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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







J Sports Med Phys Fitness. 2002 Dec;42(4):481-7.
Lymphocyte apoptosis in ovariectomized mice given progesterone and voluntary exercise.

Hoffman-Goetz L, Fietsch CL.

Department of Health Studies and Gerontology, Faculty of Applied Health Sciences, University of Waterloo, Waterloo, Ontario, Canada. lhgoetealthy.uwaterloo.ca

BACKGROUND: At menopause, many women begin both exercise programs and hormone replacement therapy (HRT). Although the effects of estrogen on exercise behavior and immune functions have been well characterized, less is known about the behavioral and immunological consequences of progesterone (P) administration. The purpose of the present study was to describe the effect of P on running behavior and on lymphoid tissue cell viability and apoptosis in ovariectomized female mice. METHODS: Adult female B6D2F1 mice were ovariectomized, allowed to recover for 1 week and implanted subcutaneously with 25 mg progesterone (n=42) or placebo pellet (n=42). Within hormone treatment, mice were randomized to running wheels or no running wheel conditions. After 21 days of wheel running and hormone exposure, mice were sacrificed for measurements of body weight, tissue weights, and thymocyte and splenocyte apoptosis, necrosis and viability with annexin-V FITC and propidium iodide by flow cytometry. RESULTS: P treated mice were heavier than placebo controls at sacrifice (p<0.001). Irrespective of hormone condition, mice increased the volume of spontaneous activity over time (p<0.001). Within the thymus, there were no differences by hormone or running condition on percent apoptosis, necrosis and viability. In the spleen, P marginally increased percent apoptosis (p<0.05) and reduced percent viability (p<0.001). Serum levels of P were higher in the hormone replaced mice compared with placebo mice (p<0.001) and in running compared with sedentary mice (p<0.01). CONCLUSIONS: P replacement in ovariectomized mice does not alter running volume relative to placebo animals. P alone was associated with a small increase in splenocyte apoptosis. The clinical relevance for postmenopausal women of lymphocyte viability changes needs to be determined.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391444&dopt=Abstract



Hematol J. 2002;3(5):264-70.
Hemoglobin induces the expression and secretion of vascular endothelial growth factor from human malignant cells.

Siddiqui FA, Desai H, Siddiqui TF, Francis JL.

Center for Hemostasis and Thrombosis, Clinical and Research Laboratories, Florida Hospital Cancer Institute, Orlando, Florida, USA. farooq.siddiqulhosp.org

Vascular endothelial growth factor (VEGF) is an angiogenic hormone that increases the growth of many malignant tumors. Tissue factor (TF), the initiator of blood coagulation, is implicated in VEGF regulation. We recently reported that hemoglobin (Hb) upregulates TF on malignant cells. Therefore, to explore the role of Hb in angiogenesis, we examined its effect on VEGF production in A375 melanoma and J82 bladder carcinoma (TF+) and KG1 myeloid leukemia (TF-) cells. Hb (0.50 mg/ml) induced VEGF expression and secretion in TF+ malignant cells. VEGF secretion was inhibited by cycloheximide (85%) and the specific inhibitors of protein tyrosine kinase, genistein (71+/-0.74 and 55+/-4.90%) and mitogen-activated protein (MAP)-kinase, PD098059 (82+/-2.0 and 59+/-6.7%) in A375 and J82 cells respectively. In contrast, Hb (2.0 mg/ml) did not increase VEGF in KG1 cells. Hb-induced VEGF was purified from the culture medium of J82 cells using immunoaffinity chromatography and two isoforms (46 and 30 kd) identified. We conclude that Hb-induced synthesis of VEGF in TF-bearing malignant cells is mediated by protein tyrosine kinase and by MAP-kinase pathways.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391545&dopt=Abstract [PubMed - in process]



J Neurosci Res. 2002 Nov 1;70(3):514-8.
Elevated luteinizing hormone expression colocalizes with neurons vulnerable to Alzheimer's disease pathology.

Bowen RL, Smith MA, Harris PL, Kubat Z, Martins RN, Castellani RJ, Perry G, Atwood CS.

Voyager Pharmaceutical Corporation, Raleigh, North Carolina, USA.

In individuals with Alzheimer's disease (AD), there is a two-fold elevation in the serum concentrations of the gonadotropins, luteinizing hormone (LH), and follicle stimulating hormone compared to age-matched controls. Whether this plays a role in disease pathogenesis is unclear. Nonetheless, gonadotropins are known to cross the blood brain barrier and the highest density of gonadotropin receptors in the brain are found within the hippocampus. We report for the first time the localization of LH in the cytoplasm of pyramidal neurons. In addition, we find a significant increase in LH in the cytoplasm of pyramidal neurons and neurofibrillary tangles of AD brain compared to age-matched control brain. Whereas the functional consequences of increased neuronal LH are unknown, it is notable that LH is primarily localized to those neurons that are known to be vulnerable to Alzheimer's disease-related neurodegeneration. Elevated serum and cortical neuron levels of LH, coupled with the decline in sex steroid production, could play important roles in the pathogenesis of AD. 2002 Wiley-Liss, Inc.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391612&dopt=Abstract



Arch Tierernahr. 2002 Jun;56(3):237-44.
Intestinal function and reproductive capacity of Tegel pullets in response to exogenous oestrogen.

Saki AA, Iji PA, Tivey DR.

Department of Animal Science, Bou-Ali Sina University, Hamadan, Iran.

The effects of varying levels of exogenous oestrogen (E2) (0, 10 or 100 micrograms E2/kg BW) on the development of 18-week old pullets were tested over a 28-day period. The hormone had no significant effects on feed intake, body growth, feed conversion ratio or weight of the oviduct. Similarly, there were no significant effects of the hormone on egg production and egg weight but eggshell thickness and weight of shell per unit area were increased (P < 0.05) at a lower level of administration (10 micrograms E2/kg BW), compared to the control and the highest level of hormone. The morphometry of the jejunal mucosa and some enzymes associated with Ca transport were similar between the three groups. Oestrogen treatment, however, intensely enhanced the expression of calbindin D22K, although this was not quantified.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12391908&dopt=Abstract



Exp Physiol. 2002 Jul;87(4):447-52.
Influence of castration on isoprenaline-induced amylase release in parotid gland from male rats.

Busch L, Borda E.

Pharmacology Unit, School of Dentistry, University of Buenos Aires, Argentina. lucilarmaco.odon.uba.ar

The purpose of this study was to determine the influence of testosterone, the male sex hormone, on beta-adrenergic agonist-induced amylase secretion from rat parotid glands. Isoprenaline (isoproterenol)-induced amylase secretion was measured in vitro from the parotid glands of control and castrated rats with and without testosterone replacement. The isoprenaline-induced amylase release was reduced in parotid glands from castrated rats compared to controls. The reduction of amylase release by isoprenaline in parotid glands of castrated rats, could be reversed by administration of testosterone. Furthermore, beta-adrenergic receptor density and the level of isoprenaline-evoked cAMP in parotid glands from castrated rats was lower compared to intact rats. Using SQ-22536 (an adenylyl cyclase inhibitor), dibutyryl cAMP (a cAMP analogue) and verapamil (a calcium channel blocker), we conclude that the impairment of amylase release from parotid glands after castration was not related to either adenylyl cyclase activity or cAMP accumulation. Amylase release from the parotid glands of castrated rats appears to be mediated by an increase in calcium ion influx.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12392108&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.














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