A special medical device for the treatment of congenital megacolon is designed.This device is made of avirulent and high-intensity plastics.The resultant which formed by up and down curve arm detained lateral anus can spur the up and down leaf of the ring clamp device.Under the continuous pressurized condition,it can clamp the rectum and the downward pull-through colon,then the colon becames necrosis,so that the aim of confluence is achieved.This device is disposable.

BACKGROUND:Transformation growth factor-β(TGF-β) and brain-derived neurotrophic factor (BDNF) are the main regulatory factors in the process of spinal cord injury. There are many researches for TGF-βand BDNF pathogenesis in the spinal cord injury, but the regulation of Ginsenoside Rg1 intervention on TGF-βand BDNF in the spinal cord injury is rarely reported.
OBJECTIVE:To observe the effect of Ginsenoside Rg1 intervention on TGF-βand BDNF expression at themolecular protein levels, and to study the protection effect of Ginsenoside Rg1 on the spinal cord and nerve function after spinal cord injury.
METHODS:Experimental rats were randomly divided into blank control group, model group and Ginsenoside Rg1 group. In the model and Ginsenoside Rg1 groups, spinal cord injury model was established with the impact method in rats. In the Ginsenoside Rg1 group, rats were intraperitoneal y injected with 10 mg/kg Ginsenoside Rg1 24 hours after modeling, once per day, for 14 days. Rats in the blank control and model groups were injected with equal saline.
RESULTS AND CONCLUSION:Compared with the control group, serum malondialdehyde levels increased, the content of superoxide dismutase decreased, TGF-βexpression levels in spinal cord tissue increased, and BDNF expression levels decreased in the model and Ginsenoside Rg1 groups. Compared with the model group, serum malondialdehyde levels decreased, the content of superoxide dismutase increased, TGF-βexpression levels in spinal cord tissue decreased, and BDNF expression levels increased in the Ginsenoside Rg1 group. Ginsenoside Rg1 can protect the injury spinal cord in rats after spinal cord injury.

BACKGROUND:Chinese herb extracts can restore and protect the nervous system of rats through intervention of neural stem cels. OBJECTIVE:To explore the role of ginsenosides Rg1 in the proliferation and protection of neural stem cels. METHOD:Sprague-Dawley rats at pregnant 19 days were dissected to take out fetal rats, and then the hippocampal tissues from fetal rats were isolated to extract neural stem cels. Neural stem cels were co-cultured with DMEM/F12 medium containing 50 g/L ginsenosides Rg1 as intervention group, with DMEM/F12 medium as blank control group, and with DMEM/F12 containing 0.64% phenol as positive control group, respectively. MTT assay was used to detect the proliferation of neural stem cels in each group, and western blot method to detect the protein expression of brain-derived neurotrophic factor and transforming growth factor-β in neural stem cels. RESULTS AND CONCLUSION:Rat neural stem cels were round single cels with clear border at early period after isolation but at 2 days after inoculation, the cels were adherent and aggregated into smal cel spheres. Compared with the blank control group, the proliferative rate of neural stem cels was significantly increased in the ginsenosides Rg1 group (P < 0.05), but decreased in the positive control group (P < 0.05). Compared with the blank control group, in the ginsenosides Rg1 group, the expression of brain-derived neurotrophic factor was elevated, and the expression of transforming growth factor-β was reduced, indicating ginsenosides Rg1 has a certain effect to promote the proliferation of neural stem cels as wel as to protect the neural stem cels.

Inflammation is the key driver of liver fibrosis progression in non-alcoholic fatty liver disease (NAFLD). Unfortunately, it is often challenging to assess inflammation in NAFLD due to its dynamic nature and poor correlation with liver biochemical markers. Liver histology keeps its role as the standard tool, yet it is well-known for substantial sampling, intraobserver, and interobserver variability. Serum proinflammatory cytokines and apoptotic markers, namely cytokeratin-18, are well-studied with reasonable accuracy, whereas serum metabolomics and lipidomics have been adopted in some commercially available diagnostic models. Ultrasound and computed tomography imaging techniques are attractive due to their wide availability; yet their accuracies may not be comparable with magnetic resonance imaging-based tools. Machine learning and deep learning models, be they supervised or unsupervised learning, are promising tools to identify various subtypes of NAFLD, including those with dominating liver inflammation, contributing to sustainable care pathways for NAFLD.

Background/Aims: We aimed to determine the association between blood urea level and incident cirrhosis, hepatic decompensation, and hepatocellular carcinoma in chronic liver disease (CLD) patients. Methods: The association between blood urea level and liver fibrosis/liver-related events were evaluated on continuous scale with restricted cubic spline curves based on generalized additive model or Cox proportional hazards models. Then, the above associations were evaluated by urea level within intervals. Results: Among 4,282 patients who had undergone liver stiffness measurement (LSM) by transient elastography, baseline urea level had a U-shaped association with LSM and hepatic decompensation development after a median follow-up of 5.5 years. Compared to patients with urea of 3.6–9.9 mmol/L, those with urea ≤3.5 mmol/L (adjusted hazard ratio [aHR], 4.15; 95% confidence interval [CI], 1.68–10.24) and ≥10 mmol/L (aHR, 5.22; 95% CI, 1.86–14.67) had higher risk of hepatic decompensation. Patients with urea ≤3.5 mmol/L also had higher risk of incident cirrhosis (aHR, 3.24; 95% CI, 1.50–6.98). The association between low urea level and incident cirrhosis and hepatic decompensation was consistently observed in subgroups by age, gender, albumin level, and comorbidities. The U-shaped relationship between urea level and LSM was validated in another population screening study (n=917). Likewise, urea ≤3.5 mmol/L was associated with a higher risk of incident cirrhosis in a territory-wide cohort of 12,476 patients with nonalcoholic fatty liver disease at a median follow-up of 9.9 years (aHR, 1.27; 95% CI, 1.03–1.57). Conclusions We identified a U-shaped relationship between the urea level and liver fibrosis/incident cirrhosis/hepatic decompensation in patients with CLD.

Nasopharyngeal carcinoma (NPC) is a common malignant tumor in China. Radiotherapy is the first-line treatment. After appropriate radiotherapy, about 5%-15% patients experience recurrence. In view of the poor efficacy and high incidence of severe late toxicities associated with re-irradiation, salvage surgery by the transnasal endoscopic approach is recommended for recurrent NPC (rNPC). Compared with re-irradiation, endoscopic surgery can better prolong survival, improve the quality of life, and reduce complications and medical expenses of patients with rNPC. However, the complexity of the nasopharyngeal skull base enhances the difficulty and risk of surgery. Expanding the boundary of surgical resection remains a clinical challenge for otolaryngologists. In this regard, to help more advanced patients with rNPC, the surgical innovative system of NPC needs to be established by multi-disciplinary cooperation, involving skull base anatomy-based investigation, appropriate administration of the internal carotid artery (ICA), repair of skull base defect, and establishment of various types of endoscopic endonasal nasopharyngectomy.