By O. Masil. Saint Lawrence University. 2018.

Beneath • large intestine the enamel is dentin order 25mg hydroxyzine free shipping, the main structure of the • rectum tooth hydroxyzine 10mg low cost. Undigested waste materials not absorbed by the Tongue blood are then eliminated from the body through The (3) tongue assists in the chewing process by defecation. Included in the digestive system are the manipulating the bolus of food during chewing accessory organs of digestion: the liver, gallbladder, and moving it to the back of the mouth for swal- and pancreas. Rough projections on the surface of the tongue called papillae con- Mouth tain taste buds. The registered by chemical stimulation of the taste mouth, also known as the (1) oral cavity or buccal buds are sweet, sour, salty, and bitter. It is formed by the taste perceptions are combinations of these four (7) Uvula (5) Soft palate (4) Hard palate (1) Oral cavity Laryngopharynx (2) Teeth (3) Tongue Food bolus (6) Pharynx (10) Epiglottis (9) Esophagus (8) Trachea Figure 6-1. Sagittal view of the head showing oral, nasal, and pharyngeal components of the digestive system. Anatomy and Physiology 107 Anatomy and Physiology Key Terms This section introduces important terms, along with their definitions and pronunciations. Pronunciation Help Long Sound a—rate ¯ e—rebirth¯ ¯ı—isle o—over¯ u—unite¯ Short Sound a—alone ˘ e—ever ˘ ˘ı—it o—not˘ u—cut˘ basic flavors. At all other cately linked with sense of smell, making taste times, the epiglottis remains upright, allowing air perception very complex. It prevents the Pharynx, Esophagus, stomach contents from regurgitating back into the esophagus. The (4) body of the stomach, the large and Stomach central portion, together with the (5) fundus, the As the bolus is pushed by the tongue into the upper portion, are mainly storage areas. Most (6) pharynx (throat), it is guided by the soft, fleshy, digestion takes place in the funnel-shaped termi- V-shaped structure called the (7) uvula. The lowest portion of folds called (7) rugae that gradually unfold as the the pharynx divides into two tubes: one that leads stomach fills. This sphincter regulates the speed and movement of The large intestine is about 5 feet long. It begins at chyme into the small intestine and prohibits back- the end of the ileum and extends to the anus. The only by coordinated, rhythmic muscle contractions secretion is mucus in the colon, which lubricates called peristalsis. The first 2 or 3 inches of the Small Intestine large intestine is called the (6) cecum, a small pouch that hangs inferior to the ileocecal valve. Projecting The small intestine is a coiled, 20-foot long tube downward from the cecum is a wormlike structures that begins at the pyloric sphincter and extends at called the (7) appendix. The main functions of the colon are which is about 10 inches long to absorb water and minerals and eliminate undi- • (2) jejunum, which is approximately 8 feet gested material. The colon is divided into ascend- long ing, transverse, descending, and sigmoid portions: • (3) ileum, which is about 12 feet long • The (8) ascending colon extends from the Digestion is completed in the small intestine with cecum to the lower border of the liver and the help of additional enzymes and secretions turns abruptly to form the (9) hepatic flexure. Nutrients in • The colon continues across the abdomen to chyme are absorbed through microscopic, finger- the left side as the (10) transverse colon, like projections called villi. Nutrients enter the curving beneath the lower end of the bloodstream and lymphatic system for distribu- (11) spleen to form the (12) splenic flexure. At the terminal end of • As the transverse colon turns downward, it the small intestine, a sphincter muscle called the becomes the (13) descending colon. Food bolus (1) Esophagus (5) Fundus of stomach (3) Lower esophageal Longitudinal (cardiac) sphincter muscle layer Circular muscle layer Lesser curvature Oblique (8) Pyloric sphincter muscle layer (4) Body Figure 6-2. Anterior view of (2) Duodenum Greater curvature the stomach showing muscle (6) Pylorus (7) Rugae layers and rugae of the mucosa. Anatomy and Physiology 109 Parotid gland Tongue Submandibular Salivary gland Mouth (oral cavity) glands Sublingual gland Pharynx Esophagus Food bolus (5) Liver Stomach Gallbladder (11) Spleen (1) Duodenum (12) Splenic flexure (9) Hepatic flexure (4) Pancreas (10) Transverse colon (2) Jejunum (13) Descending colon (8) Ascending colon (3) Ileum (6) Cecum (14) Sigmoid colon (7) Appendix (15) Rectum (16) Anus Figure 6-3. Liver, gallbladder, pancreas, and duodenum with associated ducts and blood vessels. Some of its important functions include: enzymes that pass into the duodenum through the (3) pancreatic duct. The pancreatic duct • producing bile, used in the small intestine to extends along the pancreas and, together with the emulsify and absorb fats (4) hepatic duct from the liver, enters the (5) duo- • removing glucose (sugar) from blood to synthe- denum. The digestive enzymes produced by the size glycogen (starch) and retain it for later use pancreas contain trypsin, which breaks down pro- • storing vitamins, such as B12,A,D,E,andK teins; amylase, which breaks down carbohydrates; • destroying or transforming toxic products and lipase, which breaks down fat. Bile is Pancreas also drained from the liver through the (8) right The (2) pancreas is an elongated, somewhat flat- hepatic duct and the (9) left hepatic duct. These tened organ that lies posterior and slightly inferi- two structures eventually form the hepatic duct.

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This is an association with representatives from more than 20 different countries 25 mg hydroxyzine fast delivery. This can be concluded from the resistance situation in developing countries such as Bangladesh order hydroxyzine 10 mg amex, Nigeria, Sri Lanka, and Vietnam, where the con- sumption of antibiotics per inhabitant is less than a tenth of that in the industrialized world. Still, as described from sporadic reports, the resistance situation is much worse. This is due to the fact that antibiotic therapy cannot be well aimed because of insufficient resources for bacterial diagnosis and resistance determinations. Furthermore, antibiotics can be bought freely in the local market and are therefore often used incorrectly against insusceptible pathogens and in inadequate doses. As mentioned in Chapter 1, sulfonamide was the first selectively acting agent that could be used systemically. Of course, many different antibiotics have been launched and marketed dur- ing the long period since 1970, but all of them have been related to already existing antibiotics and have then become members of one or the other of the main antibiotic families (Chapter 11). The medical reasons for marketing these new family members have been that they have shown different spectra of activity: that is, higher efficiency toward specific pathogenic bacteria, and also, among these those that showed resistance against other members of the particular antibiotic family. However, in the latter case there are examples which show that the resistance Antibiotics and Antibiotics Resistance, First Edition. The simple and inexpensive sulfonamides have been widely used and appreciated for many years. Resistance against them among pathogenic bacteria is now very common, however, and this development can be used as a clear and instructive example of the devaluation of the health care value of antibacterial agents by resistance. Next, we describe in detail mechanisms of sul- fonamide resistance to illustrate the complexity of the resistance evolution at the molecular level. This description should also demonstrate the experimental approaches that can be used to elucidate mechanisms of resistance. The very large distribution of antibiotics has meant a toxic shock, a dramatic environmen- tal change for the microbial world. We can look at it as Darwinian evolution in front of our eyes, which is accelerating, with further genetic mechanisms being selected for the horizon- tal spread of resistance genes. The bacterial world, including the pathogens, has developed molecular mechanisms for inac- tivating our antibacterial agents or evading their effect. The development of resistance among pathogenic bacteria has gen- erally been astonishingly fast, which could be explained by the rapid growth of bacteria, allowing them to undergo evolution in a short time. This resistance evolution is not constant, but some resistance events have taken a long time to occur. This is an innate form of genetic engineering in which bacteria are able to adapt and use genetic mechanisms that have evolved earlier for general environmental adaptation, for the new purpose of spreading resistance genes between bacteria. This development has meant that many infec- tious diseases which earlier were easily handled with antibiotics are now more difficult to treat. The great triumph of medicine fades and we are forced to realize that the health standard that we have become used to regarding infectious diseases is not stable. This process proceeds continuously and the general pattern is that resistance generally occurs between one or two years after the clinical introduction of a new antibiotic. This expe- rience naturally curbs the interest of the pharmaceutical industry in pursuing research in this area. From an anthropomorphic per- spective, however, no microbiologist can keep from admiring the ingenuity and efficiency that bacteria show in protecting them- selves from the toxic effects of our antibiotics. How does this resistance evolution work, and what are the precise molecular mechanisms for antibiotics resistance? New antibiotics in the true sense—that is, antibacterial agents with new points of attack at the molecular level—have been very limited in number in later years, and this is probably due to the tepid interest of the pharmaceutical industry in this area, for understandable reasons. If the antibacterial agent is effective, the infection heals quickly, and treatment can be terminated. As mentioned earlier, resistance as a rule occurs within one or two years after the introduction of a new antibacterial agent. These circumstances mean that antibiotics are not very interesting from a marketing point of view. Mammalian cells, our cells, are not endowed with that sequence of enzymic reactions necessary to synthesize folic acid, but rely on folic acid as a vitamin in our nourishment. Specifically, sulfonamides (formula 3-1)were shown to interfere with the bacterial formation of folic acid by its structural similarity to the intermediate p-aminobenzoic acid (3-2). Sulfonamide is generally mentioned in the plural form because dozens of derivatives (modifications at the amino group at the sulfon residue) of Domag’s original sulfanilamide have been synthesized through the years. In Scandinavia, the distribution of sulfonamides as a single drug for systemic use is presently nil. Aside from preparations for external use, as in ointments, the minimal distribution of sulfonamides that still occurs is in combination with trimethoprim.

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Plate 14 is a fecal specimen unstained seen under shell and the embryo at the opposing poles cheap hydroxyzine 10mg amex. Threadworm (Strongyloides) produces Parasites/2 similar ova order hydroxyzine 25mg fast delivery, but these hatch in the intestine, releasing 15. Plate 15 is an iodine-stained fecal specimen the rhabditoid larvae that are found in the feces. Te Pinworm (Enterobius) ova are approximately the plate shows the ovum of which parasite? Whipworm Microbiology/Identify microscopic morphology/ Parasites/2 Chapter 10 | Photomicrographs and Color Plate Examination 541 16. Plate 16 is an unstained fecal specimen seen Answers to Questions 16–20 under 400× using brightfield microscopy. Fasciola, Paragonimus, and Fasciolopsis all produce large, yellow-brown operculated ova. Opisthorchis viverrini small shoulders adjacent to the operculum of Microbiology/Identify microscopic morphology/ Paragonimus ova. What condition is spirochetes are sometimes seen in the blood of suspected from this field? Lead poisoning recurrentis and other species that cause relapsing Microbiology/Identify microscopic morphology/ fever. Borrelia burgdorferi, the causative agent of Spirochete/2 Lyme disease, is rarely seen in Wright’s-stained blood films and is usually diagnosed by enzyme-linked 19. They may Parasites/2 also cause primary amoebic meningoencephalitis, although they are isolated less often than Naegleria 20. Mature trophozoite of Plasmodium malariae amoeba-like cytoplasm and Schüffner’s dots, C. Mature gametocyte stage of Plasmodium ovale Microbiology/Identify microscopic morphology/ Parasites/3 542 Chapter 10 | Photomicrographs and Color Plate Examination 21. Plate 21 is a modified acid-fast stain with Answers to Questions 21–25 malachite green counterstain of a stool specimen, 1,000× magnification. B All of the organisms listed are coccidian parasites field are approximately 5 μ in diameter. The oocysts are round, about 5 μ in diameter, and Microbiology/Identify microscopic morphology/ deep pink. Schistosoma haematobium ovum epithelia that contain a high concentration of neutral B. Fecal contaminant and the fat globules produce a Maltese cross effect Body fluids/Identify microscopic morphology/Urine under a polarizing microscope. Oval fat bodies occur sediment/2 in conditions associated with increased urinary lipoprotein excretion such as the nephrotic 24. Hippuric acid Calcium oxalate crystals are usually colorless Body fluids/Identify microscopic morphology/Urine octahedrons. Ammonium magnesium phosphate sediment/2 crystals are long, colorless six-sided prisms, and hippuric acid crystals are colorless long, flat, 25. Triple phosphate crystals may form calculi in the renal pelvis appearing on an Body fluids/Identify microscopic morphology/Urine x-ray as an outline of the calyces and referred to as sediment/2 “stag-horn” calculi. Plate 26 is a urinary sediment viewed under Answers to Questions 26–30 400× magnification using a brightfield microscope. Coarse and fine granular casts have the same significance as cellular casts and point to glomerular Body fluids/Identify microscopic morphology/Urine damage. Plate 27 shows a urinary sediment viewed under colorless uniform six-sided hexagonal plates in 400× magnification using brightfield microscopy. Calcium phosphate crystals form Tis colorless crystal is presumptively identified as: in neutral to alkaline urine and appear as thin A. Hippuric acid Hippuric acid crystals form long six-sided prisms in Body fluids/Identify microscopic morphology/Urine acid urine. Cystine crystals must be differentiated sediment/2 from uric acid on the basis of solubility, polarized 28. Mesothelial cell small numbers in normal pleural, pericardial, and Body fluids/Identify microscopic morphology/Pleural ascites fluids. They are often seen in increased fluid/2 numbers when there is an inflammatory injury involving the serous membranes. Plate 29 is a Wright’s-stained smear of pleural mononuclear or binucleate cells with an open fluid prepared by cytocentrifugation. Te largest chromatin pattern and abundant agranular cell in this field (see arrow) is identified as a: cytoplasm. Metastatic cell from the breast Body fluids/Identify microscopic morphology/Pleural 29. Plate 30 is from a Wright’s-stained peripheral of the nucleus against the cell wall, usually caused by blood film, 1,000×. Which of the following best large vacuoles that form after phagocytosis of describes the cells in this plate? Plate 31 is a Wright’s-stained peripheral blood Answers to Questions 31–35 film, 1,000×.

Early in 2008, Sue Clark brought a handful of epigenetics researchers from Australia together to form the Australian Epigenetics Alliance. The AEpiA has now grown to a membership of nearly 300, with members spanning not only Australasia, but the globe. Last year we hosted our seventh flagship conference, Epigenetics 2017 in Brisbane, QLD, and the WA team are already busy preparing for Epigenetics 2019 – watch this space!

Past Epigenetics meetings:

2005 – Canberra, ACT
2007 – Perth, WA
2009 – Melbourne, VIC
2012 – Adelaide, SA
2013 – Shaol Bay, NSW
2015 – Hobart, TAS
2017 – Brisbane, QLD