What are the sciences of relationship-centered primary care

Steroidogenic acute regulatory protein (StAR), a 30-kDa protein involved in the transport of cholesterol to inner mitochondrial membrane during stimulation of steroid hormone biosynthesis, has recently been cloned from human adrenals and MA-10 mouse Leydig tumor cells. We examined the regulation of StAR mRNA accumulation upon induction of steroidogenesis in immortalized rat granulosa cells. Granulosa cells were transfected with SV40 DNA alone (POGS5); with SV40 DNA and Ha-ras oncogene (POGRS1); with SV40 DNA, Ha-ras oncogene and LH/CG receptor (GLHR15) or with FSH receptor (GFSHR17) or with the beta 2-adrenergic receptor (G beta 2AR13) expression plasmids. Cells were cultured to confluency and then stimulated for 24 h with oFSH (4 nM), hCG (2.4 nM), isoproterenol (10 microM) or forskolin (50 microM). By quantitative RT-PCR, StAR mRNA was undetectable in non-steroidogenic cells (transfected with SV40 DNA alone, POGS5) either in the presence or in the absence of forskolin. In contrast, variable amount of the message was detected in all steroidogenic cell lines cotransfected with SV40 DNA and Ha-ras. Moreover, an increase in the StAR mRNA expression was evident in all steroidogenic cells upon stimulation with their respective agonists, concomitantly with enhanced progesterone production. The RT-PCR product was sequenced and the 379 base pairs of rat StAR were found to be 93% and 86% identical to mouse and human cDNA, respectively. The deduced 126 amino acid sequence was 95%, 88% and 88% identical to the mouse, human and bovine deduced protein sequences. We conclude that StAR message is expressed only in the steroidogenic rat granulosa cells and can be upregulated by FSH, hCG, isoproterenol and forskolin in the appropriate cell lines. In addition, we find that the rat StAR cDNA exhibit a high degree of homology with the mouse and human sequences.     

Simvastatin suppresses glomerular cell proliferation and macrophage infiltration in rats with mesangial proliferative nephritis

Inhibition of 3-hydro-3-methylglutaryl coenzyme A reductase inhibits the production of mevalonate and has been shown to suppress proliferation in many cell types. Therefore, 3-hydro-3-methylglutaryl coenzyme A reductase inhibitors may have a beneficial effect in glomerular disease, because glomerular cell proliferation is a central feature in the active glomerular injury. This study examines the effect of simvastatin on glomerular pathology in a rat mesangial proliferative glomerulonephritis (GN) induced by anti-thymocyte antibody (anti-Thy 1.1 GN). There was no difference in the degree of the antibody and complement-mediated initial injuries between simvastatin-treated and control GN rats. The most pronounced feature of simvastatin-treated GN was the suppression of the early glomerular cell proliferation. The proliferative activity was maximal at day 4 after disease induction (26.5+/-7.0 of proliferating cell nuclear antigen-positive cells/glomerulus); however, approximately 70% of proliferation was suppressed by simvastatin treatment. At day 4 after disease induction, simvastatin administration also decreased alpha-smooth muscle actin expression in the glomerulus, which is a marker for mesangial cell activation. Inhibition of monocyte/macrophage recruitment into glomeruli by simvastatin was also a prominent feature. There was a 30% decrease in the number of glomerular ED-1+ cells by simvastatin treatment at day 2 after disease induction. Furthermore, simvastatin remarkably suppressed subsequent mesangial matrix expansion and type IV collagen accumulation in glomeruli. We also found that the platelet-derived growth factor expression was reduced in simvastatin-treated nephritic rats, which might simply reflect the reduction in mesangial cell proliferation and mesangial cellularity. There was no significant difference in plasma cholesterol or triglyceride levels between simvastatin- and vehicle-treated nephritic rats at day 2 and day 4, which corresponded to the times when simvastatin treatment resulted in a reduction in mesangial cell proliferation. In conclusion, this is the first report to find that mesangial cell proliferation and matrix expansion have been blocked by simvastatin in vivo. The protective effect of simvastatin in the matrix expansion in anti-Thy1.1 GN was partly by inhibition of mesangial cell proliferation and monocyte/ macrophage recruitment into glomeruli, which were independent of a change in circulating lipids.     

Application of ultrasound method for hemorrhagic digestive disease]

Ultrasonography for the digestive diseases are consisted of abdominal ultrasonography (US), endoscopic ultrasonography (EUS) and color Doppler endoscopic ultrasonography (CDEUS). These play a supplementary role in comparison with the roentgenography and endoscopy. The information of the ultrasonography is different from these examinations. By US the collateral shunts of esophago-gastric varices are observed. EUS is useful for diagnosis of the properties of esophago-gastric varices and judgement of effects of treatment for these varices, gastric ulcer and vessels in ulcer base and hemorrhagic bowel diseases. CDEUS can show blood streams of esophago-gastric varices and hemorrhagic ulcer.     

High speed data collection system for magnetic field imaging by CTtechnique

A method of high-speed data collection used in imaging the magnetic-field distribution leaking from magnetic devices along any plane is proposed. The method uses the computed tomography (CT) technique. A high-speed data collection system developed for demonstrating the method is described. An image of the magnetic field is reconstructed from projection data provided by the voltage induced in the sensors of a line conductor and a rectangular coil moving in the plane of observation. Rotational scanning of the sensors is used for collecting the projections so that data-acquisition time can be reduced. To demonstrate the performance of the system, the reconstructed images of the magnetic-field distributions made by some permanent magnets are shown     

Direct conversion mechanism of fluorine-GIC into poly(carbon monofluoride), (CF)n

The reaction mechanisms of a stage-1 fluorine-graphite intercalation compound (GIC), C_2.5F, with 0.10 MPa of fluorine gas have been studied at 573-773 K. The original stage-1 structure of C_2.5F with semi-ionic C-F bonds and planar sp² carbon sheets is maintained in most part of the compound after the reaction at 573 K, although a large number of covalent C-F bonds are formed on the surface. This compound is partially or completely converted to poly(carbon monofluoride), (CF)_n, with covalent C-F bonds and puckered sp³ carbon sheets at 673 or 773 K, respectively. Single-phase (CF)_n obtained at 773 K possesses remarkably small BET specific surface area, 61 m²/g carbon, almost unchanged from the value of the precursor C_2.5F (69 m²/g carbon). In this reaction, the accommodation of fluorine atoms supplied from the atmosphere into the galleries of C_2.5F is facilitated by the rearrangement of originally intercalated fluorine atoms in the GIC, forming (CF)_n with fewer defects compared to those by the conventional direct fluorination of graphite.     

Glycothermal synthesis of vanadium(III) phosphate hydrates

Glycothermal reaction of various vanadium compounds with triethyl phosphate yielded two hydrate phases of vanadium(III) phosphate having tetragonal (Phase 1) and monoclinic (Phase 2) crystal systems, depending on the reaction conditions such as phosphorus/vanadium ratio, vanadium starting material, reaction temperature and solvent. Thermal treatment of Phase 2 in an anaerobic condition caused transformation to Phase 1 which finally transformed to VPO₄ through an intermediate phase (Phase M). Heat treatment of both the phases in an aerobic condition caused the formation of β-VOPO₄.     

Two siblings of type 3 GM1 gangliosidosis with different clinical features and different ages of onset

We experienced two siblings of type 3 GM1 gangliosidosis. A 33-year-old woman developed dysarthria, dysbasia and bradykinesia at around the age of 30. Her 28-year-old brother showed locomotor retardation and skeletal deformity in infancy. He lost the ability to stand walk at childhood, and developed progressive dystonia. The major neurologic manifestations were parkinsonian symptoms in the elder sister, and progressive dystonia in her brother. Both had markedly reduced beta-galactosidase activity in peripheral blood lymphocyte and were diagnosed as having type 3 GM1 gangliosidosis. Gene analysis revealed that these patients were homozygotes of the adult type mutant gene. The two siblings are unique in that the clinical manifestations and the age of onset of symptoms differed markedly between them despite the same mutant gene in both cases.     

High concentration of glucose increases mitogenic responsiveness to heparin-binding epidermal growth factor-like growth factor in rat vascular smooth muscle cells

The effect of a high extracellular glucose concentration on the mitogenic response of rat vascular smooth muscle cells (SMCs) to heparin-binding epidermal growth factor-like growth factor (HB-EGF) was investigated. The mitogenic effect of HB-EGF was significantly greater in SMCs cultured in high glucose (25 mmol/L) than in cells cultured in low glucose (5.5 mmol/L) or at high osmolarity (5.5 mmol/L glucose plus 19.5 mmol/L mannitol). The mitogenic effect of epidermal growth factor (EGF), which shares the EGF receptor with HB-EGF, was not affected by glucose concentration. The mitogenic effect of HB-EGF was greater when incubated with heparan sulfate (HS) isolated from SMCs cultured in high glucose than with HS from cells cultured in low glucose. HS synthesized by cells in high glucose was of smaller molecular size and less sulfated than HS synthesized by cells in low glucose. The abundance of mRNA encoding HS-N-deacetylase/N-sulfotransferase (HS-NdAc/NST), a regulatory enzyme in the biosynthesis of HS, was decreased by high glucose in a protein kinase C-independent manner. These observations suggest that the enhanced mitogenic response to HB-EGF in SMCs cultured in high glucose may be attributable to changes in cell-associated HS. Downregulation of HS-NdAc/NST gene expression by high glucose may be related to the altered HS biosynthesis.