The Change of Interleukin-6 and Tumor Necrosis Factor in Patients with Obstructive Sleep Apnea Syndrome

The levels of lipopolysaccharide (LPS) induced interleukin 6 (IL 6) and tumor necrosis factor α (TNF α) expression in culture of peripheral blood mononuclear cells (PBMC) and the plasma levels of IL 6 and TNF α in the patients with obstructive sleep apnea syndrome (OSAS) were measured and the relationship between OSAS and IL 6 or TNF α expression studied. Both IL 6 and TNF α were detected by using ELISA in 22 patients with OSAS and 16 normal controls. The levels of LPS induced IL 6 (787.82±151.97 pg/ml) and TNF α (4165.45±1501.43 pg/ml) expression in the supernatant of the culture of PBMC and plasma level of IL 6 (50.67±4.70 pg/ml) and TNF α (299.09±43.57 pg/ml) in the patients with OSAS were significantly higher than those in the normal controls (in the supernatant of the culture of PBMC: 562.69±197.54 pg/ml and 1596.25±403.08 pg/ml respectively; in the plasma: 12.69±2.75 pg/ml and 101.88±21.27 pg/ml respectively). There were significantly positive correlation between the levels of IL 6 and TNF α and the percentage of time of apnea and hyponea, as well as the percentage of time spending at SaO 2 below 90 % in the total sleep time. It was concluded that LPS induced IL 6 and TNF α levels as well as plasma IL 6 and TNF α levels in the patients with OSAS were up regulated, which may be associated with the pathogenesis of OSAS.

DETERMINATION OF URINE TUMOR NECROSIS FACTOR, IL-6, IL-8 AND SERUM IL-6 IN PATIENTS WITH HEMORRHAGIC FEVERS WITH RENAL SYNDROME

Objective To explore the roles of cytokines in the pathogenesis of hemorrhagic fever with renal syndrome（HFRS）. Methods Double-antibody sandwich ELISA was used to determine serum interleukin （IL）-6, urine tumor necrosis factor （TNF）, IL-6 and IL-8 levels in 56 patients with HFRS. Results Serum IL-6, urine TNF, IL-6 and IL-8 concentrations in HFRS patients were significantly higher than those in control group, respectively （P<0.001）. The concentrations increased at fever stage, then continued to increase during hypotension stage and peaked at oliguria stage. The concentrations of serum IL-6, urine TNF, IL-6 and IL-8 increased in accord with the severity of the disease and differed greatly among different types of the disease. Serum IL-6 had remarkable relationships with serum specific antibodies. It was positively related to serum β2-microglobulin （β2-MG）, blood ureanitrogen （BUN） and creatinine （Cr）. Significant positive relationships were also found both between urine IL-6 and TNF, and between IL-6 and IL-8 （r=0.5768, P<0.05; r=0.3760, P<0.01）. Conclusion TNF, IL-6 and IL-8 activated during the course of the disease. IL-6 is associated with the immunopathological lesions caused by the hyperfunction of humoral immune response. IL-6, IL-8 and TNF are involved in the renal immune impairment. Determining them might, in certain extent, be used in predicting the prognosis and outcome of patients with HFRS.

Tumor necrosis family receptor superfamily member 9/tumor necrosis factor receptor-associated f

Hepatitis C virus(HCV)infection is an excellent immunological model for understanding the mechanisms developed by non-cytopathic viruses and tumors to evade the adaptative immune response.The antigen-specific cytotoxic T cell response is essential for keeping HCV under control,but during persistent infection,these cells become exhausted or even deleted.The exhaustion process is progressive and depends on the infection duration and level of antigenemia.During high antigenic load and long duration of infection,T cells become extremely exhausted and ultimately disappear due to apoptosis.The development of exhaustion involves the impairment of positive co-stimulation induced by regulatory cytokines,such as transforming growth factor beta 1.This cytokine downregulates tumor necrosis factor receptor(TNFR)-associated factor 1(TRAF1),the signal transducer of the T cell co-stimulatory molecule TNFR superfamily member 9(known as 4-1BB).This impairment correlates with the low reactivity of T cells and an exhaustion phenotype.Treatment with interleukin-7 in vitro restores TRAF1 expression and rescues T cell effector function.The process of TRAF1 loss and its in vitro recovery is hierarchical,and more affected by severe disease progression.In conclusion,TRAF1 dynamics on T cells define a new pathogenic model that describes some aspects of the natural history of HCV,and sheds light on novel immunotherapy strategies for chronic viral infections and cancer.

Effects of increased human tumor necrosis factor-like molecule 1A expression in peripheral blood of children with acute Guillain-Barre syndrome on interferon-gamma secretion

BACKGROUND:Human tumor necrosis factor-like molecule 1A(hTL1A) is a strong T helper cell type 1(Th1) co-stimulator.Guillain-Barre syndrome(GBS) is an autoimmune disorder of the nervous system,which is mediated by Th1 cells. OBJECTIVE:To determine hTL1A expression in peripheral blood T lymphocytes of acute GBS children and the effects of hTL1 A on secretion of interferon-γ. DESIGN,TIME AND SETTING:A randomized,controlled,neuroimmunological in vitro study was performed at the Central Laboratory of First Hospital of Jilin University,China from November 2005 to November 2007. MATERIALS:Venous blood samples were obtained from 6 healthy donors,aged 6-12 years(all routine blood examination items were normal),and 6 additional children with acute GBS,aged 6-12 years.The GBS children fell ill within 1 week and were not treated with hormones or immunoglobulin. Purified recombinant human soluble tumor necrosis factor-like molecule 1A(rhsTL1A,1 mg/mL, relative molecular mass 22 000,6×His tag,soluble form) was supplied by the Central Laboratory of First Hospital of Jilin University,China. METHODS:Peripheral blood mononuclear cells were isolated from healthy donors using the standard Ficoll gradient centrifugation and were incubated in 96-well culture plates.The cells were assigned to the following groups:control(2μg/mL phytohemagglutinin),2μg/mL phytohemagglutinin + 25,100 and 400 ng/mL rhsTL1A.T cell proliferation was quantified using the tritiated thymidine(~3H-TdR) method.Serum interferon-γlevels in acute GBS children were detected by enzyme-linked immunosorbent assay(ELISA).The ratio of hTL1 A-positive T cells to CD3-positive T cells in peripheral blood of acute GBS children was determined using flow cytometry. Following in vitro pre-activation of peripheral blood mononuclear cells by 2μg/mL phytohemagglutinin,the peripheral blood mononuclear cells were treated with 400 ng/mL exogenous rhsTL1A.Finally,peripheral blood mononuclear cell-secreted interferon-γlevels were measured by ELISA. MAIN OUTCOME MEASURES:The following parameters were measured:rhsTL1A stimulation index to stimulate proliferation of T cells;the serum interferon-γlevels in acute GBS children;the ratio of hTL1A-positive cells to CD3-positive cells;the levels of interferon-γsecreted by peripheral blood mononuclear cells in acute GBS children,as well as rhsTL1A-stimulated interferon-γlevels. RESULTS:T cell proliferation assay revealed that the stimulation index in each rhsTL1A group was greater than the control group.The stimulation index of the 400 ng/mL rhsTL1A group was the greatest.Serum interferon-γlevels in acute GBS children were significantly greater than the control group(P<0.05).The ratio of hTL1 A^+ CD3^+ T cells to CD3^+ T cells in acute GBS children was significantly greater than the control group(P<0.01).Phytohemagglutinin stimulated peripheral blood mononuclear cells to a greater extent than 400 ng/mL rhsTL1A in the acute GBS group,and the secreted interferon-γlevels were significantly increased(P<0.05). CONCLUSION:In T cells pre-activated with 2μg/mL phytohemagglutinin,proliferation was effectively increased with 400 ng/mL rhsTL1A treatment.Expression of hTL1 A was increased in activated T cells from peripheral blood of acute GBS children,followed by increased interferon-γsecretion.These mechanisms are considered to be part of the pathological process that induces the secretion of inflammatory cytokines in GBS syndrome.

Relationship of Tumor Necrosis Factor-α and Nitrogen Oxide with Treatment of Frequent Relapse Nephrotic Syndrome by Shenkangling(肾康灵)Granule in Children

Objective: To observe the relationship of tumor necrosis factor-α (TNF-α) and nitrogen oxide (NO) with the treatment of frequent relapse nephrotic syndrome (FRNS) and to explore the pathogenesis of FRNS and the therapeutic mechanism of Shenkangling(肾康灵，SKL) Granule in children.Methods: Sixty children suffering from FRNS were randomly divided into the treated group and control group, 30 in each, and the other 30 healthy children were taken as healthy group. The patients were treated with prednisone for a long-term course, and those with no effect or partial effect shown were treated with additional Tripterygium or Cytoxan in the control group, while in the treated group patients were treated with prednisone and additional SKL. The two groups were compared as to their changes of TNF-α,NO before and after treatment, and the relapses after treatment. Results: The levels of TNF-α and NO in the sick children before treatment were markedly higher than those after treatment and normal group (P＜0. 01). The positive correlation between TNF-α of FRNS cases and relapse risk displayed more significance than that between the relapse of FRNS and NO. The difference between treated group and control group was significant (P＜0. 01). Conclusion: TNF-α can be regarded as the monitoring parameter of the active phase in FRNS, and the higher the level, the more possible the relapse would occur. SKL could markedly reduce the relapse rate of FRNS in children.

Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia

Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest(CA). In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet(CV) and Fluore-Jade B(F-J B) staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1(Iba-1), glial fibrillary acidic protein(GFAP), and tumor necrosis factor-alpha(TNF-α) immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA(about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA). Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day postCA, and they were activated(enlarged cell bodies with short and thicken processes) in all layers 2 days postCA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.

Tumor necrosis factor-alpha in experimental autoimmune neuritis

Tumor necrosis factor-α (TNF-α) plays a key role in the pathogenesis of experimental autoimmune neuritis (EAN) as well as Guillain-Barrè syndrome. The proposed pathogenesis of TNF-α associated neuropathies involves immune-mediated attack to blood-nerve barrier, aggravated production of pro-inflammatory cytokines, and the induction of Schwann cells apoptosis. TNF-α may play a regulatory role by increasing production of interleukin-1 in macrophages, attenuating T cell receptor signaling and regulating apoptosis of potentially autoreactive T cells in EAN. The data suggest that antagonizing TNF-α functions or suppressing TNF-α production may be useful in the acute phase of EAN treatment, but further studies are required.

Tumor-related cytokine release syndrome in a treatment-naïve patient with lung adenocarcinoma:A case report

BACKGROUND Cytokine release syndrome(CRS)is defined as systemic inflammation that usually occurs following chimeric antigen receptor T-cell therapy administration;however,it has not been reported in patients with untreated non-small cell lung cancer to date.CASE SUMMARY A 44-year-old nonsmoking woman presented to the hospital due to fever,palpitation,nausea,and cough for 1 mo and was diagnosed with stage cT3N3M0(IIIc)adenocarcinoma of the lung.Auxiliary examinations revealed elevated cytokine[tumor necrosis factor-α,interleukin(IL)-1β,and IL-6]and inflammatory factor levels,which decreased after treatment with corticosteroids and immunoglobulin and when tumor growth was controlled following chemotherapy,radiotherapy,and antiangiogenesis therapy.However,tumor recurrence was observed.After administration of nivolumab as third-line treatment,the patient’s condition was transiently controlled;however,CRS-like symptoms suddenly emerged,which led to a resurgence of cytokines and inflammatory factors and rapid death.CONCLUSION CRS can develop in treatment-naïve lung cancer patients.Patients with tumorrelated CRS may be at risk of CRS recurrence,aggravation,and onset of immune checkpoint inhibitor-related adverse events.

Apoptosis and Expression of Protein TRAIL in Granulosa Cells of Rats with Polycystic Ovarian Syndrome

The relationship between apoptosis of granulosa cells and follicle development arrest in polycystic ovarian syndrome (PCOS) rats, and the contribution of tumor necrosis factor related apoptosis inducing ligand (TRAIL) in apoptosis of granulosa cells were explored. By using sodium prasterone sulfate rat PCOS model was induced. The apoptosis of granulosa cells in ovaries of rats was observed by TdT-mediated dUTP-biotin nick end-labeling (TUNEL), and the expression of TRAIL protein and mRNA in granulosa cells was detected by using immunhistochemical staining and reverse transcription polymerase chain reaction (RT-PCR) respectively. The apoptotic rate and the expression of protein TRAIL in granulosa cells were significantly higher in antral follicles from the PCOS rats than in those from the control rats (P<0.01, P<0.05). There was no significant difference in apoptotic rate and the expression of TRAIL protein in granulosa cells of preantral follicles between the PCOS rats and the control rats (P>0.05). No apoptosis and the expression of TRAIL protein in granulosa cells of primordial follicles were found in the two groups. The expression of TRAIL mRNA was significantly stronger in granulosa cells from the PCOS rats than in those from the con- trol rats (P<0.01). It was suggested that the apoptotic rate in granulosa cells was significantly higher in antral follicle from the PCOS rats than in those from the control rats. TRAIL played a role in regu- lating the apoptosis of granulosa cells in PCOS rats.

Alterations of biliary biochemical constituents and cytokines in infantile hepatitis syndrome

AIM: To investigate the biliary biochemical constituents and cytokines in infantile hepatitis syndrome (IHS). METHODS: From 42 IHS subjects and 21 controls, serum and biliary biochemical constituents, including total bilirubin (TBIL), direct bilirubin (DBIL), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (γ-GT), total bile acid (TBA), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) both in bile and serum, were assayed. The subjects with IHS were divided into a cholestasis group (n = 21) and a hepatitis group (n = 21). RESULTS: In the cholestasis group, serum TBIL, DBIL, ALT, γ-GT, TBA, IL-6 and TNF-α levels were higher than those in the control (P < 0.01); and also the biliary TBIL, DBIL, γ-GT and TBA levels were lower than those in the control, whereas biliary IL-6 and TNF-α levels were higher than those in the control (P < 0.01). In the cholestasis group, serum IL-6 and TNF-α levels were lower than those in bile (P < 0.01). In the hepatitis group, serum DBIL, ALT, γ-GT, TBA, IL-6 and TNF-α levels were higher than those in the control (P < 0.01 or 140.57 ± 70.32 vs 79.06 ± 35.25, P < 0.05), while biliary TBIL, DBIL, γ-GT and TBA levels were lower than those in the control (P < 0.01), and biliary IL-6 and TNF-α levels were higher than those in the control (P < 0.01). In the hepatitis group, serum IL-6 and TNF-α levels were also lower than those in bile (P < 0.01). Serum TBIL, DBIL, γ-GT, IL-6 and TNF-α levels in the cholestasis group were higher than those in the hepatitis group, while biliary IL-6 and TNF-α levels in the cholestasis group were higher than those in the hepatitisgroup. Biliary IL-6 and TNF-α were found to be more significantly increased than serum IL-6 and TNF-α in IHS (P < 0.01). The biliary IL-6 and TNF-α levels were positively correlated with serum DBIL, TBA and γ-GT levels in IHS subjects. CONCLUSION: Biliary biochemical constituents alter in coincidence with pathological changes in hepatocellular injury. Cholestasis is more serious in IHS patients of cholestasis subtype. Assay of biliary IL-6 and TNF-α levels can be specific and sensitive to determine the inflammatory status of impaired liver in IHS.

Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a mitochondria-dependent pathway mediated by cytochrome c oxidase subunit Ⅱ

Background:Tumor necrosis factor receptor-associated protein 1(TRAP1)plays a protective effect in hypoxic cardiomyocytes,but the precise mechanisms are not well clarified.The study is aimed to identify the mechanism of TRAP1 on hypoxic damage in cardiomyocytes.Methods:In this study,the effects of TRAP1 and cytochrome c oxidase subunit Ⅱ(COXⅡ)on apoptosis in hypoxia-induced cardiomyocytes were explored using overexpression and knockdown methods separately.Results:Hypoxia induced cardiomyocyte apoptosis,and TRAP1 overexpression notably inhibited apoptosis induced by hypoxia.Conversely,TRAP1 silencing promoted apoptosis in hypoxic cardiomyocytes.Further investigation revealed that the proapoptotic effects caused by the silencing of TRAP1 were prevented by COXⅡ overexpression,whereas COXⅡ knockdown reduced the antiapoptotic function induced by TRAP1 overexpression.Additionally,changes in the release of cytochrome c from mitochondria into the cytosol and the caspase-3 activity in the cytoplasm,as well as reactive oxygen species production,were found to be correlated with the changes in apoptosis.Conclusions:The current study uncovered that TRAP1 regulates hypoxia-induced cardiomyocyte apoptosis through a mitochondria-dependent apoptotic pathway mediated by COXⅡ,in which reactive oxygen species presents as an important component.

NF-κB Controls Resistance of Human Salivary Gland (HSG) Cells to Apoptosis in an <i>in Vitro</i>Model of Sjogren’s Syndrome

Aim: To elucidate the anti-apoptotic properties of nuclear factor kappa light-chain-enhancer of activated B cells (NF-κB) and feedback regulation of NF-κB by nuclear factor of kappa light-chain-enhancer of activated B-cells inhibitor alpha (IκBα). Methods: We developed an in vitro model of Sjogren’s syndrome by transfecting human salivary gland (HSG) and acinar cells (NS-SV-AC) with a plasmid-encoding IκBαM (pCMV-IκBαM), a degradation-resistant IκBα (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha)-mutant, and examined TNF-induced apoptosis and anti-apoptotic properties of NF-κB. Apoptosis and induction of pro-apoptotic and anti-apoptotic genes were investigated by cDNA arrays, RT-PCR, electrophoretic mobility shift assays, and western blot. Results: In the presence of NF-κB inhibitors, TNF-induced apoptosis was markedly increased in both salivary gland and acinar cells. Increased caspase-3 activity was present in both HSG and NS-SV-AC cells. IκBαM-transfected salivary gland cells were more sensitive to TNF-induced apoptosis than IκBαM-transfected acinar cells. Transcription of pro-apoptotic genes was confirmed in both HSG and NS-SV-AC cells that were transfected with IκBαM. Results from caspase-3 activity assay confirmed previous experiments showing an apoptotic role for NF-κB. Conclusion: Data from gene expression arrays suggest that different mechanisms may operate during TNF-induced apoptosis in salivary gland ductal and acinar cells.

瓜石汤联合当归芍药散对多囊卵巢综合征合并胰岛素抵抗小鼠的影响

目的:探讨瓜石汤联合当归芍药散对多囊卵巢综合征联合胰岛素抵抗(PCOS-IR)小鼠模型性激素和内膜炎症介质的影响。方法:用来曲唑和高脂饮食构建PCOS-IR模型小鼠,观察小鼠动情周期变化及检测小鼠空腹血糖、空腹胰岛素评价模型成功是否。将小鼠随机分为对照组、模型组、中药组,中药组造模成功后给予瓜石汤联合当归芍药散中药方灌胃,对照组及模型组给予等体积纯净水。干预21 d后用酶联免疫吸附试验(ELISA)法测定血清卵泡刺激素(FSH)、促黄体生成素(LH)、总睾酮(T)水平,检测内膜组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)的水平。结果:造模后对照组小鼠动情周期正常,模型组小鼠动情周期紊乱,多数位于动情间期;对照组小鼠胰岛素抵抗指数(HOMA-IR)均小于2.69,而模型组均大于2.69。给药21 d后,中药组小鼠血清LH、T、LH/FSH较模型组低(P<0.05),内膜组织TNF-α、IL-1β、IL-6 mRNA和蛋白表达水平较模型组低(P<0.05)。结论:瓜石汤联合当归芍药散能改善PCOS-IR小鼠血清激素水平,降低内膜炎症介质水平,改善内膜炎症。

自动腹膜透析治疗对老年心肾综合征患者的疗效

目的探讨自动腹膜透析治疗对老年心肾综合征(CRS)患者的疗效。方法回顾性分析2019年1月至2022年1月佛山市南海区人民医院治疗的老年CRS患者260例,根据随机数字表法,按照1?1将研究对象分为观察组和对照组,每组130例。对照组给予常规基础治疗和对症治疗,观察组在此基础上进行自动腹膜透析治疗。比较2组心功能指标、肾功能指标、炎性因子、平均动脉压(MAP)及心率。结果观察组治疗后左心室收缩末期内径、左心室舒张末期内径、左心房内径、N末端B型钠尿肽前体、尿素、胱抑素C、肌酐、肿瘤坏死因子α、高敏C反应蛋白水平低于对照组[(26.29±1.19)mm vs(29.59±1.84)mm,(47.43±1.39)mm vs(51.81±1.34)mm,(30.74±1.15)mm vs(33.11±0.88)mm,(1034.74±313.61)ng/L vs(2634.02±853.67)ng/L,(16.69±3.57)mmol/L vs(32.67±4.54)mmol/L,(0.47±0.13)mg/L vs(0.61±0.15)mg/L,(254.74±41.15)μmol/L vs(394.09±38.61)μmol/L,(144.14±23.16)mg/L vs(183.97±23.37)mg/L,(4.09±1.03)μg/L vs(5.45±1.17)μg/L,P<0.01],左心室射血分数水平高于对照组[(39.14±4.48)%vs(35.64±5.27)%,P<0.01]。2组治疗前、治疗后心率及MAP比较无显著差异(P>0.05)。结论自动腹膜透析治疗能够改善老年CRS患者的心功能、肾功能,降低炎性反应,对于改善预后具有积极意义。

多囊卵巢综合征人群血清CTRP7水平的变化及影响因素分析

目的探讨多囊卵巢综合征(PCOS)女性血清C1q肿瘤坏死因子相关蛋白7(CTRP7)水平的变化,并分析CTRP7与胰岛素抵抗(IR)的关系。方法选择2022年9月—2023年9月于本院内分泌科就诊的255例PCOS患者(PCOS组)和同期在本院体检中心体检的126名年轻健康女性(对照组)作为研究对象。PCOS组按BMI=25 kg/m^(2)为切点将PCOS患者又分为肥胖亚组(146例)和非肥胖亚组(109例);对照组按BMI=25 kg/m^(2)为切点又分肥胖亚组(12例)和非肥胖亚组(114例)。38例初诊的PCOS患者接受6个月单药司美格鲁肽改善胰岛素抵抗的治疗。采用酶联免疫吸附法(ELISA)检测血清CTRP7水平,分析血清CTRP7与相关代谢指标的关系。结果PCOS组血清CTRP7水平高于对照组[(165.07±65.04)vs(109.64±39.97)μg/L,P<0.05];PCOS肥胖亚组血清CTRP7水平高于PCOS非肥胖亚组[(189.09±65.19)vs(134.67±50.76)pg/ml,P<0.05]。38例肥胖PCOS患者连续使用司美格鲁肽单药治疗6个月后,治疗后的CTRP7水平较治疗前有显著下降[(174.31±61.724)vs(205.29±69.63),P<0.05]。相关性分析显示,CTRP7与BMI、WHR、FPG、2h-PG、FIns、2 h-Ins、HOMA-IR、TC、LDL-C、FAT、TEST成正相关(P<0.05),多元线性逐步回归分析表明,BMI、HOMA-IR是血清CTRP7水平的影响因素(R^(2)=0.311、0.353,F=169.68、103.17,P<0.05)。结论血清CTRP7水平在新诊断PCOS及肥胖人群中升高,可能与IR有关,PCOS患者使用司美格鲁肽改善胰岛素抵抗治疗后血清CTRP7水平较治疗前明显降低。

来曲唑联合尿促性素治疗多囊卵巢综合征不孕患者的疗效及其对IL-6、CRP及TNF-α水平的影响

【目的】探讨来曲唑联合尿促性素治疗多囊卵巢综合征不孕患者的疗效及其对白细胞介素-6(IL-6)、C反应蛋白(CRP)、肿瘤坏死因子(TNF-α)的影响。【方法】收集2019年1月至2021年1月在安康市中医医院诊治的94例多囊卵巢综合征不孕患者,按照随机数字表法分为观察组和对照组,每组47例。对照组给予来曲唑治疗,观察组在对照组基础上联合尿促性素治疗。比较两组排卵和妊娠情况及治疗前后子宫内膜容受性[子宫内膜厚度、血流阻力指数(RI)、血流搏动指数(PI)]、炎症因子(IL-6、CRP、TNF-α)、性激素[雌二醇(E_(2))、睾酮(T)、卵泡刺激素(FSH)、黄体生成素(LH)]水平。【结果】与对照组比较,观察组排卵率、妊娠率均较高(P<0.05);治疗后,两组子宫内膜厚度均增加,且观察组子宫内膜厚度大于对照组(P<0.05);治疗后,两组RI、PI水平比较,差异无统计学意义(P>0.05);治疗后,两组血清IL-6、CRP、TNF-α水平均降低,且观察组低于对照组(P<0.05);治疗后,两组E_(2)、FSH、LH水平均升高,T水平均降低,且观察组E_(2)、FSH、LH水平高于对照组,T水平低于对照组(P<0.05)。【结论】来曲唑联合尿促性素治疗多囊卵巢综合征不孕患者,可改善患者性激素水平和子宫内膜容受性,减轻慢性炎症,提高排卵率和妊娠率,值得临床推广应用。

炎症因子和代谢综合征患者肌少症的相关性分析

目的分析炎症因子和代谢综合征患者肌少症的相关性。方法纳入驻马店市中心医院2019年1月至2022年1月收治的代谢综合征患者共187例进行研究,依据是否合并肌少症分两组,其中57例患者合并肌少症设为肌少症组,其余130例患者未合并肌少症设为非肌少症组。对两组患者的各项资料进行单因素分析,对有统计学意义的因素行Logistic多因素分析,分析代谢综合征患者合并肌少症的危险因素,并分析炎症因子对代谢综合征患者合并肌少症的预测效果。结果肌少症组患者的男性占比、年龄、营养风险/不良占比、病程、糖化血红蛋白、C反应蛋白、白细胞介素-6、肿瘤坏死因子-α水平均高于非肌少症组,体重指数(BMI)、左小腿围、右小腿围、左上臂中点围、右上臂中点围、骨骼肌指数四肢骨骼肌质量指数(ASMI)、握力、步速均低于非肌少症组(P<0.05)。以代谢综合征患者合并肌少症为应变量,赋值1=合并肌少症,0=未合并肌少症。各因素均来源于P<0.05的指标,取所有样本的中位值为自变量,建立非条件Logistic回归模型,结果显示,C反应蛋白≥2.2 mg/L、白细胞介素-6≥6 ng/L、肿瘤坏死因子-α≥2.5 pg/mL均为代谢综合征患者合并肌少症的危险因素(P<0.05)。C反应蛋白、白细胞介素-6、肿瘤坏死因子-α水平对代谢综合征患者合并肌少症均有一定预测价值。结论C反应蛋白、白细胞介素-6、肿瘤坏死因子-α水平为代谢综合征患者合并肌少症的危险因素,且对肌少症的发生有一定预测价值。

解郁宁神汤联合草酸艾司西酞普兰对抑郁性神经症肝气郁结证患者血清DA、5-HT、NE及TNF-α的影响

目的:研究解郁宁神汤联合草酸艾司西酞普兰治疗抑郁性神经症肝气郁结证患者的临床疗效及对其血清多巴胺(DA)、5-羟色胺(5-HT)、去甲肾上腺素(NE)及肿瘤坏死因子-α(TNF-α)的影响,同时分析血清DA、5-HT、NE及TNF-α与汉密尔顿抑郁量表(HAMD)评分的关系,探讨解郁宁神汤抗抑郁可能的作用机制。方法:将60例抑郁性神经症肝气郁结证患者随机分为治疗组和对照组各30例,对照组患者予草酸艾司西酞普兰治疗,治疗组患者予解郁宁神汤联合草酸艾司西酞普兰治疗,治疗时间均为6周。分别记录患者治疗前后HAMD评分、不良反应发生情况,检测血清DA、5-HT、NE及TNF-α水平,并评价临床疗效。结果:治疗组总有效率为86.67%(26/30),对照组总有效率为60.00%(18/30),治疗组疗效优于对照组,差异有统计学意义(P<0.05)。治疗组不良反应发生率低于对照组,差异有统计学意义(P<0.05)。两组患者治疗后HAMD评分均较治疗前降低(P<0.05),且治疗组患者治疗后HAMD评分低于对照组(P<0.05)。两组患者治疗后血清DA、5-HT、NE水平均较治疗前升高,且治疗后治疗组患者血清DA、5-HT、NE水平均高于对照组(P<0.05)。两组患者治疗后血清TNF-α均较治疗前降低(P<0.05),且治疗组患者治疗后血清TNF-α低于对照组(P<0.05)。Spearman相关分析显示,血清5-HT水平与HAMD评分呈明显负相关(r=-0.958,P<0.05)。结论:解郁宁神汤联合草酸艾司西酞普兰治疗抑郁性神经症肝气郁结证患者的临床疗效优于单纯草酸艾司西酞普兰治疗,可减少不良反应发生率,同时解郁宁神汤联合草酸艾司西酞普兰可升高血清DA、5-HT、NE水平,降低血清TNF-α水平。

丹芪精颗粒对急进高原人员的防护作用研究

背景 急进高原作训如果缺少阶梯习服或低氧预适应训练,会增加急性高原病(acute mountain sickness,AMS)的发生风险。AMS是因急性缺氧而引起的潜在致命性疾病,可直接导致作训减员。因此,积极进行药物研发,预防AMS发生具有十分重要的意义。目的 观察口服丹芪精颗粒对快速进入高原地区人员急性高原反应的防护作用。方法 以2022年6月某部参加高原训练分队的男性官兵为研究对象,采用前瞻性、随机、对照临床试验设计,共纳入80例18~35岁官兵,随机分为治疗组和对照组,每组40例。治疗组口服丹芪精颗粒(主要由黄芪、丹参、黄精等药物组成),对照组口服红景天胶囊(主要成分为红景天),于进驻高原前7 d开始口服,共给予14 d。比较两组在进驻高原后第1天(T1)、第3天(T2)、第7天(T3)时一般情况、中医证候分级量化表和AMS量表评分、血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)、IL-8水平及药物安全性指标。结果 两组受试者的收缩压、舒张压、心率、血氧饱和度在各个时间点比较无统计学意义(P>0.05)。两组进驻高原后第7天中医证候积分与第1天比较均显著下降(P<0.05),组间比较治疗组低于对照组,但差异无统计学意义(P=0.088)。与进驻第1天比较,在进驻第3天、第7天时两组TNF-α、IL-6水平均降低(P<0.01),且治疗组优于对照组(P<0.05)。IL-8水平及AMS发生率组间差异无统计学意义(P>0.05)。肝、肾等指标两组均未见异常。结论 丹芪精颗粒可减少中医证候分级量化表评分,改善急进高原人员临床症状;可能通过降低血清TNF-α、IL-6水平,对急性高原暴露人员发生AMS起到防护作用。