[A case report of death from toxic encephalopathy caused by emamectin·chlorfenapyr].

Emamectin·chlorfenapyr is insecticide compounded by emamectin benzoate and chlorfenapyr. There is no special antidote after poisoning, and the mortality rate of patients is very high. We admitted a case of toxic encephalopathy caused by oral administration of emamectin·chlorfenapyr. The clinical manifestations of patient were gastrointestinal symptoms, profuse sweating, high fever, changes in consciousness. After admitted to the hospital, despite active comprehensive treatment, the patient died of ineffective rescue eventually.

[Three cases of acute chlorfenapyr poisoning].

This paper reported 3 cases of poisoning caused by chlorfenagyr. Chlorfenapyr poisoning has gradually increased in clinical practice. The early stage after poisoning is digestive tract symptoms, followed by sweating, high fever, changes in consciousness, changes in myocardial enzymology, etc. Its main mechanism of intoxication is uncoupling oxidative phosphorylation. Since there is no specific antidote after poisoning, the fatality rate of chlorfenapyr poisoning remains high. The therapeutic measures are early gastrointestinal decontamination, symptomatic and supportive treatments, and early blood purification may be an effective treatment.

[Current status of influencing factors for postoperative anastomotic leakage in low rectal cancer].

The incidence of anastomotic leakage, a common and serious postoperative complication of low rectal cancer, remains high. Clarifying the risk factors for anastomotic leakage in patients with low rectal cancer after surgery can help guide clinical treatment and help patients improve their prognosis. The current literature suggests that the risk factors affecting the occurrence of anastomotic leakage after low rectal cancer include three aspects: (1) individual factors: male gender, high body mass index, malnutrition, smoking, alcoholism, and metabolic diseases; (2) tumor factors: the lower margin of tumor <5 cm from the anal verge, tumor diameter >2.5 cm, late tumor stage, high level of tumor markers and preoperative intestinal obstruction; (3) surgical factors: long operative time (>180 min), intraoperative bleeding (≥70 ml), more than 2 cartridges of stapling for anastomosis, contamination of the operative field, epidural analgesia and intraoperative hypothermia. Notably, the surgical approach (laparoscopic, open and hand-assisted laparoscopic surgery) was not a factor influencing the occurrence of postoperative anastomotic leakage in low rectal cancer. The findings on the effects of receiving neoadjuvant therapy, gut microbiota,intestinal bowel preparation, insufficient time for preoperative antibiotic prophylaxis, left colonic artery dissection, intraoperative blood transfusion, pelvic drainage, transanal drainage and combined organ resection, and postoperative diarrhea on postoperative anastomotic leakage in low rectal cancer are controversial. However, clinical workers can still take measures to reduce the risk of anastomotic leakage according to the above risk factors by making a good assessment before surgery, actively avoiding them during and after surgery, and taking measures for each step, so as to bring maximum benefits to patients.

Long noncoding RNA LINC00511 promoted cell proliferation and invasion via regulating miR-124-3p/EZH2 pathway in gastric cancer.

OBJECTIVE: Growing evidence has shown that long non-coding RNAs (lncRNAs) can serve as prospective markers for survival in patients with gastric cancer (GC). In this study, we mainly focused on the potential roles of LINC00511 in the development process of GC. PATIENTS AND METHODS: RT-PCR was used to detect the expressions of LINC00511 and miR-124-3p in GC tumor tissues, adjacent tissues and GC cell lines. Furthermore, correlations between LINC00511 with miR-124-3p, and miR-124-3p with EZH2, were analyzed by Correlation analysis. Moreover, the overall survival (OS) of patients was analyzed using Kaplan-Meier method. Additionally, proliferation ability was measured by CCK-8 assay and invasion ability of GC cell line was detected by transwell assay. Besides, Western blot was performed to measure protein levels of GC tissues and GC cell lines. Finally, Dual-Luciferase reporter assay was performed to prove the potential binding sites between LINC00511 and miR-124-3p, miR-124-3p and EZH2. RESULTS: We found that LINC00511 was significantly increased in GC tissues and GC cell lines, which was associated with tumor growth, metastasis and predicted poor diagnosis of GC patients. MiR-124-3p was decreased in GC tissues and GC cell lines, which was negatively correlated with LINC00511 and EZH2. Furthermore, EZH2 was increased in GC tissues and GC cell lines, which was positively correlated with LINC00511. Moreover, LINC00511 inhibition repressed cell proliferation and invasion in MKN28 cells, the protein levels of Cyclin D1, ICAM-1, VCAM-1 and N-cadherin were repressed, while E-cadherin was increased. Besides, Luciferase gene reporter assay indicated that LINC00511 could sponge with miR-124-3p, which could directly target at EZH2, an oncogenic gene. We found that miR-124-3p/EZH2 axis regulated cell proliferation and invasion in MKN28 cells. Finally, the inhibited cell proliferation and invasion abilities were eliminated following with miR-124-3p inhibition in MKN28 cells with LINC00511 knockdown. CONCLUSIONS: According to the results, we found that LINC00511 was increased in GC tissues, which was associated with the poor OS in patients with GC. We uncovered a previously unappreciated LINC00511/miR-124-3p/EZH2 signaling axis in promoting cell proliferation and invasion in GC patients and GC cell lines, which suggested that it might be a potential target for treating human GC.

Glycogen synthase kinase-3 reduces acetylcholine level in striatum via disturbing cellular distribution of choline acetyltransferase in cholinergic interneurons in rats.

Cholinergic interneurons, which provide the main source of acetylcholine (ACh) in the striatum, control the striatal local circuits and deeply involve in the pathogenesis of neurodegenerative diseases. Glycogen synthase kinase-3 (GSK-3) is a crucial kinase with diverse fundamental functions and accepted that deregulation of GSK-3 activity also plays important roles in diverse neurodegenerative diseases. However, up to now, there is no direct proof indicating whether GSK-3 activation is responsible for cholinergic dysfunction. In the present study, with combined intracerebroventricular injection of Wortmannin and GF-109203X, we activated GSK-3 and demonstrated the increased phosphorylation level of microtubule-associated protein tau and neurofilaments (NFs) in the rat striatum. The activated GSK-3 consequently decreased ACh level in the striatum as a result of the reduction of choline acetyltransferase (ChAT) activity. The alteration of ChAT activity was due to impaired ChAT distribution rather than its expression. Furthermore, we proved that cellular ChAT distribution was dependent on low phosphorylation level of NFs. Nevertheless, the cholinergic dysfunction in the striatum failed to induce significant neuronal number reduction. In summary, our data demonstrates the link between GSK-3 activation and cholinergic dysfunction in the striatum and provided beneficial evidence for the pathogenesis study of relevant neurodegenerative diseases.