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981.

Background

Both major depression and posttraumatic stress disorder (PTSD) are characterized by inflammation, increased concentration levels of proinflammatory cytokines, decreased neurogenesis followed by neuroprogression, as well as mitochondrial and the hypothalamic-pituitary-adrenal axis dysfunction. Elevated levels of oxidative stress caused by an increased activity of prooxidants over antioxidants are also observed. Based on several reports, depressive episodes can lead to the sensitization of immune-inflammatory pathways. Thus, depression, PTSD, and depression comorbid with PTSD are associated with immune-inflammatory markers. The study aimed at evaluating concentration levels of iNOS, HO-1, IL-33, and MIP-1β in depression with and without PTSD.

Methods

A total number of participants enrolled in the study was 460. Out of them, 420 subjects with various levels of depression severity constituted the study group (210 males and 210 females), and 40 subjects (20 males and 20 females) constituted the control group. Each study group comprised 60 patients (30 males and 30 females) with mild depression (MD), moderate depression (MOD), severe depression (SeD), MD and PTSD (MD + PTSD), MOD and PTSD (MOD + PTSD), SeD and PTSD (SeD + PTSD), and with PTSD alone. At 7:00 a.m., all patients had serum concentrations of iNOS, HO-1, IL-33, MIP-1β determined using ELISA.

Results

Both depression exacerbation and PTSD comorbidity led to elevated levels of iNOS, HO-1, IL-33, and MIP-1β.

Conclusion

Depression both with and without PTSD leads to elevated levels of inflammation and an oxidant/antioxidant imbalance. Alterations in both cytokines and oxidative stress are related to the mechanisms responsible for the development of depressive symptoms.  相似文献   
982.
Graphene oxides possess unique physicochemical properties with important potential applications in electronics, pharmaceuticals, and medicine. However, the toxicity following inhalation exposure to graphene oxide has not yet been clarified. Therefore, this study conducted a short-term graphene oxide inhalation toxicity analysis using a nose-only inhalation exposure system and male Sprague–Dawley rats. A total of four groups (15 rats per group) were exposed: (1) control (fresh air), (2) low concentration (0.76?±?0.16?mg/m3), (3) moderate concentration (2.60?±?0.19?mg/m3), and (4) high concentration (9.78?±?0.29?mg/m3). The rats were exposed to graphene oxide for 6?h/day for 5 days, followed by recovery for 1, 3, and 21 days. No significant body or organ weight changes were noted after the short-term exposure or during the recovery period. Similarly, no significant systemic effects of toxicological importance were noted in the hematological assays, bronchoalveolar lavage fluid (BAL) inflammatory markers, BAL fluid cytokines, or blood biochemical assays following the graphene oxide exposure or during the post-exposure observation period. Moreover, no significant differences were observed in the BAL cell differentials, such as lymphocytes, macrophages, or polymorphonuclear cells. Graphene oxide-ingested alveolar macrophages as a spontaneous clearance reaction were observed in the lungs of all the concentration groups from post 1?day to post 21 days. Histopathological examination of the liver and kidneys did not reveal any significant test-article-relevant histopathological lesions. Importantly, similar to previously reported graphene inhalation data, this short-term nose-only inhalation study found only minimal or unnoticeable graphene oxide toxicity in the lungs and other organs.  相似文献   
983.
To extend the applications of engineered nanomaterials, such as graphene oxide (GO), it is necessary to minimize cytotoxicity. However, the mechanisms underlying this cytotoxicity are unclear. Dynamic chromosomal interactions have been used to illustrate the molecular bases of gene expression, which offers a more sensitive and cutting-edge technology to elucidate complex biological processes associated with epigenetic regulations. In this study, the role of GO-triggered chromatin interactions in the activation of cox2, a hallmark of inflammation, was investigated in normal human cells. Using chromosome conformation capture technology, we showed that GO triggers physical interactions between the downstream enhancer and the cox2 promoter in human embryonic kidney 293T (293T) via p65 and p300 complex-mediated dynamic chromatin looping, which was required for high cox2 expression. Moreover, tumor necrosis factor-α (TNF-α), located upstream of the p65 signaling pathway, contributed to the regulation of cox2 activation through dynamic chromatin architecture. Compared with pristine GO and aminated GO (GO-NH2), poly (acrylic acid)-functionalized GO (GO-PAA) induced a weaker inflammatory response and a weaker effect on chromatin architecture. Our results mechanistically link GO-mediated chromatin interactions with the regulation of cox2 and suggest that GO derivatives may minimize toxicity in practical applications.  相似文献   
984.

Background

Colitis, a colonic inflammatory condition, showed a linkage with hepatobiliary disorders such as cirrhosis. It has been reported that both endogenous opioids and nitric oxide (NO) play critical roles in colitis pathogenesis. Moreover, opioid and NO levels showed elevation in patients with cirrhosis. The aim of this study was to evaluate the effect of cirrhosis on the experimental model of colitis and the possible involvement of opioidergic/nitrergic systems in rats.

Methods

Colitis was induced by acetic acid 28 days after bile duct ligation (BDL). L-NAME, as an inhibitor of NO synthase and naltrexone, as an antagonist of opioid receptors were administered intraperitoneally to animals during 3 days after induction of colitis. Macroscopic colitis lesion area, inflammatory mediators change, NO metabolite levels, and colon microscopic injuries were assessed 3 days after induction.

Results

Cirrhosis significantly reduced the severity of damages to the colon. Administration of L-NAME (10 mg/kg), naltrexone (10 mg/kg) and co-administration of L-NAME (1 mg/kg) and naltrexone (5 mg/kg) significantly decreased the protective effect of BDL on colitis. Nitrite elevated levels in BDL rats were significantly diminished in L-NAME- and naltrexone-treated animals. Histopathology parameters and cytokines level alterations in the colon of acetic acid-treated animals after BDL was reversed after injection of L-NAME, naltrexone, and co-administration of L-NAME (1 mg/kg) + naltrexone (5 mg/kg).

Conclusion

Cirrhosis improved the intestinal damages induced by acetic acid in rats which may be mediated through interaction of nitrergic and opioidergic systems.  相似文献   
985.
一氧化氮作为血管平滑肌细胞舒张的信使分子,吸入一氧化氮(inhaled nitric oxide, iNO)能够扩张肺部血管,降低肺血管阻力,从而降低肺动脉压力,而对体循环压力没有影响。国内外指南均推荐iNO用于足月儿和晚期早产儿,已证实对足月儿和晚期早产儿持续肺动脉高压和低氧性呼吸衰竭具有明显效果。但是近年来的研究显示,iNO用于胎龄<34周早产儿的超适应证治疗越来越多。该文就iNO治疗胎龄<34周早产儿的有效性、安全性、应用时机、剂量、撤离方式和与血管活性药物联合使用的国内外研究进展作一综述,以期为临床应用提供参考。  相似文献   
986.
目的 探讨反复喘息学龄前儿童呼出气一氧化氮(fractional exhaled nitric oxide,FeNO)水平与血清免疫球蛋白E(immunoglobulin E,IgE)水平的关系。方法 回顾性分析2019年6月至2021年5月南充市中心医院收治的132例学龄前喘息患儿的临床资料,根据6岁以下儿童哮喘诊断标准模型分为哮喘组(n=67)和非哮喘组(n=65),检测并比较两组患儿的FeNO、IgE水平,分析两组患儿FeNO与IgE的关系。结果 哮喘组患儿的FeNO、IgE水平均显著高于非哮喘组,差异均有统计学意义(P<0.05)。哮喘组和非哮喘组患儿的FeNO与IgE均呈正相关(r>0),FeNO水平对IgE水平有显著正向影响。结论 哮喘患儿的FeNO、IgE水平均明显升高,且两者呈正相关,FeNO和IgE联合检测有利于学龄前儿童哮喘的早期识别。  相似文献   
987.
988.
目的:观察提壶揭盖法治疗糖尿病合并便秘的临床疗效及对患者血清P物质(SP)、一氧化氮(NO)水平的影响。方法:选取70例糖尿病合并便秘患者,按随机数字表法分为治疗组和对照组,每组35例,治疗期间2组共脱落3例,最终纳入治疗组34例,对照组33例。治疗组在常规降血糖基础上基于提壶揭盖法组方治疗,对照组在常规降血糖基础上给予乳果糖联合枸橼酸莫沙必利治疗,2组均连续治疗8周。比较2组临床疗效、症状积分、排便情况、心理状态及血清SP、NO水平。结果:治疗组愈显率为91.18%,高于对照组的72.73%(P<0.05)。治疗后,2组大便干结、排便不畅、腹胀、里急后重及腹痛积分均较治疗前降低(P<0.05),治疗组大便干结、排便不畅、腹胀、里急后重及腹痛积分均低于对照组(P<0.05)。与治疗前比较,治疗后2组排便时间均缩短,排便频率均降低,大便性状均有改善(P<0.05);治疗组排便时间短于对照组,排便频率低于对照组,大便性状改善情况优于对照组(P<0.05)。治疗后,2组焦虑自评量表(SAS)、抑郁自评量表(SDS)评分均较治疗前降低(P<0.05),治疗组SAS、SDS评分均低于对照组(P<0.05)。治疗后,2组血清SP水平均较治疗前升高,血清NO水平均较治疗前降低(P<0.05);治疗组血清SP水平高于对照组,血清NO水平低于对照组(P<0.05)。结论:基于提壶揭盖法治疗糖尿病合并便秘,可以较好地改善患者的临床症状,改善其肠道动力及心理状态,促进排便。  相似文献   
989.
AIMS: This study examined the long-term effects of nitrous oxide anaesthesia on serum levels of cobalamin and folate, red cell folate levels and haematological parameters, and neurological status in elderly Omani patients. METHODS: Sixty-nine consecutive patients undergoing ophthalmic surgery were randomly and double-blind assigned to nitrous oxide or propofol anaesthesia. They met the following entry criteria: age 55 years or above, no major organ failure, no clinical signs or symptoms of cobalamin or folate deficiency, mean cell volume (MCV) 相似文献   
990.
目的:观察微波照射对兔肝脏缺血再灌注损伤中的肝功能ALT、AST、LDH、肝组织匀浆一氧化氮(NO)、一氧化氮合酶(NOs)的变化,并探讨其保护机制。方法:32只新西兰大白兔被随机分为A、B、C、D共4组。各组于术后2h、4h抽血查ALT、AST、LDH。实验结束处死获取肝脏标本,检测各组的NO、NOs并行HE染色。结果:B、C、D三组的ALT、AST、LDH显著高于A组。而C、D组的NO、NOS显著低于A、B两组,其中D组又显著低于C组。C组病理改变明显轻于D组。结论:适宜条件的微波照射预处理能明显改善缺血再灌注损伤的肝功能,减轻肝细胞损伤,而NO是该保护机制中的一个重要因素。  相似文献   
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