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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

Prostate. 2002 Sep 15;53(1):1-8.
Androgens block interleukin-1 beta-induced promatrilysin expression in prostate carcinoma cells.

Stratton MS, Greenstein B, Udayakumar TS, Nagle RB, Bowden GT.

Department of Radiation Oncology, Arizona Cancer Center, Tucson, Arizona 85724, USA.

BACKGROUND: We have shown previously that interleukin (IL) -1 beta- and IL-6-induced promatrilysin expression is mediated by an indirect pathway that requires NF kappa B-dependent synthesis of IL-6 and STAT3 signaling. We now demonstrate that IL-1 beta-induced but not IL-6-induced promatrilysin expression can be blocked by androgens in the prostate carcinoma cell line LNCaP (lymph node-derived carcinoma cells of the prostate). METHODS: By using enzyme-linked immunosorbent assay analyses, promatrilysin was measured in LNCaP cells stimulated with IL-1 beta or IL-6 LNCaP-treated cells pretreated with testosterone. In addition, promatrilysin message was measured by using Northern analyses after IL-6-treated cells pretreated with testosterone. RESULTS: In LNCaP treated with testosterone before IL-1 beta stimulation induced promatrilysin expression was completely abrogated. Furthermore, testosterone completely abrogated NF kappa B transactivation activity and induction of IL-6 protein expression and mRNA. Testosterone and 5 alpha-dihydrotestosterone did not have an inhibitory effect on IL-6-induced promatrilysin expression. Testosterone also had no effect on basal promatrilysin expression or basal NF kappa B transactivation activity. CONCLUSION: From these data, we conclude that testosterone blocks IL-1 beta-induced promatrilysin expression by inhibition of NF kappa B transactivation activity, which in turn, blocks IL-6 expression. These data suggest a mechanism in vivo by which invasive and metastatic prostatic carcinoma cell clones refractory to hormone ablation therapy may develop after chemical or surgical castration. Furthermore, these data suggest that, perhaps, upstream targets such as the cytokines IL-1 beta and IL-6 may provide alternative drug targets for inhibiting prostate cancer progression. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12210475&dopt=Abstract

Prostate. 2002 Sep 15;53(1):60-4.
Loss of heterozygosity at 7q31.1 and 12p13-12 in advanced prostate cancer.

Kawana Y, Ichikawa T, Suzuki H, Ueda T, Komiya A, Ichikawa Y, Furuya Y, Akakura K, Igarashi T, Ito H.

Department of Urology, Graduate School of Medicine, Chiba University, Chiba, Japan.

BACKGROUND: Allelic losses on chromosome arms 2q, 3p, 5q, 6q, 7q, 8p, 9p, 10p, 10q, 11p, 11q, 12p, 13q, 16q, 17p, 17q, 18q, and 21q are reportedly associated with progression and/or initiation of prostate cancer. In the present study, we performed a polymerase chain reaction (PCR) analysis of polymorphic microsatellite loci on the human chromosomes 7 and 12p13-12 in prostate cancer tissue to investigate the extent of involvement of these regions, which may contain putative tumor suppressor genes. METHODS: Tissue samples were obtained at autopsy from 17 men who died of hormone-refractory prostate cancer at Chiba University, Japan, and affiliated hospitals between June of 1992 and June of 1995. DNA from normal tumor or metastatic tissue was used as the template for PCR amplification of a set of 16 polymorphic microsatellite loci on human chromosome 7 and 6 loci on the human chromosome region 12p13-12. RESULTS: The frequencies of cases with loss of heterozygosity (LOH) at 7q31.1 were 8% in primary tumor tissue and 11% in metastatic tissue. The frequencies of cases with LOH at 12p13-12 were 12% in primary tumor tissue and 25% in metastatic tumor tissue. CONCLUSIONS: In the present study, the frequencies of LOH at 7q31.1 were lower than in Western patients, suggesting that LOH in this region is not related to progression of prostate cancer in Japanese patients. The frequency of LOH at 12p13-12 was similar to that reported in Western countries, indicating that 12p13-12 may contain a tumor suppressor gene of prostate cancer. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12210480&dopt=Abstract

Prostate. 2002 Sep 1;52(4):319-29.
Resveratrol induces apoptosis in LNCaP cells and requires hydroxyl groups to decrease viability in LNCaP and DU 145 cells.

Morris GZ, Williams RL, Elliott MS, Beebe SJ.

Department of Chemistry and Biochemistry, Old Dominion University, Norfolk, Virginia, USA.

BACKGROUND: This study was conducted to determine the effects of resveratrol on prostate cancer cell viability through apoptosis induction and the significance of the three hydroxyl groups on resveratrol to the measured effect. METHODS: Hormone-sensitive LNCaP cells and hormone-insensitive DU 145 cells were treated with resveratrol, tri-methoxy-resveratrol, or diethylstilbestrol (DES; the positive control for toxicity and apoptosis). Cell viability was determined by using an MTS assay. Apoptosis was determined by the appearance of apoptotic morphology, annexin V-FITC-positive intact cells, and caspase activation. RESULTS: Resveratrol and DES decreased viability in LNCaP cells, but only resveratrol-treated cells expressed apoptotic morphology, annexin V-FITC-positive cells, and caspase activation. Tri-methoxy-resveratrol had no effect on DU 145 cell-viability and was less toxic to LNCaP cells than resveratrol. CONCLUSION: Resveratrol was toxic to cells regardless of whether the cells were hormone-responsive or -unresponsive. This finding suggests that the cell's hormone responsive status is not an important determinant of the response to resveratrol. Furthermore, the hydroxyl-groups on resveratrol are required for cell toxicity. Finally resveratrol but not DES induced caspase-mediated apoptosis. 2002 Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12210493&dopt=Abstract

Stat Med. 2002 Aug 30;21(16):2331-44.
Periodograms and pulse detection methods for pulsatile hormone data.

Grambsch P, Meller WH, Grambsch PV.

Division of Biostatistics, University of Minnesota, Minneapolis, MN 55455, USA. paiostat.umn.edu

Pulse detection algorithms and spectral analysis are the two most common methods for analysing pulsatile hormone data. We compared a popular high quality pulse detection algorithm (CLUSTER) to spectral analysis on a data set comparing luteinizing hormone data in depressed and control women. For these data, periodogram analysis methods, in particular Fisher's periodicity test, were superior in distinguishing the groups. Extending the pulse detection method to include measures of intra-individual variability improved its discriminatory performance. The two methods complement each other. 2002 John Wiley & Sons, Ltd.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12210618&dopt=Abstract

J Cell Biochem. 2002;86(4):678-87.
Characterization of a 1,25(OH)2-vitamin D3-responsive capacitative Ca2+ entry pathway in rat osteoblast-like cells.

Baldi C, Vazquez G, Boland R.

Departamento de Biologia, Bioquimica y Farmacia, Universidad Nacional del Sur, San Juan 670, (8000) Bahia Blanca, Argentina.

We investigated the existence of a capacitative Ca2+ entry (CCE) pathway in ROS 17/2.8 osteoblast-like cells and its responsiveness to 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3]. Depletion of inner Ca2+ stores with thapsigargin or 1,25(OH)2D3 in the absence of extracellular Ca2+ transiently elevated cytosolic Ca2+ ([Ca2+]i); after recovery of basal values, Ca2+ re-addition to the medium markedly increased Ca2+ entry, reflecting pre-activation of a CCE pathway. Recovery of the Ca2+ overshoot that followed the induced CCE was mainly mediated by the plasma membrane Ca2+-ATPase. Addition of 1,25(OH)2D3 to the declining phase of the thapsigargin-induced CCE did not modify further [Ca2+]i, indicating that steroid activation of CCE was dependent on store depletion. Pre-treatment with 1 microM Gd3+ inhibited 30% both thapsigargin- and 1,25(OH)2D3-stimulated CCE, whereas 2.5 microM Gd3+ was required for maximal inhibition ( approximately 85%). The activated CCE was permeable to both Mn2+ and Sr2+. Mn2+ entry sensitivity to Gd3+ was the same as that of the CCE. However, 1-microM Gd3+ completely prevented capacitative Sr2+ influx, whereas subsequent Ca2+ re-addition was reduced only 30%. These results suggest that in ROS 17/2.8 cells CCE induced by thapsigargin or 1,25(OH)2D3 is contributed by at least two cation entry pathways: a Ca2+/Mn2+ permeable route insensitive to very low micromolar (1 microM) Gd3+ accounting for most of the CCE and a minor Ca2+/Sr2+/Mn2+ permeable route highly sensitive to 1 microM Gd3+. The Ca2+-mobilizing agonist ATP also stimulated CCE resembling the Ca2+/Sr2+/Mn2+ permeable entry activated by 1,25(OH)2D3. The data demonstrates for the first time, the presence of a hormone-responsive CCE pathway in an osteoblast cell model, raising the possibility that it could be an alternative Ca2+ influx route through which osteotropic agents influence osteoblast Ca2+ homeostasis. Wiley-Liss, Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12210734&dopt=Abstract

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Hair Loss, or alopecia is a concern for increasing number of folks in aging society. Loss of hair is a visible problem, and affects the appearance and changes identity of a person.
The phenomenon of hair thinning and hair loss is most commonly associated with natural aging, although there are many other causes of hair loss, which include inherited or genetic conditions, illnesses, malnutrition, stress, hormonal problems, chemotherapy, and use of some drugs.
Hair growth is a sophisticated biological process, which has not yet been completely understood. A multitude of therapeutic measures, including drugs, surgery, and suppelements have been made available, and used. However, due to the heterogeneity in the underlying cause, there is no perfect cure for all hair loss cases. Most of chemical drugs and hair transplantation surgeries are not free from varying degrees of undesirable side effects on health.

Hair Million is an alternative solution to hair loss problems. Anecdotally, it shows prositive results and improvement for age-related hair thinning and hair loss for a fraction of people who take it. We do not know the mechanisms of action as to how Hair Million works to help stop hair loss, and promote hair growth. We only know by anecdotal observations. There has been no clinical trials nor placebo controlled statistical analysis on the efficacy of Hair Million on hair loss and hair growth. However, there are two merits in this hair restoration herbal formula:
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