No abstract

BackgroundApoptosis plays a critical role in controlling the proliferation and differentiation of germ cells during spermatogenesis. Dysregulation of the fine-tuned balance may lead to the onset of testicular diseases. In this study, we investigated the activation status of apoptosis pathways in the testicular tissues under the background of an asthmatic mouse model.MethodsTen BALB/c mice were divided into two groups: the acute asthma group and the control group. In the acute asthma group, ovalbumin (OVA)-sensitized mice were challenged with aerosolized OVA for 7 days, while the control group was treated with physiological saline. After that, both epididymis and testis were collected to determine the sperm count and motility. Apoptosis in the testis was evaluated by DNA ladder, immunochemistry and further by PCR array of apoptosis-related genes. Finally, the cleavage of caspase-3 and poly ADP-ribose polymerase (PARP) was determined by western blot and the enzymatic activities of caspase-9 and 3/7 were assessed using Caspase-Glo kits.ResultsCompared with control mice, significant decreases in the body weight, testis weight, sperm count and motility were seen in the experimental group. DNA ladder and immunochemistry showed significant increase in apoptotic index of the asthmatic testis, whereas a decrease in mRNA expression of Bcl-2 and increases in Bax, BNIP3, caspase-9, and AIF were observed in the asthma group. Furthermore, protein levels of AIF were significantly upregulated, while the translational expression of Bcl-2 was downregulated markedly. Consistently, caspase-9 activity in the testis of asthma mice was significantly higher than that of the control group.ConclusionCollectively, these results showed that Bcl-2-caspase-9 apoptosis pathway was clearly activated in the testis of asthmatic mice with the increased expression of apoptosis-related genes and proteins. To our knowledge, this is the first report demonstrating that asthma could lead to the activation of the mitochondrial apoptosis signaling pathway in the mouse testis.

No abstract

The current study aimed to investigate the imaging characteristics and pathogenesis of intracranial artery stenosis in patients with acute cerebral infarction. In total, 84 patients diagnosed with acute cerebral infarction were recruited. Magnetic resonance angiography was performed to detect the existence of intracranial artery stenosis or occlusion. In addition, magnetic resonance imaging and diffusion weighted imaging were employed to analyze the infarction types and characteristics. In the majority of patients, the infarction resulted from internal carotid stenosis (77 cases; 91.7%), while it was caused by vertebral artery stenosis in a small number of cases (7 cases; 8.3%). Multiple infarction was identified the most common type of infarction among all cases (69.0%). The most common types of infarctions in the internal carotid system were multiple infarction implicating both the cortex and centrum ovale (23.4%), and internal watershed infarction (22.1%). Although the number of cases was relatively small, multiple infarction was observed to have a high incidence in the vertebral artery system. Bedside electrocardiogram was also recorded to determine the sinus rhythm and examine the abnormal hemodynamics. The sinus bradycardia rate of patients with multiple infarction was markedly greater in comparison with that in single infarction patients (χ=0.01, P<0.05). Transcranial Doppler plus microembolus monitoring was utilized to explore the possible pathogenesis of all types of infarctions, such as arterial embolization. As compared with the single infarction patients, the embolus rate in patients with multiple infarction was notably increased by ~3.7-fold (χ=8.65, P<0.05). In conclusion, the cerebral infarction was common in the internal carotid system, with multiple infarction observed in the majority of cases. The pathogenesis of cerebral infarction included arterial embolization and inadequate hemoperfusion.