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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

Kidney Int Suppl. 2002 Dec;(82):73-80.
Cardiovascular calcification in patients with end-stage renal disease: A century-old phenomenon.

Qunibi WY, Nolan CA, Ayus JC.

Division of Nephrology, Department of Medicine, University of Texas Health Sciences Center at San Antonio,San Antonio, Texas, USA.

Cardiovascular calcification in patients with end-stage renal disease: A century-old phenomenon. The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12410860&dopt=Abstract [PubMed - in process]

Zhonghua Fu Chan Ke Za Zhi. 2002 Aug;37(8):472-4.
[Expression of macrophage colony-stimulating factor in human luteinized granulosa cells]

[Article in Chinese]

Zhang Z, Salmassi A, Mettler L.

Department of Gynecology, Obstetrics and Gynecology Hospital of Zhejiang Medical College, Zhejiang University, Hangzhou 310006, China.

OBJECTIVE: To detect and localize the expression of macrophage colony-stimulating factor (M-CSF) in human luteinized granulosa cells and investigate the effects of follicle stimulating hormone (FSH) on M-CSF production by human luteinized granulosa cells in vitro. METHODS: Human luteinized granulosa cells were isolated from follicular fluid of superovulated infertile patients undergoing intracytoplasmatic sperm injection. Some of the luteinized granulosa cells were used for detecting M-CSF by immunocytochemical staining (ABC method). Most of them were cultured with HAM's F-10 medium alone or plus various concentrations of FSH (2, 5, 15, 25 IU/ml). The media were collected after 72 hours and their M-CSF contents were measured by a solid phase enzyme-linked immunosorbant assay. RESULTS: About 80% of the luteinized granulosa cells were positively stained for M-CSF antibody. The immunoreactive signals of M-CSF were specially located in the cytoplasma of the luteinized granulosa cells. No immunoreactivity of M-CSF was observed in vaginal squamous epithelial cells through contaminations during transvaginal oocyte retrieval. The concentration of M-CSF in cultured luteinized granulosa cells medium without FSH stimulation was low. However, addition of 2, 5, 15, 25 IU/ml concentrations of FSH caused significant dose-dependent increases of M-CSF production after 72 hours culture by luteinized granulosa cells (P < 0.01). CONCLUSIONS: Human luteinized granulosa cells can synthesize and secrete M-CSF. FSH can directly stimulate M-CSF secretion by human luteinized granulosa cells. The mechanism of FSH regulating follicular development may partially via M-CSF/receptor pathway.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411027&dopt=Abstract

Zhonghua Fu Chan Ke Za Zhi. 2002 Aug;37(8):475-7.
[In vitro study on hormonal regulation of human endometrial stroma cell decidualization]

[Article in Chinese]

Su A, Mi R, Zhang S, Tu C, Zhang Y.

Department of Obstetrics and Gynecology, Tianjin First Central Hospital, Tianjin 300192, China.

OBJECTIVE: To investigate the roles of luteinizing hormone releasing-hormone (LHRH), follicle stimulating hormone (FSH), human chorionic gonadotropin (hCG) and ovary steroids in regulation of human endometrial stroma cell (ESC) decidualization. METHODS: Stroma cells derived from human endometrium during the proliferative phase were cultured in vitro and treated with physiological doses of estradiol (E(2)), testosterone (T), progesterone (P) or LHRH, FSH and hCG. Their morphologic changes and prolactin (PRL) production in the media were examined and compared. RESULTS: Addition of E(2) or T or P stimulated ESC proliferation, resulting in increase of the saturation density. The fibroblast- morphologic changes to polygonal shape and began to express PRL simultaneously after treatment of P or T. P in presence of E(2) or T significantly enhanced PRL production (P < 0.01), suggesting a synergistic action between them in stimulating ESC decidualization. LHRH, FSH or hCG also induced morphologic changes and PRL production by ESC in the presence of E(2) + P. Among them the impact of hCG is most remarkable, especially in this culture system. CONCLUSIONS: E(2), T and P play an important role in proliferation and differentiation of the ESC. LHRH, FSH, hCG also directly exert an effect on ESC decidualization.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411028&dopt=Abstract

Zhonghua Liu Xing Bing Xue Za Zhi. 2002 Aug;23(4):250-3.
[Study on the neonate umbilical cord blood thyroid stimulating hormone level in the universal iodized salt areas and its application]

[Article in Chinese]

Dong H, Zheng Q.

Department of Iodine Deficiency Disorders, Institute for Infectious Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing 100020, China.

OBJECTIVE: To investigate the neonatal umbilical cord blood thyroid stimulating hormone (TSH) level in the universal iodized salt areas and put forward the cut-point, then analyze its application. METHODS: Seven provinces were selected where the pregnant women having satisfied urinary iodine levels, then the urinary samples of pregnant women and the neonates cord blood were collected for urine iodine and TSH tests, and the relative factors were also recorded. RESULTS: Total 1 524 urine and cord blood samples were collected from pregnant women and their new borns respectively. The median urinary iodine of pregnant women was 246.0 micro g/L, and the median TSH was 3.58 mU/L. The TSH level among seven areas and the neonatal delivery type varied significantly. CONCLUSIONS: The neonatal cord blood TSH was influenced by several factors and could not be controlled, thus not be suitable as a iodine deficiency disorders surveillance indicator.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411066&dopt=Abstract

Chin Med J (Engl). 2002 Sep;115(9):1336-40.
Effect of surgical castration on risk factors for arteriosclerosis of patients with prostate cancer.

Xu T, Wang X, Hou S, Zhu J, Zhang X, Huang X.

Department of Urology, Peking University People's Hospital, Beijing 100044, China.

OBJECTIVE: To analyze the effect of castration on risk factors for arteriosclerosis of patients with prostate cancer. METHODS: Thirty patients with primary regional prostate adenocarcinoma limited to the prostate theca were selected in this study. Serum levels of testosterone (T), free testosterone (FT), dehydroepiandrosterone (DHEA), sex hormone-binding globulin (SHBG), prostatic specific antigen (PSA), triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), apoprotein alpha(1) (APOalpha(1)) and apoprotein beta (APObeta), insulin, plasma fibrinopeptide A (FPA), plasminogen activator inhibitor-1 (PAI-1) and fibrinogen were determined just prior to, 1 week and 1, 4 and 8 months after castration. RESULTS: T, FT and PSA decreased significantly 1 week after castration (21.12 +/- 15.11 ng/ml vs 383.9 +/- 62.6 ng/ml, P < 0.001; 4.08 +/- 3.29 pmol/L vs 34.11 +/- 11.59 pmol/L, P < 0.001; 14.34 +/- 7.77 ng/ml vs 23.51 +/- 6.57 ng/ml, P = 0.001, respectively) and continued to decrease until reaching their lowest levels 8 months after castration. DHEA and SHBG did not undergo any changes. TG, fasting insulin and glucose, 2-hour insulin and glucose levels were significantly elevated 1 month after castration (1.84 +/- 0.61 mmol/L vs 1.30 +/- 0.40 mmol/L, P < 0.05; 18.16 +/- 5.57 mU/L vs 9.47 +/- 3.81 mU/L, P < 0.05; 4.77 +/- 0.66 mmol/L vs 3.92 +/- 0.34 mmol/L, P < 0.05; 65.52 +/- 14.78 mU/L vs 36.94 +/- 17.12 mU/L, P < 0.01; 6.98 +/- 0.79 mmol/L vs 6.01 +/- 0.23 mmol/L, P = 0.001, respectively). TC, LDL-C, FPA and PAI-1 levels were elevated 4 months after castration (6.56 +/- 0.99 mmol/L vs 5.29 +/- 0.75 mmol/L, P < 0.01; 4.09 +/- 0.86 mmol/L vs 3.04 +/- 0.15 mmol/L, P < 0.01; 3.39 +/- 1.67 nmol/L vs 1.48 +/- 0.50 nmol/L, P < 0.01; 27.02 +/- 5.98 ng/ml vs 21.78 +/- 3.16 ng/ml, P < 0.05, respectively), continuing to increase after that point. Insulin sensitive index (ISI) decreased significantly 1 month after surgery (-4.42 +/- 0.36 vs -3.50 +/- 0.39, P < 0.001), and continued to decrease from that point forward. HDL-C, APOalpha(1), APObeta and fibrinogen remained at pre-operative levels. There was a negative linear correlation between FT and TG, TC, LDL-C, PAI-1, FPA, fasting insulin and glucose, 2-hour insulin and glucose (r = -0.311, -0.384, -0.385, -0.339, -0.353, -0.381, -0.303, -0.460 and -0.395, respectively; P < 0.05). A similar phenomenon occurred with T (r = -0.308, -0.309, -0.356, -0.320, -0.430, -0.453, -0.435, -0.483 and -0.512, respectively; P < 0.05). T and FT were positively associated with ISI (r = 0.555 and 0.501; P < 0.001). CONCLUSIONS: At 8 months follow-up of the study subjects, we found that lower androgen levels have adverse effects on lipid metabolism, coagulative function and insulin sensitivity, related to arteriosclerosis in men.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411107&dopt=Abstract

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