Objective To study the feasibility of using morphological changes of bronchioles and lymph nodes in rats for estimating the postmortem interval(PMI).Methods Thirty-five 8-week-old male SD rats were sacrificed by cervical dislocation and placed in a constant temperature and humidity box.Lung tissues of 5 rats were extracted at each time point within 24 hours after death for routine HE and PHH3 immunohistochemical staining.Image J was used to measure mucosal area,extramucosal area,luminal area of small bronchi,Then calculate the ratio of mucosal area to luminal area,extramucosal area to extramucosal,extramucosal area to mucosal area.imageJIHCprofiler was used to measure the positive degree of PHH3 immunohistochemical staining in lymph node nuclei,and the above calculation results and the positive degree of PHH3 staining were statistically analyzed by GraphPad Prism 9.5.Results The ratio of mucosal area to lumen area showed an overall downward trend with the increase of PMI(0h was statistically different compared with 18h and 24h,P<0.05).The ratio of extramucosal to lumen area and extramucosal to mucosa area showed an upward trend with the increase of PMI(0h was statistically different from other time points,P<0.05),the positive degree of PHH3 immunohistochemical staining was significantly decreased at 24 h after death(P<0.05).Conclusion The morphological changes of pulmonary bronchiole and lymph nodes showed a certain regularity within 24h after death,which was helpful to infer the early PMI,lymph node nucleus PHH3 was expected to be a critical index to distinguish early and late PMI.

Objective To study the feasibility of using morphological changes of bronchioles and lymph nodes in rats for estimating the postmortem interval(PMI).Methods Thirty-five 8-week-old male SD rats were sacrificed by cervical dislocation and placed in a constant temperature and humidity box.Lung tissues of 5 rats were extracted at each time point within 24 hours after death for routine HE and PHH3 immunohistochemical staining.Image J was used to measure mucosal area,extramucosal area,luminal area of small bronchi,Then calculate the ratio of mucosal area to luminal area,extramucosal area to extramucosal,extramucosal area to mucosal area.imageJIHCprofiler was used to measure the positive degree of PHH3 immunohistochemical staining in lymph node nuclei,and the above calculation results and the positive degree of PHH3 staining were statistically analyzed by GraphPad Prism 9.5.Results The ratio of mucosal area to lumen area showed an overall downward trend with the increase of PMI(0h was statistically different compared with 18h and 24h,P<0.05).The ratio of extramucosal to lumen area and extramucosal to mucosa area showed an upward trend with the increase of PMI(0h was statistically different from other time points,P<0.05),the positive degree of PHH3 immunohistochemical staining was significantly decreased at 24 h after death(P<0.05).Conclusion The morphological changes of pulmonary bronchiole and lymph nodes showed a certain regularity within 24h after death,which was helpful to infer the early PMI,lymph node nucleus PHH3 was expected to be a critical index to distinguish early and late PMI.

Intestinal microbiota is closely related to the human health. The unhealthy state is often associated with disorders in intestinal microbiota. Intestinal microbiota modulators such as probiotics, prebiotics and synbiotics, which can restore and improve intestinal microbiota balance, are thus drawing wide attention. This paper reviewed the research progress of modulators of intestinal microbiota.

Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage electric foot shock for about 1 h at 10 s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress cardiomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.
Animals ; Cardiomyopathies ; metabolism ; Myocytes, Cardiac ; metabolism ; Neuropeptide Y ; metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Rats ; Rats, Sprague-Dawley ; Stress, Physiological ; physiology ; Transcription Factors ; metabolism

Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage electric foot shock for about 1 h at 10 s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress cardiomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.