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21.
Thirty-seven wild plants as food for Asian elephants in the field in Simao, Yunnan province, China and five cultivated plants
as food for captive elephants in the Beijing Zoo were collected and analyzed for their main nutrient components. Protein,
fat, fiber, dry material, ash as well as major microelements: calcium, kalium, zincum, sodium in the food were analyzed by
standard methodology. No significant differences were found between the wild plants taken in the field and forage provided
in captivity. However, the calcium content in the forage is significantly less than the average of those in the wild plants.
It is suggested that the increase in calcium intake may contribute to the relief of low plasma calcium diseases of elephants
in captivity.
Translated from Journal of Beijing Normal University (Natural Science), 2006, 42(2): 184–188 [译自: 北京师范大学学报 (自然科学版)] 相似文献
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Rong‐rong Zhu Qian Chen Zhi‐bo Liu Han‐guang Ruan Qi‐cai Wu Xue‐liang Zhou 《Journal of cellular and molecular medicine》2020,24(14):7907-7914
Increased expression and activity of cardiac and circulating cathepsin D and soluble fms‐like tyrosine kinase‐1 (sFlt‐1) have been demonstrated to induce and promote peripartum cardiomyopathy (PPCM) via promoting cleavage of 23‐kD prolactin (PRL) to 16‐kD PRL and neutralizing vascular endothelial growth factor (VEGF), respectively. We hypothesized that activation of Hes1 is proposed to suppress cathepsin D via activating Stat3, leading to alleviated development of PPCM. In the present study, we aimed to investigate the role of Notch1/Hes1 pathway in PPCM. Pregnant mice between prenatal 3 days and postpartum 3 weeks were fed with LY‐411575 (a notch inhibitor, 10 mg/kg/d). Ventricular function and pathology were evaluated by echocardiography and histological analysis. Western blotting analysis was used to examine the expression at the protein level. The results found that inhibition of Notch1 significantly promoted postpartum ventricular dilatation, myocardial hypertrophy and myocardial interstitial fibrosis and suppressed myocardial angiogenesis. Western blotting analysis showed that inhibition of Notch1 markedly increased cathepsin D and sFlt‐1, reduced Hes1, phosphorylated Stat3 (p‐Stat3), VEGFA and PDGFB, and promoted cleavage of 23k‐D PRL to 16‐kD PRL. Collectively, inhibition of Notch1/Hes1 pathway induced and promoted PPCM via increasing the expressions of cathepsin D and sFlt‐1. Notch1/Hes1 was a promising target for prevention and therapeutic regimen of PPCM. 相似文献
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Self-assembled DNA nanostructures have shown remarkable potential in the engineering of biosensing interfaces, which can improve the performance of various biosensors. In particular, by exploiting the structural rigidity and programmability of the framework nucleic acids with high precision, molecular recognition on the electrochemical biosensing interface has been significantly enhanced, leading to the development of highly sensitive and specific biosensors for nucleic acids, small molecules,proteins, and cells. In this review, we summarize recent advances in DNA framework-engineered biosensing interfaces and the application of corresponding electrochemical biosensors. 相似文献
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Chai Qian Meng Ziang Lu Dexue Zhang Ziying Liu Meili Wu Weihua 《Molecular and cellular biochemistry》2021,476(6):2479-2489
Molecular and Cellular Biochemistry - Cardiomyocyte death is an important pathogenic process in cardiac complications of diabetes. Diabetic patients often suffer glycemic variability. Pyroptosis is... 相似文献
29.
Dong Haoru Shu Xinhua Xu Qiang Zhu Chen Kaufmann Andreas M. Zheng Zhi-Ming Albers Andreas E. Qian Xu 《中国病毒学》2021,36(6):1284-1302
Virologica Sinica - Human papillomavirus (HPV) infection identified as a definitive human carcinogen is increasingly being recognized for its role in carcinogenesis of human cancers. Up to... 相似文献
30.
Wan Qiangyou Kong Deping Liu Qian Guo Shumin Wang Chenchen Zhao Yan Ke Zun-Ji Yu Ying 《中国科学:生命科学英文版》2021,64(7):1068-1076
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin (PG) formation by targeting cyclooxygenase (COX) 1 and 2.Long-term use of NSAIDs that selectively inhibit COX2 increases the risk for thrombotic events,cardiac failure,and hypertension.However,the underlying mechanisms remain unclear.In this study,COX1- and COX2-deficient rats were created via Cas9/RNA-mediated gene targeting.DNA genotyping and Western blot analysis confirmed successful generation of COX1~(-/-)and COX2~(-/-)rats.Adult COX1~(-/-)rats grew normally,while more than 70%of COX2~(-/-)rats after wean died within 2 months.Echocardiography showed markedly reduced left ventricular ejection fraction and fractional shortening in adult COX2~(-/-)rats compared to those in wildtype (WT) controls.Histological analysis revealed accumulation of inflammatory cells and severe interstitial and perivascular fibrosis in COX2~(-/-)cardiac tissues.Moreover,cardiac ATP and acetyl-Co A production was dramatically decreased in COX2~(-/-)rats.Consistently,the expression of genes related to mitochondrial oxidation,such as those that encode for subunits of pyruvate dehydrogenase complex and acyl Co A dehydrogenases,were downregulated,while glycolytic hexokinase 1 (HK1) was upregulated in COX2~(-/-)heart tissues.These observations indicate that COX2-deficient rats developed spontaneously heart failure,likely as a result of dysregulated cardiac energy metabolism. 相似文献