By R. Umbrak. Westwood College Georgia. 2018.
Endocytosis refers to absorbed by Na -dependent cotransport buy sildenafil 100mg with mastercard. Endocy- With the return of Na to the cytoplasm generic 50mg sildenafil visa, tosis is further classified as phagocytosis if the vesicle forms around particulate water efflux from the cell into the intestinal matter (such as whole bacterial cells or metals and dyes from a tattoo), and pinocy- lumen decreases. Receptor- mediated endocytosis is the name given to the formation of clathrin-coated vesicles that mediate the internalization of membrane-bound receptors in vesicles coated on the intracellular side with subunits of the protein clathrin (Fig. Potocytosis is the name given to endocytosis that occurs via caveolae (small invaginations or ācavesā), which are regions of the cell membrane with a unique lipid and protein The vitamin folate provides an example of a compound trans- composition (including the protein caveolin-1). LYSOSOMES compounds such as membrane hormone receptors occurs through clathrin-coated Lysosomes are the intracellular organelles of digestion enclosed by a single pits. The receptors are targeted for these pits membrane that prevents the release of its digestive enzymes into the cytosol. Ligands entering the cell through recep- tor-mediated endocytosis bind to receptors that cluster in an area of the membrane. Adaptor proteins bind to the receptor tails and to the clathrin molecules to enclose the budding mem- brane in a cage-like clathrin coat. Molecules of a monomeric G protein called dynamin (from the Rab family) constrict the neck of the vesicle and pinch it off from the membrane as GTP is hydrolyzed. CHAPTER 10 / RELATIONSHIP BETWEEN CELL BIOLOGY AND BIOCHEMISTRY 169 infectious bacteria and yeast, recovery from injury, tissue remodeling, involution of tissues during development, and normal turnover of cells and organelles. Lysosomal Hydrolases The lysosomal digestive enzymes include nucleases, phosphatases, glycosi- dases, esterases, and proteases called cathepsins (Fig. These enzymes are all hydrolases, enzymes that cleave amide, ester, and other bonds through the addition of water. Many of the products of lysosomal digestion, such as the amino acids, return to the cytosol. Lysosomes are therefore involved in recycling compounds. Most of these lysosomal hydrolases have their highest activity near a pH of Lysosomal storage diseases. The cytosol and other cellular compartments have a pH nearer 7. Endocytosis, Phagocytosis, and Autophagy verted to residual bodies. The accumulation may be so extensive that normal cellular Lysosomes are formed from digestive vesicles called endosomes, which are function is compromised, particularly in involved in receptor-mediated endocytosis. They also participate in digestion of for- neuronal cells. Genetic diseases such as the eign cells acquired through phagocytosis and the digestion of internal contents in Tay-Sachs disease (an accumulation of par- the process of autophagocytosis. RECEPTOR-MEDIATED ENDOCYTOSIS glycogen particles in lysosomes) are caused by the absence or deficiency of specific lyso- Lysosomes are involved in the digestion of compounds brought into the cells in somal enzymes. These vesicles fuse to form multivesicular bodies called early endosomes. The early endosomes mature into late endosomes as they recycle clathrin, lipids, and other Lysosome Mucopolysaccharides Triacylglycerols Phosphoacylglycerols Proteins Polysaccharides DNA & RNA Lipases Phospholipases OligosaccharidesOligosaccharides Deoxyribonucleases ProteasesProteases GlycosidasesGlycosidases Ribonucleaseses Diacylglycerols Glucuronidases Nucleotides Phosphatases Sulfatases Monoacylglycerols Lysozyme Phosphatases Amino acids Monosaccharides Nucleosides Inorganic Fatty acids Glycerol Inorganic Head group phosphate phosphate molecules (P)i (P)i (choline, etc. Most lysosomal enzymes are hydrolases, which cleave peptide, ester, and glycosidic bonds by adding the components of water across the bond. These enzymes are active at the acidic pH of the lysosome and inactive if accidentally released into the cytosol. Lysosomes in receptor-mediated endocytosis via clathrin-coated pits. Neutrophils, the media- membrane components back to the plasma membrane in vesicles called recycling tors of the acute inflammation that followed, endosomes. The late endosomes mature into lysosomes as they progressively accu- attempted to phagocytose the urate crystals. Because urate crystals are parti- their full digestive power until after sorting of membrane lipids and proteins for cles that cannot be degraded by any of the recycling.
These include dopaminergic buy 50 mg sildenafil amex, serotonergic order sildenafil 75mg amex, and noradrenergic neurons. Parkinsonian motor symptoms are due to the progressive loss of dopaminergic neurons in the substantia nigra that innervate the striatum. Dopamine denervation is by far the most severe, best Copyright 2003 by Marcel Dekker, Inc. In contrast, it appears that the less severe serotonergic and noradrenergic denervation may mediate the frequent psychiatric symptoms of PD such as depression and anxiety. Once present, these symptoms may become a source of major disability. Psychotic symptoms may be mediated by the chronic effects of dopaminomimetic therapy superimposed on slowly accumulating cortical Lewy body pathology (5,6). COGNITIVE IMPAIRMENT Mild to moderate cognitive dysfunction affects may nondemented patients with PD. Although this dysfunction has been termed bradyphrenia, the cognitive equivalent of bradykinesia, it is now clear that the dysfunction extends beyond a mere slowing of cognition to include aspects of working memory, attention, mental ļ¬exibility, visuospatial function, word ļ¬uency, and executive functions. The latter include anticipation, planning, initiation, and the monitoring of goal-directed behaviors. The biochemical basis for these deļ¬cits is thought to be, at least in part, due to denervation of the dopaminergic and noradrenergic inputs to the frontal lobes. Other factors include basal ganglia dysfunction, which can independently impair selected aspects of attention and mental ļ¬exibility. Iatrogenic factors that can affect cognition in PD include the use of dopaminomimetic therapy to treat motor symptoms. This drug effect is complex and variable, with levodopa being unable to compensate for all the cognitive deļ¬cits observed in PD (7). It depends on the duration of illness, the severity of motor signs, the presence of dementia, sleep disturbances, and possibly depression. For instance, in the early stages of PD, levodopa treatment can improve executive functions normally regulated by the prefrontal cortex. However, this improvement is incomplete and task speciļ¬c. As the disease advances, patients with a stable clinical response to levodopa fail to exhibit a notable improvement in vigilance and executive function, and patients who exhibit motor ļ¬uctuations tend to exhibit transient deterioration in these functions (8). Finally, the effect of these drugs in patients with PD and dementia is likely to be more notable and complex. Other negative iatrogenic inļ¬uences on cognitive function in PD include the use of drugs like anticholinergics and amantadine, often used to treat tremor and dyskinesias, and psychotropics used to treat sleep disturbances and affective symptoms. These drugs can negatively affect different aspects of memory and attention, particularly in already demented patients. Like these drug effects, many intercurrent medical illnesses and Copyright 2003 by Marcel Dekker, Inc. DEMENTIA: THE PD/AD/LBD OVERLAP SYNDROMES Dementia occurs in approximately 20ā30% of PD patients. It represents a major risk factor for the development of many behavioral disturbances, including psychotic symptoms. Dementia appears to be associated with the combined effect of age and the severity of extrapyramidal symptoms (9). Pathologically, up to 40% of autopsy cases with a primary diagnosis of PD have comorbid ļ¬ndings consistent with senile dementia of the Alzheimerās type (SDAT) (10,11). Conversely, up to 30ā40% of patients with SDAT have comorbid parkinsonian features and harbor Lewy body pathology that extends beyond the dopamine neurons in the brainstem to involve the frontal cortex, hippocampus, amygdala, and basal forebrain (12). These defects conspire with aminergic deļ¬cits to increase disability and the incidence of psychotropic-induced side effects. They also contribute to the progression of parkinsonian motor symptoms by narrowing the therapeutic window of all antiparkinsonian agents. Lewy body dementia (LBD) is an increasingly recognized syndrome in which dementia is accompanied by spontaneous parkinsonian features, depressive features, and apathy (5,13). Unlike SDAT, this form of dementia exhibits signiļ¬cant ļ¬uctuations in arousal ranging from āānarcoleptic-likeāā sleep attacks to delirium in advanced cases. Sleep is often disrupted by sleep fragmentation due to rapid eye movement (REM)ārelated behavioral disorders. Patients have spontaneous features of PD and are extremely sensitive to drug-induced parkinsonism.
O Starch O O Salivary and pancreatic Ī±āamylase O O O HO O OH HO OH Maltose Isomaltose O O O O O O HO O O OH HO O O OH Trisaccharides Ī±āDextrins (and larger oligosaccharides) (oligosaccharides with Ī±ā1 quality sildenafil 75 mg,6 branches) Fig 25mg sildenafil sale. CHAPTER 27 / DIGESTION, ABSORPTION, AND TRANSPORT OF CARBOHYDRATES 497 The acidic gastric juice enters the duodenum, the upper part of the small intes- Amylase activity in the gut is abun- tine, where digestion continues. Secretions from the exocrine pancreas (approxi- dant and is not normally rate limit- mately 1. Alcohol-induced pancreatitis or surgical These secretions contain bicarbonate (HCO3 ), which neutralizes the acidic pH of removal of part of the pancreas can decrease stomach contents, and digestive enzymes, including pancreatic -amylase. Pancreatic exocrine Pancreatic -amylase continues to hydrolyze the starches and glycogen, forming secretion into the intestine also can be the disaccharide maltose, the trisaccharide maltotriose, and oligosaccharides. These decreased through cystic fibrosis, in which oligosaccharides, called limit dextrins, are usually four to nine glucosyl units long and mucus blocks the pancreatic duct, which contain one or more -1,6 branches. The two glucosyl residues that contain the -1,6 eventually degenerates. However, pancreatic glycosidic bond will eventually become the disaccharide isomaltose, but -amylase exocrine secretion can be decreased to 10% of does not cleave these branched oligosaccharides all the way down to isomaltose. In contrast, protein and fat digestion is more strongly affected in cystic fibrosis. Disaccharidases of the Intestinal Brush-Border Membrane The dietary disaccharides lactose and sucrose, as well as the products of starch diges- tion, are converted to monosaccharides by glycosidases attached to the membrane in CH2OH CH2OH the brush-border of absorptive cells (Fig. The different glycosidase activities O O are found in four glycoproteins: glucoamylase, the sucraseāmaltase complex, the smaller glycoprotein trehalase, and lactase-glucosylceramidase (Table 27. These O O OH OH glycosidases are collectively called the small intestinal disaccharidases, although glucoamylase is really an oligosaccharidase. GLUCOAMYLASE Can the glycosidic bonds of the structure shown above be hydrolyzed by -amylose? Glucoamylase and the sucraseāisomaltase complex have similar structures and exhibit a great deal of sequence homogeneity (Fig. A membrane-spanning domain near the N-terminal attaches the protein to the luminal membrane. The long polypeptide chain forms two globular domains, each with a catalytic site. In glu- Individuals with genetic defi- coamylase, the two catalytic sites have similar activities, with only small differences ciencies of the sucrase-isomal- in substrate specificity. The protein is heavily glycosylated with oligosaccharides tase complex show symptoms that protect it from digestive proteases. It begins at the nonreducing end of a polysaccharide activity in the glucoamylase complex, and or limit dextrin, and sequentially hydrolyzes the bonds to release glucose monosac- residual activity in the sucrase-isomaltase charides. It will digest a limit dextrin down to isomaltose, the glucosyl disaccharide complex (which is normally present in with an ā1,6-branch, that is subsequently hydrolyzed principally by the isomaltase excess of need) is apparently sufficient to activity in the sucraseāisomaltase complex. SUCRASEāISOMALTASE COMPLEX The structure of the sucraseāisomaltase complex is very similar to that of glu- coamylase, and these two proteins have a high degree of sequence homology. How- ever, after the single polypeptide chain of sucraseāisomaltase is inserted through the 1 membrane and the protein protrudes into the intestinal lumen, an intestinal protease 2 clips it into two separate subunits that remain attached to each other. Each subunit has a catalytic site that differs in substrate specificity from the other through non- O O O O covalent interactions. The sucraseāmaltase site accounts for approximately 100% of O O O HO HO the intestineās ability to hydrolyze sucrose in addition to maltase activity; the iso- 3 4 5 maltaseāmaltase site accounts for almost all of the intestineās ability to hydrolyze -1,6-bonds (Fig. Together, these sites account Which of the bonds in the structure above for approximately 80% of the maltase activity of the small intestine. The remainder are hydrolyzed by the sucraseāisomaltase of the maltase activity is found in the glucoamylase complex. The Different Forms of the Brush Border Glycosidases A Villi Complex Catalytic Sites Principal Activities -Glucoamylase -Glucosidase Split -1,4 glycosidic bonds between glucosyl units, beginning sequentially with the residue at the tail end (nonreducing end) of the chain. Substrates include Submucosa amylase, amylopectin, glycogen and maltose. Absorptive and goblet -Glycosidase Glucosylāceramidase Splits -glycosidic bonds between glucose cells (Phlorizin hydrolase) or galactose and hydrophobic residues, such as the glycolipids glucosylceramide and galactosylceramide Lactase Splits the -1,4 bond between glucose and galactose. To a lesser extent also splits the -1,4 bond between some cellulose disaccharides. Trehalase Trehalase Splits bond in trehalose, which is 2 glucosyl C units linked -1,1 through their anomeric Nutrients carbons. TREHALASE complexes) Trehalase is only half as long as the other disaccharidases and has only one catalytic site.
When erythrocytes are lost or destroyed purchase 75mg sildenafil visa, as from chronic bleeding or some form of hemolytic anemia order 100mg sildenafil, red blood cell pro- duction is āstepped upā to compensate for the loss. Greater num- bers of reticulocytes are then released into the blood before reaching full maturity, and counts increase above normal. Some ribosomes and rough ER appear as a net- other hand, a decrease in the number of circulating reticulocytes work in a late stage of erythrocyte development. The list of blood chemistry tests is extensive and is constantly increasing. One machine, the Sequential Multiple Analyzer mins, antibodies, and toxic or therapeutic drug levels. Tests for elec- trolytes, such as sodium, potassium, chloride, and bicar- Coagulation Studies bonate, may be performed at the same time along with tests for blood glucose, and nitrogenous waste products, Before surgery and during treatment of certain diseases, such as blood urea nitrogen (BUN), and creatinine (kre- hemophilia for example, it is important to know that co- AT-in-in). Increased levels of cause clotting is a complex process involving many reac- CPK (creatine phosphokinase), LDH (lactic dehydroge- tants, a delay may result from a number of different causes, nase), and other enzymes indicate tissue damage, such as including lack of certain hormonelike substances, calcium damage that may occur in heart disease. The amounts of the various clotting fac- kaline phosphatase (FOS-fah-tase) could indicate a liver tors are evaluated by percentage to aid in the diagnosis and disorder or metastatic cancer involving bone (see Table 3 treatment of bleeding disorders. Additional tests for coagulation include tests for Blood can be tested for amounts of lipids, such as cho- bleeding time, clotting time, capillary strength, and lesterol, triglycerides (fats), and lipoproteins, or for platelet function. Many of these tests help in evaluating disorders that may involve various vital or- Bone Marrow Biopsy gans. For example, the presence of more than the normal amount of glucose (sugar) dissolved in the blood, a con- A special needle is used to obtain a small sample of red dition called hyperglycemia (hi-per-gli-SE-me-ah), is marrow from the sternum, sacrum, or iliac crest in a pro- found most frequently in patients with unregulated dia- cedure called a bone marrow biopsy. Sometimes, several sugar evaluations are done after from the sternum, the procedure may be referred to as a the administration of a known amount of glucose. Examination of the cells gives valuable procedure is called the glucose tolerance test and is usu- information that can aid in the diagnosis of bone marrow ally given along with another test that determines the disorders, including leukemia and certain kinds of ane- amount of sugar in the urine. Learning the meanings of these parts can help you remember words and interpret unfamiliar terms. WORD PART MEANING EXAMPLE Blood Constituents erythr/o red, red blood cell An erythrocyte is a red blood cell. Hemostasis -gen producing, originating Fibrinogen converts to fibrin in the formation of a blood clot. Blood Types -lysis loosening, dissolving, A recipientās antibodies to donated red cells can cause hemolysis separating of the cells. Uses of Blood and Blood Components cry/o cold Cryoprecipitate forms when blood plasma is frozen and then thawed. Blood Disorders āemia (from āhemia) blood Anemia is a lack (an-) of red cells or hemoglobin. Transportationāof oxygen, carbon dioxide, nutrients, 1. Erythrocytes (red cells)ācarry oxygen bound to hemo- minerals, vitamins, hormones, waste globin B. Regulationāof pH, fluid balance, body temperature 2. Leukocytes (white cells)ādestroy invading organisms C. Protectionāagainst foreign organisms, blood loss and remove waste a. Proteinsāalbumin, clotting factors, antibodies, comple- a. The formed elementsāproduced in red bone marrow from 1. Blood disorders (1) Procoagulantsāpromote clotting A. Anemiaālack of hemoglobin or red cells (2) Anticoagulantsāprevent clotting 1. Deficiency anemia (1) Prothrombinase converts prothrombin to b.
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