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J Periodontal Res. 2002 Jun;37(3):192-5.
Morphological evaluation of combined effects of cyclosporin and nifedipine on gingival overgrowth in rats.
Spoildorio LC, Spolidorio DM, Neves KA, Gonzaga HF, Almeida OP.
Department of Oral Pathology, Dental School, Araraquara, University of the State of Sao Paulo, Brazil. lcoar.unesp.br
It has previously been shown that, while cyclosporin A (CsA) and nifedipine both cause gingival overgrowth in the rat, the combined use of these drugs increases the severity of overgrowth. The aim of this study was to describe the histometry and densities of fibroblasts, collagen fibers and vessels in the gingival tissue of rats that were treated with CsA and nifedipine, either alone or in combination. Rats were treated for 60 days with a daily subcutaneous injection of 10 mg/kg body weight of CsA and/or with 50 mg/kg body weight of nifedipine added to the chow. The results confirmed that CsA causes a more severe overgrowth than nifedipine, and that the combined use of these drugs increases the overgrowth severity. All the rat groups that were studied showed that, as the severity of overgrowth increased, there was a parallel increase in fibroblasts and collagen, and a decrease in vessel content. Therefore, independently of whether the gingival overgrowth was caused by CsA alone, nifedipine alone, or both treatments in combination, the fibroblast and collagen density increased in parallel with the severity of the overgrowth.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12113553&dopt=Abstract
J Nephrol. 2002 May-Jun;15(3):320-3.
Hereditary nephritis with macrothrombocytopenia: phenotypic variety and the genotypic defect.
Basile C, Schiavone P, Heidet L, Grunfeld JP.
Division of Nephrology, Hospital of Martina Franca, Italy. nefromartinopvideo.net
A number of patients present to nephrologists with end-stage renal failure of unknown cause and many have small kidneys, making renal biopsy inadvisable. A small number may have clues to the diagnosis of hereditary nephritis, as in the patient we present here. The propositus was a 22-year-old man, who was admitted to our nephrology ward because of recently discovered renal insufficiency. Ultrasound examination revealed bilateral small kidneys. He was severely hypertensive; audiometry and ophthalmic examinations were normal. Thrombocytopenia with giant platelets was observed in peripheral blood smears. Basophilic cytoplasmic inclusions (Dohle-like bodies) were present in neutrophil and basophilic granulocytes. A family history of nephropathy associated with macrothrombocytopenia was obtained. Epstein syndrome was diagnosed, a rare autosomal dominant disorder. He started hemodialysis and subsequently received a living donor kidney transplant (from his mother). Molecular genetics has considerably clarified the field of hereditary nephritis associated with macrothrombocytopenia by demonstrating that these syndromes involve a similar molecular defect. It was first shown that these syndromes were linked to the same locus on chromosome 22q. Then the gene involved--encoding non-muscle myosin heavy chain 9 (MYH9)--was identified. This entity ("MYH9 disease") must be clearly differentiated from Alport syndrome (type IV collagen disease). In conclusion, this case serves to remind us: 1) that in patients presenting late to nephrologists with bilateral small kidneys, the diagnosis can still be made in some instances on the basis of other clinical signs known to be associated with recognized inherited syndromes; 2) that there are various types of inherited thrombocytopenia associated with nephritis; screening for nephritis is mandatory in all of them.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12113606&dopt=Abstract
Zhonghua Gan Zang Bing Za Zhi. 2002 Jun;10(3):200-3.
[Effects of genistein on the fenestrae, proliferation and nitric oxide synthesis of liver sinusoidal endothelial cells from carbon tetrachloride-induced experimental hepatic fibrosis rats]
[Article in Chinese]
Liu X, Huang M, Cheng N, Xiao W, Wang Y.
Lab of Department of Internal Medicine, West China Hospital, Sichuan University, Chengdu 610041, China.
OBJECTIVE: To investigate the effects of genistein, a tyrosine protein kinase inhibitor, on the fenestrae, proliferation and nitric oxide (NO) synthesis of the liver sinusoidal endothelial cells from CCl(4)-induced hepatic fibrosis rats in vitro. METHODS: By in situ collagenase perfusion and two-step percoll gradient centrifugation, SECs were isolated and cultured from normal and CCl(4)-treated Wistar rats. The fenestrae of SECs were observed by the scanning electron microscopy, and the SECs cell proliferation was determined by the MTT assay. The concentrations of NO in the cultured medium of SECs were detected indirectly by measurement of nitrates and nitrites (the stable products of NO) using the nitrate reduction method. RESULTS: Scanning electron microscopic studies revealed that the number of fenestrae in SECs from all stage of hepatic fibrotic rats was decreased markedly as compared with the SECs from normal controls; however, no obvious changes in the fenestrae of SECs were observed after treated with genistein (100 mumol/L) for 24 hours. After treated with 100 mumol/L genistein for 24 hours, the cell proliferation rates of SECs from all stages of hepatic fibrosis were decreased significantly was compared with the control group (P<0.05). The synthesis of NO by SECs from all stages of hepatic fibrosis was markedly lower than those of normal controls. Treatment with 100 mumol/L genistein for 24 hours could increase the synthesis of NO by SECs from the early stage (stage I) of fibrosis; however, this effect of genistein was not observed in SECs from stage II or III of fibrosis at this concentration. CONCLUSIONS: The results suggest that genistein may play an important role in regulating the function of SECs.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12113679&dopt=Abstract
Zhonghua Gan Zang Bing Za Zhi. 2002 Jun;10(3):204-6.
[Luteolin inhibits proliferation and collagen synthesis of hepatic stellate cells]
[Article in Chinese]
Zhao W, Liang C, Chen Z, Pang R, Zhao B, Chen Z.
Medical Laboratory of KUNMING General Hospital, Chengdu Military Command, KUNMING 650032, China.
OBJECTIVE: To investigate the effect of luteolin on the proliferation and collagen expression of hepatic stellate cells. METHODS: The effect of luteolin on proliferation and collagen synthesis of hepatic stellate cells isolated from the liver of Wistar rats were determined by (3)H-TdR and (3)H-Pro, and procollagen gene expression was also detected by DIG-labeled gene probe and in situ hybridization. RESULTS: The proliferation and collagen synthesis were significantly and dose-dependently inhibited by luteolin when the concentrations reached 10 micromol/L and 20 micromol/L respectively (t=2.542, P<0.05; t=3.650, P<0.01). The type I, III procollagen mRNA expression was decreased by 25 micromol/L luteolin, in which the type I procollagen mRNA was reduced with statistical significance (x(2)=6.850, P<0.01). CONCLUSIONS: Luteolin inhibits the proliferation and collagen expression of hepatic stellate cells in vitro. It may have a preventive or therapeutic role in liver fibrosis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12113680&dopt=Abstract
Lancet. 2002 Jul 6;360(9326):57-8.
Adiponectin and development of type 2 diabetes in the Pima Indian population.
Lindsay RS, Funahashi T, Hanson RL, Matsuzawa Y, Tanaka S, Tataranni PA, Knowler WC, Krakoff J.
National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 1550 East Indian School Road, Phoenix, AZ 85014, USA. rlindsaail.nih.gov
Adiponectin is a collagen-like circulating protein secreted by adipocytes that is proposed to mediate obesity-related resistance to insulin. In a case-control series, we assessed the role of adiponectin in later development of type 2 diabetes in 70 patients who later developed type 2 diabetes and 70 controls, matched for body-mass index, age, and sex. Cases and controls were taken from the longitudinal study of health in the Pima Indian population. At baseline, the concentration of adiponectin was lower in cases than in controls (p=0.01) and individuals with high concentrations of this protein were less likely to develop type 2 diabetes than those with low concentrations (incidence rate ratio 0.63 [95% CI 0.43-0.92]; p=0.02).
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12114044&dopt=Abstract
The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes
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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