34. D. de Walque, J. Hum. Resour. 45, 682-717 (2010). 35. C. E. Finch, E. M. Crimmins, Science 305, 1736-1739 (2004). ACKNOWLEDGMENTS We thank M. Barbieri, A. Case, A. Deaton, J. Goldstein, I. Kuziemko, R. Lee, and K. Wachter, as well as seminar participants at Berkeley, the Chicago Federal Reserve, Fundação Getúlio Vargas São Paulo, Bonn University, University of Munich, Princeton University, ETH Zurich, and the University of Zurich for comments. Supported by Princeton Center for Translational Research on Aging grant 2P30AG024928. Data and code are available at http://dx.doi.org/10.7910/DVN/C2VYNM. SUPPLEMENTARY MATERIALS www.sciencemag.org/content/352/6286/708/suppl/DC1 Materials and Methods Figs. S1 to S8 Tables S1 to S4 References (36-38) 22 December 2015; accepted 17 March 2016 Published online 21 April 2016 10.1126/science.aaf1437 NEURODEVELOPMENT Complement and microglia mediate early synapse loss in Alzheimer mouse models Soyon Hong,1 Victoria F. Beja-Glasser,1* Bianca M. Nfonoyim,1* Arnaud Frouin,1 Shaomin Li,2 Saranya Ramakrishnan,1 Katherine M. Merry,1 Qiaogiao Shi,2 Arnon Rosenthal, 3,4,5 Ben A. Barres,6 Cynthia A. Lemere,2 Dennis J. Selkoe,2,7 Beth Stevens1,8+ Synapse loss in Alzheimer's disease (AD) correlates with cognitive decline. Involvement of microglia and complement in AD has been attributed to neuroinflammation, prominent late in disease. Here we show in mouse models that complement and microglia mediate synaptic loss early in AD. C1q, the initiating protein of the classical complement cascade, is increased and associated with synapses before overt plaque deposition. Inhibition of C1q, C3, or the microglial complement receptor CR3 reduces the number of phagocytic microglia, as well as the extent of early synapse loss. C1q is necessary for the toxic effects of soluble ß-amyloid (AB) oligomers on synapses and hippocampal long-term potentiation. Finally, microglia in adult brains engulf synaptic material in a CR3-dependent process when exposed to soluble Aß oligomers. Together, these findings suggest that the complement-dependent pathway and microglia that prune excess synapses in development are inappropriately activated and mediate synapse loss in AD. Downloaded from http://science.sciencemag.org/ on January 2, 2020 G enome-wide association studies impli- cate microglia and complement-related pathways in Alzheimer's disease (AD) (1). Previous research has demonstrated both beneficial and detrimental roles of com- plement and microglia in plaque-related neuro- pathology (2, 3); however, their roles in synapse loss, a major pathological correlate of cognitive decline in AD (4), remain to be identified. Emerg- ing research implicates microglia and immune- related mechanisms in brain wiring in the healthy 1F.M. Kirby Neurobiology Center, Boston Children's Hospital (BCH) and Harvard Medical School (HMS), Boston, MA 02115, USA. 2Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital (BWH) and HMS, Boston, MA 02115, USA. 3Alector Inc., 953 Indiana Street, San Francisco, CA 94107, USA. 4Annexon Biosciences, 280 Utah Avenue Suite 110, South San Francisco, CA 94080, USA. 5Department of Anatomy, University of California San Francisco (UCSF), San Francisco, CA 94143, USA. Department of Neurobiology, Stanford University School of Medicine, Palo Alto, CA 94305, USA. 7Prothena Biosciences, Dublin, Ireland. "Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. *These authors contributed equally to this work. +Corresponding author. Email: beth.stevens@childrens.harvard.edu brain (1). During development, C1q and C3 local- ize to synapses and mediate synapse elimination by phagocytic microglia (5-7). We hypothesized that this normal developmental synaptic pruning pathway is activated early in the AD brain and mediates synapse loss. The degree of region-specific synapse loss is a stronger correlate of cognitive decline in AD than counts of plaques, tangles, and neuronal loss (8, 9). To determine how early synapse loss occurs, we used superresolution structured illu- mination microscopy (SIM) (10) to quantify syn- apse density in hippocampal CA1 stratum radiatum of familial AD-mutant human amyloid precursor protein (hAPP) ("J20") transgenic mice (11). Quan- tification of colocalized pre- and postsynaptic puncta [synaptophysin and postsynaptic den- sity 95 (PSD95) (Fig. 1A); synaptotagmin and homer (fig. S1, A to D)] revealed a significant loss of synapses in J20 hippocampus at 3 to 4 months old (mo), an age that precedes plaque deposition (11, 12). Synapse loss in preplaque J20 CA1 was confirmed by electron microscopy (fig. S1G). Con- focal imaging also showed synapse loss in CA1, CA3, and dentate gyrus of 3 mo J20 hippo- campus but not in striatum (fig. S1E). Synapse 712 6 MAY 2016 . VOL 352 ISSUE 6286 sciencemag.org SCIENCE RESEARCH | REPORTS A WT J20 Synaptophysin + PSD95 Physin PSD95 150 Individual or Colocalized Puncta *** *** WT 100- % WT 50- 0 J20 B DG FC STR CRB Physin PSD95 Physin+PSD95 C1q DAP 150- *** WT WT J20 *** 100- 50- ns J20 C1q Intensity Levels (A.U.) T ns T 0 DG FC STR CRB C C1q PSD95 D C1g PSD95 % PSD95 Colocalized with C1q 250- * 200- Downloaded from http://science.sciencemag.org/ on January 2, 2020 % WT 150- 100- 50 0 WT J20 E WT J20 WT J20 Aß DAPI C1g Aß Levels in J20 DG C1q Levels in J20 DG 150- 150- * Veh % Vehicle-Rx ** 100- T % Vehicle-Rx $ 100- 50 50- CpdE 0 0 Veh CpdE Veh CpdE Fig. 1. C1q up-regulation and deposition onto synapses precede pre- plaque synapse loss in J20 mice. (A) Superresolution SIM images of synaptophysin (green)- and PSD95 (red)-immunoreactive puncta in stratum radiatum of 3 mo J20 or WT hippocampus (CA1). Quantification of synaptic puncta or their apposition using Imaris indicates selective loss of PSD95 in J20 hippocampus as compared to their WT littermate controls. See fig. S1. (B) Region-specific up-regulation of C1q (green) in 1 mo J20; DG, dentate gyrus; FC, frontal cortex; STR, striatum; CRB, cerebellum; DAPI, 4',6-diamidino-2-phenylindole. See fig. S2. (C) Orthogonal view of SIM image showing colocalization of C1q (green) and PSD95 (red). (D) Higher percentage of PSD95 colocalized with C1q in 1 mo J20 dentate gyrus versus WT. (E) Compound E reduces deposited soluble Aß (red) and Clq (green) in 1 mo J20 dentate gyrus, with minimal effect on C1q levels in WTmice. Scale bar, 2 um (A, C, and D) or 10 um (B and E). Means ± SEM; n = 3 or 4 mice per genotype or per treatment group per genotype. * P < 0.05, ** P < 0.01, or *** P < 0.001 using two-way analysis of variance (ANOVA) followed by Bonferroni posttest (A and B), two-tailed one-sample t test (D), or two- tailed unpaired t test (E). levels were not altered in 1 mo J20 brains ver- sus wild-type (WT) littermates (fig. S1F), sug- gesting that the hippocampal synaptic loss at 3 mo is likely not a result of abnormal synaptic development. We asked whether the classical complement cascade is up-regulated in preplaque brains when synapses are already vulnerable. C1q immuno- reactivity (13) (antibody now available at Abcam) was elevated in J20 brains as early as 1 mo and preceding synapse loss (Fig. 1B and fig. S1). C1q elevation was region-specific, particularly in the hippocampus and frontal cortex, two regions vulnerable to synapse loss (14) (Fig. 1B and fig. S2A). C1q immunoreactivity was comparable be- tween J20 and WT mice at postnatal day 21 (P21) (fig. S2B), suggesting that elevated levels at 1 mo are likely not a developmental artifact. C1q was also similarly increased in the hippocampus of another model of AD, the APP/PS1 (presenilin 1) mice (15) (fig. S2C). Notably, SIM demonstrated colocalization of C1q with PSD95-positive puncta in 1 mo J20 hippocampus (Fig. 1C). A higher percentage of PSD95 colocalized with C1q in the hippocampus of J20 mice than in that of WT littermates (Fig. 1D and fig. S3), suggesting that the C1q-associated synapses may be marked for elimination. Punctate Aß was found deposited in J20 hip- pocampus at 1 mo (fig. S4), long before Aß plaques deposit (11, 12), raising the question of whether C1q increase in these preplaque brains is dependent on soluble Aß levels. To test this hypothesis, we injected the mice with compound E, a y-secretase inhibitor that rapidly decreases Aß production (12). Compound E markedly re- duced soluble Aß levels in J20 mice; there was a corresponding reduction of C1q deposition (Fig. 1E), suggesting that Aß up-regulates Clq. SCIENCE sciencemag.org 6 MAY 2016 . VOL 352 ISSUE 6286 713 RESEARCH | REPORTS A Control Aß Monomer Aß Oligomer B C1q PSD95 % PSD95 Colocalized With C1q C1q 250- * 200- % WT 150- 100- 50- 0 Mon. Rx Olig. Rx C Control Aß Monomer Aß Oligomer % CD68 Occupancy in C1qa WT Microglia CD68 60- ** Iba1 % Total Microglia ## Control Rx AB Monomer Rx 40- AB Oligomer Rx T 20- 0 0 1 2 3 100- I D % Total Microglia % CD68 Occupancy in C1qa KO Microglia Control Rx 80- JAB Monomer Rx 60- Aß Oligomer Rx Downloaded from http://science.sciencemag.org/ on January 2, 2020 Fig. 3. Complement is necessary for synapse loss and dysfunction in AD models. (A) Aß oli- gomers induced loss of colocalized synapsin- and PSD95-immunoreactive puncta in the contralateral hippocampus of 3 mo WT mice (left panel); however, they failed to do so in C1qa KO mice (right panel). (B) Coinjection of Aß oligomers with the function- blocking antibody against C1q, ANX-M1, but not with its IgG isotype control, prevented synapse loss in WT mice. (C) Pretreatment of hippocampal slices with the anti-Clq antibody, ANX-M1, prevented Aß- mediated LTP inhibition (green) versus IgG (red). IgG alone had a minimal effect (blue) versus artificial cerebrospinal fluid (aCSF) vehicle (black). n = 6 to 11 slices per group. (D) Percentage of PSD95 co- localized with C3 is increased in APP/PS1 hippo- campus versus that of WT mice. (E and F) Genetic deletion of C3 prevents synapse loss in 4 mo APP/ PS1 mice. Quantification of colocalized immuno- reactive puncta for synaptotagmin and homer in dentate gyrus (E) or synaptophysin and PSD95 in CA1 stratum radiatum (F) of WT, APP/PS1, APP/ PS1xC3 KO, and C3 KO hippocampi. Means ± SEM; n = 3 to 5 mice per genotype or per treatment group per genotype. * P < 0.05, ** P < 0.01, or *** P < 0.001 using two-tailed one-sample t test (D), one- way (A, C, E, F) or two-way (B) ANOVA followed by Bonferroni posttest. ns, not significant. A Synapsin + PSD95 Colocalized Puncta 40- 20- 2 NOCH 1 0 0 1 T 3 %CD68 within Iba1+ Microglia Fig. 2. Oligomeric AB increases Clq and microglial phagocytic activity. (A and B) Soluble AB oligomers in WT mice led to elevation of Clq (green) (A) and a higher percentage of PSD95 (red) colocalization with Clq versus monomers (B). (C and D) oAß induced high levels of CD68 (green) immunoreactivity in Ibal-positive (red) microglia in WTmice (C), but not in those of C1qa KO mice (D). Both had negligible changes in morphology. See fig. S10. Scale bar, 10 um (A), 5 um (B), or 20 um (C). Means ± SEM; n = 3 to 5 mice per treatment group per genotype. * P < 0.05 using two-tailed t test (B) or *P < 0.05, ** P < 0.01 versus control-treated or ##P < 0.01 versus Aß monomer-treated using two-way ANOVA followed by Bonferroni posttest (C). B Synapsin + PSD95 Colocalized Puncta in WT Mice 400- 200- 200- ns Control ns lgG Ctrl % Control 150- 150- Aß Mon. % Control Aß Olig. % oAB-Rx 300- C1q Ab * ** 100- 100- T 200- 50- 50- 100- 0 0 0 C1qa WT C1qa KO PBS oAB PBS OAB C 250- aCSF +- IgG+aCSF % Baseline at 55 min of LTP Induction -IgG+oAB fEPSP slope (%) 200 C1qAb+oAB 200- LTP Magnitudes 180- ns *** 150 *** 160- 140- 100- 120- HFS 50- 100- -20 0 20 40 60 aCSF lgG+ lgG C1q Ab Time (min) aCSF +0Aß +0Aß D % PSD95 Coloc. With C3 Synaptotagmin + Homer in DG F Synaptophysin + PSD95 in CA1 250- * 150 ns 150 ns ns 200- ns * * % WT 150- % WT 100- % WT 100- 100- 50- 50- 50- O 0 WT APP/PS1 WT APP/PS1 APP/PS1 C3 KO WT APP/PS1APP/PS1 C3 KO 0 xC3 KO xC3 KO 714 6 MAY 2016 . VOL 352 ISSUE 6286 sciencemag.org SCIENCE RESEARCH | REPORTS A B Homer-GFP Homer-GFP Iba1 Iba1 15- % Engulfment *** 10- 5. 0- Aß Mon. AB Olig. C % Homer-GFP Engulfment by Microglia D Synaptotagmin + Homer Colocalized Puncta 250- 250- PBS 150- 150- PBS * 200- 200- oAB ns OAß % PBS-Rx % PBS-Rx % PBS-Rx ** % PBS-Rx 150- 150- 100- 100- ns 100- 100- 50- 50- 50- 50- 0 0 Homer-GFP Homer-GFP r0 0- xCR3 WT xCR3 KO To further address whether the increase of C1q is dependent on soluble Aß, and if so, which species, we injected soluble Aß oligomers or monomers into lateral ventricles of WT mice. Hippocampus contralateral to the injection site was examined to avoid any surgery-related ef- fects. Oligomeric Aß (oAß), which is prefibrillar in nature and acts as a mediator of synapse loss and dysfunction in AD (4), but not the relatively innocuous monomeric Aß or vehicle, induced C1q deposition (Fig. 2A and fig. S5). A higher percentage of PSD95 colocalized with C1q in oAß-injected versus monomer-injected mice (Fig. 2B), in a manner similar to this colocalization in J20 mice. Together, these findings show an early and aberrant increase and synaptic localization of C1q in multiple AD model systems. Further- more, fluorescent in situ hybridization (FISH) demonstrated up-regulated C1qa expression in microglia (fig. S6), implicating microglia as a major source of C1q in these preplaque brains. To test whether Clq and oAß act in a common pathway to eliminate synapses, we injected oAß into lateral ventricles of C1qa knockout (KO) mice (16). Soluble oAß induced a significant loss of co- localized synapsin- and PSD95-immunoreactive puncta in WT mice within 72 hours (Fig. 3A, left panel) (17). In contrast, oAß failed to induce syn- apse loss in C1qa KO mice (Fig. 3A, right panel), suggesting that Clq is required for oAß-induced synapse loss in vivo. To determine whether local, acute inhibition of C1 activation could similarly blunt the synaptotoxic effects of oAß, we used an antibody against C1q (anti-C1q) (ANX-M1, Annexon Biosciences), which blocks the classical complement cascade (see fig. S7 and supplemen- tary methods). Coadministration of the ANX-M1 anti-C1q antibody, but not its immunoglobulin G (IgG) isotype control, prevented oAß from inducing synapse loss in WT mice (Fig. 3B). Thus, block- ing C1 activation by either genetic or antibody- mediated means lessened oAB's synaptotoxic effects. To determine whether C1q is associated with synaptic dysfunction, we asked whether the established ability of oAß to potently inhibit long-term potentiation (LTP) (4) was depen- dent on C1q. We tested the functional effects of the ANX-M1 anti-C1q antibody in acute hippo- campal slices treated with oAB. IgG alone had negligible effects on LTP induction in WT mouse hippocampal slices and on the ability of oAß to inhibit LTP; however, pretreatment of hippo- campal slices with the anti-C1q antibody signif- icantly prevented the impairment of LTP by oAß (Fig. 3C). Neither ANX-M1 nor its IgG control altered basal synaptic neurotransmission (fig. S8). Collectively, these results in hippocampal slices and in mice support C1q as a key mediator of oAß-induced synaptic loss and dysfunction. In the healthy developing brain, C1q promotes activation of C3, which opsonizes subsets of synapses for elimination, a process that is down- regulated in the mature brain (5, 6). However, oAß induced a significant C3 deposition in WT adult mice (fig. S7A, upper panel). This was sig- nificantly reduced in both the C1qa KO (fig. S7A, lower panel) and the ANX-M1 anti-Clq antibody- treated WT mice (fig. S7B), suggesting that the C3 deposition in this model is downstream of the classical complement cascade. Consistent with these findings, a higher percentage of PSD95 colocalized with C3 in J20 and APP/PS1 brains (Fig. 3D and fig. S9). To determine whether C3 is necessary for early synapse loss in AD genetic models, we crossed APP/PS1 mice, which, simi- lar to the J20 mice, had a significant increase and localization of C1q and C3 onto hippocampal synapses (figs. S2C and S9), to C3-deficient mice (18). Quantification of colocalized pre- and post- synaptic puncta demonstrated synapse loss in 4 mo APP/PS1 hippocampus as compared to WT; however, APP/PS1xC3 KO mice did not display this synapse loss (Fig. 3, E and F). Together, our data indicate that genetic deletion of C3 amelio- rates synapse loss in APP/PS1 mice, providing further evidence that the classical complement cascade mediates early synapse loss in AD mouse models. Downloaded from http://science.sciencemag.org/ on January 2, 2020 CR3 WT CR3 KO Fig. 4. Microglia engulf synapses via CR3 upon oligomeric Aß challenge. (A) Orthogonal view of high-resolution confocal image shows colocalization of homer-GFP and Iba1 (red). (B) Three-dimensional reconstruction and surface rendering using Imaris demonstrate larger volumes of homer-GFP puncta inside microglia of oAß-injected contralateral hippo- campus versus those of monomer-injected. (C) Mi- croglia of homer-GFPxCR3 KO mice (right panel) show less engulfment of homer-GFP when chal- lenged with oAB versus those of homer-GFP mice (left panel). (D) Aß oligomers failed to induce syn- apse loss in the contralateral hippocampus of CR3 KO mice (right panel) as they did in WT mice (left panel). Scale bar, 5 um (A and B). Means ± SEM; n = 3 mice per treatment group per genotype (n = 6 to 17 microglia analyzed per mouse). * P < 0.05, ** P < 0.01, or *** P < 0.0001 using two-tailed t test (B) or two-tailed one-sample t test (C and D). ns, not significant. Microglia express complement receptors and mediate synaptic pruning in the developing brain (1, 6), raising the question of whether this normal developmental pruning pathway could be acti- vated to mediate synapse loss in the preplaque AD brain. Consistent with this hypothesis, mi- croglia had increased amounts of the lysosomal protein CD68 in J20 hippocampus compared to WT and less so in striatum, a less vulnerable region (figs. S1C and S10). Furthermore, in WT mice challenged with oAß, microglia had sig- nificantly increased levels of CD68 immuno- reactivity (Fig. 2C). However, in C1qa KO mice in which synapse loss was rescued, oAß failed to induce such an increase (Fig. 2D), suggesting that microglia eliminate synapses through the complement pathway. To directly test whether phagocytic microg- lia engulf synaptic elements, we adapted our in vivo synaptic engulfment assay (19) using in- tracerebroventricular injections of Aß in homer- GFP (green fluorescent protein) mice (20) (Fig. 4.A). oAß induced a significantly higher volume of internalized homer-GFP in microglia than monomeric Aß controls did at the contralateral hippocampus (Fig. 4B), indicating that microglia engulf synaptic elements when challenged with oAB. Internalized homer-GFP often colocalized SCIENCE sciencemag.org 6 MAY 2016 . VOL 352 ISSUE 6286 715 RESEARCH | REPORTS with CD68 (fig. S11A), suggesting that the en- gulfed synapses are internalized into lysosom- al compartments in a manner similar to that of developmental synaptic pruning (6). Notab- ly, oAß failed to increase synaptic engulfment in microglia lacking CR3 (21), a high-affinity receptor for C3 expressed on macrophages [homer-GFPxCR3 KO versus homer-GFP mice, which received tail vein injections of phosphate- buffered saline (PBS) or oAß (Fig. 4C)]. These data demonstrate that CR3 is necessary for oAß-dependent engulfment of synapses by microglia. To test whether inhibition in microglial en- gulfment leads to protection against oAß-induced synapse loss, we performed tail vein injections of oAB into WT and CR3 KO mice. oAß induced synapse loss in the hippocampus of WT mice but not in that of CR3 KO mice (Fig. 4D). All CR3-positive microglia were P2RY12-positive (fig. S11), indicating that they are resident cells (22). Altogether, these results suggest that resi- dent microglia engulf synaptic material when chal- lenged by oAß through a complement-dependent mechanism. Synaptic deficits occur in early AD and mild cognitive impairment before onset of plaques and are some of the first signs of the neuronal de- generative process (4, 23-25). Here we identify critical synaptotoxic roles of complement and microglia in AD models before plaque forma- tion and neuroinflammation, in regions of the hippocampus undergoing synapse loss. Using multiple experimental approaches, we demon- strate a region-specific increase of phagocytic microglia and accumulation of C1q and C3 on synapses in preplaque brains. Microglia in the adult brain, when challenged with synapto- toxic, soluble Aß oligomers, engulf synapses in the absence of plaque aggregates; deletion of CR3 blocks this process. Finally, inhibiting C1q, C3, or CR3 activity rescues synaptic loss and dysfunction. Our data suggest a local activation of a de- velopmental pruning pathway (5, 6) as a key mechanism underlying oAß-induced synapse loss in preplaque AD brain. C1q is aberrantly increased by diffusible oAß in a region-specific manner and deposits onto synapses, triggering the activation of downstream classical comple- ment pathway and phagocytic microglia. Block- ing Aß production in J20 mice significantly ameliorated C1q deposition in the hippocampus, and genetic or antibody-mediated inhibition of complement blocks oAß from inducing microg- lial synaptic engulfment, synapse loss, and LTP inhibition. These complementary findings have direct therapeutic relevance. We propose a model in which Clq and oAß operate in a common pathway to activate the complement cascade and drive synapse elimi- nation by microglia through CR3 (fig. S12). This could occur in multiple ways: Soluble oAß asso- ciates with synaptic membranes and other syn- aptic markers (4, 26); thus, oAß bound to synapses may anchor Clq directly. Alternatively, oAß binding to synapses may weaken the synapse (4) and expose a C1q receptor. Although spe- cific receptors for C1q at synapses are not yet known, we have shown that C1q binds syn- apses in vulnerable regions undergoing syn- apse loss (5, 27). It is also plausible that oAß and C1q may work indirectly to mediate syn- apse loss through cytokines such as trans- forming growth factor-ß (7), through microglial or astrocytic activation, or through other mech- anisms, including major histocompatibility complex class I (MHCI)-PirB, another immune pathway critical for synapse elimination in de- velopment and AD (28-30). Finally, our studies show that resident mi- croglia in the adult central nervous system phagocytose synapses when challenged by syn- aptotoxic oAß, implicating microglia as poten- tial cellular mediators of synapse loss. Although microglia and complement activation are pro- minently involved in plaque maintenance and related periplaque neuropathology, their roles have heretofore been largely regarded as a sec- ondary event related to neuroinflammation (2). Our studies directly challenge this view and sug- gest that microglia and immune-related path- ways can act as early mediators of synapse loss and dysfunction that occur in AD models be- fore plaques form. Although the complement pathway may not be involved in all patholog- ical routes to AD, including plaque-associated synapse loss, the work reported here provides new insights into how synapses are lost in AD. It will be important in future studies to examine whether this microglia or the complement- dependent pathway also plays a role in plaque- associated synapse loss or in other synaptopathies, including tauopathies and Huntington's dis- ease. If so, our findings may suggest comple- ment and microglia as potential early therapeutic targets in AD and other neurodegenerative dis- eases involving synaptic dysfunction and memory decline. REFERENCES AND NOTES 1. S. Hong, L. Dissing-Olesen, B. Stevens, Curr. Opin. Neurobiol. 36, 128-134 (2016). 2. T. Wyss-Coray, J. Rogers, Cold Spring Harb. Perspect. Med. 2, a006346 (2012). 3. M. E. Benoit et al., J. Biol. Chem. 288, 654-665 (2013). 4. L. Mucke, D. J. Selkoe, Cold Spring Harb. Perspect. Med. 2, a006338 (2012). 5. B. Stevens et al., Cell 131, 1164-1178 (2007). 6. D. P. Schafer et al., Neuron 74, 691-705 (2012). 7. A. R. Bialas, B. Stevens, Nat. Neurosci. 16, 1773-1782 (2013). 8. S. T. DeKosky, S. W. Scheff, Ann. Neurol. 27, 457-464 (1990). 9. R. D. Terry et al., Ann. Neurol. 30, 572-580 (1991). 10. S. Hong, D. Wilton, B. Stevens, D. S. Richardson, Structured Illumination Microscopy for the investigation of synaptic structure and function. Methods in Molecular Biology; Synapse Development: Methods and Protocols. 11. L. Mucke et al., J. Neurosci. 20, 4050-4058 (2000). 12. S. Hong et al., J. Neurosci. 31, 15861-15869 (2011). 13. A. H. Stephan et al., J. Neurosci. 33, 13460-13474 (2013). 14. J. A. Harris et al., J. Neurosci. 30, 372-381 (2010). 15. J. L. Jankowsky et al., Hum. Mol. Genet. 13, 159-170 (2004). 16. M. Botto et al., Nat. Genet. 19, 56-59 (1998). 17. D. B. Freir et al., Neurobiol. Aging 32, 2211-2218 (2011). 18. M. R. Wessels et al., Proc. Natl. Acad. Sci. U.S.A. 92, 11490-11494 (1995). 19. D. P. Schafer, E. K. Lehrman, C. T. Heller, B. Stevens, J. Vis. Exp. 88, 51482 (2014). 20. T. Ebihara, I. Kawabata, S. Usui, K. Sobue, S. Okabe, J. Neurosci. 23, 2170-2181 (2003). 21. A. Coxon et al., Immunity 5, 653-666 (1996). 22. O. Butovsky et al., Nat. Neurosci. 17, 131-143 (2014). 23. D. J. Selkoe, Science 298, 789-791 (2002). 24. S. W. Scheff, D. A. Price, F. A. Schmitt, E. J. Mufson, Neurobiol. Aging 27, 1372-1384 (2006). 25. S. W. Scheff, D. A. Price, F. A. Schmitt, S. T. DeKosky, E. J. Mufson, Neurology 68, 1501-1508 (2007). 26. S. Hong et al., Neuron 82, 308-319 (2014). 27. A. H. Stephan, B. A. Barres, B. Stevens, Annu. Rev. Neurosci. 35, 369-389 (2012). 28. A. Datwani et al., Neuron 64, 463-470 (2009). 29. T. Kim et al., Science 341, 1399-1404 (2013). 30. H. Lee et al., Nature 509, 195-200 (2014). ACKNOWLEDGMENTS We thank B. Sabatini (HMS), T. Bartels (BWH), and members of the Stevens laboratory for critical reading of the manuscript; L. Dissing-Olesen (BCH) for help with the conceptual figure (fig. S12), M. Ericsson [HMS electron microscopy (EM) facility] for EM imaging, K. Kapur (BCH) for advice on statistics, D. M. Walsh (BWH) for Aß oligomers (S26C), S. Okabe (University of Tokyo) for homer-GFP mice, and M. Leviten and T. Yednock (Annexon Biosciences) for characterization and advice on the ANX-M1 anti-C1q antibody; D. Richardson (Harvard Center for Biological Imaging), A. Hill BCH Intellectual and Developmental Disabilities Research Center Cellular Imaging Core NIH-P30-HD-18655, and H. Elliot and T. Xie (HMS Image and Data Analysis Core) for assistance with imaging and data analysis; and S. Kim (BWH), K. Colodner (BCH), and S. Matousek (BWH) for assistance with mice. The J20 mice, C1qa KO mice, P2RY12 antibody, and the ANX-M1 C1q function-blocking antibody are available from L. Mucke, M. Botto, O. Butovsky, and A. Rosenthal under material transfer agreements with UCSF Gladstone, Imperial College London, BWH, and Annexon Biosciences, respectively. A.R. is a cofounder, consultant, and chairman of the board of directors; B.A.B. is a cofounder and chairman of the scientific advisory board; and B.S. serves on the scientific advisory board of Annexon LLC. A.R., B.A.B., and B.S. are minor shareholders of Annexon LLC. All other authors declare no competing financial interests related to this project. The following patents related to this project have been granted or applied for: PCT/2015/010288 (S.H. and B.S.), US14/988387 and EP14822330 (S.H., A.R., and B.S.), and US8148330, US9149444, US20150368324, US20150368325, US20150368326, and US20120328601 (B.S. and B.A.B.). This work was funded by an Edward R. and Anne G. Lefler Fellowship (S.H.), Coins for Alzheimer's Research Trust (B.S.), Fidelity Biosciences Research Initiative (F-Prime) (B.S. and C.A.L.), JPB Foundation (B.A.B.), the National Institutes of Health AG000222 (S.H.), National Institute of Neurological Disorders and Stroke-NIH R01NS083845 (D.J.S.), National Institute on Aging-NIH 1RF1AG051496A (B.S.). Supplementary materials contain additional data, including materials and methods. S.H. and B.S. designed the study and wrote the manuscript, with help from all authors. S.H. performed most experiments and data analysis; V.F.B .- G. and B.M.N. performed microglial activation and engulfment experiments along with immunohistochemistry; S.R. and K.M.M. performed C1q immunohistochemistry; A.F. performed FISH; S.L. performed electrophysiology; Q.S. and C.A.L. assisted with design and collection of APP/PS1 tissue; A.R. and B.A.B. designed and characterized the ANX-M1 anti-C1q antibody; and D.J.S. contributed in the discussions and experimental design. SUPPLEMENTARY MATERIALS www.sciencemag.org/content/352/6286/712/suppl/DC1 Materials and Methods Figs. S1 to S12 10 November 2015; accepted 18 March 2016 Published online 31 March 2016 10.1126/science.aad8373 716 6 MAY 2016 . VOL 352 ISSUE 6286 sciencemag.org SCIENCE Downloaded from http://science.sciencemag.org/ on January 2, 2020 Science Complement and microglia mediate early synapse loss in Alzheimer mouse models Soyon Hong, Victoria F. Beja-Glasser, Bianca M. Nfonoyim, Arnaud Frouin, Shaomin Li, Saranya Ramakrishnan, Katherine M. Merry, Qiaoqiao Shi, Arnon Rosenthal, Ben A. Barres, Cynthia A. Lemere, Dennis J. Selkoe and Beth Stevens Science 352 (6286), 712-716. DOI: 10.1126/science.aad8373originally published online March 31, 2016 Too much cleaning up The complement system and microglia seek out and destroy unwanted cellular debris for the peripheral immune system as well as excess synapses in the developing brain. Hong et al. now show how the system may go haywire in adults early in the progression toward Alzheimer's disease (AD). Aberrant synapse loss is an early feature of Alzheimer's and correlates with cognitive decline. In mice susceptible to AD, complement was associated with synapses, and microglial function was required for synapse loss. The authors speculate that aberrant activation of this "trash disposal" system underlies AD pathology. Science, this issue p. 712 ARTICLE TOOLS http://science.sciencemag.org/content/352/6286/712 SUPPLEMENTARY MATERIALS http://science.sciencemag.org/content/suppl/2016/03/30/science.aad8373.DC1 http://stm.sciencemag.org/content/scitransmed/7/309/309ra164.full RELATED CONTENT http://stm.sciencemag.org/content/scitransmed/6/241/241cm5.full http://stm.sciencemag.org/content/scitransmed/6/226/226ra30.full http://stke.sciencemag.org/content/sigtrans/8/402/ec329.abstract http://stke.sciencemag.org/content/sigtrans/5/238/ra61.full http://stke.sciencemag.org/content/sigtrans/8/373/ec100.abstract http://stke.sciencemag.org/content/sigtrans/9/427/ra47.full http://stke.sciencemag.org/content/sigtrans/9/427/pc11.full http://stke.sciencemag.org/content/sigtrans/10/470/eaan1468.full http://stm.sciencemag.org/content/scitransmed/7/278/278ra33.full REFERENCES This article cites 29 articles, 11 of which you can access for free http://science.sciencemag.org/content/352/6286/712#BIBL PERMISSIONS http://www.sciencemag.org/help/reprints-and-permissions Use of this article is subject to the Terms of Service Science (print ISSN 0036-8075; online ISSN 1095-9203) is published by the American Association for the Advancement of Science, 1200 New York Avenue NW, Washington, DC 20005. The title Science is a registered trademark of AAAS. Copyright @ 2016, American Association for the Advancement of Science Downloaded from http://science.sciencemag.org/ on January 2, 2020See Answer
  • Q6: BIOL 334 Neurobiology Journal Article Perspective Papers This semester you will write two critical perspective papers on journal articles we read and discuss in class Journal Clubs. The purpose of these is to give you practice in summarizing the important points of scientific papers and in critically evaluating their quality. The first article we will discuss is: Chan et al., Nature 2007: "Rejuvenation" protects neurons in mouse models of Parkinson's disease. You will not write a paper on this article yet. Read it closely and be prepared to talk about key figures (see below) during our class Journal Club. After our discussion, I'll post an example perspective paper to guide you in your writing later. The main paper, supplementary text, and helpful background info are posted on Moodle under Journal Clubs. You will only be responsible for the figures in the main text (Fig. 1-5) and Supplementary Fig S1, S6, and S7. Don't worry about being familiar with the other figures. If you need a refresher on how approach a primary literature article, please see the other clearly- marked helpful resources I've posted to Moodle under Journal Clubs. For all our papers, I recommend reading the paper 2-3 times before beginning your assignment. Please feel free to discuss the papers with each other. If there are things you don't understand, ask questions! – to each other or to me. You should also do some digging on your own. However, assignments should be written individually in your own words (also do not quote or paraphrase from the paper). Your Perspective Paper will have two main parts (see below for details): 1. Summary statement: ~1 page 2. Perspective statement on one of the two options below (choose one: "A” or “B”): ~1 page A. paper quality B. implications/extensions of this work For your summary statement, address the following questions: What specific question/hypothesis were the researchers attempting to address? What are the most important experiments in the paper that addressed this question? (DO NOT try to discuss all the experiments—choose the ones that you feel are most important) What methods/techniques did the researchers use in these experiments? What conclusions did the authors draw based on these results? How did the conclusions address the researchers' original question/hypothesis? For your position sections, support your position as critically as possible, drawing upon information from class, the textbook, and other sources as appropriate. Depending on whether you are addressing the quality or implications, address the following questions: 2A. Paper quality How well were the experiments described? What (if anything) could the authors have done to make the experimental design clearer? How well did the data support the author's conclusions? What additional experiments or controls are needed for you to be fully convinced? How appropriate were the methods for the research question? Are there other techniques that would have been more appropriate to use? BIOL 334 Neurobiology 2B. Implications What further lines of inquiry are suggested by these studies? How did the work contribute to extending or transforming what was already known? What do you think is the next most logical experiment based on the new results? How would you design this experiment? What are specific ways in which the research can be extended to other model systems or other important questions that will make it even more impactful? Formatting Word document (NOT a PDF) titled as follows: Last name_paper (ex: Luth_Chan 2007) 2 pages maximum - keep your writing concise! I will not accept any paper longer than 2 pages. 1.5 spaced 12-point Arial 1-inch margins Item Hypothesis/research question, important results, and Points 15 conclusions, for 2-3 experiments are clearly and concisely stated Methods details for experiments are accurately described 10 Connections between the research question, experiments, and conclusions are made 5 Your position on the paper is clearly stated Critical analysis refers to specific elements of the paper Position is supported with course material and/or outside sources Suggestions for alternative methods (quality) or additional experiments (implications) are present Ideas logically presented with effective transitions 10 15 10 10 10 Reader can distinguish between the paper's findings and your interpretations and opinions 5 Few grammar or spelling mistakes 50 In-text citations and bibliography are in correct format 5 Total 100See Answer
  • Q7: INSTRUCTIONS : Link given in the file https://www.usatoday.com/story/news/health/2021/05/04/hospitals-overuse-elective-procedur es-before-pandemic-report-finds/4921660001/ Need to do it in 100 words APA Style/n2:31 To Do Assignment Details Surgical Technology Practicum III Discussion #2: USA Today Surgery Article 100 pts Not Submitted Due Apr 25, 2024 at 11:59 PM Submission Types Discussion Comment III 5G Description Apr 25, 2024 at 12:34 PM Discussion Question: Based on this USA Today's Article- Will Elective Surgery continue to be overused or abused? Will it be more difficult for elective surgery to be booked? https://www.usatoday.com/story/news/health/20 21/05/04/hospitals-overuse-elective-procedures- before-pandemic-report-finds/4921660001/ View Discussion 4 Dashboard Calendar To Do Notifications InboxSee Answer
  • Q8: Instructions Title is surgical technologist Based on this profession you have to answer the questions Need to do it in 50 - 60 words each Reference and intext citation needed, do your own research for it patient care technician, phlebotomist, pharmacy technician and I have my CPR certification.. (You can take information from here alsoi)/n 5:05 .II 5G JOB INTERVIEW QUESTIONS 12_5_22-... in relation to them. Addressing why your background makes you a good fit will let employers know why your traits and qualifications make you well prepared. . Why do you want to work here? Tips: Interviewers often ask this question to determine whether you took the time to research the company and to learn why you see yourself as a good fit. The best way to prepare for this question is to do your homework and learn about the products, services, mission, history, and culture of this workplace. In your answer, mention the aspects of the company that appeal to you and align with your career goals. Explain why you are looking for these things in an employer. . What motivates you? Tips: Employers ask this question to gauge your level of self-awareness and ensure your sources of motivation align with the role. To answer, be as specific as possible, provide real-life examples and tie your answer back to the job role. • What credentials do you have that qualify you as a surgical technologist? Any applicant who qualifies for the position has completed a surgical technology degree program. By completing other certification programs, the potential employee may have additional credentials with a skill. Pay attention to extra credentials they discuss and determine if the individual meets your prerequisite requirements for the position. What to look for in an answer: • • Has at least an associate degree Possesses board certification Experience working in a medical facility Why is it necessary to account for all medical equipment and waste after a patient's treatment? The potential employee explains why the protocol is in place and steps that they followed in the field. This step has prevented medical office and doctors from facing medical malpractice lawsuits. It is critical that the worker comprehends how to prevent risks and keep all patients safe. What to look for in an answer: Ability to pay attention to details and help reduce serious liabilities for the hospital • • Compliance with OSHA protocol Desire to protect the patient from further negative outcomes Dashboard Calendar To Do Notifications Inbox 5:04 .II 5G JOB INTERVIEW QUESTIONS 12_5_22-... PCD 201 PROFESSIONAL CAREER DEVELOPMENT Job Interview Questions: . How would you describe yourself? Tips: When an interviewer asks you to talk about yourself, they're looking for information about how your qualities and characteristics align with the skills they believe are required to succeed in the role. If possible, include quantifiable results to demonstrate how you use your best attributes to drive success. . What makes you unique? Tips: Employers often ask this question to identify why you might be more qualified than other candidates they're interviewing. To answer, focus on why hiring you would benefit the employer. Since you don't know the other applicants, it can be challenging to think about your answer in relation to them. Addressing why your background makes you a good fit will let employers know why your traits and qualifications make you well prepared. . Why do you want to work here? Tips: Interviewers often ask this question to determine whether you took the time to research the company and to learn why you see yourself as a good fit. The best way to prepare for this question is to do your homework and learn about the products, services, mission, history, and culture of this workplace. In your answer, mention the aspects of the company that appeal to you and align with your career goals. Explain why you are looking for these things in an employer. What motivates you? Tips: Employers ask this question to gauge your level of self-awareness and ensure your sources of motivation align with the role. To answer, be as specific as possible, provide real-life examples and tie your answer back to the job role. • What credentials do you have that qualify you as a surgical technologist? Any applicant who qualifies for the position has completed a surgical technology degree program. By completing other certification programs, the potential employee may have additional credentials with a skill. Pay attention to extra credentials they discuss and determine if the individual meets your prerequisite requirements for the position. What to look for in an answer: • Has at least an associate degree Dashboard Calendar To Do Notifications InboxSee Answer
  • Q9: Homework #1: Osmolarity/Tonicity Problem: A patient has the following volumes of distribution: deuterium oxide: 40 liters inulin: 13 liters Evans blue: 2.8 liters Her plasma Osmolarity is 285mOsM. 1. How much solute (osmoles) exists in each of the above compartments? Using the data above as the initial conditions in each case, determine the effects of the following procedures on the water and solute in the ECF and ICF after equilibrium has occurred. You should be able to give the numerical values for volume and osmolarity of the ECF and ICF. Briefly explain your rationale for solving each problem. (Treat each solution below as a separate problem; do not make them additive.) 2. Patient ingests 1 L of water, which is absorbed totally from the digestive tract. 3. Patient ingests 0.18 moles of NaCl, all of which is absorbed into the body. Use dissociation constant of 2 for NaCl in all problems. 4. Patient receives an intravenous infusion of 2 L of 0.9% NaCl solution. 5. Patient ingests 1 L of water containing 0.3 moles of urea, all of which is absorbed. Instructions 1. Use this template and write your answers in neatly. 2. Rounding as instructed or your answers may not be correct. For volume, round to 0.1 L For solute, round to 0.001 osmoles For osmolarity, use mOsm (e.g., 300 mOsM) 3. Explanations should be brief and should largely address rationale for distribution of solute and water. Scanned with CamScanner 1. (10pts) Vol L Sol osmol mosM 2. (20pts) 3. (20pts) Total Vol L Sol osmol mosM Explanation: Vol L Total Total ECF ECF ECF ICF ICF ICF Plasma Scanned with CamScanner Sol osmol mOsM Explanation: 4. (20pts) Total Vol L Sol osmol mosM Explanation: Vol L ECF 5. (30pts) Work in 2 steps. Step1: Add water only, not penetrating particles yet. Remember to explain why? Total ECF ICF 40 Sol osmol q mOsM Explanation: ICF 13 27 d 3.705 7.698 + 285 Scanned with CamScanner Step2: Add penetrating particles and calculate new osmolarity. Total ECF ICF Vol L Sol osmol mOsM Scanned with CamScannerSee Answer
  • Q10: Introduction Despite what the $60 Billion diet industry has told you your whole life, restrictive dieting doesn't work (see article here: https://rightasrain.uwmedicine.org/body/healthy- weight/diets-dont-workLinks to an external site.). Remember the reality tv show The Biggest Loser? Every contestant has gained the weight back. And some weigh more than they were before going on the show! This is because strict, restrictive diets focused on rapid weight loss slow down your metabolism. Your body is designed to fight change. Your body interprets a restrictive diet as a famine. "There was a drought and the crops have died," your body thinks. You are descended from survivors. Your body is going to slow everything way down to weather the storm. So when you go off the diet even a little bit, your body is going to store those calories up in case there's another "famine". This is not a great strategy for the 21st century, where high calorie foods are everywhere. So are all diets bad? Turns out there are "fad diets" and then there are lifestyle choices. Restrictive fad diets focus on weight loss. But there are "diets" that instead focus on listening to your body, preventing disease, long term healthy choices and lifestyle habits. These tend to be more successful. Our class will be evaluating 6 popular diets to assess their long term effectiveness. Each student was put into a discussion group last week. This week, you will be working with your group to choose a popular diet. For the next few weeks, you'll be researching and evaluating this diet. You'll compare this diet to other popular diets and the present your findings to the rest of the class. You are not expected nor even encouraged to try out the diet on your own. Right now, let's work on picking out a diet to evaluate. You'll work with your group to choose one. I'll make sure each group is researching a different diet, so your group might not get its first choice. You might choose to go with one of the big fads right now like Keto, Intermittent Fasting, or, good ol trusty WW. But there are some more creative options here: Latest DietsLinks to an external site. Links to an external site. Initial Post In your initial post, I want each of you to suggest one popular diet to your group. Include a sentence or two on why you chose it. If anyone has posted before you, you have to pick a different plan to suggest. The goal is to have 5-6 choices to vote on. Reply Posts and Voting On Tuesday, read what your classmates posted. Now it's your turn to vote. Make another post in the discussion board with your Top 3 choices, ranked. You can leave it at that, or you can continue the discussion and come to a consensus. If not, I'll tally the votes and choose one for you. I will then reply to the group with the popular diet you'll be researching for the next couple of weeks. You might not get your first choice because I need to make sure every group in the class is doing a different diet. I'll let you know which diet your group will ultimately research next week. I'll also put that information in next week's discussion. Do not proceed with any research until I officially assign a diet to your group.See Answer
  • Q11:INSTRUCTIONS I need you to draw that graph, and find it the protein of whole milk, low fat milk and egg he doesn't have to change the name of the graph just he has to use mine that I showed you under You have to name, the whole milk, low fat milk, and egg in the graph/nProfein my 12. 0 0.3 0.6 Ab sonlance of 560 mm 0.9 1-2 1.5 Absorbance 66onm 0 0.365 0.776 1.187 1.589 1.993 1.263 (whole milk) 1.284 (low fat milk) (egg) Standard Curve of Protein Concentration. 1.342 (Protein mg/L).See Answer
  • Q12: Discussion Assignment Week 7: Evaluating your chosen diet plan - Discussion Group 5: Carnivore Now that your group has been assigned a popular diet to research, it's time to evaluate it. I've provided some criteria for evaluation. I want EACH student to answer the 16 questions about the group's assigned diet. Once everyone has posted, look for discrepancies between your posts and discuss those. For example, if one student thinks it's an expensive diet but another doesn't, talk it out a bit. I'd like there to be a general consensus about each of these issues. In a couple of weeks, you'll be presenting the diet to the class, so it's a good idea to work things out now so that you can come up with a summary later. It would be helpful if everyone made their initial posts before Sunday so you have some time to discuss. Initial Post Do some internet research on your assigned diet. Make sure you look through multiple sources so you're not getting information from just one place. 1. What's the eating plan for this diet? What do you eat, how much and how often? 2. Does the program systemically eliminate one group of foods from a person's eating pattern? If so, what do you think the consequences of this are? 3. Does the program encourage specific supplements or foods that can be purchased only from selected distributors? If so, do you think this is a barrier? Why or why not? 4. Do you think this diet plan is expensive to follow? Why or why not? 5. Is this program time intensive? Is there a lot of research or cooking involved? 6. Does the program tout magic or miracle foods or products that burn fat? If so, do you think this will be effective? 7. Does the program have rigid menus? If so, do you think this makes it easier or harder to follow? 8. Is it safe for anyone to follow this plan? Does the program provide a warning to people with diabetes, high blood pressure, or other health problems? 9. Are there any long-term health consequences to this plan (this might take some digging!)? 10. Does the program encourage or promote increased physical activity? 11. Does the program encourage an intake that is very low in calories (below 800 a day)? If so, do you think this is safe? 12. How culturally biased is this diet? Will people of different cultures/religions have difficulty following this diet? 13. Is there a social component to this plan? How are people kept accountable? 14. Can a person be on this diet and still have a dinner at a restaurant or a holiday meal with their family? 15. Does this program have staying power? What percentage of people stick with it for the long term? 16. What is your overall impression of this diet? Reply Posts Reply to each of your fellow group members pointing out areas where you disagree. I'd like to see an actual discussion here, and I'd like you to come to a general consensus about each of the evaluation criteria./nSee Answer
  • Q13:Description Week 4 --Student is required to do a cover letter. Instructions: 1. Choose one cover letter from the sample below, please replace the information with your information. 2. Save and submit----upload using MS WORD/PDF format. Two sample cover letters/nSee Answer
  • Q14: 1. Activity: ✓ Activity Analysis Form CATEGORY Activities of daily living Instrumental activities of daily living Health management Rest and sleep Education Work Play Leisure Social participation 2. Relevance and importance: - 1- SUBCATEGORY From Thomas H. Occupational and Activity Analysis, Third Edition. SLACK Incorporated; 3. Objects used and their properties: Tools: Supplies: Equipment: Resources: 4. Space demands: 5. Social demands: 6. Sequencing and timing demands: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. Activity Analysis From Thomas H. Occupational and Activity Analysis, Third Edition. SLACK Incorporated; 2 7. Body functions required: FUNCTIONS Specific Mental Functions Higher level cognitive: Judgment, concept formation, metacognition, executive func- tions, praxis, cognitive flexibility, insight Attention: Sustained shifting and divided attention, concentration, distractibility Memory: Short-term, long- term, and working memory Perception: Discrimination of sensations (e.g., auditory, tactile, visual, olfactory, gustatory, vestibular, proprioceptive) Thought: Control and content of thought, awareness of reality vs. delusions, logical and coherent thought Mental functions of sequencing complex movement: Regulating speed, response, quality, and time of motor production Emotional: Regulation and range of emotions; appropriateness of emotions Experience of self and time: Awareness of one's identity (including gender identity), body, and position in the reality of one's environment and time NONE Activity Analysis MINIMALLY MODERATELY GREATLY CHALLENGED CHALLENGED CHALLENGED From Thomas H. Occupational and Activity Analysis, Third Edition. SLACK Incorporated; 3 HOW IT IS USED (continued) FUNCTIONS Global Mental Functions Consciousness: State of awareness and alertness, including the clarity and continuity of the wakeful state Orientation: Orientation to person, place, time, self, and others Psychosocial: Integration of mental functions to form personal and interpersonal skills to esestablisheciprocal social interactions Temperament and personality: Extroversion, introversion, agreeableness, conscientiousness, emotional stability, openness to experience self-control, self-expression, confidence, motivation, impulse control, appetite Energy: Energy level, motivation, appetite, craving, impulse control Sleep: Physiological process, quality of sleep Sensory Functions Visual functions: Quality of vision, visual acuity, visual stability, visual field Hearing functions: Sound detection and discrimination; aware- ness of location and distance of sounds NONE Activity Analysis MINIMALLY MODERATELY GREATLY CHALLENGED CHALLENGED CHALLENGED From Thomas H. Occupational and Activity Analysis, Third Edition. SLACK Incorporated; HOW IT IS USED (continued) FUNCTIONS Vestibular functions: Sensation related to position, balance, and secure movement against gravity Taste functions: Association of taste qualities of bitterness, sweetness, sourness, and saltiness Smell functions: Sensing of odors and smells Proprioceptive functions: Awareness of body position and space Touch functions: Feeling of being touched, touching various textures Interoception: Internal detection of changes in one's internal organs Pain: Localized and generalized pain Sensitivity to temperature and pressure: Thermal awareness (hot and cold), sense of force applied to the skin (thermoreception) Neuromusculoskeletal and Movement-Related Functions Functions of Joints and Bones Joint mobility: Joint range of motion Joint stability: Structural integrity of joints, physiologi- cal stability of joints related to structural integrity Muscle Functions Muscle power: Strength Muscle tone: Degree of muscle tension Activity Analysis NONE MINIMALLY MODERATELY GREATLY CHALLENGED CHALLENGED CHALLENGED From Thomas H. Occupational and Activity Analysis, Third Edition. SLACK Incorporated; 5 HOW IT IS USED (continued)See Answer
  • Q15: Human reproductive Biology 1. Describe the structure of the male and female reproductive systems, relating structure to function. (200 words): Functions of male reproductive system: Describe the functions of each of these parts. 1. Testis 2. Epididymis 3. Vas deferens 4. Scrotum 5. Prostate gland 6. Seminal Vesicles Functions of female reproductive system: Describe the functions of each of these parts. 1. Ovary 2. Fallopian tubes 3. Uterus 4. Cervix 5. Vagina 2. Describe one function, brought about by the process of meiosis that spermatogenesis and oogenesis have in common. (100 words): 14th – 15th February 2024 Please write the similarities between spermatogenesis and oogenesis in a paragraph rather than a table. Please discuss the process mentioning differentiation, multiplication and division. How many stages of meiosis do they go through. Please mention if haploid or diploid cells are formed. 3. Describe how the end product cells of spermatogenesis and oogenesis differ. (100 words): 16th 17th February 2024 Write a paragraph on the differences between spermatogenesis and oogenesis. Please mention how many sperms and eggs are formed after the process. Discuss the size of the resulting cells. Mobility of the cells. 4. Name THREE hormones involved in the control of the female menstrual cycle and describe their function. (200 words): 18th - 20th February 2024 List three hormones and state what their function in the menstrual cycle are. You can choose any of the ones mentioned below GnRF (Gonadotropin Releasing Factor) FSH (Follicle Stimulating Hormone) LH (Luteinizing hormone) Oestrogen Progesterone Please write three separate paragraphs, one for each hormone and its function in detail. Please mention how they are regulated and whether they stimulate/inhibit other hormones. 5. Summarise the timeline of events in embryonic and foetal development. (600 words) 21st - 23rd February 2024 Name the three stages of fetal/prenatal development (Germinal, Embryonic and fetal) Explain the major events in each stage. For this section, please include aspects like what stage the cells multiply to form a blastocyst. When the neural tubes form. When the nervous system forms. When all the major organs are formed. When the reflexes start to take place. When the foetus puts on weight. 6. Explain the relationship between structure and function of the placenta. (100 words) 24th February 2024 Explain how the placental structure is suited to carry out its function. General function of the placenta mention a few of the functions. Focus on how the placenta acts as an exchange surface for at least one structure to function point. 7. Explain the importance of the changes to the foetal circulation, lungs and liver in the readiness for birth. (300 words) 25th - 26th February 2024 For this section the changes to fetal circulation in the lungs and liver before and after birth needs to be discussed. An example of before birth has been provided for Foremen Ovale, however you need to re-write this in your own words and not copy and paste what has been provided. For this section you need to concentrate on why these events take place. For example mention why the pulmonary arch is present before birth and why it closes after. a. Foramen ovale In the Foetus: Opening between atria in the heart. Allows oxygenated blood to flow from right atria to the left atria and then to the aorta via the left ventricle Changes after birth: b. Ductus arteriosus In the Foetus. Changes after birth: c. Ductus venosus In the Foetus: 8. Identify and explain the function of the stages of birth. (400 words) 27th - 28th February 2024 Changes after birth: d. Umbilical arteries In the Foetus: Changes after birth: e. Umbilical vein In the Foetus: Changes after birth: List the three stages of birth and explain what the function of each stage is. References Question 1 Male Reproductive System https://microbenotes.com/male-reproductive-system/ https://www.healthline.com/human-body-maps/male-reproductive-organs-internal#1 https://www.webmd.com/sex-relationships/guide/male-reproductive-system#1 Female Reproductive System https://patient.info/news-and-features/the-female-reproductive- system#:~:text=The%20main%20function%20of%20the,the%20ova%20of%20a%20 woman https://bio.libretexts.org/Bookshelves/Human Biology/Book%3A_Human Biology ( Wakim and Grewal)/22%3A Reproductive System/22.06%3A Structures of the Female Reproductive System https://courses.lumenlearning.com/boundless-ap/chapter/the-female-reproductive- system/ Question 2 and 3 https://www.vedantu.com/biology/differences-between-spermatogenesis-and- oogenesis http://bioninja.com.au/summaries/11.4%20Gametogenesis.pdf https://bio.libretexts.org/Bookshelves/Human Biology/Book%3A_Human Biology ( Wakim and Grewal)/22%3A_Reproductive System/22.08%3A Functions of the F emale Reproductive System Question 4 https://www.bbc.co.uk/bitesize/guides/zs9hb82/revision/2 https://openstax.org/books/biology-2e/pages/43-4-hormonal-control-of-human- reproduction Question 5 https://www.verywellmind.com/stages-of-prenatal-development-2795073 https://courses.lumenlearning.com/suny-ap2/chapter/embryonic-development/ https://www.msdmanuals.com/en-gb/home/women-s-health-issues/normal- pregnancy/stages-of-development-of-the-fetus https://www.hli.org/resources/miracle-fetal-development/ https://www.tes.com/teaching-resource/fetal-development-worksheet-7524244 Question 6 https://www.biologydiscussion.com/human-development/placenta-structure-and- functions-explained-with-diagram/5163 https://my.clevelandclinic.org/health/body/22337-placenta Question 7 https://www.khanacademy.org/test-prep/nclex-rn/nclex-rn-circulatory-system/fetal- circulation-ddp/v/fetal-circulation-right-before-birth Fetal Circulation (Ductus Venosus, Foramen Ovale & Ductus Arteriosus) - Sarah Clifford Illustration srity bypasses the VENOSUS PULMONARY ARTERIES miringa FETAL https://www.youtube.com/watch?v=c_EZRaOLPnc https://www.youtube.com/watch?v=wH6xWTWwzZw https://www.youtube.com/watch?v=v3HRUnPKFS8 RA CIRCULATION Question 8 and-newborn-90-P02362 PORAMEN OVALE Mixed blood anters the high in 0₂1 65 Some of this enters the exits via the pulmonar T TO GET TH https://www.clinicalanatomy.ca/embryology/FetalCirculation/story.html labor/art-20046545 Most of this https://www.stanfordchildrens.org/en/topic/default?id=fetal-circulation-90-P01790 https://medlineplus.gov/ency/article/002395.htm#:~:text=Once%20the%20baby%20t akes%20the, absorbed%20from%20the%20respiratory%20system https://www.stanfordchildrens.org/en/topic/default?id=blood-circulation-in-the-fetus- Dovie and travels to LUF full NOT S GAS G https://www.nichd.nih.gov/health/topics/labor-delivery/topicinfo/stages https://www.mayoclinic.org/healthy-lifestyle/labor-and-delivery/in-depth/stages-of- https://www.babycentre.co.uk/a177/the-stages-of-childbirth https://bio.libretexts.org/Bookshelves/Human Biology/Book%3A Human Biology ( Wakim_and_Grewal)/22%3A Reproductive System/22.08%3A_Functions of the F emale Reproductive SystemSee Answer
  • Q16:Module 05 Written Assignment - Sexually Tr... Assignment Content Select a sexually transmitted infection (STI) and do research on it. Write a 3-5 page paper about the condition/issue. In the paper discuss the concepts below: • What is the pathophysiology of one STI • What is the etiology of the selected STI • What are the clinical manifestations of the selected STI • What is the treatment for the selected STI Use at least one scholarly source to support your findings. Examples of scholarly sources include academic journals, textbooks, reference texts, and CINAHL nursing guides. Be sure to cite your sources in-text and on a References page using APA format. You can find useful reference materials for this assignment/n Sexually Transmitted Diseases: Chlamydia Quick Lesson By: Tanja Schub, BS Cinahl Information Systems, Glendale, CA Patricia Lawrence, RN, MS, BSN, BS, CIC Cinahl Information Systems, Glendale, CA Edited by: Diane Pravikoff, RN, PhD, FAAN Cinahl Information Systems, Glendale, CA Chlamydia is a common infectious disease caused by the gram- negative bacterium Chlamydia trachomatis (C. trachomatis). Chlamydia is the most common sexually transmitted disease (STD) and the most common cause of acquired infertility in the United States; it is transmitted primarily by vaginal, anal, and oral sex, but can also be transmitted to a neonate while in the birth canal during vaginal delivery. When C. trachomatis is introduced into the rectum, oropharynx, or genital tract through sexual contact, it is engulfed by epithelial vacuoles. Avoiding lysosomal destruction, the bacteria survive and multiply, often producing no symptoms. Over time, the infection can spread to surrounding tissues and organs. Inflammation and related damage can lead to serious effects on reproductive and genitourinary health. Complications of untreated chlamydia in women include pelvic inflammatory disease (PID) and subsequent tubal infertility, genital tract infection, lymphogranuloma venereum, ectopic pregnancy, and chronic pelvic pain. Acute perihepatitis, or Fitz-Hugh-Curtis syndrome, is an unusual outcome of PID and is believed to develop as a result of chlamydia or gonorrheal infection. In pregnant women, infection can lead to pre-eclampsia, premature delivery, and infection in the newborn. In men, chlamydia can cause urethritis, epididymitis, and prostatitis. Studies suggest a likely relationship between chlamydial infection in males and infertility. Reactive arthritis-a complication of chlamydial infection consisting of arthritis, urethritis, and conjunctivitis -can affect both genders but is more prevalent among men. Chlamydial infection increases the risk for contracting and transmitting human immunodeficiency virus (HIV) infection in both women and men. In the neonate, chlamydial infection can lead to pneumonia, nasopharyngitis, chlamydial conjunctivitis, and chronic trachoma (i.e., infection of the eye; for more information, see ) that can lead to blindness. Diagnosis is based on clinical presentation, patient history, and results of nucleic acid amplification tests (NAATS) or bacterial culture; NAATS are the test of choice. The differential diagnosis includes gonorrheal infections and nongonococcal urethritis. Treatment is curative, involving a short course of antibiotics. Education on adherence to medical treatment and the practice of safe sex are important public health components of the treatment plan. Worldwide, chlamydia is the most common bacterial sexually transmitted disease, with prevalence estimated over 140 million infected individuals. In 2016, approximately 1.6 million new cases of chlamydia were reported to the CDC, which corresponds to a rate of 497.3 cases per 100,000 people. In the U.S., the highest chlamydial infection rates are seen in young people; the incidence in 2016 was 1,929.2 cases per 100,000 in those aged 15-19 years and 2,643.8 cases per 100,000 in those aged 20-24 years. The incidence of chlamydia is substantially higher in females than in males (657.3 cases per 100,000 vs. 330.5 cases per 100,000), but at least part of this disparity is thought to be because of increased screening among in women. Approximately, 25% of infected males and 80% of infected females are asymptomatic. Antibiotic treatment is effective in 95% of cases of chlamydia. Without treatment, 10-20% of females with chlamydia develop pelvic inflammatory disease (PID) and 5 −10% of those will develop Fitz-Hugh-Curtis syndrome. PID can cause infertility, ectopic pregnancy, and chronic pelvic pain. Sexually active individuals, especially those with multiple sexual partners, are at risk for acquiring chlamydia. Chlamydia occurs most frequently in adolescents, women under the age of 25 years, and individuals who engage in unprotected sex. The use of oral contraceptives and IV drugs, cervical displacement, having a new sexual partner, frequent douching, being non-White (i.e., Black, Hispanic, Native American, Alaskan Native ethnicity), being unmarried, having a history of sexually transmitted diseases, and early age of first sexual experience have all been associated with an increased risk for acquiring chlamydial infection. For additional information on risk factors for chlamydial infection, see Evidence-Based Care Sheet: Sexually Transmitted Diseases: Chlamydia -- Risk Factors. Known as the "silent disease," chlamydia is often asymptomatic. If symptoms occur, they usually appear 1-3 weeks after exposure. In women, the clinical presentation includes a yellow, purulent vaginal discharge, difficult or frequent urination, postcoital bleeding, abdominal or pelvic pain, and irregular uterine bleeding. Signs and symptoms in men include urethritis, painful or difficult urination, discharge, scrotal pain or tenderness, and urethral burning or itching. Both genders can experience conjunctivitis, pharyngitis, or both from oral sex. Individuals who engage in receptive anal sex can experience proctitis with rectal pain, discharge, and/or bleeding. • Patient History • Review sexual history, including age at first sexual experience, number of sexual partners, history of sexually transmitted diseases, and HIV infection status o Ask if the patient uses protection and/orever has unprotected sex • Laboratory Tests o NAATS (e.g., polymerase chain reaction [PCR]), or nucleic acid hybridization tests will identify Chlamydia Trachomatis bacteria; NAAT results can remain positive up to 3 weeks after completion of antibiotic therapy; in general, NAAT should not be used to test-for-cure, except when monitoring treatment efficacy in pregnant women. The incubation period (1-5 days) for Chlamydia Trachomatis should be observed before getting tested ■ Swab culture (e.g., endocervical, rectal, pharyngeal, urethral) samples will identify Chlamydia Trachomatis bacteria; it grows on columnar cells found in the urethra and cervix; pooled vaginal secretions should not be utilized for swabbing ▪ Direct fluorescent antibody (DFA) testing of swab culture (e.g., urethral, rectal, neonates conjunctival, endocervical) samples will identify Chlamydia Trachomatis ▪ Urine sample testing can identify Chlamydia Trachomatis bacteria; patients should not urinate for an hour before providing sample and female patients should not clean labia before providing sample o A positive Enzyme-linked immunosorbent blood test (ELISA) indicates a new infection O o Cytologic analysis of ocular fluid can be ordered for patients with ocular complaints for whom conjunctivitis or ocular trachoma are suspected o An elevated CBC level indicates infection • Other Tests of interest o CT and ultrasonography can be ordered if Fitz-Hugh-Curits syndrome is suspected o Ultrasonography can be ordered to assess for tubo-ovarian abscess o Chest X-ray can be ordered for patients with difficulty breathing to assess for pneumonia • Administer Prescribed Medications and Monitor Treatment Efficacy o Assess vital signs and all physiologic systems (especially reproductive and urinary systems); notify the treating clinician of laboratory test results once available • Assess for pain using a facility-approved pain assessment tool; administered prescribed analgesics, as ordered o Administer prescribed antibiotics (e.g., doxycycline, azithromycin, ofloxacin), as ordered Erythromycin or amoxicillin can be prescribed in pregnancy o Monitor for and educate on potential adverse effects ofSee Answer
  • Q17:5) What does DRG stand for and what order of neurons pass through it? (1st, 2nd, 3rd order neuron)See Answer
  • Q18: Unit 4 Part A - Biomolecules - Guidance Title: Biomolecules and key biological principles Credits: 6 (Graded) Part A Deadline: Please use the Ascentis workbook and links provided to read on the topic to be written about and then rephrase the information into your own words. Day 1-2 1. With reference to the graph below, answer the following: a. Describe the effect of increasing substrate concentration on enzyme activity in the reaction. What happens to the rate of enzyme reaction as substrate concentration increases? b. Give an explanation for the term 'enzyme-substrate complex'. What is the role of an enzyme in a chemical reaction? What is a substrate in relation to enzymes? How do substrates and enzymes interact to form a complex? Make sure to mention the active site. c. Label 'Z' on the graph at a point where the active sites of the enzyme are not fully saturated with substrate molecules. Insert a 'Z' on the line of the graph at any point where the enzymes are not fully saturated with substrate molecules. Rate of Enzyme Controlled Reaction Substrate Concentration Day 3 2. Write a definition for each of the characteristics below Characteristic Phenotype Diploid cell Gene Locus Sex Linkage Homozygous Day 4 Definition 3. Place a tick in the corresponding boxes to link with the described features Features Contains Sulphur Is a Monomer Contains Peptide bonds Formed by a condensation reaction Is a storage molecule Contains Glycerol Day 5 Glucose Sucrose Protein Starch Fat Glycogen 4. Explain the meaning of the terms: a. Gene What is a gene and where are they located? What is the role of genes? What is the importance of genes in inheritance and traits? Give an example. b. Mutation What is a mutation and how do they occur? What is the significance of mutations in genetics? Give an example. Day 6-7 5. a. State the meaning of the term polymer. What is a polymer and how are they formed? b. Identify an energy storage polymer found in muscle cells. Name an energy storage polymer that can be found in muscle cells. c. Explain why monosaccharide molecules are not suitable as storage molecules within cells. Explain what a monosaccharide is and how they are used in the cells. Explain why monosaccharides are not suitable as storage molecules and give some examples. Resources Enzymes https://www.khanacademy.org/science/ap-biology/cellular-energetics/enzyme- structure-and-catalysis/a/enzymes-and-the-active-site https://www.youtube.com/watch?v=qgVFkRn8f10 Genetics https://www.youtube.com/watch?v=CBezq1fFUEA https://www.khanacademy.org/science/ms-biology/x0c5bb03129646fd6:inheritance- and-variation/x0c5bb03129646fd6:genes-proteins-and-traits/a/genes-proteins-and- traits-ms https://www.khanacademy.org/science/ms-biology/x0c5bb03129646fd6:inheritance- and-variation/x0c5bb03129646fd6: chromosomes/a/chromosomes-and-genes-ms https://www.bbc.co.uk/bitesize/guides/zc499j6/revision/2/nSee Answer

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