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J Pharmacol Exp Ther. 2002 Dec;303(3):1255-64.
Stimulated tyrosine phosphorylation of phosphatidylinositol 3-kinase causes acidic pH-induced contraction in spontaneously hypertensive rat aorta.

Rohra DK, Yamakuni T, Furukawa K, Ishii N, Shinkawa T, Isobe T, Ohizumi Y.

Department of Pharmaceutical Molecular Biology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.

Acidic pH induced a contraction (APIC) in isolated aortas from spontaneously hypertensive (SHR) and Wistar Kyoto rats, but failed to produce any response in age-matched Wistar rat aorta. This study was conducted to test the hypothesis that tyrosine phosphorylation of proteins is a molecular mechanism underlying the APIC. Tyrosine kinase inhibitors, genistein and tyrphostin 23 inhibited the APIC in a concentration-dependent manner. APIC was inhibited by phosphatidylinositol 3-kinase (PI3-kinase) inhibitors, LY-294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one hydrochloride] and wortmannin. Consistent with the results from tension measurement experiments, Western blot analysis showed that acidic pH induced an appreciable increment of tyrosine phosphorylation of 85-kDa protein (p85) in SHR aorta, which was completely inhibited by tyrphostin 23, whereas in Wistar rat aorta, the protein tyrosine phosphorylation was not observed. Further investigations using immunoprecipitation followed by Western blotting confirmed an increase in the tyrosine phosphorylation of p85. Analysis by SDS-polyacrylamide gel electrophoresis followed by silver staining of the gel revealed that amounts of multiple proteins with molecular sizes of 120, 130, 210, and 225 kDa were increased at acidic pH, which were immunoprecipitated with anti-phosphotyrosine antibody. Western blotting using a specific anti-PI3-kinase antibody identified the p85 as the regulatory subunit of PI3-kinase, whereas 120-, 130-, and 225-kDa proteins were identified by mass spectrometry as pro-alpha2 (I) collagen, collagen alpha1 (I) chain, and fibernectin I, respectively. As assayed by Western blotting using anti-myosin light chain (MLC) antibody, acidic pH induced a stimulation of MLC phosphorylation, and the stimulated MLC phosphorylation was abolished by tyrphostin 23 and LY-294002. These results suggest that acidic pH induces an increase in tyrosine phosphorylation of PI3-kinase, resulting in the MLC phosphorylation-dependent contraction of SHR aorta.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12438550&dopt=Abstract

Pediatr Res. 2002 Dec;52(6):900-6.
Alterations in adult rat heart after neonatal dexamethasone therapy.

de Vries WB, van der Leij FR, Bakker JM, Kamphuis PJ, van Oosterhout MF, Schipper ME, Smid GB, Bartelds B, van Bel F.

Department of Neonatology, University Medical Center/Wilhelmina Children's Hospital, Utrecht, The Netherlands.

Glucocorticoid treatment in preterm babies to prevent chronic lung disease causes myocardial hypertrophy and increased myocardial protein content. Although these changes are thought to be transient, there is evidence that dexamethasone (DEX) induces permanent myocardial abnormalities as well. We investigated whether a therapeutic course of neonatal DEX in rat pups produces anatomic and biochemical alterations in rat hearts during adult life. Twenty-four rat pups were treated with DEX on d 1, 2, and 3 (0.5, 0.3, and 0.1 micro g/g) of life, with doses proportional to those used in preterm babies. Twenty-four control pups were treated with saline. At d 7, wk 8, or wk 45 (n = 8 per group) rats were killed. The anatomic parameters measured were body weight (Bw, in grams), heart (myocardial) weight (Hw, in milligrams), and the Hw:Bw ratio. Myocardial total protein (Prot) and DNA content were determined, and the Prot:DNA ratio was calculated. Histopathology and morphometry were performed on 45-wk-old rat hearts. In DEX-treated rat pups, at d 7, Bw and Hw were lower and the Hw:Bw ratio was increased. DNA content was lower, Prot higher, and Prot:DNA ratio was increased. In 8-wk-old rats Bw, Hw, DNA content, Prot content or Prot:DNA ratio did not differ between groups, but the Prot:DNA ratio still tended to be higher in DEX-treated rats. In 45-wk-old rats Hw and Hw:Bw ratio were significantly lower and Prot:DNA ratio higher in DEX-treated rats. Histopathologic analysis showed larger cardiomyocyte volume, length, and width, indicating hypertrophy, and increased collagen, indicating early degeneration of individual myocytes. In conclusion, neonatal DEX treatment in rat pups causes a permanent decrease in heart weight, as well as hypertrophy and early degeneration of cardiomyocytes during adulthood.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12438668&dopt=Abstract

Cell Physiol Biochem. 2002;12(5-6):325-34.
Mixed lineage kinase 3 inhibits platelet-derived growth factor-stimulated DNA synthesis and matrix mRNA expression in mesangial cells.

Parameswaran N, Hall CS, Bock BC, Sparks HV, Gallo KA, Spielman WS.

Department of Physiology, Michigan State University, East Lansing 48824, USA. paramessu.edu

Mixed lineage kinase 3 (MLK 3) is a recently described member of the MLK subfamily of Ser/Thr protein kinases that interacts with MAPK pathways. The aim of this study was to test the potential interaction of MLK 3 with signaling pathways stimulated by PDGF in rat mesangial cells. We have established a stable cell line expressing human MLK 3 in rat glomerular mesangial cells. The effects of PDGF on proliferation and matrix mRNA expression were examined. In control (vector-transfected) mesangial cells PDGF increased [(3)H]-thymidine incorporation significantly in a concentration-dependent manner. In mesangial cells expressing MLK 3, PDGF-induced increase in DNA synthesis was significantly reduced. PDGF also induced fibronectin and collagen I mRNA expression in control cells, the effects of which were also significantly blocked in MLK 3-transfected cells. To understand the potential interaction of MLK 3 over expression with the MAPK pathways and to examine the potential mechanism of the effects of MLK 3 over expression on proliferation and matrix expression, activation of ERK2, JNK1 and p38 were examined. ERK2 activation was increased several fold by PDGF in control cells but was attenuated significantly in MLK 3 expressing cells. PDGF did not have any effect on JNK and p38 activation, in either cell types. Using the same stable-transfected cell line, identical results were obtained on proliferation and matrix expression with sarafotoxin-s6b (endothelin receptor agonist) another potent mitogenic and sclerotic agent for mesangial cells. These results indicate an important role for MLK 3 in the regulation of growth and matrix expression in mesangial cells. 2002 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12438768&dopt=Abstract

Blood Coagul Fibrinolysis. 2002 Oct;13(7):627-36.
A study of platelet activation in paroxysmal, persistent and permanent atrial fibrillation.

Kamath S, Chin BS, Blann AD, Lip GY.

Haemostatis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.

We hypothesized that the 'residual' thromboembolic risk in therapeutically anticoagulated patients undergoing cardioversion could potentially be related to abnormal haemorheology and platelet activation. To test this hypothesis, we firstly investigated the role of haemorheology and platelet activation in patients with paroxysmal and persistent atrial fibrillation (AF), who were compared with healthy controls and patients with permanent AF. Second, we compared these indices in patients with persistent AF, before and after successful cardioversion. We measured indices of haemorheology (haematocrit, plasma viscosity, and fibrinogen), fibrin D-dimer (an index of thrombogenesis and fibrin turnover) and platelet activation (as assessed by platelet aggregation and plasma levels of beta-thromboglobulin, and soluble P-selectin) in 29 patients with paroxysmal AF, 87 patients with permanent AF and 29 healthy controls in sinus rhythm. The effects of cardioversion were studied in 20 patients with persistent AF, who maintained sinus rhythm at 2 months follow-up. Plasma levels of beta-thromboglobulin (P = 0.03) and fibrin D-dimer (P = 0.001) were higher in patients with AF, when compared with controls; the highest levels were seen in those with permanent AF (Tukey's test, < 0.05). Plasma viscosity was significantly higher in the patients with paroxysmal AF compared with healthy controls (P = 0.02). Plasma soluble P-selectin levels and platelet aggregation responses to all four platelet agonists (adenosine diphosphate, collagen, epinephrine and thrombin) in patients with paroxysmal AF and permanent AF were similar to controls. Plasma fibrinogen, viscosity and other markers of platelet activation (including platelet aggregation) were not significantly different in patients with paroxysmal AF, during episodes of AF and sinus rhythm (P = not significant), although mean haematocrit was significantly higher during the episodes of AF compared with episodes of sinus rhythm (P = 0.03). Among the patients with persistent AF who remained in sinus rhythm at 2 months following successful cardioversion, there was a significant decrease in the plasma levels of soluble P-selectin at 2 weeks and 2 months, when compared with baseline (pre-cardioversion) levels (P < 0.001). Haemorheology and platelet aggregation response to agonists did not change significantly, except for a transient increase in platelet aggregation response to collagen at 2 weeks (P = 0.045). In conclusion. abnormal haemostatic and platelet activation in patients with permanent AF are not consistently observed in patients with paroxysmal and persistent AF. Abnormal haemorheology appears to play an important role in patients with paroxysmal AF, especially during the paroxysms of AF. Cardioversion of persistent AF to sinus rhythm appears to decrease the platelet activation, but whether this translates into a beneficial reduction in thromboembolic risk requires further study.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12439149&dopt=Abstract [PubMed - in process]

Laryngoscope. 2002 Nov;112(11):2025-32.
Integrins in head and neck squamous cell carcinoma invasion.

Dyce OH, Ziober AF, Weber RS, Miyazaki K, Khariwala SS, Feldman M, Ziober BL.

Department of Otorhinolaryngology, University of Pennsylvania Medical Center, Philadelphia 19104, USA.

OBJECTIVE: To relate the invasive properties of different squamous cell cancer cell lines to the function and expression of the integrins. STUDY DESIGN: A series of in vitro and in vivo experiments were designed to assess and compare integrin expression and function in two different head and neck squamous cell carcinoma cell lines. METHODS: Invasive properties of two squamous cell carcinoma cell lines (UM-SCC-1 and JHU-022-SCC) were assessed using an in vitro artificial matrix assay as well as an in vivo system with orthotopically implanted tumor cells in mice. Whole cell and surface expression levels of integrin subunits (alpha2, alpha3, alpha5, alpha6, beta1, and beta4) were determined for each cell line using Western blot analysis and flow cytometry. We compared the ability of JHU-022-SCC and UM-SCC-1 cells to bind the extracellular matrix elements collagen IV, fibronectin, laminin 5, and laminin10 using an in vitro adhesion assay. Contributions of the different integrins to the adhesive properties were determined by selective antibody blocking of different subunits. RESULTS: The UM-SCC-1 cell line is 50% more invasive in vitro and displays a greater propensity for perineural and lymphatic invasion in vivo. The UM-SCC-1 cells exhibited greater adherence to fibronectin than JHU-022-SCC cells. Alpha6 and beta4 expression is approximately twofold greater in the JHU-022-SCC cells. Alpha2, alpha3, and beta1 expression appears to be upregulated in UM-SCC-1 cells. CONCLUSION: The UM-SCC-1 carcinoma cells are more invasive than JHU-022-SCC cells and may be related to differential expression of the integrins alpha6beta4, alpha3beta1, and alpha2beta1.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12439174&dopt=Abstract

Hair loss is a problem in modern soceity. Examining the factors of hair growth may shed light on how hair loss might occur. How long can hair grow before it stops growing eventually if it does? Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of hair growth as well as The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.

DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.

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