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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







Cancer Causes Control. 2002 May;13(4):299-305.
Transient increase in breast cancer risk after giving birth: postpartum period with the highest risk (Sweden).

Liu Q, Wuu J, Lambe M, Hsieh SF, Ekbom A, Hsieh CC.

Division of Biostatistics and Epidemiology, Cancer Center, University of Massachusetts Medical School, Worcester 01605, USA.

OBJECTIVE: Identify time-points when the elevated postpartum maternal breast cancer risk peaks. METHODS: A case-control study nested within the Swedish Fertility Register included 34,018 breast cancer cases from the Swedish Cancer Register between 1961 and 1995. From the Fertility Register, 170,001 eligible subjects matched to the cases by age were selected as controls. Analysis contrasted risk between uniparous (7084 cases and 31,703 controls) and nulliparous (5411 cases and 22,580 controls) women and between biparous (13,239 cases and 65,858 controls) and uniparous women. Logistic regression analysis included indicator variables representing each year of age, ages at delivery, and time since delivery. RESULTS: Comparing uniparous with nulliparous women the transient increase in maternal breast cancer risk peaked 5 years following delivery (odds ratio= 1.49, 95% confidence interval 1.01-2.20) and leveled off 15 years postpartum. Biparous women had a transient increase in risk that was lower at its peak than that of uniparous women, occurring about 3 years following second delivery. CONCLUSIONS: A time window of 5 years postpartum when maternal breast cancer risk is highest was observed. Establishing timing of peak transient increase in postpartum breast cancer risk may define the latent period required for pregnancy hormones in promoting progression of breast cells that have undergone early stages of malignant transformation.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074499&dopt=Abstract



Cancer Causes Control. 2002 May;13(4):307-16.
Prospective study of IGF-I, IGF-binding proteins, and breast cancer risk, in northern and southern Sweden.

Kaaks R, Lundin E, Rinaldi S, Manjer J, Biessy C, Soderberg S, Lenner P, Janzon L, Riboli E, Berglund G, Hallmans G.

Unit of Nutrition and Cancer, International Agency for Research on Cancer, Lyon, France. kaakarc.fr

OBJECTIVE: To examine the possible relationships of breast cancer risk to prediagnostic plasma levels of insulin; insulin-like growth factor-I (IGF-I); and IGF-binding proteins -1, -2, and -3. METHODS: Within two prospective cohorts in Umea and Malmo we measured plasma concentrations of insulin, IGF-I, and IGFBPs for a total of 513 incident breast cancer cases and 987 matched controls. RESULTS: Globally, risk was unassociated with levels of IGF-I, IGFBP-3, or IGF-I adjusted for IGFBP-3. When breaking down the analysis by subgroups of age at blood donation, an increase in risk was observed for increasing levels of IGF-I in women aged 55 or older, in the Umea cohort only (odds ratios of 1.00, 1.73, 1.76, 1.90; Ptrend = 0.05). This effect weakened, however, when the analysis was restricted to subjects who did not use exogenous hormones for the treatment of menopausal symptoms. Levels of IGF-I and IGFBP-3 were not related to risk in younger women, recruited before age 50, contrary to observations from previous studies. In a subcohort where blood samples had been collected after at least four hours of fasting, breast cancer risk showed no clear associations with levels of insulin, IGFBP-1, or IGFBP-2. CONCLUSIONS: Our results do not confirm earlier findings of an association of plasma IGF-I levels with breast cancer risk especially in young women, but suggest a possible association with postmenopausal breast cancer risk, possibly among ERT/HRT users only. Our results do not support the hypothesis that elevated plasma insulin levels, and reduced levels of IGFBP-I and IGFBP-2, are associated with increased breast cancer risk.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074500&dopt=Abstract



Cancer Causes Control. 2002 May;13(4):353-63.
Lifestyle and nutritional determinants of bioavailable androgens and related hormones in British men.

Allen NE, Appleby PN, Davey GK, Key TJ.

Cancer Research UK Epidemiology Unit, University of Oxford, UK. naomi.alleancer.org.uk

OBJECTIVE: To investigate the lifestyle and nutritional determinants of serum bioavailable androgens and their related hormones in men. METHODS: This study is based on a sample of 696 men with a wide range of nutrient intakes, whose diet and lifestyle characteristics were assessed with a questionnaire and serum sex hormones measured using immunoassays. RESULTS: Men aged 70 years or older had 12% lower testosterone and 40% lower free-testosterone (FT) and androstanediol glucuronide (A-diol-g) concentrations than men who were 20-29 years of age. Conversely, sex hormone-binding globulin (SHBG) and luteinizing hormone (LH) concentrations were 90% and 49% higher in the oldest age group compared with the lowest, respectively. Men who had a body mass index (BMI) of 30+ kg/m2 had 30% lower testosterone, 45% lower SHBG, 22% lower LH and 5% lower FT concentrations compared with men with a BMI of <20 kg/m2. Conversely, A-diol-g concentration was 15% higher in the highest BMI category compared with the lowest. A high waist circumference was further associated with a 12% lower testosterone and SHBG concentration, after adjusting for BMI. Compared with never-smokers, smoking 10+ cigarettes/day was associated with 15% higher testosterone, 22% higher SHBG and 17% higher LH concentrations; FT and A-diol-g were not associated with smoking. Compared with no exercise, vigorous exercise of 3+ hours/week was associated with 11% higher testosterone and 16% higher SHBG concentrations, whilst LH, FT, and A-diol-g were not associated with vigorous exercise. Dietary factors were not strongly associated with hormones, although saturated fat intake was negatively associated with SHBG (r = -0.10; p = 0.01) and alcohol intake was positively associated with A-diol-g (r = 0.11; p = 0.004). No dietary factors were associated with testosterone, FT, or LH. CONCLUSIONS: Age is the strongest determinant of serum bioavailable androgens. BMI and some lifestyle and dietary factors influence SHBG and testosterone concentrations, but have no strong association with FT, suggesting that homeostasis is effective. A-diol-g shows broadly similar associations to FT, with the exception of the effect of BMI and alcohol.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074505&dopt=Abstract



Dev Biol. 2002 Jul 1;247(1):137-48.
Distinct patterns of downstream target activation are specified by the helix-loop-helix domain of proneural basic helix-loop-helix transcription factors.

Talikka M, Perez SE, Zimmerman K.

Laboratory of Developmental Neurobiology, The Rockefeller University, 1230 York Avenue, New York, New York 10021, USA.

Both gain- and loss-of-function analyses indicate that proneural basic/helix-loop-helix (bHLH) proteins direct not only general aspects of neuronal differentiation but also specific aspects of neuronal identity within neural progenitors. In order to better understand the function of this family of transcription factors, we have used hormone-inducible fusion constructs to assay temporal patterns of downstream target regulation in response to proneural bHLH overexpression. In these studies, we have compared two distantly related Xenopus proneural bHLH genes, Xash1 and XNgnr1. Our findings indicate that both Xash1 and XNgnr1 induce expression of the general neuronal differentiation marker, N-tubulin, with a similar time course in animal cap progenitor populations. In contrast, these genes each induce distinct patterns of early downstream target expression. Both genes induce expression of the HLH-containing gene, Xcoe2, at early time points, but only XNgnr1 induces early expression of the bHLH genes, Xath3 and XNeuroD. Structure:function analyses indicate that the distinct pattern of XNgnr1-induced downstream target activation is linked to the XNgnr1 HLH domain, demonstrating a novel role for this domain in mediating the differential function of individual members of the proneural bHLH gene family. (c) 2002 Elsevier Science (USA).


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074558&dopt=Abstract



Eur Urol. 2002 Jun;41(6):655-9.
Bone mineral content and related biochemical variables in patients with ileal bladder substitution and colonic Indiana pouch.

Sevin G, Kosar A, Perk H, Serel TA, Gurbuz G.

Department of Urology, Medical School, University of Suleyman Demirel, PK 37, Isparta, Turkey.

OBJECTIVES: To evaluate the effects of ileal bladder substitution or colonic Indiana pouch on skeletal bone density and various biochemical parameters related to bone metabolism. PATIENTS AND METHODS: In 27 patients with urinary diversion and 14 controls with benign urologic disease, bone mineral density (BMD), assessed by dual-photon absorptiometry; serum electrolyte, creatinine, alkaline phosphatase and parathyroid hormone levels were determined, and capillary blood gas analysed. BMD was measured in the lumbar spine and the femur neck. The mean time since surgery was 33.6+/-10.1 months in 17 patients with an ileal bladder substitution and 56+/-9.1 months in 10 patients with a colonic Indiana pouch (p=0.001). RESULTS: Although BMD did not change in the colonic Indiana pouch group, it was reduced in the patients with ileal bladder substitution compared to control group. The mean pH value was not statistically significant different in the both groups from the control group (p>0.2).The mean base excess value reduced in the substitution group (p<0.01). While alkaline phosphatase levels increased in both groups compared to control group (p<0.05), the mean parathyroid hormone level decreased only in the patients with ileal bladder substitution (p<0.05). The other biochemical parameters were similar in patients and control subjects. There was a statistically significant correlation between the base excess values and BMD values of the patients in both groups. CONCLUSION: Although there is decreased BMD in patients with an ileal bladder substitute, there is no change in BMD in the patients with Indiana pouch. Alkaline phosphatase levels increased in both patient groups indicating increased bone turnover.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12074784&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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