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The corpus luteum is composed primarily of granulosa cells but also of theca cells arrhythmia recognition poster purchase lanoxin, capillaries arteria maxilar generic 0.25 mg lanoxin amex, and fibroblasts prehypertension blood pressure treatment 0.25 mg lanoxin free shipping. The corpus luteum synthesizes and secretes steroid hormones, which are necessary for implantation and maintenance of the zygote should fertilization occur. If fertilization does occur, the corpus luteum will secrete steroid hormones until the placenta assumes this role, later in pregnancy. Systemically, the ovarian steroid hormones act on a variety of target tissues including uterus, breast, and bone. The functional unit of the ovaries is the single ovarian follicle, which comprises one germ cell surrounded by endocrine cells. When fully developed, the ovarian follicle serves several critical roles: It will provide nutrients for the developing oocyte; release the oocyte at the proper time (ovulation); prepare the vagina and fallopian tubes to aid in fertilization of the egg by a sperm; prepare the lining of the uterus for implantation of the fertilized egg; and, in the event of fertilization, maintain steroid hormone production for the fetus until the placenta can assume this role. Oogenesis In the developing ovaries, primordial germ cells produce oogonia by mitotic divisions until gestational weeks 2024. Beginning at gestational weeks 89, some of these oogonia enter the prophase of meiosis and become primary oocytes. The meiotic process continues until approximately 6 months after birth, at which point all oogonia have become oocytes. The oocytes remain in a state of suspended prophase; the first meiotic division will not be completed until ovulation occurs many years later. At birth, only 2 million oocytes remain; by puberty, only 400,000 oocytes remain; by menopause (which marks the end of the reproductive period), few, if any, oocytes remain. Whereas males continuously produce spermatogonia and spermatocytes, females do not produce new oogonia and function from a declining pool of oocytes. If fertilization occurs, the corpus luteum secretes steroid hormones and supports the developing zygote. If no fertilization occurs, the corpus luteum regresses and becomes the corpus albicans. Synthesis and Secretion of Estrogen and Progesterone the ovarian steroid hormones, progesterone and 17estradiol, are synthesized by the ovarian follicles through the combined functions of the granulosa cells and the theca cells. Virtually all steps in the biosynthetic pathway are the same as those discussed previously for the adrenal cortex and the testes. Recall that the adrenal cortex produces all intermediates up to the level of androstenedione, but because it lacks the enzyme 17-hydroxysteroid dehydrogenase, it does not produce testosterone. Recall also that the testes, having 17-hydroxysteroid dehydrogenase, produce testosterone as their major hormonal product. In the ovaries, all steps in the biosynthetic pathway are present including aromatase, which converts testosterone to 17-estradiol, the major ovarian estrogen. Progesterone and 17-estradiol are synthesized as follows: Theca cells synthesize and secrete progesterone. Every 28 days a sequence of follicular development, ovulation, and formation and degeneration of a corpus luteum is repeated in the menstrual cycle. The first 14 days of the menstrual cycle involve follicular development and are called the follicular phase. The last 14 days of the menstrual cycle are dominated by the corpus luteum and are called the luteal phase. At the midpoint of the cycle, between the follicular and luteal phases, ovulation occurs. In the granulosa cells, androstenedione is converted to testosterone and testosterone is then converted to 17estradiol. In females, the hypothalamic-pituitary axis is controlled by both negative and positive feedback, depending on the phase of the menstrual cycle. The follicular and luteal phases are characterized by negative feedback of estradiol and progesterone, respectively, on the anterior pituitary. Midcycle is characterized by positive feedback of estradiol on the anterior pituitary. Thus the follicular phase is dominated by negative feedback effects of estradiol on the hypothalamicpituitary axis. Estradiol levels rise sharply as a result of the proliferation of follicular cells and the stimulation of estradiol synthesis that occurred during the follicular phase. In the luteal phase of the menstrual cycle, the major hormonal secretion of the ovaries is progesterone. Thus the luteal phase is dominated by negative feedback effects of progesterone on the hypothalamic-pituitary axis.
Is the item substantially more costly than a medically appropriate and realistically feasible alternative pattern of care? Does the item serve essentially the same purpose as equipment already available to heart attack wiki order lanoxin overnight the beneficiary? The acceptance of an assignment binds the supplier-assignee to arrhythmia uti discount lanoxin 0.25 mg with amex accept the payment for the medically required equipment or service as the full charge and the supplier-assignee cannot charge the beneficiary the differential attributable to blood pressure medication heart rate lanoxin 0.25mg amex the equipment actually furnished. See the Medicare Program Integrity Manual, Chapters 5 and 6, for medical review guidelines. The same concept applies even if the patient resides in a bed or portion of the institution not certified for Medicare. If the patient is at home for part of a month and, for part of the same month is in an institution that cannot qualify as his or her home, or is outside the U. However, do not pay for repair, maintenance, or replacement of equipment in the frequent and substantial servicing or oxygen equipment payment categories. Repairs To repair means to fix or mend and to put the equipment back in good condition after damage or wear. Repairs to equipment which a beneficiary owns are covered when necessary to make the equipment serviceable. However, do not pay for repair of previously denied equipment or equipment in the frequent and substantial servicing or oxygen equipment payment categories. If the expense for repairs exceeds the estimated expense of purchasing or renting another item of equipment for the remaining period of medical need, no payment can be made for the amount of the excess. This includes items in the frequent and substantial servicing, oxygen equipment, capped rental, and inexpensive or routinely purchased payment categories which are being rented. The owner is expected to perform such routine maintenance rather than a retailer or some other person who charges the beneficiary. Thus, hiring a third party to do such work is for the convenience of the beneficiary and is not covered. This might include, for example, breaking down sealed components and performing tests which require specialized testing equipment not available to the beneficiary. Do not pay for maintenance of purchased items that require frequent and substantial servicing or oxygen equipment. Since renters of equipment recover from the rental charge the expenses they incur in maintaining in working order the equipment they rent out, separately itemized charges for maintenance of rented equipment are generally not covered. Payment may not be made for maintenance of rented equipment other than the maintenance and servicing fee established for capped rental items. Replacement Replacement refers to the provision of an identical or nearly identical item. Situations involving the provision of a different item because of a change in medical condition are not addressed in this section. Equipment which the beneficiary owns or is a capped rental item may be replaced in cases of loss or irreparable damage. Irreparable wear refers to deterioration sustained from day-to-day usage over time and a specific event cannot be identified. Replacement of equipment due to irreparable wear takes into consideration the reasonable useful lifetime of the equipment. The reasonable useful lifetime of durable medical equipment is determined through program instructions. In the absence of program instructions, carriers may determine the reasonable useful lifetime of equipment, but in no case can it be less than 5 years. Computation of the useful lifetime is based on when the equipment is delivered to the beneficiary, not the age of the equipment. Replacement due to wear is not covered during the reasonable useful lifetime of the equipment. During the reasonable useful lifetime, Medicare does cover repair up to the cost of replacement (but not actual replacement) for medically necessary equipment owned by the beneficiary. Such supplies include those drugs and biologicals which must be put directly into the equipment in order to achieve the therapeutic benefit of the durable medical equipment or to assure the proper functioning of the equipment. However, the coverage of such drugs or biologicals does not preclude the need for a determination that the drug or biological itself is reasonable and necessary for treatment of the illness or injury or to improve the functioning of a malformed body member.
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Having developed such a tissue-specific colonizing ability blood pressure kid generic lanoxin 0.25 mg amex, the cells in metastatic colonies may proceed to blood pressure chart daily cheap lanoxin 0.25mg overnight delivery disseminate further hypertension icd 9 code 2013 lanoxin 0.25mg line, not only to new sites in the body, but also back to the primary V d the i G R 32 Principles of oncology tumors in which their ancestors arose. Accordingly, tissue-specific colonization programs that are evident among certain cells within a primary tumor may originate not from classical tumor progression occurring entirely within the primary lesion, but instead from immigrants that have returned home. Implicit in this self-seeding process is another notion: the supportive stroma that arises in a primary tumor and contributes to its acquisition of malignant traits provides a hospitable site for reseeding and colonization by circulating cancer cells released from metastatic lesions. Clarifying the regulatory programs that enable metastatic colonization represents an important agenda for future research. Substantial progress is being made, for example, in defining sets of genes (metastatic signatures) that correlate with and appear to facilitate the establishment of macroscopic metastases in specific tissues. For these reasons, the process of colonization is likely to encompass a large number of cell-biologic programs that are, in aggregate, considerably more complex and diverse than the preceding steps of metastatic dissemination that allow carcinoma cells to depart from primary tumors to sites of lodging and extravasation throughout the body. Reprogramming Energy Metabolism the chronic and often uncontrolled cell proliferation that represents the essence of neoplastic disease involves not only deregulated control of cell proliferation but also corresponding adjustments of energy metabolism in order to fuel cell growth and division. Under aerobic conditions, normal cells process glucose, first to pyruvate via glycolysis in the cytosol and thereafter via oxidative phosphorylation to carbon dioxide in the mitochondria. Under anaerobic conditions, glycolysis is favored and relatively little pyruvate is dispatched to the oxygen-consuming mitochondria. Otto Warburg first observed an anomalous characteristic of cancer cell energy metabolism153155: Even in the presence of oxygen, cancer cells can reprogram their glucose metabolism, and thus their energy production, leading to a state that has been termed aerobic glycolysis. The existence of this metabolic specialization operating in cancer cells has been substantiated in the ensuing decades. This reliance on glycolysis can be further accentuated under the hypoxic conditions that operate within many tumors: the hypoxia response system acts pleiotropically to upregulate glucose transporters and multiple enzymes of the glycolytic pathway. According to one long-forgotten163 and a recently revived and refined hypothesis,164 increased glycolysis allows the diversion of glycolytic intermediates into various biosynthetic pathways, including those generating nucleosides and amino acids. In turn, this facilitates the biosynthesis of the macromolecules and organelles required for assembling new cells. Moreover, Warburg-like metabolism seems to be present in many rapidly dividing embryonic tissues, once again suggesting a role in supporting the large-scale biosynthetic programs that are required for active cell proliferation. Interestingly, some tumors have been found to contain two subpopulations of cancer cells that differ in their energy-generating pathways. One subpopulation consists of glucose-dependent (Warburg-effect) cells that secrete lactate, whereas cells of the second subpopulation preferentially import and utilize the lactate produced by their neighbors as their main energy source, employing part of the citric acid cycle to do so. Although this provocative mode of intratumoral symbiosis has yet to be generalized, the cooperation between lactatesecreting and lactate-utilizing cells to fuel tumor growth is in fact not an invention of tumors, but rather again reflects the co-opting of a normal physiologic mechanism, in this case one operative in muscle165,167,168 and the brain. Finally, the notion of the Warburg effect needs to be refined for most if not all tumors exhibiting aerobic glycolysis. The effect does not involve a switching off oxidative phosphorylation concurrent with activation of glycolysis, the latter then serving as the sole source of energy. Finally, this capability for reprograming energy metabolism, dubbed to be an emerging hallmark in 2011,2 is clearly intertwined with the hallmarks conveying deregulated proliferative signals and evasion of growth suppressors, as discussed earlier. As such, its status as a discrete, independently acquired hallmark remains unclear, despite growing appreciation of its importance as a crucial component of the neoplastic growth state. V d the i G R Evading Immune destruction the eighth hallmark reflects the role played by the immune system in antagonizing the formation and progression of tumors. A longstanding theory of immune surveillance posited that cells and tissues are constantly monitored by an ever alert immune system, and that such immune surveillance is responsible for recognizing and eliminating the vast majority of incipient cancer cells and, thus, nascent tumors. The role of defective immunologic monitoring of tumors would seem to be validated by the striking increases of certain cancers in immune-compromised individuals. In recent years, however, an increasing body of evidence, both from genetically engineered mice and from clinical epidemiology, suggests that the immune system operates as a significant barrier to tumor formation and progression, at least in some forms of nonvirus-induced cancer. The results indicated that, at least in certain experimental models, both the innate and adaptive cellular arms of the immune system are able to contribute significantly to immune surveillance and, thus, tumor eradication. Such weakly immunogenic cells can thereafter successfully colonize both immunodeficient and immunocompetent hosts. Conversely, when arising in immunodeficient hosts, the immunogenic cancer cells are not selectively depleted and can, instead, prosper along with their weakly immunogenic counterparts. When cells from such nonedited tumors are serially transplanted into syngeneic recipients, the immunogenic cancer cells are rejected when they confront, for the first time, the competent immune systems of their secondary hosts.
The A chains and B chains are released pulse pressure 60 mmhg discount lanoxin line, now inactive arteria maxillaris generic 0.25mg lanoxin with amex, and are excreted in the urine heart attack fever buy lanoxin 0.25mg overnight delivery. Increases in blood glucose concentration rapidly stimulate the secretion of insulin. Because of the preeminence of glucose as a stimulant, it is used to describe the mechanism of insulin secretion by the cell, as illustrated in Figure 9. The circled numbers in the figure correlate with the steps described as follows: 1. Once inside the cell, glucose is phosphorylated to glucose6-phosphate by glucokinase (Step 2), and glucose6-phosphate is subsequently oxidized (Step 3). Two disulfide bridges link the A chain to the B chain, and a third disulfide bridge is located within the A chain. The synthesis of insulin is directed by a gene on chromosome 11, a member of a superfamily of genes that encode related growth factors. The signal peptide is cleaved early in the biosynthetic process (while the peptide chains are still being assembled), yielding proinsulin. Proinsulin is then shuttled to the endoplasmic reticulum, where, with the connecting peptide still attached, disulfide bridges form to yield a "folded" form of insulin. Briefly, when the K+ channels close, K+ conductance decreases and the membrane potential moves away from the K+ equilibrium potential and is depolarized. Ca2+ channels, also in the cell membrane, are regulated by changes in voltage; they are opened by depolarization and closed by hyperpolarization. Ca2+ flows into the cell down its electrochemical gradient and the intracellular Ca2+ concentration increases (Step 7). Increases in intracellular Ca2+ concentration cause exocytosis of the insulin-containing secretory granules (Step 8). Insulin is secreted into pancreatic venous blood and then delivered to the systemic circulation. C peptide is secreted in equimolar amounts with insulin and is excreted unchanged in the urine. Therefore the excretion rate of C peptide can be used to assess and monitor endogenous cell function. Recall from Chapter 8 that oral glucose is a more powerful stimulant for insulin secretion than intravenous glucose. The insulin receptor is a tetramer composed of two subunits and two subunits. The subunits lie in the extracellular domain, and the subunits span the cell membrane. A disulfide bond connects the two subunits, and each subunit is connected to a subunit by a disulfide bond. Insulin binds to the subunits of the tetrameric insulin receptor, producing a conformational change in the receptor. Activated tyrosine kinase phosphorylates several other proteins or enzymes that are involved in the physiologic actions of insulin including protein kinases, phosphatases, phospholipases, and G proteins. Phosphorylation either activates or inhibits these proteins to produce the various metabolic actions of insulin. The insulin receptor is either degraded by intracellular proteases, stored, or recycled to the cell membrane to be used again. Insulin down-regulates its own receptor by decreasing the rate of synthesis and increasing the rate of degradation of the receptor. In addition to the previously described actions, insulin also binds to elements in the nucleus, the Golgi apparatus, and the endoplasmic reticulum. For example, the stimulatory effects of amino acids and fatty acids on insulin secretion utilize metabolic pathways parallel to those utilized by glucose. Glucagon activates a Gq protein coupled to phospholipase C, which leads to a rise in intracellular Ca2+. When the availability of nutrients exceeds the demands of the body, insulin ensures that excess nutrients are stored as glycogen in the liver, as fat in adipose tissue, and as protein in muscle. These stored nutrients are then available during subsequent periods of fasting to maintain glucose delivery to the brain, muscle, and other organs. The effects of insulin on nutrient flow and the resulting changes in blood levels are summarized in Table 9.