The research progress of the actions of mast cells in sepsis / 实用医学杂志

Sepsis is a life-threatening organ dysfunction,which is caused by the body's uncontrolled immune response to infection.Tissue masts cells(MC),derived from blood mast cell progenitors,are one of the classical effector cells in inflammatory response.MC plays an important role in sepsis via secreting a variety of inflammatory mediators and cytokines.Here,we summarized the potential roles of MC in sepsis,which is expected to provide novel ideas for the future research on the novel mechanisms of MC in sepsis.

Research progress of ICU-acquired weakness / 中华危重病急救医学

ICU-acquired weakness (ICU-AW) is a common complication in the intensive care unit (ICU). The occurrence of ICU-AW directly leads to prolonged ICU stays for critically ill patients, and in severe cases, it continues to affect their quality of life even after discharge. This article provides a comprehensive review of the research progress on ICU-AW based on domestic and foreign studies, aiming to provide a scientific overview of ICU-AW, including its definition, pathophysiology, diagnosis, screening tools, influencing factors, and potential intervention strategies, so as to promote timely planning and implementation of relevant screening and intervention measures.

Roles of mitochondrial pathway-mediated apoptosis in intracranial aneurysm initiation in rabbits / 中国脑血管病杂志

Objective Toinvestigatethemolecularmechanismsofmitochondrialpathway-mediated apoptosisinintracranialaneurysminitiationinrabbits.Methods FifteenNewZealandwhiterabbitswere divided into 3 groups using the computer random method. After using bilateral carotid artery ligation for modeling basilar artery aneurysm,they were divided into a 2-day group (n=3),a 7-day group (n=6)(3 of them were used for real-time quantitative polymerase chain reaction [PCR]analysis),and a sham operation group (n=6)(3 of them were used for real-time quantitative PCR analysis). The tissue of apex of basilar artery was harvested and the histopathological changes in the vascular wall were observed. TUNEL staining was used to detect apoptotic cells and immunohistochemical staining,and quantitative analysis was used to analyze inflammatory cell distribution. Real-time quantitative PCR was used to detect the expression of apoptosis-related protein mRNA. Results (1 )After modeling,the apoptotic cells were found at the apex of basilar artery in rabbits (the site of internal elastic layer lesion )of the 2-day group and 7-day group. In the 2-day group after operation,the numbers of apoptotic cells (4. 02 ± 0. 21)were significantly higher than those of the basilar artery trunk (0. 40 ± 0. 13),the left posterior cerebral artery (0. 41 ± 0.22),and the right posterior cerebral artery (0. 29 ± 0. 11). The differences were statistically significant (P<0. 05). After modeling,the numbers of apoptotic cells (5. 01 ± 0. 29)of the 7-day group were significantly higher than those of the basilar artery trunk (0. 49 ± 0. 21),the left posterior cerebral artery (0. 31 ± 0. 12),and the right posterior cerebral artery (0. 41 ± 0. 19)(P<0. 05). The internal elastic layer lesions and apoptotic cells were not observed in the rabbits of the sham operation group. (2)After modeling, the expression levels of caspase 9 (1. 97 ± 0. 23)and caspase-3 mRNA (2. 31 ± 0. 40)at the apex of basilar artery in rabbits of the 7-day group were increased significantly compared with that of the sham group (P<0.01).Conclusion Apoptosisisinvolvedintheearlyprocessofaneurysmsinsimple hemodynamics-induced basilar terminus aneurysm formation. Its molecular mechanisms are activated by Bcl-2-mediated mitochondrial pathway through caspase-9.

Role of N-cadherin in cranial neural crest delamination during chick embryogenesis / 中国病理生理杂志

AIM: To investigate the role of N-cadherin in the delamination of neural crest cells. METHODS: The normal expression of N-cadherin in neural tube was identified using in situ hybridization. The cells with N-cadherin over expression were obtained by transfection of wild-type N-cadherin (wt-N-cadherin) ,and the cells with N-cadherin silencing expression were obtained by transfection of dominant-negative N-cadherin (dn-N-cadherin). The migration of cranial neural crest cells was determined by the technique of immunohistochemistry. RESULTS: Either overexpression or down-regulation of N-cadherin significantly affected the migration of cranial neural crest cells. CONCLUSION: Delamination and migration of the cranial neural crest cells rely on the relative N-cadherin expression in the neural tube during neurulation.