Objective To observe the effect of exercise on insulin resistance induced by a high fat diet and to explore the underlying mechanism.Methods Thirty healthy male Wistar rats were randomly divided into a normal control group (NC group) and a high-fat group (HF group),fed with normal chow and a high fat diet respectively.Eighteen weeks later,insulin resistance had appeared in the HF group.The HF group was then randomly subdivided into a high-fat diet control group (HC group,fed a high fat diet) and an exercise group (HE group,fed a high fat diet and subjected to swimming training for 6 weeks).After 24 weeks,an insulin sensitivity index was calculated.Serum free fatty acid (FFA) and skeletal muscle triglyceride (TG) were detected.Phosphorylation of adenosine monophosphate kinase-α (AMPKα) in skeletal muscle was detected by Western blotting.Results At twenty-four weeks the insulin sensitivity of the HC group had decreased significantly compared to the NC group.Serum FFA level and skeletal muscle TG content had both increased.Average phosphorylation of AMPKα in the HC group decreased to 48.7% of the NC group average.Compared to the HC group,insulin sensitivity and phosporylation of AMPK-α were elevated significantly in the HE group.Serum FFA level and skeletal muscle TG content were both lower.However,compared to the NC group,both serum FFA level and skeletal muscle TG content had increased in the HE group,while insulin sensitivity and phosphorylation of AMPKα had significantly decreased.Conclusions Exercise can significantly improve insulin resistance induced by a high-fat diet through decreasing serum FFA level and ectopic li-pid accumulation in skeletal muscle.

Objective To observe the effect of exercise on the expression of TNF-α in the adipose tissue of insulin resistant rats fed a high fat diet. Methods Thirty healthy male rats were randomly divided into a high fat di- et group and a normal chow group. Eighteen weeks later, the high fat group was randomly divided into a resting group fed with the high fat diet only, and an exercise group fed the high fat diet, but receiving swimming training for 6 weeks. Changes in their metabolism of glucose and lipids were observed, and the insulin sensitivity index was calcu-lated. Meanwhile, the level of TNF-α mRNA in their adipose tissue was detected with a real-time fluorescence quan-titative polymerase chain reaction (PCR), and protein in the adipose tissue was measured using Western blotting. Results After 18 weeks of high fat diet feeding, the insulin sensitivity index of the high fat diet group decreased sig-nificantly as compared to the normal chow group, suggesting that insulin resistance had been acquired in the high fat diet group. 24 weeks later, the insulin sensitivity index of the resting group had decreased further, again significantly when compared to the normal chow group. Compared to the resting group, the insulin sensitivity index of exercise group was significantly higher, and the expression of TNF-α mRNA and protein in their adipose tissue was significant- ly increased. Conclusion Insulin resistance can be induced by high fat diet feeding. Exercise can improve insulin resistance by increasing the expression of TNF-α in adipose tissue.

Objective To observe the effects of exercise on serum adiponectin and adiponectin receptor (AdipoR) level in skeletal muscle of insulin-resistant rats. Methods A total of 30 healthy male rats were randomly divided into a control group ( NC, n = 8) and a high-fat group ( HF, n = 22), fed with normal chow and high fat diet, respectively. Eighteen weeks later, the high-fat group was randomly divided into a high-fat diet control group (HC, n = 10) and an exercise group (HE, n = 12). The HC and HE group were continually fed with high fat diet, while the HE group was administered with swimming training for 6 weeks in addition at the same time. After 24 weeks, the insulin sensitivity index was calculated, and serum adiponectin level was detected by using ELISA. The expressions of AdipoR mRNA in skeletal muscle were detected with real-time fluorescence quantitative polymerase chain reaction (PCR). Results After 18 weeks, compared to NC group, the insulin sensitivity index of HF group decreased significantly. It suggested that insulin resistance appeared in HF group. Twenty-four weeks later, compared to NC group, the ISI of HC group was significantly decreased, meanwhile the level of serum adiponectin, expression of AdipoR1 and AdipoR2 mRNA in skeletal muscle of HC group were 71.9% , 59.9% and 69.2% of those of the NC group, respectively; compared to HC group, the ISI was increased significantly by exercise, meanwhile the expression of AdipoR1 mRNA in skeletal muscle was significantly increased by 1.33 times, however the level of serum adiponectin and the expression of AdipoR2 mRNA in skeletal muscle were not altered in HE group. Conclusion Six weeks of exercise improves insulin sensitivity through increasing the expression of AdipoRI mRNA in skeletal muscle.

Objective: To investigate chromosome abnormality rate and related factors of spontaneous abortion in early pregnancy. Methods: A total of 831 tissue samples of spontaneous abortion in early pregnancy were collected from June 2015 to August 2018 in the First Affiliated Hospital of Nanjing Medical University. Chromosomal copy number was analyzed by next generation sequencing (NGS). The relationships between chromosome abnormality and maternal age, in vitro fertilization-embryo transfer (IVF-ET) pregnancy, number of previous spontaneous abortions, history of live birth were analyzed by statistical methods. Results: Among 831 tissue samples of spontaneous abortion in early pregnancy, 461 (55.5%, 461/831) were found to have chromosome abnormalities. Maternal age (OR=1.107, 95%CI: 1.070- 1.145) and history of live birth (OR=1.909, 95%CI: 1.182-3.083) were the positive correlative factors of chromosome abnormality. Times of previous spontaneous abortion (OR=0.807, 95%CI: 0.702-0.928) and IVF-ET pregnancy (OR=0.554, 95%CI: 0.404-0.760) were the negative correlative factors of chromosome abnormality. Conclusions Chromosome abnormality is an important cause of spontaneous abortion in early pregnancy. The rate of chromosome abnormality increases with the increase of maternal age and the history of live birth, and decreases with the increase of number of previous spontaneous abortion and IVF-ET pregnancy.

Objective To investigate chromosome abnormality rate and related factors of spontaneous abortion in early pregnancy. Methods A total of 831 tissue samples of spontaneous abortion in early pregnancy were collected from June 2015 to August 2018 in the First Affiliated Hospital of Nanjing Medical University. Chromosomal copy number was analyzed by next generation sequencing (NGS). The relationships between chromosome abnormality and maternal age, in vitro fertilization?embryo transfer (IVF?ET) pregnancy, number of previous spontaneous abortions, history of live birth were analyzed by statistical methods. Results Among 831 tissue samples of spontaneous abortion in early pregnancy, 461 (55.5%, 461/831) were found to have chromosome abnormalities. Maternal age (OR=1.107, 95%CI: 1.070-1.145) and history of live birth ( OR=1.909, 95%CI : 1.182-3.083) were the positive correlative factors of chromosome abnormality. Times of previous spontaneous abortion (OR=0.807, 95%CI: 0.702-0.928) and IVF?ET pregnancy ( OR=0.554, 95%CI : 0.404-0.760) were the negative correlative factors of chromosome abnormality. Conclusions Chromosome abnormality is an important cause of spontaneous abortion in early pregnancy. The rate of chromosome abnormality increases with the increase of maternal age and the history of live birth, and decreases with the increase of number of previous spontaneous abortion and IVF?ET pregnancy.

Interactions between brain-resident and peripheral infiltrated immune cells are thought to contribute to neuroplasticity after cerebral ischemia. However, conventional bulk sequencing makes it challenging to depict this complex immune network. Using single-cell RNA sequencing, we mapped compositional and transcriptional features of peri-infarct immune cells. Microglia were the predominant cell type in the peri-infarct region, displaying a more diverse activation pattern than the typical pro- and anti-inflammatory state, with axon tract-associated microglia (ATMs) being associated with neuronal regeneration. Trajectory inference suggested that infiltrated monocyte-derived macrophages (MDMs) exhibited a gradual fate trajectory transition to activated MDMs. Inter-cellular crosstalk between MDMs and microglia orchestrated anti-inflammatory and repair-promoting microglia phenotypes and promoted post-stroke neurogenesis, with SOX2 and related Akt/CREB signaling as the underlying mechanisms. This description of the brain's immune landscape and its relationship with neurogenesis provides new insight into promoting neural repair by regulating neuroinflammatory responses.
Humans ; Ischemic Stroke ; Brain/metabolism* ; Macrophages ; Brain Ischemia/metabolism* ; Microglia/metabolism* ; Gene Expression Profiling ; Anti-Inflammatory Agents ; Neuronal Plasticity/physiology* ; Infarction/metabolism*