Vulcan carbon was pre-treated at 850 o C at a ramp rate of 5 o C/min and maintained for 24 hours under 5% H2 in Ar. Cs-Ru modified MgO and AC preparationTypically, Ru3(CO)12 was dispersed in THF for 2 hours under sonication. The mixture was then transferred to the MgO or activated carbon (AC) and allowed to sonicate at ambient
A significant decrease in tissue pH or acidosis is a common feature of numerous diseases, including RA (rheumatoid arthritis). Cartilage homoeostasis is profoundly affected by local acidosis in the joints. The diuretic, amiloride, is neuroprotective in models of cerebral ischaemia, a property attributable to the inhibition of ASICs (acid-sensing ion channels) by the drug. However, little is known about the effect of amiloride on apoptosis induced by extracellular acid in articular chondrocytes. We have found that amiloride could restrain the acid-induced apoptosis of rat articular chondrocytes in vitro. Primary rat articular chondrocytes were isolated, cultured and induced to apoptose by exposure to extracellular solution (pH 6.0), while simultaneously treated with 50-200 μM amiloride. Apoptotic rate, mitochondrial function, levels of apoptosis-related gene Bcl-2 family mRNA and activity of caspase 3/9 in chondrocytes were examined. Amiloride inhibited chondrocyte apoptosis in a dose-dependent manner. Furthermore, amiloride partly restored the levels of mitochondrial membrane potential by regulation of Bcl-2 family gene mRNA expression, and activity of caspase 3/9 in chondrocytes induced by extracellular acid. Our results indicated that amiloride protected against acid-induced apoptosis in rat articular chondrocytes by increasing anti-apoptotic ability and down-regulation of pro-apoptotic factors, thus protecting mitochondrial function.
Objective To investigate the clinical significance of the detection of bone mineral density (BMD) and bone turnover markers (BTM) in older women with osteoporosis, and to compare their predictive power for osteoporotic fractures (OF). Methods In this retrospective study, 96 patients with OF and 107 patients with osteoporosis who were hospitalized in the Department of Orthopedics at the First Affiliated Hospital of Chengdu Medical College were examined from October 2017 to February 2019. All selected patients were divided into either the fracture group (96 cases, 47.3%) or the non‐fracture group (107 cases, 52.7%). BMD was measured by dual‐energy X‐ray absorptiometry (DXA). BTM were detected by electrochemical luminescence: aminoterminal propeptide of type I procollagen (PINP), β‐cross‐linked C‐telopeptide of type I collagen (β‐CTX), and molecular fragment of osteocalcin N terminal (N‐MID). Bone metabolism‐related indicators were detected, including alkaline phosphatase (ALP), calcium (Ca), and phosphorus (P). Independent‐samples t‐tests were used to compare the measurement data between the two groups, one‐way ANOVA to compare the gaps between groups, and binary logistic regression to analyze the correlation of BMD and BTM with OF. Results There were no significant differences in age, weight, height, body mass index, age, and time of menopause between the two groups. There were a total of 71 cases (35.0%) in group A (60–70 years), 80 cases (39.4%) in group B (71–80 years), and 52 cases (25.6%) in group C (81–90 years). The fracture group was compared with the non‐fracture group for BMD in the lumbar (0.75 ± 0.05 vs 0.88 ± 0.13, 0.75 ± 0.16 vs 0.87 ± 0.09, 0.74 ± 0.21 vs 0.87 ± 0.12 g/cm2; P < 0.05), BMD in the hip (0.62 ± 0.16 vs 0.74 ± 0.14, 0.61 ± 0.15 vs 0.73 ± 0.0, 0.58 ± 0.13 vs 0.73 ± 0.08 g/cm2; P < 0.05), PINP (83.7 ± 5.7 vs 74.8 ± 5.0, 80.7 ± 4.1 vs 72.1 ± 5.1, 81.2 ± 7.0 vs 68.7 ± 6.3 ng/mL, P < 0.05), and β‐CTX (829.7 ± 91.5 vs 798.8 ± 52.2, 848.1 ± 71.2 vs 812.4 ± 79.0, 867.3 ± 53.1 vs 849.1 ± 67.2 pg./mL, P < 0.05). N‐MID (19.0 ± 6.7 vs 21.3 ± 9.7, 16.2 ± 7.0 vs 18.0 ± 5.3 ng/mL, P < 0.05) in the fracture cases was lower than in the non‐fracture cases for groups B and C, and there was statistical significance. Among the fracture cases, PINP in group A was higher than in group B and C, and β‐CTX in group C was higher than in group A and B (P < 0.05). There was no significant difference in the ALP, P, and Ca between the two groups (P > 0.05). Binary logistic regression analysis showed that for BMD in the lumbar and hip, β‐CTX and OF were significantly correlated (respectively, odds ratio [OR] = −4.182, 95% confidence interval [CI] 1.672–3.448; OR = 6.929, 95% CI 2.586–12.106; OR = 7.572, 95% CI 1.441–3.059), and the differences were statistically significant. PINP and N‐MID were correlated with OF (respectively, OR = 4.213, 95% CI 0.978–1.005; OR = 2.510, 95% CI 1.070–1.134, P > 0.05), the difference was not statistically significant. Conclusion Osteoporotic older women, with lower bone density and hig...
Background: Carnitine palmitoyltransferase 1C (CPT1C) is a critical enzyme that catalyzes carnitinylation of fatty acids for transport into mitochondria for β-oxidation. No previous studies have been conducted to explore the prognostic and oncogenic role of CPT1C in gastric cancer (GC).Methods: Public RNA-sequencing data and micro-array data were extracted from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases respectively. Survival analysis was performed in TCGA and GSE62254 cohorts. RT-qPCR and Western blot analyses were used to determine genes expression in GC cells. Fatty acid oxidation (FAO) assay kit was used to examine cell FAO rate. The cell proliferation ability and cell cycle were tested by using CCK-8 and cell cycle assay kits.Results: In the both TCGA and GSE62254 cohorts, high expression of CPT1C was significantly associated with poor overall (OS) (P<0.001) and disease free survival (DFS) of GC patients (P<0.001). Silence of CPT1C significantly inhibited cell FAO rate, suppressed cell proliferation and induced cell cycle arrest, while enforced CPT1C expression had the opposite effects. However, etomoxir treatment completely restricted the increase of FAO rate, cell viability and the phase of DNA synthesis caused by enhanced CPT1C expression. Of note, CPT1C expression was transcriptionally activated by hypoxia inducible factor-1α.Conclusions: High expression of CPT1C induced by hypoxia was closely associated with poor prognosis and can promote proliferation of GC cells.
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