다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

The transmembrane kinase Ire1p is required for activation of the unfolded protein response (UPR), the increase in transcription of genes encoding endoplasmic reticulum (ER) resident proteins that occurs in response to the accumulation of unfolded proteins in the ER. Ire1p spans the ER membrane (or the nuclear membrane with which the ER is continuous), with its kinase domain localized in the cytoplasm or in the nucleus. Consistent with this arrangement, it has been proposed that Ire1p senses the accumulation of unfolded proteins in the ER and transmits the signal across the membrane toward the transcription machinery, possibly by phosphorylating downstream components of the UPR pathway. Molecular genetic and biochemical studies described here suggest that, as in the case of growth factor receptors of higher eukaryotic cells, Ire1p oligomerizes in response to the accumulation of unfolded proteins in the ER and is phosphorylated in trans by other Ire1p molecules as a result of oligomerization. In addition to its kinase domain, a C-terminal tail domain of Ire1p is required for induction of the UPR. The role of the tail is probably to bind other proteins that transmit the unfolded protein signal to the nucleus.

Oligomerization and phosphorylation of the Ire1p kinase during intracellular signaling from the endoplasmic reticulum to the nucleus.

At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, how...

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Free Radicals in the Physiological Control of Cell Function

Cell signaling by receptor-tyrosine kinases

https://sites.bu.edu/chenlab/files/2014/01/38_McBeathDevCell_04.pdf

Cell shape, cytoskeletal tension, and rhoa regulate stem cell lineage commitment

Musculoskeletal regeneration research network : A global initiative

The spur valve jejunal interposition in choledochus cystectomy. A clinical and experimental study.

The existence of toxic and carcinogenic pentavalent antimony in water is a great safety problem. In order to remove antimony(V) from water, the purpose of this study was to prepare a novel graphene nano iron zinc (rGO/NZV-FeZn) photocatalyst via hydrothermal method followed by ultrasonication. Herein, weakly magnetic nano-Fe-Zn materials (NZV-FeZn, GACSP/NZV-FeZn, and rGO/NZV-FeZn) capable of rapid and efficient Sb(V) adsorption from water were prepared and characterised. In particular, rGO/NZV-FeZn was shown to comprise franklinite, Fe0, and graphite. Adsorption data were fitted by a quasi-second-order kinetic equation and Langmuir model, revealing that among these materials, NZV-FeZn exhibited the best Sb removal performance (543.9 mgSb gNZV-FeZn-1, R2 = 0.951). In a practical decontamination test, Sb removal efficiency of 99.38% was obtained for a reaction column filled with 3.5 g of rGO/NZV-FeZn. Column regenerability was tested at an initial concentration of 0.8111 mgSb L-1, and the treated water obtained after five consecutive runs complied with the GB5749-2006 requirement for Sb. rGO/NZV-FeZn was suggested to remove Sb(V) through adsorption-photocatalytic reduction and flocculation sedimentation mechanisms and, in view of its high cost performance, stability, and upscalable synthesis, was concluded to hold great promise for source water and wastewater treatment.

/pdf/highly-efficient-removal-of-sb-v-from-water-by-franklinite-4989g5ijup.pdf

Highly efficient removal of Sb(V) from water by franklinite-containing nano-FeZn composites.

The insufficiency of compensatory angiogenesis in the heart of hypertension patients contributes to heart failure transition. The HIF1α-VEGF signaling cascade controls responsive angiogenesis. One of the challenges in reprograming the insufficient angiogenesis is to achieve a sustainable tissue exposure to the pro-angiogenic factors, such as HIF1α stabilization. In this study, we identified Rnd3, a small Rho GTPase, as a pro-angiogenic factor participating in the regulation of the HIF1α-VEGF signaling cascade. Rnd3 physically interacted with and stabilized HIF1α, and consequently promoted VEGFA expression and endothelial cell tube formation. To demonstrate this pro-angiogenic role of Rnd3 in vivo, we generated Rnd3 knockout mice. Rnd3 haploinsufficient (Rnd3+/−) mice were viable, yet developed dilated cardiomyopathy with heart failure after transverse aortic constriction stress. The post-stress Rnd3+/− hearts showed significantly impaired angiogenesis and decreased HIF1α and VEGFA expression. The angiogenesis defect and heart failure phenotype were partially rescued by cobalt chloride treatment, a HIF1α stabilizer, confirming a critical role of Rnd3 in stress-responsive angiogenesis. Furthermore, we generated Rnd3 transgenic mice and demonstrated that Rnd3 overexpression in heart had a cardio-protective effect through reserved cardiac function and preserved responsive angiogenesis after pressure overload. Finally, we assessed the expression levels of Rnd3 in the Correspondence to: Jiang Chang, MD, PhD; jchang@ibt.tamhsc.edu; Phone: (713) 677-7603, Fax: (713) 677-7410, Mailing address: Texas A&M University Health Science Center, Institute of Biosciences and Technology, 2121 W. Holcombe Blvd., Houston, TX 77030. †These authors contributed equally to this work. Disclosure None. HHS Public Access Author manuscript Hypertension. Author manuscript; available in PMC 2017 March 01. Published in final edited form as: Hypertension. 2016 March ; 67(3): 597–605. doi:10.1161/HYPERTENSIONAHA.115.06412. A uhor M anscript

Rnd3/RhoE Modulates HIF1α/VEGF Signaling by Stabilizing HIF1α and Regulates Responsive Cardiac Angiogenesis

Objective To investigate the reliability of urea as the internal reference of ankle irrigating fluid in correction of synovial fluid and related factor concentration dilution times, and to further determine the factor expression level in synovial fluid. Patients and methods A total of 91 patients, including 20 cases of non-posterior median foot lesions and 71 cases of unilateral ankle osteoarthritis, were enrolled in this study. AOFAS score, Takakura staging and visual analogue pain scale were given; the venous blood was collected and the ankle fluid and irrigating fluid were obtained from the affected side via puncture. The urea in serum, synovial fluid and irrigating fluid was quantified using an AU5800 biochemical instrument (Beckman Coulter). Statistical analysis was performed for the correlation between urea in serum and synovial fluid; the levels of TNF-α, IL-1β, IL-6, IGF-1 and HELIX-II in irrigating fluid quantified by enzyme linked immunosorbent assay (ELISA) were further corrected. Results There was a good linear relationship between urea contents in synovial fluid and serum (R2=0.89), and the regression slope was 0.927. The levels and ratio of urea in serum and synovial fluid were independent of Takakura staging or pain degree. The expressions of IL-1β (p=0.000), IGF-1 (p=0.000) and HELIX-II (p=0.010) were significantly increased in synovial fluid in patients with ankle osteoarthritis. There was no significant difference in expression of IL-1β (p=0.514), and TNF-α was not detected in synovial fluid. Conclusions This study confirmed the dynamic stability of urea in the ankle fluid, and it is not affected by the progression of arthritis, age and other factors, which is the standard internal reference of correcting ankle irrigating fluid dilution times. The occurrence mechanism of ankle osteoarthritis may be different from that of other osteoarthritis, and IL-6 and IGF-1 are associated with the progression of the disease. Increased HELIX-II is an independent factor of predicting cartilage injury.

Lei Wei

Papers

Musculoskeletal regeneration research network : A global initiative

The spur valve jejunal interposition in choledochus cystectomy. A clinical and experimental study.

Highly efficient removal of Sb(V) from water by franklinite-containing nano-FeZn composites.

Rnd3/RhoE Modulates HIF1α/VEGF Signaling by Stabilizing HIF1α and Regulates Responsive Cardiac Angiogenesis

Clinical research on correction of ankle arthritis-related factor levels via urea