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Objective To investigate the preventive effect of specific knockdown of X box-binding protein 1（XBP-1） in smooth muscle cells on cardiopulmonary injury in hypoxia-induced pulmonary hypertension（HPH） mice. Methods Sixty 8-week-old male C57BL/6 mice were selected and randomly divided into control group（NC), HPH group, HPH +shCtrl group, and HPH + shXBP-1 group, respectively. Mice in the control group was placed in normal pressure and oxygen environment, and mice in the HPH group, HPH+shCtrl group, and HPH+shXBP-1 group were placed in low pressure and low oxygen environment for HPH modeling. At 3 weeks prior to model construction, mice in the HPH+shXBP-1 group were injected with smooth muscle specific XBP-1 knockdown adeno-associated virus serotype 9（AAV9） virus through the tail vein, and mice in the HPH+shCtrl group were injected with control virus. After anesthesia, right ventricular systolic pressure（RVSP） was measured by cardiac catheter. Right ventricular internal diameter（RVID） and thickness of right ventricle anterior wall（RVAW） were measured with small animal ultrasound instrument. The heart was isolated and right ventricular hypertrophy index（RVHI） was evaluated. Right ventricular myocardium was collected and masson was performed to calculate collagen volume fraction（CVF). The blood of mice was collected from periorbital area, and endothelin-1（ET-1） was detected by enzyme-linked immunosorbent assay（ELISA） and the levels of nitric oxide（NO), nitric oxide synthase（NOS） and induced nitric oxide synthase（iNOS） were detected by colorimetry. Alveolar lavage was performed on the left lung, and the bronchoalveolar lavage fluid（BALF） was collected. Interleukin-1β（IL-1β), interleukin-6（IL-6), tumor necrosis factor-α（TNF-α） were detected by ELISA. HE staining was performed on the middle and posterior lobe of the right lung, and the distal pulmonary artery wall thickness ratio（WT%） and pulmonary artery wall area ratio（WA%） were evaluated. The total protein of the right anterior lobe lung was extracted, and the expression of XBP-1 protein was detected by Western blotting. Results The RVSP of the HPH and HPH+shCtrl groups were higher than that of the control group, and the RVSP of the HPH+shXBP-1 group was lower than that of the HPH and HPH+shCtrl group（all P＜0. 05). Compared with the control group, RVID of the HPH group and HPH+shCtrl group decreased, while RVAW and RVHI increased. Compared with the HPH group and HPH+shCtrl group, RVID increased, while RVAW and RVHI decreased in the HPH+shXBP-1 group（all P＜0. 05). The CVF of the HPH group and HPH+shCtrl group was higher than that of the control group, and the CVF was lower in the HPH+shXBP-1 group than in the HPH group and HPH+shCtrl group（all P＜0. 05). The plasma ET-1 levels of the HPH group and HPH+shCtrl group were higher, and the levels of NO, NOS and iNOS were lower than those of the control group（all P＜0. 05). The plasma ET-1 level was lower in the HPH+shXBP-1 group than in the HPH group and HPH+shCtrl group, and the levels of NO, NOS and iNOS were higher than those of the HPH group and HPH+shCtrl group（all P＜0. 05). The levels of IL-1β, IL-6 and TNF-α in BALF of the HPH and HPH+shCtrl groups were higher than those in the control group, and the levels of IL-1β, IL-6 and TNF-α in the HPH+shXBP-1 group were lower than those in the HPH group and HPH+shCtrl groups（all P＜0. 05). WT% and WA% of the HPH group and HPH+shCtrl group increased in comparison with those of the control group, and the WT% and WA% of the HPH+shXBP-1 group decreased in comparison with those of the HPH group and HPH+shCtrl group（all P＜0. 05). Compared with the control group, the expression of XBP-1 protein increased in the HPH group and HPH+shCtrl group; compared with the HPH group and HPH+shCtrl group, the expression of XBP-1 protein decreased in HPH+shXBP-1 group（all P＜0. 05). Conclusions Specific knockdown of XBP-1 can reduce pulmonary artery pressure and improve heart function, myocardial fibrosis, pulmonary artery remodeling, homeostasis of vasoactive substances and intrapulmonary inflammation in HPH mice. XBP-1 may be involved in the process of cardiopulmonary injury in HPH mice. [ABSTRACT FROM AUTHOR]

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Copyright of Basic & Clinical Medicine is the property of Editorial Office of Basic & Clinical Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To evaluate the efficacy and safety of evolocumab, a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, in lowering LDL-C levels in patients with coronary heart disease complicated with mild renal insufficiency. Methods Clinical data of patients diagnosed with coronary heart disease complicated with mild renal insufficiency in Department of Cardiology (estimated glomerular filtration rate (eGFR) 60-90 mL/(min · 1.73 m²)) were retrospectively collected. All patients were divided into two groups according to the LDL-C lowering strategy. In the experimental group (n=50, patients were treated with evolocumab, a PCSK9 inhibitor, combined with statins (rosuvastatin calcium tablets), and their counterparts in the control group (n=42) were treated with statins (rosuvastatin calcium tablets) alone. LDL-C level, renal function indicators, side effects and adverse cardiovascular events at 1 and 3 months were observed between two groups. Results Compared with the control group, the LDL-C level at 1 month was significantly lower in the experimental group ((1.27±0.90) mmol/L vs. (1.75±0.82) mmol/L, P < 0.05, and the LDL-C level 3 months was even lower ((0.94±0.44) mmol/L vs. (1.53±0.53) mmol/L, P < 0.05. However, no significant differences were noted in the changes of renal function indicators at l and 3 months between two groups (all P > 0.05. During 3-month treatment period, no adverse reactions, such as new-onset diabetes mellitus and neurocognitive dysfunction, were observed in both groups. The incidence of cardiovascular events (readmission for unstable angina, acute myocardial infarction and repeated percutaneous coronary intervention) and other adverse reactions (rash and myalgia) did not significantly differ between two groups (all P > 0.05. Conclusions In coronary heart disease patients complicated with mild renal insufficiency, evolocumab combined with rosuvastatin can significantly reduce LDL-C levels at 1 and 3 months and maintain high safety compared with compared to rosuvastatin alone. [ABSTRACT FROM AUTHOR]

Copyright of Basic & Clinical Medicine is the property of Editorial Office of Basic & Clinical Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Remote Sensing is the property of Editorial Office of Journal of Remote Sensing & Science Publishing Co. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal on Communication / Tongxin Xuebao is the property of Journal on Communications Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Physical Education / Tiyu Xuekan is the property of Journal of Physical Education Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective： To explore the effects and mechanism of dihydromyricetin on hypoxia-induced inflammatory response and apoptosis in cardiomyocytes. Methods： H9C2 cells were randomly divided to four groups： control group, control ＋ dihydromyricetin group, hypoxia group, hypoxia ＋ dihydromyricetin group. Control ＋ dihydromyricetin group and hypoxia ＋ dihydromyricetin group were treated with dihydromyricetin (5 μmol/L), while control group and hypoxia group were treated with DMSO in the absence or presence of hypoxia for 24 h. The mRNA levels of CD40, IL-1β, IL-6, TNF-α and miRNA-145-5p were evaluated by real-time PCR. The concentrations of IL-1β, IL-6 and TNF-oL were measured by ELISA assay. The MTT assay was used to analyze the living cells. Apoptotic index of cardiomyocytes was examined by Tunel. Western blot was used to determine the expression of Cleaved Caspase3. Results： Compared with control group and control ＋ dihydromyricetin group, the mRNA levels of CD40, IL-1β, IL-6 and TNF-α and the concentrations of IL-1β, IL-6 and TNF-α increased significantly (P<0.05), with attenuated miRNA-145-5p mRNA and cell viability (P<0. 05), as well as increased apoptotic index (P<0.05), and the expressions of Cleaved Caspase3 were upregulated (P<0.05) in hypoxia group. Compared with those in hypoxia group, inflammatory cytokines reduced significantly (P<0.05) and miRNA-145-5p mRNA increased significantly (P<0.05), with restored cell viability (P<0.05), as well as decreased apoptotic index (P<0.05), and there was a reduction of level of Cleaved Caspase3 (P<0.05) by the treatment with dihydromyricetin in hypoxia ＋ dihydromyricetin group. Conclusion： Dihydromyricetin can significantly decrease hypoxia-induced inflammatory response and apoptosis in cardiomyocytes, possibly by upregulating miRNA-145-5p and further inhibiting CD40-mediated inflammatory response and apoptosis. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)