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As the newly released egg is drawn into the Fallopian tube prehypertension pregnancy discount labetalol 100mg with visa, microscopic cilia push the cell through the fluid-filled tube pulse pressure 50-60 100 mg labetalol with amex, toward the uterus. As the egg moves through the Fallopian tube, the cells of the ruptured follicle change. The follicle turns yellow and is now known as the corpus luteum (kawr pus loot ee um), which means "yellow body" in Latin. The corpus luteum continues to release estrogens but also begins to release another steroid hormone called progesterone. Progesterone also stimulates the growth and development of the blood supply and surrounding tissue in the already-thickened uterine lining. Menstruation At the start of the new follicular phase, low estrogen levels also cause the lining of the uterus to detach from the uterine wall. This tissue, along with blood and the unfertilized egg, are discharged through the vagina. The menstrual cycle continues, on average, until a female is in her late forties to early fifties. At this time, the production of estrogens declines, and ovulation and menstruation stop. During the first two days of the luteal phase, immediately following ovulation, the chances that an egg will be fertilized are the greatest. This is usually from 14 to 18 days after the completion of the last menstrual cycle. If a sperm fertilizes an egg, the fertilized egg completes meiosis and immediately undergoes mitosis. After several divisions, a ball of cells will form and implant itself in the lining of the uterus. Within a few days of implantation, the uterus and the growing embryo will release hormones that keep the corpus luteum functioning for several weeks. This allows the lining of the uterus to nourish and protect the developing embryo and prevents the menstrual cycle from starting again. In Your Notebook Draw a cycle diagram to represent the phases and days of the menstrual cycle. Endocrine and Reproductive Systems 993 Sexually Transmitted Diseases What are some of the most commonly reported sexually transmitted diseases? Chlamydia, which damages the reproductive tract and can lead to infertility, is caused by a bacterium that is spread by sexual contact. The safest course to follow is to abstain from sexual contact before marriage, and for both partners in a committed relationship to remain faithful. The next safest course is to use a latex condom, but even condoms do not provide 100 percent protection. Compare and Contrast Compare and contrast the sexual development of male embryos to that of female embryos. Use what you learned about mitochondria in Chapter 7 to explain how mitochondria might influence sperm activity. The embryo goes through round after round of cell division, producing the trillions of cells in a newborn baby. But how do these cells arrange themselves so beautifully into the tissues and organs of the body, and how does an individual cell "know" to become an embryonic skin, heart, or blood cell? These are some of the most important questions in all of biology, and we are only beginning to learn the answers. Key Questions What takes place during fertilization and the early stages of human development? Vocabulary zygote · blastocyst · implantation · gastrulation · neurulation · placenta · fetus Fertilization and Early Development What takes place during fertilization and the early stages of human development? Taking Notes Flowchart As you read, draw a flowchart that shows the steps from fertilized egg to newborn baby. The story of human development begins with the gametes-sperm produced in the testes and egg cells produced in the ovaries. Sperm and egg must meet, so that the two gametes can fuse to form a single the cell. Fertilization During sexual intercourse, sperm are released when semen is ejaculated through the penis into the vagina.

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An inadequate response to daily doses 300 mcg/day is rare and may indicate poor compliance blood pressure readings chart 100mg labetalol amex, malabsorption heart attack 5 hour energy purchase labetalol 100mg on line, and/or drug interactions. The recommended starting dose of levothyroxine sodium in elderly patients with cardiac disease is 12. In patients with severe hypothyroidism, the recommended initial levothyroxine sodium dose is 12. In patients with secondary (pituitary) or tertiary (hypothalamic) hypothyroidism, the levothyroxine sodium dose should be titrated until the patient is clinically euthyroid and the serum free- T4 level is restored to the upper half of the normal range. Newborns the recommended starting dose of levothyroxine sodium in newborn infants is 10-15 mcg/kg/day. In infants with very low (< 5 mcg/dL) or undetectable serum T4 concentrations, the recommended initial starting dose is 50 mcg/day of levothyroxine sodium. Infants and Children Levothyroxine therapy is usually initiated at full replacement doses, with the recommended dose per body weight decreasing with age (see Table 3). However, in children with chronic or severe hypothyroidism, an initial dose of 25 mcg/day of levothyroxine sodium is recommended with increments of 25 mcg every 2-4 weeks until the desired effect is achieved. Hyperactivity in an older child can be minimized if the starting dose is one-fourth of the recommended full replacement dose, and the dose is then increased on a weekly basis by an amount equal to one-fourth the full-recommended replacement dose until the full recommended replacement dose is reached. Subclinical Hypothyroidism- If this condition is treated, a lower levothyroxine sodium dose. Patients who are not treated should be monitored yearly for changes in clinical status and thyroid laboratory parameters. In the treatment of well-differentiated (papillary and follicular) thyroid cancer, levothyroxine is used as an adjunct to surgery and radioiodine therapy. Myxedema Coma ­ Myxedema coma is a life-threatening emergency characterized by poor circulation and hypometabolism, and may result in unpredictable absorption of levothyroxine sodium from the gastrointestinal tract. Therefore, oral thyroid hormone drug products are not recommended to treat this condition. Thyroid hormone products formulated for intravenous administration should be administered. Nutritional, behavioral, and reproductive processes are intricately regulated by endocrine systems, as are growth (including bone growth/remodeling), gut, cardiovascular, and kidney function and responses to all forms of stress. Disorders of any of the endocrine systems, involving both overactive and underactive hormone secretion, result inevitably in disease, the effects of which may extend to many different organs and functions and are often debilitating or life-threatening. Viewed from this general perspective, the threat posed from environmental chemicals with endocrine activity (either agonist or antagonistic) is potentially serious. However, the fact that humans and wildlife are exposed to such chemicals does not necessarily mean that clinically manifest disturbance of the relevant endocrine system will result, because much depends on the level and duration of exposure and on the timing of exposure. Currently, our concept of "endocrine" has been broadened by the discovery of other chemical regulators, such as chemicals secreted into the blood by neurons, that are sometimes termed neurohormones. The term "cytocrine" has been applied to numerous local or intercellular chemical regulators, including growth factors. Intercellular cytocrines that travel through the extracellular fluids to other cells in a tissue also are known as paracrine and autocrine regulators, depending on whether they affect other cells or themselves, respectively. Even before allowing for the increase in complexity of "endocrinology" that has resulted from recent recognition of the many cytocrine/paracrine systems that operate, it had been realized that there were numerous "classical" endocrine systems in the body that regulate processes as diverse as blood pressure, smooth muscle contraction, fluid balance, and bone resorption. It is beyond the scope of this chapter to describe the entire endocrine system; instead, the focus will be on the three major endocrine axes that affect reproductive development and function. This restriction is based on the observations that many manifestations of endocrine disruption involve the reproductive system, particularly during its vulnerable developmental period. This restriction is arbitrary and should not imply that endocrine disruptors cannot affect other endocrine axes. It is also emphasized that the general principles on which all endocrine (and probably paracrine) axes are first set up and then operate are essentially identical, and hence, most of what is discussed below can be transferred in principle to other endocrine axes that are not described. The emphasis will be on the vertebrate endocrine system, with only minor attention paid to invertebrates. Although there are many parallels between vertebrate and invertebrate endocrine mechanisms, there are some major differences as well.

Furthermore hypertension 5 hour energy order labetalol 100 mg with mastercard, the lymph fluid passes through chains of drainage lymph nodes before it is transported back to the systemic circulation blood pressure khan academy purchase 100 mg labetalol otc, providing an important anatomic basis for the immune regulatory functions of the lymphatic system. Although it is traditionally thought that approximately 90% of the capillary ultrafiltrate and associated plasma proteins is reabsorbed at the venous end of the capillary, more recent evidence, to the contrary, supports the view that the bulk of the tissue fluid is taken up by the lymphatic vasculature. There is minimal reabsorption into the venules (63), thus underscoring the importance of the lymphatic vasculature in the maintenance of tissue fluid homeostasis (64). Lymphatic capillaries, located at the center of each of the intestinal villi, known as lacteals, serve as an essential conduit for the drainage of absorbed dietary lipids and fat-soluble vitamins. The mesenteric lymphatic tree is the main conduit that transports those molecules into the systemic circulation (66). Recent intravital imaging studies have demonstrated that the lacteal is not simply acting as a passive conduit; instead, it is able to respond to autonomic nerve stimulation to the surrounding smooth muscle cells and actively transport the absorbed lipid (67). The lymphatic vessels are critical conduits for the trafficking of leukocytes and soluble antigens from the peripheral tissue to the draining lymph nodes, where either immune priming or tolerance can take place, depending on the type of transported antigens and the immune cells (70). Interestingly, the point of entry for immune cells is often located in areas of the lymph capillary with sparse basement membrane, known as portals (75). An interesting point is that chemotactic guidance gradients, as established by chemokines, are likely able to overcome the challenge of lymph flow reduction; therefore, cellular transport is minimally affected by interstitial flow variation. By contrast, absorption of molecules such as antigens, peptides, and cytokines is sensitive to the changing velocity of lymph flow (70), suggesting that lymph stasis, or slower lymph flow, would have a greater impact on molecular than cellular transport. Lymphedema, characterized by excessive accumulation of interstitial tissue fluid as a result of impaired fluid transport through this vasculature, is the major form of lymphatic dysfunction. Based on etiology, lymphedema can be classified as primary or secondary lymphedema. Secondary lymphedema is the most common form of lymphedema, afflicting more than 120 million patients worldwide. Primary Lymphedema Primary lymphedema results from heritable defects in lymphatic vascular development or function. Heterozygous mutation of flt4 within the tyrosine kinase domain leads to receptor dysfunction and causes the congenital hypoplastic lymphedema, known as Nonne-Milroy lymphedema (89). Secondary Lymphedema Secondary lymphedema is a result of obstruction or disruption of the lymphatic vascular system, which occurs as a consequence of infection, malignancies, or trauma. The resulting lymphatic insufficiency leads to interstitial fluid accumulation distal to the disrupted lymphatic structure. The most common form of secondary lymphedema worldwide is lymphatic filariasis, a condition caused by lymphatic vessel infiltration and obstruction by the nematode parasite, predominantly Wuchereria bancrofti. The estimated incidence of filariasis ranges between 140 and 200 million people, with those afflicted individuals residing primarily in third world countries (93). In the United States, secondary lymphedema results mainly from surgical and radiation therapies, either combined or individually administered for malignant conditions. These include not only breast cancer, but also other cancers, such as prostate, testicular, uterine, and ovarian as well as lymphoma, melanoma, and various head and neck tumors (94). Radiation appears to promote surgery-induced lymphedema through promoting tissue fibrosis (95). Infection, such as cellulitis, has also been shown to be a risk factor for lymphedema development following surgery of certain tumors (96, 97). One of the identified systemic risk factors for lymphedema development in at-risk patient cohorts is obesity (98). Although the mechanism of this obesity risk is not well understood, it is recognized that obesity alone can produce impaired interstitial fluid transport, decreased immune cell migration, decreased pumping ability of the collecting lymphatic vessels, and abnormal lymph node structure (99, 100). These factors predispose obese individuals to lymphedema (101), suggesting that obesity may act as another "hit" to promote lymphedema development in cancer survivors. In parallel to illustrating the role of genetic mutations in the etiology of primary lymphedema, some studies have shown that genetic mutation may also predispose cancer patients to develop lymphedema following surgical and/or radiation treatment. Taken together, these observations suggest that multiple factors, both genetic and nongenetic, are involved in promoting the development of secondary lymphedema in those at risk for the development of the disease.

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However blood pressure nose bleed buy cheap labetalol 100 mg on-line, tumor production was eventually detected on the monocot species Asparagus officinalis and Dioscorea bulbifera (Bytebier et al heart attack blues labetalol 100 mg free shipping. As mentioned above, the first extensive investigation of a genetic basis for plant susceptibility to Agrobacterium-mediated transformation was a study conducted by Nam et al. These authors determined root transformation-susceptibility of approximately 40 different ecotypes of Arabidopsis thaliana. Gelvin It is possible to identify host "transformation competence" genes using bulk segregant analysis followed by positional cloning. Although many of the mutagenized Arabidopsis lines initially showed a rat phenotype when their roots were infected with Figure 13-1. The high initial rate of "false positive" rat mutant identification serves as a reminder that plant transformationcompetence may often be determined by physiological or environmental factors, and care must be taken in interpreting the results of screens for transformation competence or recalcitrance. In flower dip transformation (or the closely related flower vacuum infiltration method; Bechtold et al. Seeds are collected from the siliques of these dipped flowers and are plated onto medium to select for plants expressing an antibiotic/herbicide resistance marker. Several reports have indicated that the female gametophyte is the target for flower dip transformation (Ye et al. We tested a number of Arabidopsis rat mutants and recalcitrant ecotypes 488 Stanton B. Although all the tested mutants and ecotypes were highly recalcitrant to somatic (root) transformation, only the rad5 mutant (Nam et al. All other rat mutants were highly susceptible to flower dip transformation (Mysore et al. Furthermore, different cell types within plants show markedly different susceptibility to Agrobacteriummediated transformation (Sangwan et al. In some instances, tissue- or cell-specific expression of particular host genes correlated with transformation competence (Yi et al. Thus, one needs to take into consideration the host tissue being assayed for transformation competence when evaluating host susceptibility to Agrobacterium-mediated transformation. Using a low concentration of bacterial cells (105-106/ml, compared to 108/ml as used for rat mutant screening) as an inoculum, we have identified eight hat mutants (S. Current efforts include identification of hat genes and verification of their roles in transformation. Interruption of any of these steps can result in disruption of the transformation process. I shall review what is known about plant proteins involved in each of these steps. Bacterial attachment is a complex process involving bacterial exopolysaccharides and, most likely, plant cell wall proteins. All bacterial mutants which are "non-attaching" are attenuated in virulence (Matthysse, 1987; Crews et al. However, several reports have indicated that "non-wounded" plant tissue can also be infected, albeit with low efficiency (Escudero and Hohn, 1997; Brencic et al. Agrobacterium makes and secretes numerous exopolysaccharides, including a cyclic 1,2-D-glucan and cellulose (Matthysse et al. However, most bacteria do not bind directly to the plant cell surface; rather, the bacteria form a biofilm (Matthysse et al. Biofilm formation is required for efficient transformation to occur, and bacterial mutants deficient in biofilm formation are either avirulent or highly attenuated in virulence (Douglas et al. Because of the importance of biofilm formation in plant transformation, it is at times difficult to determine the role of specific plant genes and proteins in bacterial attachment directly to the plant cell. Early reports suggested a proteinaceous material on the plant surface is required for bacterial attachment (Neff and Binns, 1985; Gurlitz et al. Approximately 10 years ago, our laboratory initiated genetic studies to identify Arabidopsis ecotypes and mutants that were resistant to Agrobacterium-mediated transformation. Gelvin fied were several, including Bl-1 and Petergof, which would not support bacterial attachment (Nam et al. The mutant most severely deficient in bacterial attachment under all conditions examined was rat1. Thus, at least one arabinogalactan protein gene is required for bacterial attachment, biofilm formation, and transformation.


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