Inflammation in diabetic retinopathy: possible roles in pathogenesis and potential implications for therapy

Diabetic retinopathy, characterized as a microangiopathy and neurodegenerative disease, is the leading cause of visual impairment in diabetic patients. Many clinical features observed in diabetic retinopathy, such as capillary occlusion, acellular capillaries and retinal non-perfusion, aggregate retinal ischemia and represent relatively late events in diabetic retinopathy. In fact, retinal microvascular injury is an early event in diabetic retinopathy involving multiple biochemical alterations, and is manifested by changes to the retinal neurovascular unit and its cellular components. Currently, intravitreal anti-vascular endothelial growth factor therapy is the firstline treatment for diabetic macular edema, and benefits the patient by decreasing the edema and improving visual acuity. However, a significant proportion of patients respond poorly to anti-vascular endothelial growth factor treatments, indicating that factors other than vascular endothelial growth factor are involved in the pathogenesis of diabetic macular edema. Accumulating evidence confirms that low-grade inflammation plays a critical role in the pathogenesis and development of diabetic retinopathy as multiple inflammatory factors, such as interleukin-1β, monocyte chemotactic protein-1 and tumor necrosis factor-α, are increased in the vitreous and retina of diabetic retinopathy patients. These inflammatory factors, together with growth factors such as vascular endothelial growth factor, contribute to blood-retinal barrier breakdown, vascular damage and neuroinflammation, as well as pathological angiogenesis in diabetic retinopathy, complicated by diabetic macular edema and proliferative diabetic retinopathy. In addition, retinal cell types including microglia, Müller glia, astrocytes, retinal pigment epithelial cells, and others are activated, to secrete inflammatory mediators, aggravating cell apoptosis and subsequent vascular leakage. New therapies, targeting these inflammatory molecules or related signaling pathways, have the potential to inhibit retinal inflammation and prevent diabetic retinopathy progression. Here, we review the relevant literature to date, summarize the inflammatory mechanisms underlying the pathogenesis of diabetic retinopathy, and propose inflammation-based treatments for diabetic retinopathy and diabetic macular edema.

Inflammation-related nomogram for predicting survival of patients with unresectable hepatocellular carcinoma received conversion therapy

BACKGROUND The efficacy of conversion therapy for patients with unresectable hepatocellular carcinoma(HCC)is a common clinical concern.AIM To analyse the prognostic factors of overall survival(OS)in patients with unresectable HCC who received conversion therapy.METHODS One hundred and fifty patients who met the inclusion criteria were enrolled and divided into a training cohort(n=120)and a validation cohort(n=30).Using the independent risk factors in the training cohort,a nomogram model was constructed to predict OS for patients treated with transarterial chemoembolization following hepatic resection.The nomogram was internally validated with the bootstrapping method.The predictive performance of nomogram was assessed by Harrell’s concordance index(C-index),calibration plot and timedependent receiver operating characteristic curves and compared with six other conventional HCC staging systems.RESULTS Multivariate Cox analysis identified that albumin,blood urea nitrogen,gamma-glutamyl transpeptidase to platelet ratio,platelet to lymphocyte ratio,macrovascular invasion and tumour number were the six independent prognostic factors correlated with OS in nomogram model.The C-index in the training cohort and validation cohort were 0.752 and 0.807 for predicting OS,which were higher than those of the six conventional HCC staging systems(0.563 to 0.715 for the training cohort and 0.458 to 0.571 for the validation cohort).The calibration plots showed good consistency between the nomogram prediction of OS and the actual observations of OS.Decision curve analyses indicated satisfactory clinical utility.With a total nomogram score of 196,patients were accurately classified into low-risk and high-risk groups.Furthermore,we have deployed the model into online calculators that can be accessed for free at https://ctmodelforunresectablehcc.shinyapps.io/DynNomapp/.CONCLUSION The nomogram achieved optimal individualized prognostication of OS in HCC patients who received conversion therapy,which could be a useful clinical tool to help guide postoperative personalized interventions and prognosis judgement.

Tamanu Oil in Acne Management: Potential Anti-Inflammatory and Wound-Healing Properties for Scar Reduction

Tamanu oil, derived from the nuts of Calophyllum inophyllum, has gained increasing attention for its potential in acne management due to its purported anti-inflammatory and wound-healing properties. This analysis evaluates the efficacy of tamanu oil in acne treatment with a specific focus on its impact on inflammation and scar reduction. The novelty of this research lies in its comprehensive analysis of tamanu oil’s dual mechanism of action: reducing acne-related inflammation and promoting the healing of acne scars. Clinical trials and laboratory analyses were conducted to assess the oil’s effectiveness in diminishing erythema, swelling, and post-acne scarring compared to conventional treatments. Preliminary findings demonstrate that tamanu oil significantly reduces inflammation and accelerates wound healing, potentially offering a promising adjunct or alternative to standard acne therapies. Future research should aim to optimize formulation and application protocols, long-term effects, and comparative therapeutic efficacy with other anti-inflammatory agents. Tamanu oil offers a novel and effective approach to acne management, with potential advantages that go beyond inflammation reduction to include enhanced scar reduction, making it a subject that warrants further investigation.

Efficacy of Ulinastatin Combined with Continuous Renal Replacement Therapy in the Treatment of Sepsis Acute Kidney Injury and Its Effects on Systemic Inflammation, Immune Function and miRAN Expression

Objective: To research the effectiveness of ulinastatin in combination with continuous renal replacement therapy in treating sepsis acute kidney injury and its effect on systemic inflammation, immune function and miRAN expression. Methods: The 84 patients who were diagnosed with sepsis complicated by acute kidney injury in our hospital between May 2020 and June 2022 were chosen and randomly assigned to the study group (n = 42) and the control group (n = 42). Ulinastatin in combination with continuous renal replacement therapy was administered to the study group, whereas the control group was administered with continuous renal replacement therapy alone. Both groups’ clinical effects were observed. The levels of blood urea nitrogen (BUN), serum creatinine (SCr), tumor necrosis factor-α (TNF-α), high sensitivity Creactive protein (hs-CRP), vascular cell adhesion molecule-1 (VCAM-1), IgG, IgA, IgM, expression levels of miR-233 and miR-10a were compared among both the groups, pre-, and post-treatment. Results: The study group’s overall effectiveness rate was higher that is 95.24%, in comparison to the control group’s 78.57%, and this difference was statistically significant (P α, hs-CRP, VCAM-1, and miR-233 and miR-10a expression levels in both the study and control groups were decreased, however, the study group had reduced levels in comparison to the control group, with statistically significant differences (P P Conclusion: Ulinastatin in combination with continuous renal replacement therapy for treating sepsis acute kidney injury exhibits a positive effect and can significantly improve the systemic inflammation and immune function in patients.

Cellular Nutrition,Inflammation in Cancer Prevention and Therapy

Chronic inflammation is known to contribute to human tumorigenesis,with an estimated 20%of adult cancers being attributable to chronic inflammatory conditions caused by infectious agents as well as chronic noninfectious inflammatory diseases.Recently,chronic inflammation is regarded as an‘enabling characteristic’of human cancer.In addition,the impact of chronic inflammation is also noticed on the outcome of cancer therapy and design of new therapeutic approaches.Nutrients are necessary for maintaining general health,and most of researches have focused on their beneficial effects on immune functions.However,the effects of nutrition in regulating inflammation deserve a close attention.Naturally,the nutrition-decreased inflammation reduces the risk of cancer in healthy individuals and normalizes the physical state of cancer patients.Therefore,it is valuable to understand the cellular nutrition in modulating inflammation.In the present review,I will summarize the impacts of inflammation on tumorigenesis and discuss the benefits of nutrition in regulating inflammation and the underlying mechanisms.It is believed that nutritional approaches to regulating inflammation will open a new window for cancer prevention and therapy.

New therapeutic perspectives in irritable bowel syndrome: Targeting low-grade inflammation, immuno-neuroendocrine axis, motility, secretion and beyond

Irritable bowel syndrome(IBS)is a chronic,recurring,and remitting functional disorder of the gastrointestinal tract characterized by abdominal pain,distention,and changes in bowel habits.Although there are several drugs for IBS,effective and approved treatments for one or more of the symptoms for various IBS subtypes are needed.Improved understanding of pathophysiological mechanisms such as the role of impaired bile acid metabolism,neurohormonal regulation,immune dysfunction,the epithelial barrier and the secretory properties of the gut has led to advancements in the treatment of IBS.With regards to therapies for restoring intestinal permeability,multiple studies with prebiotics and probiotics are ongoing,even if to date their efficacy has been limited.In parallel,much progress has been made in targeting low-grade inflammation,especially through the introduction of drugs such as mesalazine and rifaximin,even if a better knowledge of the mechanisms underlying the low-grade inflammation in IBS may allow the design of clinical trials that test the efficacy and safety of such drugs.This literature review aims to summarize the findings related to new and investigational therapeutic agents for IBS,most recently developed in preclinical as well as Phase 1 and Phase 2clinical studies.

Emodin ameliorates lipopolysaccharides-induced corneal inflammation in rats

· AIM: To investigate the effect of emodin on pseudomonas aeruginosa lipopolysaccharides(LPS)-induced corneal inflammation in rats.· METHODS: Corneal infection was induced by pseudomonas aeruginosa LPS in Wistar rats. The inflammation induced by LPS were examined by slit lamp microscope and cytological checkup of aqueous humor.Corneal tissue structure was observed by hematoxylin and eosin(HE) staining. The activation of nuclear factor kappa B(NF-κB) was determined by Western blot.Messenger ribonucleic acid(m RNA) of tumor necrosis factor-α(TNF-α) and intercellular adhesion molecule-1(ICAM-1) in LPS-challenged rat corneas were measured with reverse transcription-polymerase chain reaction(RT-PCR).· RESULTS: Typical manifestations of acute corneal inflammation were observed in LPS-induce rat model,and the corneal inflammatory response and structure were improved in rats pretreated with emodin. Treatment with emodin could improve corneal structure, reduce corneal injure by reducing corneal inflammatory response. Emodin could inhibit the decreasing lever of inhibitor of kappa B alpha(IкBα) express, and the m RNA expression of TNF-α and ICAM-1 in corneal tissues was also inhibited by emodin. The differences were statistically significant between groups treated with emodin and those without treatment(P 【0.01).·CONCLUSION: Emodin could ameliorate LPS-induced corneal inflammation, which might via inhibiting the activation of NF-κB.

Development of animal models underlining mechanistic connections between prostate inflammation and cancer

The characterization of animal models has indicated that the genetic,dietary and environmental factors and hormonal imbalance may influence the risk to develop prostate inflammatory lesions and prostate cancer(PC)confirming human epidemiologic data.It is now established that the prostate inflammatory response typically results in major changes in the local microenvironment of epithelial cells of the prostate gland,including an intense stromal remodeling,activation of fibroblasts,infiltration of immune cells such as mast cells,macrophages and B and T lymphocytes and collagen deposition.The immune cells recruited at prostate inflammatory lesions and myofibroblasts may contribute to the release of numerous pro-inflammatory cytokines and chemokines that in turn can promote the oxidative stress,genomic instability and proliferation of epithelial cells.The accumulation of additional genetic and/or epigenetic alterations in prostatic stem/progenitor cells may subsequently culminate to their malignant transformation and PC initiation and progression and more particularly with advancing age.The potential mechanistic relationships between the molecular events associated with the persistent inflammatory response and prostate carcinogenesis have important implications for optimizing the current therapies against different prostatic disorders and PCs.

Effects of Religious vs. Conventional Cognitive-Behavioral Therapy on Inflammatory Markers and Stress Hormones in Major Depression and Chronic Medical Illness: A Randomized Clinical Trial

Background: Depressive disorder is often accompanied by physiological changes that may adversely affect the course of medical illness, including an increase in pro-inflammatory cytokines. Methods: We examine the effects of religious cognitive behavioral therapy (RCBT) vs. conventional CBT (CCBT) on pro-/anti-inflammatory indicators and stress hormones in 132 individuals with major depressive disorder (MDD) and chronic medical illness who were recruited into a multi-site randomized clinical trial. Biomarkers (C-reactive protein and pro-inflammatory cytokines TNF-α, IL-1β, IFN-γ, IL-6, IL-12-p70), anti-inflammatory cytokines (IL1ra, IL-4, IL-10), and stress hormones (urinary cortisol, epinephrine, norepinephrine) were assessed at baseline, 12 weeks, and 24 weeks. Differential effects of baseline religiosity on treatment response were also examined, along with effects of religiosity on changes in biomarkers over time independent of treatment group. Biomarker levels were log transformed where possible to normalize distributions. Mixed models were used to examine trajectories of change. Results: CRP increased and IL-4, IL-10, and epinephrine decreased over time, mostly in the opposite direction expected (except epinephrine). No significant difference between RCBT and CCBT was found on average trajectory of change in any biomarkers. Religiosity interacted with treatment group in effects on IL-6, such that CCBT was more effective than RCBT in lowering lL-6 in those with low religiosity whereas RCBT appeared to be more effective than CCBT in those with high religiosity. Higher baseline religiosity also tended to predict an increase in pro-inflammatory cytokines INF-γ and IL-12 (p70) and urinary cortisol over time. Conclusions: RCBT and CCBT had similar effects on stress biomarkers. CCBT was more effective in reducing IL-6 levels in those with low religiosity, whereas RCBT tended to be more effective in those with high religiosity. Unexpectedly, higher baseline religiosity was associated with an increase in several stress biomarkers.

The Akt Pathway Inhibitor Degeulin Prevents Staphylococcal Enterotoxin B Induced Splenocyte Proliferation and Inflammation

Staphylococcal Enterotoxin B (SEB) is considered a potential biological weapon. It is toxic by both inhalation and ingestion. Effects of ingestion include fever, vomiting and diarrhoea, while inhalation may additionally result in chest pain, dyspnoea, pulmonary oedema and respiratory failure. Severe exposure may be fatal and treatment relies on symptomatic support. At a cellular level, SEB up-regulates T-cell proliferation leading to a pathological inflammatory response. Deguelin, a rotenoid isolated from the African plant Mundulea sericea (Leguminosae), has been shown to reduce cellular proliferation by inhibiting the phosphoinositide 3-kinase/Akt (PI3K/Akt) signalling pathway. Using isolated murine splenocytes, we have demonstrated that treatment with deguelin reduces SEB inducing T cell proliferation by 60%. Deguelin treatment also decreased IL-2 and CCL2 secretion by splenocytes exposed to SEB. We demonstrate that targeting cellular proliferation can significantly reduce inflammation after SEB exposure and suggest that anti-proliferatives may have a role as potential generic medical counter measures if superantigens are used as biological weapons.

Proteolytic Enzyme Combination Reduces Inflammation and Oxidative Stress and Improves Insulin Sensitivity in a Model of Metabolic Syndrome

Chronic, low-level inflammation may be an independent marker of Metabolic Syndrome (MetS). Systemic Enzyme Therapy (SET), the oral administration of proteolytic enzymes, is safe and effective in the management of inflammation. Therefore, the effects of SET, as Wobenzym&reg, on the prevention and treatment of inflammation and other metabolic risk factors were assessed in a rabbit model of diet-induced MetS. Animals were fed a lipid-enriched diet for 8 weeks during which they were administered a vehicle control (control group) or Wobenzym either throughout the study period (prevention group) or beginning at the 5th week, after the development of biomarkers of MetS (treatment group). At the 8th week, both prevention and treatment groups demonstrated improved insulin sensitivity relative to the control group and reduced serum C-reactive protein (CRP) and glycosylated hemoglobin (HbA1c, P < 0.001). At 8 weeks, the prevention group, but not the treatment group, exhibited reduced total cholesterol and oxidative stress, measured as serum malondialdehyde (P < 0.001). Triglycerides and free fatty acids were reduced in both the treatment (P < 0.01) and prevention groups (P < 0.001) relative to the control group at the 8th week. Body weight and blood glucose were not affected. Enzyme therapy may have a positive effect on inflammation, insulin sensitivity, and other metabolic risk factors of MetS.

星形胶质细胞调节缺血性脑卒中的胶质瘢痕形成

背景:缺血性脑卒中是临床上主要的致死及致残性疾病之一,经血管再通获益的患者数量极其有限,故探索有效治疗手段迫在眉睫。以星形胶质细胞为主所形成的胶质瘢痕作为缺血性脑卒中的重要病理变化之一,是阻碍脑卒中后期轴突再生和神经修复的主要原因。目的:通过对缺血性脑卒中后星形胶质细胞瘢痕形成的病理过程、关键的信号调节机制和潜在治疗靶点进行分析,旨在为干预星形胶质细胞瘢痕形成以有效治疗缺血性脑卒中提供理论依据,并为促进脑卒中后康复提供新策略。方法:全面检索2010-2022年在中国知网、PubMed和Web of Science数据库收录的相关文献,中文检索词:“缺血性脑卒中、脑缺血、星形胶质细胞、胶质瘢痕、胶质增生、星形胶质细胞增多症”,英文检索词:“Ischemic stroke,Brain ischemi*,Cerebral ischemi*,Astrocyt*,Astroglia*,Glial scar,Gliosis,Astrogliosis”,经筛选后纳入78篇文献进行综述。结果与结论:①星形胶质细胞在中枢神经系统稳态的维持中具有重要作用,缺血性脑卒中发生后,星形胶质细胞从静息态转变为激活态,由于脑缺血部位损伤的严重程度的不同,其活化呈现从肿胀、增殖到胶质瘢痕形成的动态变化。②成熟的星形胶质细胞受到刺激重新进入细胞周期并发生增殖和迁移,是形成胶质瘢痕的主要细胞来源,脑室下区的神经干细胞、脑实质局部神经胶质抗原2(NG2)和室管膜细胞前体细胞也可分化为星形胶质细胞,内皮素1(ET-1)、水通道蛋白4(AQP4)、睫状神经营养因子(CNTF)和缝隙连接蛋白参与了此过程;硫酸软骨素蛋白多糖(CSPG)是细胞外基质的主要成分,同增殖的星形胶质细胞共同形成致密的胶质瘢痕屏障,阻碍了轴突的极化和延伸。③星形胶质细胞活化、增殖、迁移及促炎作用所涉及的关键信号分子的激活或者抑制调节了胶质瘢痕形成,转化生长因子β1(TGF-β1)/Smad和JAK/STAT3是经典的星形胶质细胞反应性相关通路,糖原合成酶激酶3β(GSK-3β)和受体相互作用蛋白激酶1(RIP1K)是调节炎症反应的关键分子,而关于Smad泛素化相关因子2(Smurf2)和白细胞介素17及其下游信号通路在胶质瘢痕形成中的研究相对较少,值得深入探索。④以星形胶质细胞反应性相关的信号通路、细胞增殖调控蛋白和炎症因子为靶点的药物有效抑制了缺血性脑卒中后胶质瘢痕的形成,其中临床常用药物如褪黑素和丙戊酸调节胶质瘢痕形成的作用已被发现,这使得通过抑制胶质瘢痕形成来促进神经功能恢复的药物应用于脑卒中患者成为可能。⑤然而,胶质瘢痕在脑卒中急性期发挥的神经保护作用是不可忽视的,因此如何选择合适的药物干预时机,以在保持胶质瘢痕发挥保护作用的同时促进局部微环境中的神经再生和修复是今后努力的方向。

儿童胃肠道炎性肌纤维母细胞瘤的诊断与治疗

目的总结儿童胃肠道炎性肌纤维母细胞瘤(inflammatory myofibroblastic tumor,IMT)的临床特征及诊治经验。方法回顾性分析湖南省儿童医院普外科2010年1月至2021年12月收治的11例胃肠道IMT患儿临床资料,男7例,女4例;发病年龄8个月至15岁,收集患儿临床特点、影像学检查、病理学诊断、外科治疗及随访情况等。结果11例主要以腹痛、呕吐、发热、血便及腹部肿物就诊。10例行一期手术完整切除肿瘤,其中1例术后予化疗;1例经活检确诊后未予手术,仅行化疗。11例均病理诊断明确,均获随访(随访时间6~60个月),其中9例治愈,2例带瘤生存(1例于术后2年复发)。结论儿童胃肠道IMT临床少见,手术是首选治疗方法。复发、难治性IMT的治疗亟待进一步积累经验。

乳腺熏洗方促进非哺乳期乳腺炎术后创面愈合的临床和机制研究

目的观察乳腺熏洗方熏洗对非哺乳期乳腺炎(NPM)术后创面愈合的影响,并探讨其作用机制。方法将98例NPM术后创面生肌收口期患者随机分为治疗组、对照组,每组49例,在常规换药的基础上,治疗组给予乳腺熏洗方熏洗治疗,对照组给予质量浓度为9 g/L的氯化钠溶液熏洗治疗,疗程为12 d。比较两组创腔体积缩小率、创口面积缩小率,以及创面肉芽组织状态评分、血常规[白细胞(WBC)、中性粒细胞(NEU)、中性粒细胞百分比(NEU%)、血小板(PLT)]、C反应蛋白(CRP)、红细胞沉降率(ESR)的变化情况;两组各选取5例病例,采用Western blot法检测创面组织白细胞介素-6(IL-6)、Janus激酶2(JAK2)、信号转导及转录激酶蛋白3(STAT3)蛋白表达的变化情况。结果(1)最终完成试验者94例,其中治疗组49例、对照组45例。(2)治疗组创腔体积缩小率、创口面积缩小率高于对照组(P<0.05)。(3)治疗前后组内比较,治疗组创面肉芽状态评分升高(P<0.05);组间治疗后比较,治疗组创面肉芽状态评分高于对照组(P<0.05)。(4)治疗前后组内比较,两组WBC、NEU、NEU%、PLT、CRP、ESR水平降低(P<0.05);组间治疗后比较,治疗组PLT、CRP水平低于对照组(P<0.05)。(5)治疗前后组内比较,对照组创面肉芽组织IL-6、JAK2、STAT3蛋白表达上调(P<0.05);组间治疗后比较,治疗组创面肉芽组织IL-6、STAT3蛋白表达水平低于对照组(P<0.05)。结论乳腺熏洗方熏洗能有效促进NPM术后创面愈合,其机制可能与抑制IL-6/JAK2/STAT3信号通路,进而抑制创面炎症反应有关。

益气活血法对慢性心力衰竭大鼠心肌能量代谢及炎性因子的影响

目的:基于益气活血法探讨全真一气汤合补阳还五汤对慢性心力衰竭(CHF)大鼠心肌能量代谢及炎性因子的影响。方法:将30只健康雄性SD大鼠随机分为对照组、模型组和中药组,每组10只。采用腹腔注射阿霉素制备CHF模型,中药组给予全真一气汤合补阳还五汤干预。采用酶联免疫吸附法(ELISA)检测三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)、白细胞介素6(IL-6)、N末端脑钠肽前体(NT-proBNP)水平;采用逆转录定量聚合酶链式反应(qRT-PCR)检测miR-21水平。结果:与对照组比较,模型组ATP、ADP、AMP降低(P<0.05),IL-6、NT-proBNP、miR-21表达均升高(P<0.05);与模型组比较,中药组ATP、ADP、AMP均升高(P<0.05),IL-6、NT-proBNP、miR-21表达均降低(P<0.05)。结论:益气活血法治疗可提高CHF大鼠心肌能量供应,减轻炎症反应,改善心功能。

拨针疗法联合中药对腰椎间盘突出症患者术后神经根水肿时间、疼痛介质及血清miR-141-3p的影响

目的 观察拨针疗法联合消髓化核汤对腰椎间盘突出症患者臭氧射频消融术后神经根水肿时间、疼痛介质及血清mi R-141-3p的影响。方法 将92例行臭氧联合低温等离子射频消融术的腰椎间盘突出症患者随机分为消髓化核汤组和拨针联合组,每组46例。消髓化核汤组予消髓化核汤治疗,拨针联合组在消髓化核汤组基础上予拨针疗法治疗。观察两组神经根水肿消失时间及治疗前后中医证候积分、疼痛视觉模拟量表(visual analog scale, VAS)评分、炎症指标[微小核糖核酸-141-3p(miRNA-141-3p, miR-141-3p)、可溶性肿瘤坏死因子Ⅰ型受体(soluble tumor necrosis factor receptor typeⅠ, sTNFRⅠ)、白细胞介素-17(interleukin-17,IL-17)、磷脂酶A2(phospholipase A2, PLA2)]和疼痛介质指标[甲硫氨酸脑啡肽(methionine enkephalin,Met-EnK)、缓激肽(bradykinin,BK)、 5-羟色胺(5-hydroxy tryptamine,5-HT)、 6-酮前列腺素E1α(6-keto-prostaglandin E1α, 6-keto-PGE1α)]水平的变化,并比较两组临床疗效。结果 拨针联合组总有效率为97.8%,高于消髓化核汤组的82.6%(P<0.05)。治疗后,两组中医证候积分较治疗前降低(P<0.05),且拨针联合组低于消髓化核汤组(P<0.05)。治疗后,两组VAS评分较治疗前降低(P<0.05),拨针联合组低于消髓化核汤组(P<0.05)。拨针联合组患者神经根水肿消失时间短于消髓化核汤组(P<0.05)。治疗后,两组血清IL-17、PLA2、miR-141-3p含量较治疗前降低(P<0.05),且拨针联合组低于消髓化核汤组(P<0.05);两组血清s TNFRⅠ含量较治疗前升高(P<0.05),且拨针联合组高于消髓化核汤组(P<0.05)。治疗后,两组血清Met-En K含量较治疗前升高(P<0.05),且拨针联合组高于消髓化核汤组(P<0.05);两组血清6-keto-PGE1α、5-HT、BK含量较治疗前降低(P<0.05),且拨针联合组低于消髓化核汤组(P<0.05)。结论 拨针疗法联合消髓化核汤治疗可降低腰椎间盘突出症术后血清IL-17、PLA2、miR-141-3p水平,改善疼痛介质指标,促进神经根水肿消退,提升临床疗效。

抗生素降阶梯疗法联合盐酸溴己新治疗支气管扩张伴感染的临床研究

目的:探讨抗生素降阶梯疗法联合盐酸溴己新治疗支气管扩张伴感染的疗效。方法:纳入90例支气管扩张伴感染患者作为研究对象,按照治疗方式不同将患者分为对照组(n=45)和观察组(n=45)。对照组予以常规抗生素治疗;观察组予以抗生素降阶梯疗法联合盐酸溴己新治疗。比较两组患者临床疗效、症状改善时间及住院时间、治疗前后血气分析[动脉血氧饱和度(SaO_(2))、动脉血氧分压(PaO_(2))、动脉血二氧化碳分压(PaCO_(2))]、肺功能指标[第1秒用力呼气容积实测值与预测值百分比(FEV1%pred)、FEV1与用力肺活量比值(FEV1/FVC)]和血清炎症指标[白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)]。结果:观察组患者治疗显效率高于对照组(P<0.05);观察组患者各症状改善时间及住院时间均短于对照组(P<0.05)。治疗后,两组患者SaO_(2)、PaO_(2)均升高(P<0.05),且观察组高于对照组(P<0.05);PaCO_(2)均下降(P<0.05),且观察组低于对照组(P<0.05)。治疗后,两组患者FEV1%pred、FEV1/FVC均升高,且观察组均高于对照组(P<0.05);血清IL-6、TNF-α水平均降低,且观察组均低于对照组(P<0.05)。结论:抗生素降阶梯疗法联合盐酸溴己新治疗可以更好地促进支气管扩张伴感染患者临床症状和体征消失,改善血气和肺功能,减轻气道炎症,促进患者恢复健康。

糖皮质激素短期疗法对大叶性肺炎患儿肺部炎症影响及安全性分析

目的探讨糖皮质激素短期疗法对大叶性肺炎患儿肺部炎症影响并对其安全性进行分析。方法通过随机抽签法将2020年9月—2022年10月本院收治的大叶性肺炎患儿94例分为两组,每组47例。其中,对照组采用阿奇霉素治疗,观察组则在此基础上联合糖皮质激素短期疗法。比较两组临床疗效、治疗前后肺功能、炎性因子水平、不良反应发生率。结果与对照组相比较,观察组治疗总有效率较高(P<0.05);与对照组相比较,治疗后观察组FVC、FEV_(1)、FEV_(1)/FVC、PEF水平较高,IL-6、CRP、PCT水平较低(P<0.05);与对照组相比较,观察组不良反应发生率较低(P<0.05)。结论对大叶性肺炎患儿给予糖皮质激素短期疗法,具有较高的临床疗效,同时有利于改善患儿肺功能,缓解机体炎症反应,降低不良反应发生率,具有较高的安全性。

家庭护士食疗理论在超重/肥胖代谢综合征病人饮食干预中的实证研究

目的:基于家庭护士食疗理论,探讨优化不同非营养素搭配比例的家庭护士食疗优化方案对超重/肥胖代谢综合征病人调节代谢的效果,验证家庭护士食疗理论抗炎、抗氧化的有效性。方法:招募符合标准的超重/肥胖代谢综合征受试者70例,随机分为对照组和干预组,每组各35例。对照组给予富含非营养素的家庭护士食疗方案(家庭护士®专用茶+富含非营养素的个性化饮食),干预组给予家庭护士食疗优化方案(优化非营养素的家庭护士®蛋白复配粉+家庭护士®专用茶+富含非营养素的个性化饮食)。观察干预6周后两组受试者体重、代谢指标、炎症指标及氧化应激指标。结果:干预6周后,两组体重、体质指数和腰围均有下降(P<0.05),干预组的变化值高于对照组。干预6周后,干预组低密度脂蛋白胆固醇、丙氨酸氨基转移酶、收缩压、同型半胱氨酸较干预前改善(P<0.05),两组空腹胰岛素、胰岛素抵抗指数、总胆固醇、三酰甘油、天门冬氨酸氨基转移酶、尿酸均较干预前明显改善(P<0.05)。干预6周后,干预组超敏C⁃反应蛋白、超氧化物歧化酶水平明显改善(P<0.05)。干预组饮食依从性优于对照组。结论:家庭护士食疗优化方案在减重、抗炎和抗氧化应激方面的改善效果优于富含非营养素的家庭护士食疗方案,进一步验证了家庭护士食疗理论的有效性。

家庭护士食疗理论解读

相关数据显示慢性病已成为威胁人类健康的主要因素,食疗在慢性病的治疗和康复过程中显示了积极的作用,现代医学、营养学的不断发展也赋予了食疗新的生命力,使人们获得更加健康的饮食的同时也为临床非药物慢性病干预管理提供了新思路。目前学者关注的是饮食模式或单个营养素如何作用于人体,缺乏科学系统理论的支持,而家庭护士食疗理论可以构建具有地区特色的慢性病饮食干预方案,为慢性病食疗干预提供理论依据。