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2008_05_30_16_16_54

2008_05_30_16_16_54 - T5 W0 BILD 2 2 Name KEY Winter...

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Unformatted text preview: T5 W0 BILD 2 2 Name KEY Winter Quarter, 2006 l. (5 points) In the immune system, where do B cells develop and mature? Where do T cells develop and mature? B cells develop and mature in the bone marrow; T cells originate in the bone marrow and mature in the thymus. 2. (10 points) How does an action potential differ from a postsynaptic potential with respect to initiation, propagation, and changes in size (briefly in each case)? Action potentials are initiated by a change in membrane potential (rely on voltage-gated ion channels), they are actively propagated (regenerative), and are all-or-none events (meaning a given size and they do not summate). Postsynaptic potentials are intiated by neurotransmitters (acting on receptors(, they are passively propagated (local events), and they are graded (they can summate). 3. (10 points) How, when, and where are the 3 body axes of the amphibian determined (e.g. in the sea urchin)? Diagram them (anterior-posterior; dorsal-ventral; left-right) in relation to the originaldefining landmarks at the time of determination. .- MWCMWAL fM\ Spam. MIT-7 MW M 9 meadvmw p.49, s 6‘91 W947 (9'47 Cream . (1:, but (a! mzok 4: 140 F0" 4.017405" are, W) M:- v: mg iv? M“! 4, pmeu‘ar (more? pan) 4. (10 points) How do fish gills exemplify the pripciples of a counter current exchange system? (PPM 4.146: W .tf‘f (D 0”“th WW 5. (15 points) What are the 3 general functions of bones? What are the 3 types of joints (with respect to movement)? Functions: (1) support & protection, (2) movement (serve as levers for muscles), and (3) calcium reservoir. Types of joints: (1) ball & socket, (2) hinge, and (3) pivot joints. BILD 2 3 Name KEY Winter Quarter, 2006 6. (10 points) How is C0, transported in the blood? What enzymes contribute; what do they do? Does hemoglobin contribute either directly or indirectly? If so, how? Transported as bicarbonate ion (HCO3'). The enzyme carbonic anhydrase converts C02 and H20 into H2C03 which then ionizes into HCO,‘ and H‘. The H’ binds to hemoglobin and is transported (and removed from solution at the same time). (15 points) How does neurotransmitter release occur from a presynaptic terminal? What controls it? Probably best to outline the electrical and molecular events in the terminal. Depolarization of the axon terminal by an action potential briefly opens voltage-gated calcium channels in the terminal membrane which allow a brief surge of calcium influx. This triggers exocytosis of “docked” synaptic vesicles aligned against the presynaptic membrane and loaded with transmitter. The transmitter is then dumped into the synaptic cleft while the synaptic vesicle membrane itself is subsequently retrieved and recycled. (25 points) How and where are proteins digested in the vertebrate gut? What enzymes are involved and how are they regulated? Role of hormones in this? (Detail is good.) The acid environment of the stomach denatures (unfolds) many proteins. Pepsinogen, released from Chief cells in the stomach lining, is converted to the endoprotease pepsin by the acid environment. Pepsin cleaves proteins to yield large peptides which move in the chyme to the small intestine. The pancrease secretes trypsinogen, chymotrypsinogen, and procarboxypeptidase into the small intestine. Enterokinase from cells in the small intgestinal walls cleaves trypsinogen to release the endoprotease trypsin which further breaks down (digests) proteins into peptides and at the same time activates (cleaves) chymotrypsinogen to release the endoprotease chymotrypsin which cleaves proteins to release peptides. Trypsin also cleaves procarboxypeptidase to release carboxypeptidase, an exopeptidase which cleaves proteins or peptides (one amino acid at a time) from the carboxy end. The intestinal glands secrete aminopeptidase, an exopeptidase which releases amino acids one at a time from the amino terminal end of peptides, and they secrete dipeptidase which breaks down dipeptides to release free amino acids. (Together these many proteases provide a complementary set of specificities, cleaving proteins at many sites to efficiently break them down and release the amino acids for uptake.) Food in the stomach triggers release of gastrin which acts to stimulate secreation of gastric juices (including pepsinogen) for protein digestion in the stomach. Amino acids reaching the small intestine (chyme from the stomach) triggers CCK release from the duodenum into the blood to act BILD 2 4 Name KEY Winter Quarter, 2006 on the pancreas and induce release of additional digestive enzymes to breakdown protein among other things. 9. (15 points) What is the typical receptive field for a retinal ganglion cell in the retina? How was this mapped? (Best to show the firing patterns for a spot of light in the various regions.) 0 h~C€Mva3 OF F-J'u/uuuwx If" 4 2023p 1.3.,” At .1,“ ’i W “W. (L 11 , Ody war-av) 3,414, mar-{- emf»- Mwm; Gena/n, WJAA—JM .. . - IM' -—& N H N/ 10. (15 points) How does calcium regulate muscle contraction? What are the molecules and steps involved? How is calcium availability itself regulated in muscle? Calcium in the sarcoplasm binds to troponin, causing a conformational shift in the protein which moves the attached tropomyosin filaments. This in turn exposes myosin-binding sites on the underlying actin filaments, thereby permitting the loaded myosin head groups (charged with ATP having been cleaved to ADP and retained bound in energized linkage) to bind, spring backward moving the actin filament along. and generating contraction. Calcium is normally stored in the sarcoplasmic reticulum (extensive membrane sacs) and is also available in the extracellular fluid. When the motor nerve fires and elicits an EPSP at the NMJN which, in turn, elicits an AP in the muscle , the depolarization which results activates voltage-gated calcium channels in the surface membrane thereby permitting calcium influx. Even more important, the AP travels along and down the t-tubule system, releasing calcium from the associated sarcoplasmic reticula into the cytoplasm. This calcium drives (enables) muscle contraction as described above. When the AP is gone and the membrane repolarizes, calcium pump return the calcium to the sarcoplasmic reticulum and to the extercellular solution, which terminates the muscle contraction. ll. (15 points) Where does active transport occur in the nephron. Indicate what gets actively transported and in which direction. Proximal convoluted tubule: active export of Na”, glucose, amino acids; active import of H". Ascending limb of Loop of Henle: active export of Cl'. Distal convoluted tubule: active export of Na’ and HC03'; activde uptake of K’ and H‘. BILD 2 5 Name KEY Winter Quarter, 2006 12. (20 points) Diagram the pressure curve for the left side of the human heart through one cardiac cycle beginning with the last half of diastole. Show the relative pressures in the left atrium, left ventricle, and aorta throughout the cycle. Indicate where the atrioventricular and aortic valves open and close. «4- u.»'\. 13. (15 points) Diagram a typical antibody (e.g. from the lgG class). Indicate where the antigen- binding sites are. Which regions are identical among the chains? Which regions are common to all antibodies of a given class? Which regions are unique to this antibody? S ”fix" a m z. iMth In. L154 u H L1. g SW wont»: SW 18" t5- L1. a.“ “a: :4 A. (JAM Clea! r-«Jo‘oM (#0,: “3M M M‘ 4M wm‘ v4 A ran/en Ah (it-«Lurin— Ms‘ (909144 on» mtaaoflajsn-t m Flirt- 14. (10 points) What are MHC proteins? Where are they located and what are their functions (distinguish the different classes)? MHC proteins are plasmm membrane glycoproteins that help target/activate T cells. MHC I proteins are present on all nucleated animals cells and present peptides (10-20 amino acids) on the cell exterior to be recognized by cytotoxic T cells via their T cell receptors and CD8. MHC II proteins on B cells, macrophages, and antigen-presenting cells offer up foreign peptides from invaders or foreign material in the cell. The antigen is recognized bgyh helper T cells via their receptors and CD4, activating the cells carry out their functions. BILD 2 6 Name KEY Winter Quarter, 2006 15. l6. l7. MHC III proteins assist complement protein in lysing cells. (15 points) Outline/diagram what Helper T cells do for the humoral immune response (antibody production). How do they do it? A helper T cell is activated by using its T cell receptor and CD4 to recogize an antigen presented on an MHC II molecule on a B cell, macrophage, or antigen-presenting cell. This activaton, together with cytokines form the antigen-presenting cell (or macrophage) leads to production of more cytokines by the TH cell which stimulates proliferation of the TH cell to produce a larger colony (both for immediate action and for memory cells). The activated TH cells then recognize and bind to similar antigens presented by a B cell, again via MHC II (and recognized by CD4), and secretes additional cytokines to stimulate proliferation of the B cells to form both antibody-secreting plasma cells and quiescent memory B cells for future attacks. (15 points) Adrenaline (epinephrine) mediates the ‘fight-or-flight” response. How does it do it? Indicate where adrenalin is made, what induces its release (signal and pathway), and how it achieves a whole-body coordinated response (list the many targets and effects it produces). Adrenalin is made in the adrenal cortex; its release is triggered by nerve input from the spinal cord (via the Splanchnic nerve) in response to stress or fear. It diffuses througout the cardiovascular system activating all target cells with appropriate receptors. This include in part: 1) the heart to increase heart rate, 2) major arteries to increase blood pressure, 3) liver to induce glycogen breakdown to elevate blood glucose, 4) pancreas to reduce insulin release and prevent it from lowering blood glucose, 5) vasodilate muscle, heart, & brain blood vessels to increase their blood supply, and 6) vasoconstrict blood vessels in the organs (viscera) to restrict blood in this time of emergency. These and other actions provide a coordinated response, maximizing the bodies defense. (10 points) Diagram the regulatory controls on the release of thyroxin. What induces its release initially and what ends it? (U 5 9 “‘5;th \ (fwd. . Tan yum” “A BILD 2 7 Name KEY Winter Quarter, 2006 (20 points} Outline the hormonal pattern that regulates reproductive function during puberty in the human male. What events trigger puberty, leading to the appearance of secondary sexual characteristics and the maturation of sperm? 19. (15 points) What regulates follicle cell development during the ovarian cycle, and what are the consequences of that development (both direct and indirect)? If pregnancy occurs, what continuing role does the remnants of the follicle cell play? GnRH from the hypothalamus triggers FSH release from the anterior pituitary early in the ovarian cycle. and the FSH stimulates follicle cell development which produces and releases estrogen. This in turn (I) exerts negative feedback on the anterior pituitary to reduce FSH release, (2) causes a gradual buildup of GnRH to eventually induce a surge of FSH 8!. LB, and (3) causes buildup of the uterine lining. The LH surge triggers full ovulation, i.e- release of the egg from the follicle. and converts the residual follicle to the corpus Iuteum which continues to secrete estrogen and progesterone. If fertilication does not occur. the corpus luteum (residual follicle) degenerates, causing a fall in progesterone levels and the sloughing off of the uterine buildup and the re- initiation of a new ovarian cycle. If . on the other hand, pregnancy did occur, the corpus luteum continues to secrete progesterone for a couple of months in response to stimulation by HCG from the placenta. (In short the follicle does a lot both directly and indirectly as a hormone supplier and supporter of the developoing egg.) BILD 2 8 Name KEY Winter Quarter, 2006 21. 22. 23. (10 points) What is the “cortical reaction" in a fertilized egg? How is it induced, how does it work, and what role does it play? Depolarization of the fertilized egg membrane causes calcium release from internal stores into the cytoplasm. This, in turn, triggers exocytosis of degradative enzymes from the cortical granules underlying the membrane. The enzymes digest the bindin receptors (preventing subsequent sperm from binding) and release the vitelline layer. causing formation of the fertilization envelope. This constitutes the “Slow Block to Polyspcrmy“. vastly reducing the chances of multiple fertilization of the egg. The original depolarization was induced by the fusion of the sperm cell membrane with the egg membrane which produces a slow but substantial inflow of sodium ion (hence, the depolarization). (10 points) How do the blastulas of sea urchins and frogs differ? In both cases gastrulation begins by an invagination to produce an internal cavity. Where does this occur in the two cases, and what is the development fate of the cavity that forms? Sea urchin blastulas (formed by holoblastic equal cleavage) have a uniform layer of cells encasing a fluid-filled blastocoel. Gastrulatoin begins by the blastopore invaginating at the vegetal pole. Frog blastulas (formed by holoblastic unequal cleavage) have an asymmetric distribution of small cells on top and large yolk-filled cells on the bottom; the blastula contains a fliud—filled blastocoel in the upper half. Gastrulation begins by an invagination of the blastopore at the Grey Crescent, roughly half way between the animal and vegetal poles. In both cases, the cavity that forms becomes the archenteron and subsequently the interior of the digestive tract. (10 points) Spemann’s transplant experiment showed that the dorsal lip of the embryo was the “primary organizer” because, when transplanted, it could induce a second embryo fused with the initial primary one. What was the proof that the transplant actually induced a second embryo rather than simply becoming a second embryo itself? The second embryo not only had donor cells making up key parts (e.g. the notochord and spinal cord) but it also had host cells contributing to parts they would not normally form (e.g. spinal cord though the host cells came from the ventral surface and would normally have been endoderm). Donor and host cell types could be distinguished by their different pigments. (An amazing experiment way back then: Turns out the notochord derives from the dorsal lip and plays an important role in inducing the appearance of the spinal cord normally.) (5 points) What would you like to have happen in the next couple of years? (One sentence, and don’t take long because it’s a “freebee”). -------------- It’s all yours to say -—-—-—---- ...
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