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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5





Diabetes. 2002 Nov;51(11):3151-62.
Effects of insulin deficiency or excess on hepatic gluconeogenic flux during glycogenolytic inhibition in the conscious dog.

Edgerton DS, Cardin S, Pan C, Neal D, Farmer B, Converse M, Cherrington AD.

Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. dale.edgertoanderbilt.edu

The direct acute effects of insulin on the regulation of hepatic gluconeogenic flux to glucose-6-phosphate (G6P) in vivo may be masked by the hormone's effects on net hepatic glycogenolytic flux and the resulting changes in glycolysis. To investigate this possibility, we used a glycogen phosphorylase inhibitor (BAY R3401) to inhibit glycogen breakdown in the overnight-fasted dog, and the effects of complete insulin deficiency or a fourfold rise in the plasma insulin level were assessed during a 5-h experimental period. Hormone levels were controlled using somatostatin with portal insulin and glucagon infusion. After the control period, plasma insulin infusion 1) was discontinued, creating insulin deficiency; 2) increased fourfold; or 3) was continued at the basal rate. During insulin deficiency, glucose production and the plasma level and net hepatic uptake of nonesterified free fatty acids increased, whereas during hyperinsulinemia they decreased. Net hepatic lactate uptake increased sixfold during insulin deficiency and 2.5-fold during hyperinsulinemia. Net hepatic gluconeogenic flux increased more than fourfold during insulin deficiency but was not reduced by hyperinsulinemia. We conclude that in the absence of appreciable glycogen breakdown, an acute gluconeogenic effect of hypoinsulinemia becomes manifest, whereas inhibition of the process by a physiologic rise in insulin was not evident.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12401705&dopt=Abstract



Diabetes. 2002 Nov;51(11):3229-36.
Glucagon is required for early insulin-positive differentiation in the developing mouse pancreas.

Prasadan K, Daume E, Preuett B, Spilde T, Bhatia A, Kobayashi H, Hembree M, Manna P, Gittes GK.

Laboratory of Surgical Organogenesis, Children's Mercy Hospital, Kansas City, Missouri 64108, USA.

The embryonic pancreas is thought to develop from pluripotent endodermal cells that give rise to endocrine and exocrine cells. A key guidance mechanism for pancreatic development has previously been found to be epithelial-mesenchymal interaction. Interactions within the epithelium, however, have not been well studied. Glucagon is the earliest peptide hormone present at appreciable levels in the developing pancreatic epithelium (embryonic day [E]-9.5 in mouse). Insulin accumulation begins slightly later (E11 in mouse), followed by a rapid accumulation during the "second wave" of insulin differentiation ( approximately E15). Here we found that blocking early expression and function of glucagon, but not GLP-1, an alternate gene product of preproglucagon mRNA, prevented insulin-positive differentiation in early embryonic (E11) pancreas. These results suggest a novel concept and a key role for glucagon in the paracrine induction of differentiation of other pancreatic components in the early embryonic pancreas.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12401714&dopt=Abstract



ndmctsgh.edu.tw

BACKGROUND: Metabolic acidosis was evaluated in the past as an independent variable of catabolism in haemodialysis (HD) patients. Nevertheless, it could in theory reflect a higher acid production from protein oxidation. The aim of this study was to evaluate the incidence and basis of metabolic acidosis in conjunction with a nutritional assessment in a HD population (n=120). METHODS: Three groups were identified based on three consecutive monthly predialysis plasma bicarbonate concentrations (P(HCO3)) and pH values. The effect of correction of metabolic acidosis on nutritional parameters was also studied in acidotic patients. RESULTS: The mean P(HCO3) ranged from 19.2+/- 0.4 mmol/l in group A (n=21) to 24.4+/-0.3 mmol/l in group B (n=80) and 27.5+/-0.4 mmol/l in group C (n=19). The adequency of dialysis (Kt/V) and ultrafiltration rates was comparable in the three groups. When compared with group B, group A had significantly higher body mass index (BMI), triceps skin fold thickness (TSF), dietary protein intake (DPI), normalized protein catabolic rate (nPCR) as well as serum creatinine, K(+) and intact parathyroid hormone (I-PTH). In contrast, when compared with group B, group C had a significantly lower DPI, nPCR, plasma creatinine and albumin. There was no significant difference in plasma inflammatory markers such as C-reactive protein (CRP) and interleukin 6 (IL-6) among all three groups. There was a significant negative correlation between P(HCO3) and nPCR (P<0.001), DPI (P<0.001), creatinine (P<0.001). Over a period of 6 months, the correction of metabolic acidosis in the HD patients did not affect nutritional parameters. CONCLUSION: These findings suggest that metabolic acidosis as a result of a higher protein intake does not detrimentally affect nutritional status.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12401862&dopt=Abstract



J Lipid Res. 2002 Nov;43(11):1818-28.
15-Deoxy-delta12,14-prostaglandin J2-induced apoptosis does not require PPARgamma in breast cancer cells.

Clay CE, Monjazeb A, Thorburn J, Chilton FH, High KP.

Department of Cancer Biology, Wake Forest University Baptist Medical Center, Medical Center Boulevard, Winston Salem, NC 27157, USA.

Naturally occurring derivatives of arachidonic acid are potent agonists for the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARgamma) and block cancer cell proliferation through the induction of apoptosis. We have previously reported that induction of apoptosis using cyclopentenone prostaglandins of the J series, including 15deoxydelta(12,14)PGJ(2) (15dPGJ(2)), is associated with a high degree of PPAR-response element (PPRE) activity and requires early de novo gene expression in breast cancer cells. In the current study, we used pharmacologic and genetic approaches to test the hypothesis that PPARgamma is required for 15dPGJ(2)-induced apoptosis. The PPARgamma agonists 15dPGJ(2), trogliltazone (TGZ), and GW7845, a synthetic and highly selective tyrosine-based PPARgamma agonist, all increased transcriptional activity of PPARgamma, and expression of CD36, a PPARgamma-dependent gene. Transcriptional activity and CD36 expression was reduced by GW9662, a selective and irreversible PPARgamma antagonist, but GW9662 did not block apoptosis induced by 15dPGJ(2). Moreover, dominant negative expression of PPARgamma blocked PPRE transcriptional activity, but did not block 15dPGJ(2)-induced apoptosis. These studies show that while 15dPGJ(2) activates PPRE-mediated transcription, PPARgamma is not required for 15dPGJ(2)-induced apoptosis in breast cancer cells. Other likely mechanisms through which cyclopentenone prostaglandins induce apoptosis of cancer cells are discussed.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12401880&dopt=Abstract



Horm Res. 2002;58(5):229-32.
Insulin resistance (HOMA) in relation to plasma cortisol, IGF-I and IGFBP-3. A study in normal short-statured and GH-deficient children.

Bleicher M, Hogel J, Wudy S, Wabitsch M, Homoki J, Sorgo W, Heinze E.

Department of Pediatrics, University of Ulm, Germany.

OBJECTIVE: To investigate the possible contribution of plasma cortisol and growth hormone (GH) as reflected by insulin-like growth factor-I (IGF-I)/insulin-like growth factor-binding protein-3 (IGFBP-3) on insulin action in short-statured children. METHODS: In this study, insulin resistance (HOMA) was determined in 34 normal short-statured (age 9.4 +/- 3.5 years) and in 19 GH-deficient children (age 10.4 +/- 2.2 years). HOMA was examined in relation to fasting plasma cortisol, IGF-I, IGFBP-3 and in addition to birthweight and body mass index (BMI). RESULTS: Birthweight was not correlated to insulin resistance. In GH-deficient children, BMI was significantly augmented and was associated with HOMA (p < 0.02). In both groups of patients, fasting plasma cortisol was related to HOMA (normal: r = 0.295, p < 0.05, GH-deficient: r = 0.495, p < 0.02). Only in normal short-statured children IGF-I (r = 0.338, p < 0.03) and IGFBP-3 (r = 0.493, p < 0.002) were associated with insulin resistance. CONCLUSION: The results indicated that at a young age cortisol contributed to insulin resistance in short-statured children. In normal short-statured children HOMA was associated with IGF-I and IGFBP-3. Possibly GH, a known cause of insulin resistance, contributed to HOMA as IGF-I and IGFBP-3 do not mediate insulin resistance but reflect growth hormone secretion. The results in GH-deficient children supported this conclusion as in the absence of GH insulin resistance was not associated with IGF-I/IGFBP-3. 2002 S. Karger AG, Basel


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12401942&dopt=Abstract







The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer an essential part of our body, just like appendix. What little hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

Hair Million is a blend of Asian herbs that wards off hair loss and promotes hair growth. Of various approaches to hair restoration, Hair Million offers advantages including low cost compared with other methods or drugs, and safety, because it is made of safe and healthy herbs.












DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells. Our bodies produce decreasing amount of DHEA as we get older. various health benefits: To deter aging, improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance, facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions, and treat depression.





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