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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

Reproduction. 2003 Jul;126(1):121-31.
Phospholipase C and protein kinase C involvement in mouse embryonic stem-cell proliferation and apoptosis.

Quinlan LR, Faherty S, Kane MT.

Department of Physiology, National University of Ireland, University Road, Galway, Ireland.

Activation of the phosphatidylinositol (PtdIns) signal transduction system involves stimulation of phospholipase C (PLC) by hormones and other agonists to produce two second messengers, the inositol phosphate, Ins(1,4,5)P3 which releases calcium from intracellular stores, and diacylglycerol which activates protein kinase C (PKC). This study, using activators or inhibitors of PLC and PKC and a calcium ionophore, examined the role of the PtdIns system in mouse embryonic stem (ES) cells. The PLC inhibitor, U-73122, inhibited ES-cell proliferation and also inhibited PLC activation as evidenced by a decrease in inositol phosphate formation in response to fetal calf serum stimulation. The two PKC activators, the diacylglycerol analogue 1,2, dioctanoyl-sn-glycerol (DOG) and the phorbol ester 12-O-tetra-decanoyl phorbol 13-acetate (TPA), increased cell proliferation in a dose-dependent manner, as did the calcium ionophore, ionomycin. However, co-stimulation with either ionomycin and DOG or ionomycin and TPA resulted in a reduced number of cells. The PKC inhibitor, bisindolylmaleimide II (Bis II), significantly decreased the number of ES cells, mainly due to increased apoptosis. The possible feedback effect of PKC on PLC was examined by preincubating ES cells with either the PKC inhibitor Bis II or the activator TPA before stimulation of inositol phosphate production with fetal calf serum; preincubation with Bis II increased inositol phosphate formation whereas preincubation with TPA decreased inositol formation. These results indicate that the PtdIns system is involved in the control of ES-cell proliferation and apoptosis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12814354&dopt=Abstract [PubMed - in process]

Am J Transplant. 2003 Jul;3(7):873-7.
Post transplant erythrocytosis in hypercalcemic renal transplant recipients.

Kurella M, Butterly DW, Smith SR.

Department of Medicine, Division of Nephrology, University of California San Francisco, San Francisco, CA, USA.

In vitro data suggest that calcium plays an important role in normal and disordered erythropoiesis. The purpose of this study is to determine whether there is an association between serum calcium, various hormone levels, and the development of post transplant erythrocytosis (PTE). Data were collected on 283 patients who underwent renal transplantation between 1994 and 1998. The relationship between serum calcium and PTE development was tested using the chi-square test. Univariate and multivariable adjusted models were employed to determine predictors of maximum hematocrit. Selected patients underwent measurement of intact parathyroid hormone (PTH), 1,25-dihydroxy vitamin D, and erythropoietin (EPO). Seventy-three patients (26%) developed PTE. Post transplant erythrocytosis was more common in patients with hypercalcemia compared with patients with normal serum calcium (34% vs. 18%, p = 0.002). In multivariable analyses, serum calcium was a strong independent predictor of maximum hematocrit post transplant, even after adjustment for renal function. A serum calcium of >or=10.2 mg/dL was associated with greater than two-fold increased odds of PTE. There were no differences in hormone levels between subjects with hypercalcemia and PTE, subjects with PTE alone, and subjects with hypercalcemia alone. Hypercalcemia is associated with the development of PTE in renal transplant recipients.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12814479&dopt=Abstract [PubMed - in process]

Anal Biochem. 2003 Jul 15;318(2):260-9.
Reconstituted 3-dimensional human skin of various ethnic origins as an in vitro model for studies of pigmentation.

Yoon TJ, Lei TC, Yamaguchi Y, Batzer J, Wolber R, Hearing VJ.

Pigment Cell Biology Section, Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

Reconstituted 3-dimensional human skin equivalents containing melanocytes and keratinocytes on an artificial dermal substitute are gaining popularity for studies of skin metabolism because they exhibit morphological and growth characteristics similar to human epidermis. In this study, we show that such a pigmented epidermis model can be used to assess the regulation of pigmentation by known melanogenic compounds. In monolayers or in melanocyte-keratinocyte co-cultures, melanocyte-keratinocyte interactions are missing or are spatially limited. The commercial skin equivalents used in this study were derived from epidermal cells obtained from donors of three different ethnic origins (African- American, Asian, and Caucasian), and they reflect those distinct skin phenotypes. We used these pigmented human epidermis models to test compounds for potential effects on pigmentation in a more physiologically relevant context, which allows further characterization and validation of interesting melanogenic factors. We used known melanogenic stimulators (alpha-melanocyte-stimulating hormone and 3,4-dihydroxyphenylalanine) and inhibitors (hydroquinone, arbutin, kojic acid, and niacinamide) and examined their effects on the production of melanin and its distribution in upper layers of the skin. Our studies indicate that commercial skin equivalents provide a convenient and cost-effective alternative to animal testing for evaluating the regulation of mammalian pigmentation by melanogenic factors and for elucidating their mechanisms of action.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12814630&dopt=Abstract [PubMed - in process]

Hum Mutat. 1998;11(4):333-4.
Polymorphisms in the coding exons of the human luteinizing hormone receptor gene. Mutations in brief no. 124. Online.

Wu SM, Jose M, Hallermeier K, Rennert OM, Chan WY.

Department of Pediatrics, Georgetown University Medical Center, Washington, DC., USA.

Four polymorphisms were identified in the coding exons of the human luteinizing hormone/chorionic gonadotropin receptor (hLHR) gene. A CTGCAG insertion occurred after nucleotide 54 in 8 of 34 independent chromosomes examined. The heterozygosity frequency was 0.353. This Leu-Gln dipeptide insertion in the first Leucine repeat of the hLHR extracellular domain did not affect the ligand binding affinity of the receptor. Among the 54 chromosomes analyzed, 64.8% was A and 35.2% was G at nucleotide 872 in exon 10. The heterozygosity frequency was 0.115. The A/G substitution led to the replacement of Asn by Ser in the G allele and the abolition of a potential N-glycosylation site. Another polymorphism occurred at nucleotide 935. Fifty nine percent of chromosomes examined were A and 41% were G at this site with the encoded amino acid being Ser in the former and Asn in the latter. The heterozygosity frequency was 0.192. This polymorphism did not have biological consequence. Both of the exon 10 polymorphisms showed ethnic prevalence with the 872 G allele and 935 A allele predominantly in non-Caucasians. The fourth polymorphism was neutral and occurred at nucleotide 1065 in exon 11, with C in 60% and T in 40% of the 50 chromosomes examined. These polymorphisms are useful for tracking the inheritance of specific hLHR allele.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10215412&dopt=Abstract

Eur Urol. 2003 Jul;44(1):150-4.
Polymorphisms in the vitamin D receptor gene and the risk of calcium nephrolithiasis in children.

Ozkaya O, Soylemezoglu O, Misirlioglu M, Gonen S, Buyan N, Hasanoglu E.

Department of Pediatric Nephrology, Gazi University School of Medicine, Ankara, Turkey. ozanozkayahoo.com

OBJECTIVE: Polymorphism in the Vitamin D Receptor (VDR) gene has recently been reported to be associated with calcium metabolism disorders. This study was conducted to investigate the association of VDR gene polymorphism with the risk of calcium nephrolithiasis. METHODS: We investigated the VDR ApaI, BsmI and TaqI polymorphisms, in relation to serum calcium, phosphate, intact parathyroid hormone and 1.25(OH)(2)D(3) in 64 hypercalciuric stone-forming children and 90 healthy children. DNA was isolated from peripheral blood, and genotyping was performed with PCR-based methods. RESULTS: The frequency of ApaI AA genotype was significantly higher in the children with calcium nephrolithiasis than the controls (chi(2)=9.5; p=0.008). The distribution of BsmI and TaqI genotypes in stone-forming patients was similar to those in the control group. There was a significant association between TaqI TT genotype and the strength of the family history. The patients with TT genotype were observed to have a 8 times more risk than patients with Tt/tt genotype for recurrent stone episodes (OR 8, 95%CI 1.61-39.6). CONCLUSION: VDR genotype determination may provide a tool to identify individuals who are at a risk for calcium nephrolithiasis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12814692&dopt=Abstract [PubMed - in process]

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