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关键词： 三联雾化   头孢曲松钠   IL-6   小儿支气管肺炎   WBC   hs-CRP  

摘要： 评估头孢曲松钠+三联雾化应用在小儿支气管肺炎(BP)中的效果及对白细胞计数(WBC)、白介素-6(IL-6)、超敏C反应蛋白(hs-CRP)的影响。方法 择取40例BP患儿(2023年7月—2024年11月),依据随机数表法的分组运行规则,将全部病例均分至:对照组20例(头孢曲松钠),观察组20例(增加三联雾化),评价组间生化指标(WBC、IL-6、hs-CRP)、肺功能参数[肺总容量(TLC)、肺活量(VC)、残气量(RV)/TLC]、时间指标、临床有效率、药品不良反应(ADR)。结果 治疗后,与对照组相对比,观察组WBC、IL-6、hs-CRP、RV/TLC均更低,TLC、VC、临床有效率均更高,时间指标更佳,P<0.05,ADR无差异,P>0.05。结论 对BP患儿予以头孢曲松钠+三联雾化,可以降低WBC、IL-6、hs-CRP水平,改善肺功能,优化时间指标,增强整体疗效,安全性良好。

关键词： 中西医结合   情绪调节   急性淋巴细胞白血病   化疗反应  

摘要： 探讨中西医结合护理联合情绪调节对急性淋巴细胞白血病(ALL)患者化疗反应和心理状态的影响。方法 选取我院收治的82例急性淋巴细胞白血病患者作为研究对象,以随机数字表法分为观察组及对照组,对照组应用常规护理,观察组采取中西医结合护理联合情绪调节措施,对比两组患者的的药物不良反应程度、凝血功能障碍、疲乏程度、情绪状态。结果 观察组的药物不良反应程度低于对照组(P<0.05),负性情绪评分在干预后低于对照组(P<0.05)。结论 中西医结合护理联合情绪调节措施,对于ALL患者的化疗不良反应和心理状态均有改善作用,可增强患者的化疗耐受性。

关键词： 老年患者   细菌性肺炎   IL-6   PCT   SAA   CRP  

摘要： 探讨老年肺炎患者血清IL-6、PCT、SAA、CRP指标表达及病情评估中的作用。方法 本研究聚焦于特定时间跨度,即2023年11月至2024年11月期间,于本院接受诊疗的老年肺炎患者群体。经严格筛选,最终纳入符合研究标准的老年肺炎患者共计200例。依据细菌培养这一关键检测手段所得结果,将这些患者精准划分为细菌性肺炎患者组(包含86例)以及非细菌性肺炎患者组(包含114例)。进一步地,针对细菌性肺炎患者组,采用CURB-65评分系统进行细致分层,其中得分处于0-1分区间被划定为低危组,该组患者有37例;得分在2-3分区间被划定为中危组,包含26例患者;得分达到4-5分区间被划定为高危组,有23例患者。与此同时,选取同期在本院进行健康体检的老年人群100例作为对照组。随后,对所有研究对象进行血清IL-6、PCT、SAA、CRP水平的检测工作。检测结果表明,老年细菌性肺炎患者的血清炎性因子水平显著高于非细菌性肺炎患者以及对照组,差异具有统计学意义(P<0.05)。此外,高危老年肺炎患者的血清炎性因子水平高于低危和中危患者,差异同样具有统计学意义(P<0.05)。结论 老年细菌性肺炎患者的血清炎性因子水平相对处于较高状态,且病情越严重,上述指标水平越高。

关键词： psoriasis   PsA   prevention   TNF inhibitors   narrow-band UVB phototherapy  

摘要： Objectives Conflicting data exist on TNF inhibitors' (TNFi) role in preventing PsA in psoriasis. Using propensity score matching, we compared PsA incidence in severe psoriasis patients treated with TNFi vs narrow-band ultraviolet B (nbUVB) phototherapy over a decade of *** Consecutive adults with severe psoriasis prescribed TNFi or nbUVB phototherapy between September 2005 and September 2010 were enrolled. Of 946 patients, 497 received TNFi (median follow-up 9.6 +/- 2.6 years) and 449 underwent nbUVB (9.4 +/- 5.9 years). All had rheumatologist assessment before therapy and for PsA diagnosis. PS matching was adjusted for factors linked to PsA, including arthralgia, family history, BMI, PASI and psoriasis distribution, including *** After propensity score matching, the TNFi cohort contributed 2705.5 person-years of follow-up (mean 9.1 +/- 2.9 years), and the nbUVB cohort contributed 2654.1 person-years (mean 8.9 +/- 5.4 years). The PsA incidence rate per 100 patients was 1.18 (0.84-1.52) in the TNFi group and 2.48 (2.24-2.72) in the nbUVB group, yielding an incidence rate ratio of 2.1 (1.37-2.98, P = 0.0002). A time-dependent Cox model confirmed that TNFi treatment was associated with a significantly lower risk of PsA (HR = 0.32, P < 0.0001). Arthralgia (HR = 7.68, P < 0.0001), nail psoriasis (HR = 1.93, P = 0.0004) and higher PASI score (HR = 1.03 per point, P = 0.0096) were independent predictors of *** This PS-matched study shows a clear benefit of TNFi vs nbUVB in PsA reduction in severe psoriasis patients over nearly a decade of therapy.

关键词： MHC class I chain-related gene B   MICB antibody   Allotype response   Panel reactive antibody test   Kidney transplant  

摘要： BackgroundAntibodies against non-HLA antigens, such as MICA and MICB, have emerged as potential contributors to antibody-mediated rejection and graft failure. While MICA antibodies are well characterized, MICB-specific antibodies remain poorly understood due to the lack of standardized detection tools. To address this gap, we aimed to develop a cell-based platform expressing individual MICB antigens to evaluate the feasibility of detecting allele-specific anti-MICB antibodies in pre-kidney transplant *** class I, MICA, and MICB-null human embryonic kidney (HEK)-293T cells were previously generated by CRISPR/Cas9. We established five cell lines expressing single MICB antigens (each MICB*002, *003, *004, *005:02, and *008 allele). A total of 64 pre-kidney transplant sera were tested to assess anti-MICB antibody responses to the five cell lines using flow *** successfully established and validated five HEK-293T cell lines each expressing a single MICB antigen using anti-MICB monoclonal antibody staining. No anti-MICB antibodies were detected in any of the 64 pre-transplant sera tested. This finding may reflect a low incidence of sensitization to MICB in this patient population and suggests the need for larger, more diverse cohorts in future studies to fully assess the prevalence of anti-MICB responses. The established cell lines provide a promising tool for future investigation of allele-specific anti-MICB antibody *** the present study did not detect allele-specific anti-MICB antibody responses, establishing HEK-293T cell lines expressing single MICB antigens represents a significant methodological advance. This platform enables the potential assessment of immune responses targeted to individual MICB allotypes, thus offering new avenues for the future study of MICB immunogenicity in transplantation settings.

关键词： demethylation   inflammation   lung injury   PM2.5   TET1  

摘要： PM2.5 has been linked to a variety of lung diseases. The objective of this study was to investigate the mechanism of lung inflammation caused by acute exposure to PM2.5 from the perspective of DNA methylation. Sprague-Dawley male rats were exposed to different concentrations of PM2.5 by non-exposure intratracheal instillation every other day for 3 times. Chemically modified si-Foxa1, si-Tet1, and si-NC were administered via the intratracheal instillation, followed by exposure to a medium concentration of PM2.5. Fourteen days following the final exposure, serum, bronchoalveolar lavage fluid (BALF), and lung tissues were collected for the appropriate tests. Acute exposure to PM2.5 resulted in infiltration of inflammatory cells and destruction of the alveolar structure. The levels of IL-4 and eotaxin-1 in serum and BALF were increased, while the levels of interferon-gamma (IFN-gamma) were decreased. In lung tissues, there was a decrease in the whole genome 5-mC and an increase in 5-hmC. The methylation level of the interleukin-4 (IL-4) DNA promoter CpG islands decreased, accompanied by an increase in the mRNA level. The protein expression of Forkhead box A1 (FOXA1) and ten-eleven translocation methylcytosine dioxygenase 1 (TET1) was upregulated. Downregulation of FOXA1 and TET1 levels reversed those changes. PM2.5 induced the upregulation of FOXA1 and TET1 protein expression, which subsequently affected the DNA methylation levels of IL-4. This, in turn, promoted the release of IL-4 and led to pulmonary inflammation. This study provides insights into the potential DNA methylation regulatory mechanisms underlying lung inflammation induced by acute PM2.5 exposure.

关键词： Prostate cancer   Neutrophils   Androgen receptor   IL-8   CXCL1  

摘要： The role of immune cells, particularly neutrophils, in the prostate cancer (PCa) progression remains poorly understood. In this study, we investigated the impact of neutrophils on PCa progression using an in vitro co-culture migration assay. Our findings revealed that PCa cells recruited more neutrophils than normal prostate epithelial cells. Importantly, the recruitment of neutrophils to PCa cells led to increased PCa cell proliferation. Further mechanistic investigations revealed that co-culture of PCa cells with neutrophils led to increased secretion of the chemokine CXCL1. This, in turn, stimulated neutrophils to produce the cytokine IL-8. The enhanced CXCL1/IL-8 signaling axis subsequently amplified androgen receptor (AR) signaling in PCa cells, thereby promoting their proliferation. Disruption of this pathway via IL-8 neutralizing antibodies or AR knockdown reversed the neutrophil-induced PCa cell proliferation. These findings were validated in a mouse model and further supported by clinical sample analysis. Collectively, our study highlights the therapeutic potential of targeting the newly identified signaling cascade involving infiltrating neutrophils within the PCa microenvironment. Understanding and modulating this pathway may offer novel strategies to suppress PCa progression.

关键词： Multiple sclerosis   Edaravone   Demyelination   Kynurenine pathway   NLRP3 inflammasome   Cuprizone (CPZ) model  

摘要： Multiple sclerosis (MS) is a neurodegenerative disorder involving various pathways that affect disease progression and treatment. The kynurenine pathway (KP) has gained attention in MS studies, contributing to demyelination and disease progression. This study aimed to explore the pharmacological effects of edaravone (EDV) on the corpus callosum and the spinal cord in the cuprizone (CPZ) animal model of demyelination. Male Wistar rats were randomly divided into the control, CPZ, and CPZ-EDV groups. CPZ (500 mg/kg/day) was administered via oral gavage for eight weeks, and at the start of the 5th week, EDV (5 mg/kg/day,I.P.) was initiated and continued for 4 weeks. EDV ameliorated behavioral and motor deficits in CPZ-intoxicated rats and promoted the differentiation of oligodendrocyte progenitor cells by activating OLIG2, enhancing re-myelination. This was demonstrated by increased density of myelinated nerve fibers and OLIG2+ cells co-expressing myelin basic protein (MBP), indicating enhanced OPC differentiation and remyelination. EDV also reduced the inflammatory mediators TNF-alpha and NF-& kgreen;B, and diminished the activation of NLRP3 inflammasome, inhibiting the release of IL-1 beta. Furthermore, EDV decreased indoleamine 2,3-dioxygenase-1 (IDO1) mRNA expression and activity, as well as the protein levels of kynurenine 3-monooxygenase (KMO), leading to reduced neurotoxic metabolites (quinolinic and anthranilic acid) while elevating the neuroprotective metabolite kynurenic acid (KYNA). In conclusion, EDV exerted neuroprotective effects by reducing inflammation, inhibiting the KP's neurotoxic metabolites, and promoting remyelination through OLIG2 activation. These effects are possibly attributed to EDV's action on TNF-alpha/NF-& kgreen;B/NLRP3 signaling and the KP.

关键词： autoimmune disease   ANCA-associated vasculitis   glomerulonephritis   antigen specific   T cells   anti-cytokine biologics  

摘要： Introduction This study investigates the therapeutic potential of blocking key CD4+ Th1 effector cytokines, TNF-alpha and IFN-gamma, in experimental anti-myeloperoxidase (MPO) glomerulonephritis (GN). The immunopathogenesis of MPO autoimmunity is biphasic, with an initial transient Th17 dominance followed by a sustained Th1 response, posing challenges for effective cytokine *** To evaluate anti-cytokine therapy at distinct disease phases, we induced anti-MPO autoimmunity in mice through MPO immunization and triggered GN using anti-glomerular basement membrane (GBM) globulin at early (day 20) and late (days 32 and 38) stages. Mice received anti-TNF-alpha or anti-IFN-gamma beginning 4 hours post-GN induction, with kidney injury assessed 4 or 10 days *** In early anti-MPO GN (day 20), neither anti-TNF-alpha nor anti-IFN-gamma mitigated kidney injury, consistent with Th17-driven autoimmunity at this stage. However, in late, established GN (day 32), TNF-alpha blockade significantly attenuated kidney injury, indicating its pathogenic role in Th1-driven disease. At day 32, IFN-gamma neutralization induced a Th2 phenotypic shift, increasing IL-4 production in ex vivo MPO-stimulated lymph node cells and upregulating alternatively activated M2 macrophages. Despite this immunological shift, short-term IFN-gamma blockade failed to confer renal protection. To assess whether prolonged IFN-gamma neutralization is beneficial, we extended the induced kidney injury phase to day 38. In this setting, extending anti-IFN-gamma treatment effectively attenuated kidney injury, highlighting its therapeutic potential in late-stage *** These findings highlight the dynamic role of Th1 cytokines in anti-MPO GN, with TNF-alpha blockade benefiting established disease, while IFN-gamma neutralization requires prolonged intervention. This study informs Th1-targeted strategies in MPO anti-neutrophil cytoplasmic antibody (ANCA)-associated GN.

关键词： Sea buckthorn   casuarictin   amylase   lipase   TNFalpha synthesis   ellagitannins  

摘要： This study focused on fractionation of Hippophae rhamnoides L. leaves to obtain higher added value fractions enriched with bioactive compound casuarinin and its isomer casuarictin and to isolate casuarictin and their biological properties. Fractionation with ethylacetate produced fractions enriched with predominantly casuarinin and both isomers casuarinin and casuarictin. The individual compound casuarictin (94% purity) was prepared through liquid-liquid extraction and HPLC. The structure was confirmed by 1H NMR data. In vitro tests demonstrated that the samples inhibit digestive enzymes amylase and lipase and reduce inflammation in human blood model stimulated by lipopolysaccharide. Casuarictin and the fractions showed a novel inhibitory effect on pancreatic lipase. Additionally, they strongly inhibited the synthesis of tissue necrosis factor alpha (TNFalpha) induced by LPS in human blood ex vivo. These findings suggest potential of seabuckthorn leaves as a new valuable raw material and its active component casuarictin for applications in the nutraceuticals, human diets and so on.