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Chin Med J (Engl). 2002 Sep;115(9):1376-9.
Clinical manifestations of low bone mass in amenorrhea patients with elevated follicular stimulating hormone.

Yu Q, Lin S, He F, Li B, Lin Y, Zhang T, Zhang Y.

Department of Obstetrics and Gynecology, Peking Union Medical College Hospital, Beijing 100730, China.

OBJECTIVE: To study the characteristics of low bone mass in amenorrhea patients with elevated follicular stimulating hormone (FSH). METHODS: Amenorrhea patients with elevated FSH: Primary amenorrhea 18 cases, secondary amenorrhea 171 cases and age matched controls with normal menstruation, 180 cases. The descriptive parameters were: estrogen, alkaline phosphatase, urinary excretion of calcium to creatine ratio, cortical bone mineral density at the right radius measured by single photon absorptiometry and trabecular bone mineral density at the lumbar vertebra body measured by quantitative computerized tomography. RESULTS: Average E(2) levels in amenorrhea patients is under 150 pmol/L with significantly higher alkaline phosphatase and urine calcium to creatine ratio values than the normal menstruation group. Cortical bone mineral density in the secondary amenorrhea group (655 +/- 69 mg/cm(2)) was significantly lower than that of the normal menstruation group (677 +/- 56 mg/cm(2), P < 0.01). Trabecular bone mineral density in the secondary amenorrhea group (145 +/- 26 mg/cm(3)) was significantly lower than that of the NOR group (192 +/- 28 mg/cm(3), P < 0.001). The disparity with the normal menstruation group is even greater in the primary amenorrhea group. Bone mineral density of the amenorrhea patients was negatively correlated with duration of the menopause. CONCLUSIONS: Serum estrodiol levels in amenorrhea patients was so low that bone turnover was accelerated. This led to insufficient bone accumulation and a dramatically drop in trabecular bone mineral density. The extent was closely related to age of onset of amenorrhea and the duration of ovarian failure.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411116&dopt=Abstract

Zhonghua Yu Fang Yi Xue Za Zhi. 2002 Jul;36(4):258-60.
[Changes of serum sex hormone levels in male workers exposed to cadmium]

[Article in Chinese]

Zeng X, Jin T, Kong Q, Zhou Y.

Department of Occupational Health and Toxicology, School of Public Health, Fudan University, Shanghai 200032, China.

OBJECTIVE: To investigate the changes in serum levels of sex hormones in male workers occupationally exposed to cadmium (Cd). METHODS: Eighty-five Cd-exposed workers in a cadmium refinery in the south China and 76 local healthy subjects as control were selected in the study. Air samples in the workplaces were collected and detected for Cd concentration. Urinary Cd (UCd) level of the workers was measured by graphite atomic absorption spectrometry (AAS) and adjusted by urine level of creatinine (Cr), as an indicator of Cd-burden in the body of all subjects. Also, their serum levels of testosterone (T), follicle stimulating hormone (FSH) and luteinizing hormone (LH) were determined with radioimmunoassay and enzyme immunoassay, respectively, and dose-effect relationship was evaluated. RESULTS: The serum testosterone levels in Cd-exposure group with 10.9-21.9 and > 21.9 micro mol/mol Cr were 13.00 and 11.37 nmol/L, significantly higher than that (9.31 nmol/L) in those with 0.0-2.2 micro mol/mol Cr. Significantly more increased level of LH (4.11 and 4.32 U/L) was detected in heavy exposure group in the workshop for electrolysis than in control group (2.52 U/L) and in the group with 0.0-2.2 micro mol/mol Cr of UCd (2.64 U/L). No changes in serum level of FSH were found related to Cd exposure. CONCLUSION: Occupational Cd exposure could independently contribute to the changes of serum levels of sex hormone in male workers.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411208&dopt=Abstract

Circ Res. 2002 Nov 1;91(9):814-20.
Estrogen causes dynamic alterations in endothelial estrogen receptor expression.

Ihionkhan CE, Chambliss KL, Gibson LL, Hahner LD, Mendelsohn ME, Shaul PW.

Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75390-9063, USA.

Estrogen receptor (ER)alpha mediates many of the effects of estrogen on the vascular endothelium. The purpose of the present study was to determine whether estrogen modifies endothelial ERalpha expression. In experiments in cultured ovine endothelial cells, physiological concentrations of 17beta-estradiol (E2, 10(-10) to 10(-8) mol/L) caused an increase in ERalpha protein abundance that was evident after 6 hours of hormone exposure. Shorter (2-hour) E2 treatment caused ERalpha downregulation. In contrast to the upregulation in ERalpha after long-term E2, the expression of the other ER isoform, ERbeta, was downregulated. Both nonselective ER antagonism with ICI 182,780 and the inhibition of gene transcription with actinomycin D blocked the increase in ERalpha with E2. In studies using the human ERalpha gene promoter P-1 coupled to luciferase, an increase in ERalpha gene transcription was evident in endothelial cells within 4 hours of E2 exposure. The transcriptional activation was fully blocked by ICI 182,780, whereas the specific ERbeta antagonist RR-tetrahydrochrysene yielded partial blockade. Overexpression of ERalpha or ERbeta caused comparable 10- and 8-fold increases, respectively, in ERalpha promoter activation by E2. Thus, long-term exposure to E2 upregulates ERalpha expression in endothelial cells through the actions of either ERalpha or ERbeta on ERalpha gene transcription; in contrast, E2 causes ERbeta downregulation in the endothelium. We postulate that E2-induced changes in ERalpha and ERbeta expression modify the effects of the hormone on vascular endothelium.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411396&dopt=Abstract

Br J Pharmacol. 2002 Nov;137(6):799-804.
Leptin potentiates IFN-gamma-induced expression of nitric oxide synthase and cyclo-oxygenase-2 in murine macrophage J774A.1.

Raso GM, Pacilio M, Esposito E, Coppola A, Di Carlo R, Meli R.

Department of Experimental Pharmacology, University of Naples "Federico II", via D. Montesano, 49-80131 Naples, Italy.

1. Leptin, a pleiotropic hormone believed to regulate body weight, has recently been associated with inflammatory states and immune activity. Here we have studied the effect of leptin on expression of IFN-gamma-induced nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2), both prominent markers of macrophage activation, using the murine macrophage J774A.1 cell line. 2. After 24 h of incubation, leptin (1-10 micro g ml(-1)) potently synergized with IFN-gamma (100 U ml(-1)) in nitric oxide (NO) release, evaluated as nitrite and nitrate (NO(x)), and prostaglandin E(2) (PGE(2)) production in culture medium. 3. The observed increase of NO and PGE(2) was related to enhanced expression of the respective inducible enzyme isoforms, measured in mRNA and protein by RT-PCR and Western blot analysis, respectively. 4. When cells were stimulated only with leptin, a weak induction of NO and PGE(2) release and of the expression of related inducible enzymes was observed. 5. Moreover IFN-gamma increased the expression of the functional form of leptin receptor (Ob-Rb) and this effect was potentiated by leptin in a concentration-dependent manner. 6. These data suggest that macrophages, among the peripheral immune cells, represent a target for leptin and confirm the relevance of this hormone in the pathophysiology of inflammation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411410&dopt=Abstract

Hypertension. 2002 Nov;40(5):667-72.
Long-term adrenomedullin administration in experimental heart failure.

Rademaker MT, Charles CJ, Espiner EA, Nicholls MG, Richards AM.

Christchurch Cardioendocrine Research Group, Department of Medicine, The Christchurch School of Medicine, Christchurch, New Zealand. miriam.rademakehmeds.ac.nz

Short-term administration of adrenomedullin, a recently discovered peptide with potent vasodilator, natriuretic, and aldosterone-inhibitory actions, has beneficial effects in experimental and clinical heart failure. The effects of prolonged adrenomedullin administration have not previously been assessed in this setting. Consequently, in 16 sheep with pacing-induced heart failure, we infused either adrenomedullin (10 ng/kg per minute; n=8) or a vehicle control (Hemaccel; n=8) for 4 days. Compared with control data, infusion of adrenomedullin persistently increased circulating levels of the peptide (by approximately 9.5 pmol/L; P<0.001), in association with prompt (15 minutes) and sustained (4 days) increases in cardiac output (day 4, 27%), and reductions in peripheral resistance (30%), mean arterial pressure (13%), and left atrial pressure (24%; all, P<0.001). Adrenomedullin also significantly enhanced urinary sodium excretion (day 4, 3-fold; P<0.05), creatinine excretion (1.2-fold; P<0.001), and creatinine clearance (1.4-fold; P<0.001) over the 4 days of treatment, whereas urine volume and cAMP excretion tended to be elevated (both, 0.1>P>0.05). Plasma renin activity was increased (P<0.05), whereas aldosterone levels were reduced in a sustained fashion (P<0.01). Plasma endothelin rose transiently (hours 1 to 6) after initiation of treatment (P<0.05). Despite substantial cardiac unloading, plasma concentrations of the natriuretic peptides were not significantly different from control. In conclusion, long-term administration of adrenomedullin induces pronounced and sustained cardiovascular and renal effects in experimental heart failure, including reductions in cardiac preload and afterload, as well as augmentation of cardiac output, sodium excretion, and glomerular filtration. These findings support the concept of adrenomedullin as a protective hormone during hemodynamic compromise with therapeutic potential in heart failure.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411460&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

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