Clinical Observations on the Combined Use of Hyperbaric Oxygenation and Conventional Medications in the Management of Type 2 Diabetes Mellitus Concurrent With Sudden Deafness.

Objective: The aim of this study is to investigate the effectiveness of combining hyperbaric oxygen therapy (HBOT) with conventional pharmacological interventions in the management of type 2 diabetes mellitus concurrent with sudden deafness. Methods: A cohort of 96 patients diagnosed with sudden deafness was enrolled and subsequently randomized into 2 groups: a treatment group (n = 50) and a control group (n = 46). The control group received standard conventional treatment aimed at enhancing microcirculation and nutritional support for nerves, while the treatment group underwent conventional symptomatic treatment coupled with HBOT. The evaluation encompassed the monitoring of blood glucose and blood lipid levels, clinical efficacy, and absolute hearing threshold improvement in both groups. Results: Following the intervention, noteworthy reductions in blood glucose and blood lipid levels were observed in both groups compared to their respective pretreatment values. Furthermore, posttreatment values in the treatment group exhibited a statistically significant decrease in comparison to those in the control group (P < .05). On assessing clinical efficacy posttreatment, the treatment group demonstrated a significantly higher efficacy than the control group (P < .05). In addition, the absolute hearing thresholds in both groups exhibited a significant decrease posttreatment compared to baseline values. Notably, the treatment group displayed a statistically significant reduction in absolute hearing thresholds compared to the control group posttreatment (P < .05). Conclusion: The combined therapeutic approach utilizing hyperbaric oxygen exhibits effectiveness in mitigating auditory impairment among individuals manifesting sudden deafness concomitant with type 2 diabetes mellitus. Furthermore, this treatment approach is associated with a concurrent reduction in blood glucose and blood lipid levels.

Association between hs-CRP and depressive symptoms: a cross-sectional study.

Background and aim: High-sensitivity C-reactive protein (hs-CRP) is a sensitive measure of low-grade inflammation and appears superior to conventional blood tests in assessing cardiovascular disease. The purpose of this investigation was to explore the link between high-sensitivity CRP and depressive symptoms among adults. Methods and results: Multiple logistic regression and smoothed curve fitting were used to investigate the association between hs-CRP and depressive symptoms based on data from the, 2017-2020 National Health and Nutrition Examination Survey (NHANES). Subgroup analyses and interaction tests were used to assess the stability of this relationship across populations. The study comprised 6,293 non-clinical participants, which included 549 individuals with depressive symptoms. The prevalence of depressive symptoms was found to increase with increasing levels of hs-CRP. This trend persisted even after quartetting hs-CRP levels. In the fully adjusted model, each unit increase in hs-CRP was associated with a 10% increase in the odds of depressive symptoms (OR=1.10,95%CI:1.01-1.21). Participants in the highest quartile of hs-CRP had a 39% higher prevalence of depressive symptoms compared to those in the lowest quartile (OR=1.39,95%CI:1.01-1.92). Additionally, this positive correlation was more pronounced in men. Conclusions: In adult Americans, there exists a positive association between elevated hs-CRP levels and depressive symptoms, with a more prominent manifestation of this association observed in males.

The Neuroprotective Role of Neuroserpin in Ischemic and Hemorrhagic Stroke.

Tissue plasminogen activator (tPA) is commonly used to treat acute ischemic stroke within an appropriate therapeutic window. Its inhibitor, neuroserpin (NSP), is reported to exhibit neuroprotective effects on stroke. This review aims to summarize, from literature, the available evidence, potential mechanisms, and knowledge limitations regarding the neuroprotective role of NSP in stroke. All the available evidence indicates that the regulation of the inflammatory response may play a key role in the mechanisms of NSP, which involve all the constituents of the neuroimmune axis. The neuroinflammatory response triggered by stroke can be reversed by NSP, with complicated mechanisms such as maintenance and reconstruction of the structure and function of the blood-brain barrier (BBB), protection of the cells in the central nervous system, and suppression of cell death in both ischemic and hemorrhagic stroke. Moreover, available evidence strongly suggests a tPA-independent mechanism is involved in NSP. However, there are many important issues that are still unclear and need further investigation, such as the effects of NSP on hemorrhagic stroke, the role of the tPA-independent neuroprotective mechanisms, and the clinical application prospects of NSP. We believe our work will be helpful to further understand the neuroprotective role of NSP.

Chrysophanol alleviates myocardial injury in diabetic db/db mice by regulating the SIRT1/HMGB1/NF-κB signaling pathway.

Myocardial injury induced by diabetes has become an increasing health problem. Chrysophanol (CHR) has been widely studied as a potential treatment for many diseases due to its anti-inflammatory effects, but has not been investigated in regard to diabetes-induced myocardial injury. The present study evaluated the myocardial protective effects of CHR in C57BL/KsJ-db/db diabetic mice. C57BL/KsJ-db/db and C57BLKS/J mice were treated with vehicle, metformin (100 mg/kg/day) or CHR (50 or 100 mg/kg/day) for 28 days. An oral glucose tolerance test was performed to detect blood glucose levels. Blood lipids, triglycerides, total cholesterol, myocardial function-associated enzymes, namely creatine kinase (CK) and lactate dehydrogenase (LDH), and insulin levels were analyzed. TNF-α, interleukin (IL)-1ß and IL-6 inflammatory cytokine levels in serum and myocardial tissues were determined by ELISA. Expression of silent information regulator l (SIRT1) and high mobility group box 1/NF-κB pathway-associated proteins in myocardial tissues were measured by western blot analysis and immunohistochemistry. CHR treatment at both concentrations markedly decreased blood lipid and serum insulin levels, and inhibited the myocardial enzymes CK and LDH. CHR also significantly ameliorated the cardiac pathological changes in diabetic mice. The inflammatory cytokine levels that were increased in C57BL/KsJ-db/db diabetic mice were downregulated by CHR treatment. CHR also increased SIRT1 protein expression and inhibited activation of the HMGB1/NF-κB pathway. In conclusion, the present study indicates that CHR effectively protected against diabetic myocardial injury via regulation of SIRT1 and the HMGB1/NF-κB signaling pathway.

A prospective, randomised double-blind study on the anaesthetic effect of dexmedetomidine hydrochloride in brainstem tumour surgery.

CONTEXT: Brainstem tumour surgery is difficult, and accidents can easily occur. OBJECTIVE: To explore the effect of dexmedetomidine hydrochloride on brainstem tumour surgery. DESIGN, SETTING AND PARTICIPANTS: A total of 60 patients with brainstem tumours successfully operated on by our hospital from March 2016 to March 2018 were selected as subjects. INTERVENTIONS: These patients were randomised into two groups: the research group (n = 30) and control group (n = 30). Patients in the control group were given propofol together with a placebo (0.9% sodium chloride solution) to maintain anaesthesia after general anaesthesia, while patients in the research group were supplemented with dexmedetomidine hydrochloride. MAIN OUTCOME MEASURE: Awakening time, overall stability of various indicators in the operation and adverse reactions during the awakening period were observed. RESULTS: The results revealed that patients in the research group had a longer awakening time, higher mean stability rate, higher effective rate and less incidence of adverse reactions during the awakening period than the control group; the differences were all statistically significant (P < 0.05). CONCLUSION: Dexmedetomidine hydrochloride has a good analgesic effect in intraoperative anaesthesia during brainstem tumour surgery, which significantly reduces the incidence of adverse reactions. Therefore, it can be used to assist anaesthesia during brainstem tumour operations and is worthy of clinical popularisation and application.

[Effect of fas mRNA expression on cytochrome C-induced apoptosis of HL-60 cells in vitro].

The aim of this study was to investigate the effect of cytochrome C on apoptosis of HL-60 cells and to explore the mechanism of HL-60 cell apoptosis induced by cytochrome C. The HL-60 cells were treated with different concentrations of cytochrome C for 24 hours. The concentrations of cytochrome C were as follows: 0 (control group), 9.375 mg/L, 18.75 mg/L, 37.5 mg/L, 75 mg/L and 150 mg/L. The apoptosis was analyzed by flow cytometry (FCM) after HL-60 cells were treated with different concentrations of cytochrome C for 24 hours. The fas mRNA expression changes of relevant apoptotic genes were examined by reverse transcription-polymerase chain reaction (RT-PCR) after HL-60 cells were treated with different concentrations of cytochrome C for 24 hours and were analyzed half-quantitatively. The expressions of fas involved in HL-60 treated with different concentrations of cytochrome C for 24 hours were detected by Western blot. The results indicated that the flow cytometry (FCM) (PI straining) showed obvious hypo-diploid peak before G(1) phase in the treated group, and its apoptotic ratio increased in a dose-dependent manner. The fas mRNA expression levels of the relevant apoptotic genes could be detected by RT-PCR after HL-60 cells treated with different concentrations of cytochrome C for 24 hours, and the expression of fas mRNA in HL-60 cells was increased by cytochrome C in dose-dependent manner within range of 0-37.5 mg/L. It is concluded that the cytochrome C up-regulates expressions of fas mRNA and their protein so as to induce apoptosis of the HL-60 cells.