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101.
NIMA-related kinases defective in murine models of polycystic kidney diseases localize to primary cilia and centrosomes 总被引:1,自引:0,他引:1
Mahjoub MR Trapp ML Quarmby LM 《Journal of the American Society of Nephrology : JASN》2005,16(12):3485-3489
A key feature of the polycystic kidney diseases is aberrant cell proliferation, a consequence of dysfunctional ciliary signaling. The NIMA-related kinases (Nek) Nek1 and Nek8 carry the causal mutations of two of the eight established mouse models of polycystic kidneys. Nek proteins have roles in cell cycle and may contribute to coordinate regulation of cilia and cell-cycle progression. Herein is reported that in a mouse kidney epithelial cell line, mNek1 localizes to centrosomes in interphase and remains associated with the mitotic spindle pole during mitosis. In contrast, mNek8 localizes to the proximal region of the primary cilium and is not observed in dividing cells. Knockdown of mNek8 by siRNA does not affect ciliary assembly. Taken together with the phenotypes of the mutant mice, these data suggest that mNek1 and mNek8 provide links between cilia, centrosomes, and cell-cycle regulation. 相似文献
102.
Genetic hypercalciuria 总被引:1,自引:0,他引:1
Hypercalciuria is an important, identifiable, and reversible risk factor in stone formation. The foremost and most fundamental step in dissecting the genetics of hypercalciuria is understanding its pathophysiology. Hypercalciuria is a complex trait. This article outlines the various factors that compromise the attempt to dissect the genetics of hypercalciuria, summarizes the clinical and experimental monogenic causes of hypercalciuria, and outlines the initial results from attempts in studying polygenic hypercalciuria. Finally, the problem is set in perspective of the current database, technologic advances and limitations are highlighted, and prospects of further advances in the field are speculated upon. 相似文献
103.
The incidence and magnitude of retinal hemorrhages (RH) in a group of 23 preterm infants (29-35 weeks) born spontaneously in vertex presentation have been compared with those of 23 others (28-35 weeks) born by gentle extraction with small forceps. Distribution to the groups was random. The overall frequency of RH in both groups together was low, 6%, with no statistically significant difference between the groups. No fundi with severe (grade III) hemorrhages were seen. Both the incidence and magnitude of RH were less in the preterm neonates when compared with previously reported figures in term infants born spontaneously or with forceps extraction. The study provides further evidence in support of the hypothesis that fetal head compression with venous congestion is the main cause of RH in the newborn. 相似文献
104.
Spontaneous disseminated squirrel fibroma 总被引:1,自引:0,他引:1
105.
BMK1 is activated in glomeruli of diabetic rats and in mesangial cells by high glucose conditions 总被引:4,自引:0,他引:4
Suzaki Y Yoshizumi M Kagami S Nishiyama A Ozawa Y Kyaw M Izawa Y Kanematsu Y Tsuchiya K Tamaki T 《Kidney international》2004,65(5):1749-1760
BACKGROUND: High glucose causes renal cell injury through various signal transduction pathways, including mitogen-activated protein (MAP) kinases cascades. Big MAP kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a recently identified MAP kinase family member and was reported to be sensitive to osmotic and oxidative stress. However, the role of BMK1 in diabetic nephropathy has not been elucidated yet. METHODS: We investigated whether BMK1 is activated in the glomeruli of Otsuka Long Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus in comparison with the control Long Evans Tokushima Otsuka (LETO) rats. We also examined the effect of high glucose on BMK1 activity in cultured rat mesangial cells. RESULTS: BMK1 and ERK1/2 but not p38 were activated in the glomeruli of OLETF rats, which showed diabetic nephropathy at 52 weeks of age. High glucose, in addition to a high concentration of raffinose, caused rapid and significant activation of BMK1 in rat mesangial cells. MAP kinase/ERK kinase (MEK) inhibitors, U0126 and PD98059, both inhibited BMK1 activation by high glucose in a concentration-dependent manner. Protein kinase C (PKC) inhibition by GF109203X and PKC down-regulation with long-time phorbol myristate acetate (PMA) treatment both inhibited BMK1 and Src kinase activation. Src kinase inhibitors, herbimycin A and PP2, also inhibited high glucose-induced BMK1 activation. PKC inhibitors, Src inhibitors and MEK inhibitors, all inhibited cell proliferation by high glucose. Finally, transfection of dominant-negative MEK5, which is an upstream regulator of BMK1, abolished the BMK1-mediated rat mesangial cell proliferation stimulated by high glucose. CONCLUSION: In the present study, we demonstrated that high glucose activates BMK1 both in vivo and in vitro. It was suggested that high glucose induces PKC- and c-Src-dependent BMK1 activation. It could not be denied that BMK1 activation is induced through an osmotic stress-sensitive mechanism. BMK1-mediated mesangial cell growth may be involved in the pathogenesis of diabetic nephropathy. 相似文献
106.
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109.
DeBar LL Ritenbaugh C Vuckovic N Stevens VJ Aickin M Elliot D Moe E Orwoll E Ernst D Irving LM 《Preventive medicine》2004,39(5):1047-1055
BACKGROUND: This paper describes decisions about the experimental design for the Youth, Osteoporosis, and Understanding Total Health Project (YOUTH), a trial designed to test the efficacy of a health plan-based lifestyle intervention for increasing bone mineral density among adolescent women 14 to 16 years of age. METHODS: This randomized controlled trial recruited adolescent women who were at higher risk for developing osteoporosis (body mass index 16-23) from a large HMO in the Pacific Northwest. The intervention focused on improving diet (high calcium foods, fruits, and vegetables) and increasing physical activity (high impact and spinal motion). The intervention included both group and individual activities. The primary endpoint in the study was total bone mineral density as measured by dual-energy X-ray absorptiometry (DEXA). RESULTS: Baseline data were collected on the trial cohort of 228 adolescent women and their families. This paper discusses how researchers met the following challenges in designing and implementing the trial: determining appropriate dietary and exercise targets to affect bone mineral density in adolescents; choosing suitable assessments; and developing an intervention well suited for implementation in a non-school (health plan) setting. We also discuss the rationale for the specific study population chosen (females, younger adolescents). CONCLUSIONS: The YOUTH project is one of very few preventive research interventions with adolescents conducted in a health plan setting. Many of the recruitment and intervention strategies used in this trial may be appropriate for adoption in other health plan-based prevention studies. 相似文献
110.
Ali N Yoshizumi M Tsuchiya K Kyaw M Fujita Y Izawa Y Abe S Kanematsu Y Kagami S Tamaki T 《European journal of pharmacology》2004,485(1-3):127-135
Ebselen (2-phenyl-1, 2-benzisoselenazol-3[2H]-one) is a seleno-organic compound exhibiting both glutathione peroxidase and antioxidant activity. Although it has been reported that ebselen is effective against hydrogen peroxide (H(2)O(2))-induced cell death in several cell types, its effect on endothelial cell damage has not yet been elucidated. In the present study, we examined the effect of ebselen on H(2)O(2)-induced human umbilical vein endothelial cells (HUVECs) death, and its intracellular mechanism. Our findings showed that pretreatment of HUVECs with ebselen resulted in a significant recovery from H(2)O(2)-induced cell death in a concentration-dependent manner. In addition to the inhibition of lactate dehydrogenase (LDH) leakage, ebselen inhibited H(2)O(2)-induced cytochrome c release and caspase-3 activation and the resultant apoptosis in HUVECs. Moreover, it was observed that H(2)O(2) significantly stimulated activation of mitogen-activated protein (MAP) kinases, i.e., p38 MAP kinase, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK1/2). Ebselen inhibited H(2)O(2)-induced p38 MAP kinase, but not JNK or ERK1/2 activation. Furthermore, SB203580 (4-[4-fluorophenyl]-2-[4-methylsulfinylphenyl]-5-[4-pyridyl]-1H-imidazole), a specific p38 MAP kinase inhibitor, inhibited H(2)O(2)-induced p38 MAP kinase phosphorylation, cytochrome c release, caspase-3 activation, as well as cell death in HUVECs. These findings suggest that ebselen attenuates H(2)O(2)-induced endothelial cell death through the inhibition of signaling pathways mediated by p38 MAP kinase, caspase-3, and cytochrome c release. Thus, inhibition of p38 MAP kinase by ebselen may imply its usefulness for prevention and/or treatment of endothelial cell dysfunction, which was suggested to be the first step in the development of atherosclerosis. 相似文献