Reinke's Edema: Cold Steel Versus Radiofrequency Coblation.

OBJECTIVE: This study compared the effects of radiofrequency (RF) coblation and cold steel (CS) surgery for the treatment of Reinke's edema (RE). METHODS: A retrospective analysis was conducted on 61 patients with RE, with 33 (54.1%) in the CS surgery group and 28 (45.9%) in the RF coblation group. The primary endpoints were the bilateral operation time and dyspnea severity, assessed preoperatively and at 1 and 3 months postoperatively. Secondary endpoints included subjective and objective vocal assessments, laryngovideostroboscopy (LVS) images, and Voice Handicap Index-10 (VHI-10) scores obtained before and at 1 and 3 months postoperatively. RESULTS: The average bilateral operation time was significantly shorter in the RF coblation group (24.2 ± 3.9 min) compared to the CS group (38.4 ± 5.2 min) (P = .041). All patients experienced a decrease in their Dyspnea Severity Index (DSI) scores postoperatively, with no significant differences observed between the two groups at any time point. However, improvements in the grade of hoarseness, roughness, and asthenia were significantly greater in the RF coblation group than in the CS group (P < .001). There were no statistically significant differences in breathiness and strain between the two groups. The average VHI-10 score significantly decreased from preoperative values in both groups (P < .001), with no significant differences observed between the two groups at any time point. CONCLUSIONS: The RF coblation procedure is a reliable and safe method for RE surgery, offering an effective treatment choice for RE.

Gut microbiota is correlated with gastrointestinal adverse events of metformin in patients with type 2 diabetes.

Aim: Gastrointestinal discomfort is the most common adverse event in metformin treatment for type 2 diabetes. The mechanism of action of metformin is associated with gut microbiota. However, the gut microbial community structure related to metformin-induced gastrointestinal adverse events remains unclear. This study aimed to investigate it. Methods: 50 patients with newly diagnosed diabetes were treated with metformin 1500mg/d for 12 weeks. The patients were divided into two groups according to whether gastrointestinal adverse events occurred (group B) or did not occur (group A) after treatment. The fecal bacterial communities and short-chain fatty acids (SCFAs) were sequenced and compared. 70 diabetes mice were randomly divided into 8 groups and treated with metformin (Met), clindamycin (Clin) and/or SCFA, which were the Met+/Clin+, Met+/Clin-, Met-/Clin+, Met-/Clin-, Met+/SCFA+, Met+/SCFA-, Met-/SCFA+ and Met-/SCFA- group. After 4 weeks of metformin treatment, blood glucose, food intake, fecal SCFAs, gut microbiota and gut hormones were measured. Results: Metformin increased the abundance of Phascolarctobacterium, Intestinimonas and Clostridium III. Functional prediction analysis showed that the propanoate metabolism pathway was significantly up-regulated. The concentrations of acetic acid and propanoic acid in feces were significantly increased. The abundance of Clostridium sensu stricto, Streptococcus and Akkermansia induced by metformin in group B was higher than that in group A. The propanoate metabolism pathway and propanoic acid in feces were significantly up-regulated in group B. In the animal experiments, the food intake decreased and glucose control increased in metformin groups compared with those in the control groups. The total GLP-1 level in the Met+/Clin- group was significantly higher than that in the Met-/Clin- group, while there was no statistical difference between the Met-/Clin- and Met+/Clin+ group. The total GLP-1 level in the Met-/SCFA+ group was significantly higher than that in the Met-/SCFA-group, while the levels of total GLP-1 and active GLP-1 in the Met+/SCFA- group and the Met+/SCFA+ group were significantly higher than those in the Met-/SCFA-group. Conclusions: Our data suggest that metformin promotes the secretion of intestinal hormones such as GLP-1 by increasing the abundance of SCFA-producing bacteria, which not only plays an anti-diabetic role, but also may causes gastrointestinal adverse events.

Confirmation of the Absence of Somogyi Effect in Patients with Type 2 Diabetes by Retrospective Continuous Glucose Monitoring Systems.

Background: The Somogyi effect is defined as fasting hyperglycemia secondary to nocturnal hypoglycemia. In past decades, this effect proved to be rare or absent. However, many endocrinologists still believe in this phenomenon in clinical practice. Does the Somogyi effect truly exist? We aimed to answer this question with a study based on a larger sample size. Methods: We collected retrospective CGMs data from 2,600 patients with type 2 diabetes with stable treatment of insulin. Nocturnal hypoglycemia was defined as a CGMs sensor glucose of less than 3.9 mmol/L for at least 15 min between 24:00 and 06:00. Morning fasting glucose was compared between people with nocturnal hypoglycemia and without nocturnal hypoglycemia. Results: Valid CGMs data were obtained on 4,705 of 5,200 nights. Morning fasting glucose was observed lower after nights with nocturnal hypoglycemia compared with nights without hypoglycemia (P < 0.001). 84 cases presented fasting glucose of more than 7 mmol/L after nocturnal glucose of less than 3.9 mmol/L. Only 27 cases presented fasting glucose of more than 7 mmol/L after nocturnal glucose of less than 3.0 mmol/L. Fasting glucose values below 3.9 mmol/l in the morning were associated with a 100% risk of nocturnal hypoglycemia, while fasting glucose values over 9.6 mmol/l in the morning were associated with no risk of nocturnal hypoglycemia. Correlation analysis showed that the nocturnal glucose nadir was significantly correlated with fasting glucose levels (r = 0.613, P < 0.001). Conclusions: Our data provided no support for the existence of the Somogyi effect. If fasting glucose exceeds 9.6 mmol/L, we do not have to worry about asymptomatic nocturnal hypoglycemia in patients with type 2 diabetes.

Alterations of sleep quality and circadian rhythm genes expression in elderly thyroid nodule patients and risks associated with thyroid malignancy.

To study the alterations of sleep quality and circadian rhythm genes expressions upon elderly thyroid nodule patients, the risk factors associated with thyroid malignancies, and the potential relationship involved. The elderly people enrolled in our study were divided into three groups according to the thyroid histopathology: malignant nodule group, benign nodule group, and normal group, and the clinical data and sleep quality were collected. Among the patients of surgery, 56 fresh thyroid tissues were collected for real-time PCR, immunohistochemistry and western blotting analysis of CLOCK, BMAL1, CRYs and PERs. Poor sleep quality, sleep latency and daytime dysfunction were the independent risk factors of malignant nodule after adjusted by other impacts. The expression levels of CLOCK, BMAL1 and PER2 in thyroid malignant group were significantly higher than benign and normal groups, while CRY2 was decreased, p < 0.05. In addition, CLOCK and BMAL1 protein levels were positively correlated with PSQI of corresponding patients and CRY2 was negatively correlated. Circadian rhythm genes mainly altered in malignant nodules, and sleep disorders may be involved in the occurrence of elderly thyroid malignancy through the high expressions of CLOCK and BMAL1, and low expression of CRY2.

Von Willebrand Factor Deficiency Improves Hepatic Steatosis, Insulin Resistance, and Inflammation in Mice Fed High-Fat Diet.

OBJECTIVE: The aim of this study was to investigate the effect of Von Willebrand factor (VWF) on high-fat diet (HFD)-induced hepatic steatosis, insulin resistance, and inflammation in mice. METHODS: The expression of VWF was detected in obese mice. Wild-type and VWF knockout mice were fed a normal chow diet or an HFD, and then biomedical, histological, and metabolic analyses were conducted to identify pathologic alterations. Inflammatory cytokine levels and the number of hepatic macrophages were determined in these mice fed an HFD. RESULTS: VWF expression was significantly increased in obese mice. VWF-/- mice were less obese and had improved hepatic steatosis, balance of lipid metabolism, and insulin resistance in response to HFD. Furthermore, VWF deficiency attenuated HFD-induced systemic and hepatic inflammation. In addition, VWF deficiency rescued the abnormal accumulation of hepatic macrophages. CONCLUSIONS: These data demonstrated VWF deficiency improves hepatic steatosis, insulin resistance, and inflammation. Furthermore, the protective effects are mediated via regulation of hepatic macrophages.

The Half-Life of Serum Thymidine Kinase 1 Concentration Is an Important Tool for Monitoring Surgical Response in Patients with Lung Cancer: A Meta-Analysis.

AIMS: In this meta-analysis, we evaluated the usefulness of serum thymidine kinase 1 concentration (STK1c) for monitoring the outcome of extensive open surgery in patients with lung cancer. We also compared STK1c between a healthy population and patients with benign and malignant lung tumors to assess its potential value for early detection of lung cancer and for distinguishing between benign lung disease and malignant cancer. MATERIALS AND METHODS: Related studies were retrieved from publications in PubMed, Cochrane, China National Knowledge Infrastructure, Wanfang databases, and Internet searches. Correlation was evaluated using weighted mean difference. Fixed or random effect models were selected for data analyses based on heterogeneity tested with the chi-square test. Publication bias was assessed using a funnel plot and Egger's test. RESULTS: Twenty studies were selected for analysis, which showed that STK1c was significantly (p < 0.00001) reduced by 41.7% 1 month after extensive open surgery, approximately corresponding to an STK1c half-life of 1 month. STK1c levels were significantly higher in lung cancer patients than in healthy persons (p < 0.00001) or in patients with benign lung disease (p < 0.00001). There was also a significant difference in STK1c between patients with benign and malignant lung disease (p < 0.0001). CONCLUSIONS: The half-life of STK1c may be an important tool in the clinical evaluation of surgical response in patients with lung cancer. STK1c may also be beneficial in the early detection of lung cancer.

Effects of resveratrol on the expression and DNA methylation of cytokine genes in diabetic rat aortas.

This paper studies the expression of proinflammatory cytokines such as IL-1ß, IL-6, TNF-α, and IFN-γ and anti-inflammatory cytokines such as IL-10 in diabetic rat aortas, the effects of resveratrol on these cytokines, and the potential epigenetic mechanisms involved. The experiment was performed on rats divided into four groups: normal group (NC), normal interventional group (NB), diabetic group (DM), and diabetic interventional group (DB). The NB and DB groups were treated with resveratrol. After more than 3 months, the rats' aortas were removed and analyzed for cytokines by using immunohistochemistry, Western blotting, real-time PCR, and methylation-specific PCR. Histological localization of these cytokines was mainly found in the arterial intima of diabetic rats. The protein and mRNA expression levels of IL-1ß, IL-6, TNF-α, and IFN-γ were significantly higher in the DM group than in the NC group (p < 0.05), whereas in the resveratrol-treated groups (NB and DB), the levels were relatively lower than those in the corresponding groups. The DM group showed reduced levels of DNA methylation at the specific cytosine phosphate guanosine sites of IL-1ß, IL-6, TNF-α, and IFN-γ, relative to those in the NC group (p < 0.01), and these levels were increased by resveratrol. In contrast, IL-10 was dramatically methylated and showed decreased expression in response to high glucose, and resveratrol reversed this effect. These results demonstrate that the inflammatory response is involved in diabetic macroangiopathy. Resveratrol inhibits the expression of proinflammatory cytokines and thus may have a protective effect on the aorta in hyperglycemia. Thus, DNA methylation, an epigenetic gene silencing signal, may be responsible for these two phenomena.