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Relation between disulfidptosis-related genes and prognosis or immunotherapy of pancreatic cancer: based on bioinformatics analysis

ObjectiveTo investigate the relation between disulfidptosis-related genes (DRGs) and prognosis or immunotherapy response of patients with pancreatic cancer (PC). MethodsThe transcriptome data, somatic mutation data, and corresponding clinical information of the patients with PC in The Cancer Genome Atlas (TCGA) were downloaded. The DRGs mutated in the PC were screened out from the 15 known DRGs. The DRGs subtypes were identified by consensus clustering algorithm, and then the relation between the identified DRGs subtypes and the prognosis of patients with PC, immune cell infiltration or functional enrichment pathway was analyzed. Further, a risk score was calculated according to the DRGs gene expression level, and the patients were categorized into high-risk and low-risk groups based on the mean value of the risk score. The risk score and overall survival of the patients with high-risk and low-risk were compared. Finally, the relation between the risk score and (or) tumor mutation burden (TMB) and the prognosis of patients with PC was assessed. ResultsThe transcriptome data and corresponding clinical information of the 177 patients with PC were downloaded from TCGA, including 161 patients with somatic mutation data. A total of 10 mutated DRGs were screened out. Two DRGs subtypes were identified, namely subtype A and subtype B. The overall survival of PC patients with subtype A was better than that of patients with subtype B (χ2=8.316, P=0.003). The abundance of immune cell infiltration in the PC patients with subtype A was higher and mainly enriched in the metabolic and conduction related pathways as compaired with the patients with subtype B. The mean risk score of 177 patients with PC was 1.921, including 157 cases in the high-risk group and 20 cases in the low-risk group. The risk score of patients with subtype B was higher than that of patients with subtype A (t=14.031, P<0.001). The overall survival of the low-risk group was better than that of the high-risk group (χ2=17.058, P<0.001), and the TMB value of the PC patients with high-risk was higher than that of the PC patients with low-risk (t=5.642, P=0.014). The mean TMB of 161 patients with somatic mutation data was 2.767, including 128 cases in the high-TMB group and 33 cases in the low-TMB group. The overall survival of patients in the high-TMB group was worse than that of patients in the low-TMB group (χ2=7.425, P=0.006). ConclusionDRGs are closely related to the prognosis and immunotherapy response of patients with PC, and targeted treatment of DRGs might potentially provide a new idea for the diagnosis and treatment of PC.

视网膜光化学损伤感光细胞凋亡的分子基础

视网膜光化学损伤动物模型是研究视网膜变性类疾病的良好模型，研究发现凋亡是视网膜感光细胞光化学损伤以及其它视网膜变性疾病感光细胞丢失的主要机制。本文阐述了核转录因子kappa;B（NFkappa;B）体系，arrestin蛋白家族，AP-1和神经营养因子受体P75NTR等调控感光细胞凋亡的分子机制。 （中华眼底病杂志，2004，20：396-398）

A Correlative Analysis of the Dropout in 40 Peritoneal Dialysis Patients in the Hospital

目的:调查我院腹膜透析患者死亡和转HD治疗的原因及相关影响因素。方法: 收集腹膜透析患者在我院死亡14例,转HD治疗 2 6例;查阅40例患者在我院的完整病历资料,调查其死亡及转HD治疗的原因及感染病原菌、营养等指标。结果: 14例腹膜透析死亡患者主要原因为肺部感染合并心脑血管疾病及消化道出血,均占(29%,4/14)。643%(9 / 14)的死亡患者HBlt;90 g/L,ALBlt;30 g/l;71.4%(10 / 14)的腹膜透析死亡患者合并钙磷失调。 26例腹膜透析患者转HD的首要原因和次要原因分别为腹透相关性腹膜炎(50%,13/26)和透析液引流不畅(42%,11/26)。72.7%透析液引流不畅的腹透患者经影像学诊断漂管,27.3%患者为拔管手术证实网膜堵塞管口。结论: 1.肺部感染性疾病合并合并心脑血管系统及消化系统,为腹膜透析患者死亡的主要原因,与全身营养状况不良,钙磷失调有关。 2. 腹膜透析相关性腹膜炎仍为腹膜透析患者退出转HD治疗的主要原因。 3.因透析液引流不畅而拔管为转HD治疗的第二位原因,漂管和网膜阻塞管口为透析液引流不畅的原因。

Association between C-reactive protein change and outcome after stroke

Objective To explore the association between C-reactive protein (CRP) change and the prognosis of patients with stroke. Methods Individuals who were diagnosed with stroke from the 2011 China Health and Retirement Longitudinal Study (CHARLS) registry were included. The baseline characteristics in 2011, blood tests in 2011 and 2015, and follow-up data in 2018 were collected. The patients were divided into three groups according to their CPR change from 2011 to 2015, and the cut-off values of CRP change were 0 and 5 mg/L. Logistic regression analysis was performed to evaluate the association between CRP change and the risk of death after stroke. Results A total of 1065 participants diagnosed in 2011 were enrolled. There were 383 participants in the CRP decreased group (CRP change ranging from –74.30 to –0.01 mg/L), 584 participants in the CRP stable group (CRP change ranging from 0 to 4.98 mg/L), and 98 participants in the CRP increased group (CRP change ranging from 5.00 to 79.27 mg/L). By 2018, the numbers (rates) of deaths in CRP decreased group, CRP stable group, and CRP increased group were 25 (6.53%), 33 (5.65%), and 13 (13.27%), respectively, and the difference in the mortality among the three groups was statistically significant (P=0.020). Logistic regression analysis showed that the CRP change≥5 mg/L was associated with a higher risk of death after stroke [odds ratio=2.332, 95% confidence interval (1.099, 4.946), P=0.027]. Conclusions Increasing CRP levels over time may indicate an increased risk of death in stroke patients. A 4-year increase in CRP greater than 5 mg/L may be an independent predictor of the risk of long-term death in stroke patients.

The effects of lens-specific overexpression of OSM on the eye development in the transgenic mice

Objective To determine the effects of lensspecific overexpression of OSM on the eye development. Methods A truncated mouse OSM c DNA (661 bp) was linked to the αA-crystallin promoter. Transgenic mice were characterized by routine histological and immunohistochemical techiniques. TUNEL assays were used to de tect cell death. The mRNA expression of caspase-3 was detected by in situhybridization, Rabbit anti-cleavage caspase-3 antibody was used to detectactive capase-3. Results At embryonic day (E) 14.5 and 17.5, expression of the OSM transgenic protein was detected specifically in lens fiber cells. The onset of retinal degeneration in the mid portion of the transgenic retinae was observed started from E17.5. By the time of birth 50% or more of the retinal cells were missing. The OSM transgenic retinal cells underwent apoptosis indicated by TUNEL assays. Most strikingly, activation of caspase-3 protein were observed throughout the transgenic retinas. Conclusions Lens-specific overexpression of OSM activate caspase-3, leading to abnormal eye development,apoptosis and widespread retinal degeneration. (Chin J Ocul Fundus Dis，2003，19：201-268)

氧自由基诱导培养的牛视网膜色素上皮细胞凋亡的研究

Lenvatinib + transarterial chemoembolization + PD-1 antibody in the treatment of hepatocellular carcinoma with main portal vein tumor thrombus and cavernous transformation: four case reports

Objective To summarize the effect of lenvatinib + transarterial chemoembolization (TACE) + programmed cell death protein-1 (PD-1) antibody in the treatment of hepatocellular carcinoma with main portal vein tumor thrombus and cavernous transformation. Methods In this study, we reported the clinical data of four patients with hepatocellular carcinoma with main portal vein tumor thrombus and cavernous transformation who received conversion therapy with lenvatinib combined with TACE and PD-1 antibody in West China Hospital. Results Among the four patients, two patients achieved complete response and two achieved partial response; tumor markers were significantly decreased after combination treatment. However, all four patients failed to undergo hepatectomy. ConclusionsLenvatinib + TACE + PD-1 antibody is effective for hepatocellular carcinoma with main portal vein tumor thrombus and cavernous transformation. However, there are still many problems worthy of further discussion.

Apoptosis of photoreceptors in the early stage of siderotic retinopathy in rat

Objective To demonstrate if apoptosis is one of the mechanisms of siderotic retinopathy. Methods Autoclaved iron particles were implanted in the vitreous cavities of 32 eyes of SD rats.Glass chips were implanted in 10 control eyes.The experimental eyes were enucleated at various time intervals from days 1 to 15.Retinal degeneration was examined using the TdT-mediated,dUTP-biotin nickend labeling(TUNEL)method.Electrophoresis on agarose gel was used to detect internucleosomal DNA fragmentation.Results TUNEL-positive nuclei were observed only in the outer nuclear layer beginning on day 2.The nuclei spread throughout the outer nuclear layer by the end of day 3.No TUNEL-positive nuclei were observed in other layers throughout the experimental perios.Analysis of DNA,extracted from the retinas by electrophoresis on agarose gel,revealed a typical ladder pattern of internucleosoma DNA cleavage in the experimental eyes.ConclusionApoptosis of photoreceptors occurs at the early phase of iron-induced retinopathy in the rats.

儿童癫痫的 50 年随访研究：医疗结局、发病率和药物治疗

描述儿童癫痫的长期预后，尤其侧重于癫痫发作缓解、复发、药物治疗、相关神经系统功能障碍、死亡率和死亡原因。针对 1962 年—1964 年间基于人群总数为 195 例癫痫发作儿童队列的一项前瞻性纵向研究。数据均通过医疗记录和调查问卷收集。来自最初队列 94% 的随访数据显示，无智力或神经功能障碍的患儿，无癫痫发作的长期预后最好。这些患儿发病较晚，癫痫发作的持续时间较短，且通常不使用药物。他们中仅少数曾复发。全面性而非局灶性癫痫，通常较少复发，持续用药更短。 “真正发病”组，即在 1962 年—1964 年间纳入的发病患儿，无癫痫发作的长期预后最好，90% 在 50 年后癫痫无发作。尽管该组中仅 10% 在随访时仍有发作，但 22% 仍使用抗惊厥药物，且常使用传统药物—苯巴比妥或苯妥英钠作为抗癫痫药物之一。整个组的标准化死亡率（Standardized mortality ratio，SMR）为 2.61，且在有无其他神经系统缺陷的患者之间无差异。年轻的死亡患者部分有神经系统损伤，部分死于癫痫相关的情况，而年龄较大的患者死亡通常由非癫痫相关疾病导致。发病组中无患者死于癫痫猝死（Sudden unexpected death in epilepsy，SUDEP）。我们 12 年的随访和以往的报道相比，儿童癫痫患者的 50 年长期随访总体显示出更好的癫痫无发作结局。文章报道了癫痫发作较低的复发率，癫痫发作的缓解并不意味着药物治疗的终止，SUDEP 相关的死亡率也低于以往的报道。

The associations between stress hyperglycemia ratio and all-cause/cardiovascular/diabetes-related mortality in advanced cardiovascular-kidney-metabolic syndrome

ObjectiveTo investigate the association between the stress-induced hyperglycemia ratio (SHR) and all-cause, cardiovascular, and diabetes-related mortality in patients with advanced cardiovascular-kidney-metabolic (CKM) syndrome, and to evaluate the value of SHR as an independent prognostic marker. MethodsThis retrospective cohort study used data from the 1999–2018 U.S. National Health and Nutrition Examination Survey (NHANES). A total of 2 135 patients with advanced CKM (stages 3 and 4) were included. Kaplan-Meier analysis and multivariable Cox regression models were applied to assess the relationship between SHR and mortality outcomes. Restricted cubic spline (RCS) analysis was employed to explore potential non-linear associations. Subgroup analyses were conducted to identify possible effect modifiers. ResultsOver a mean follow-up of 248 months, 674 all-cause, 198 cardiovascular, and 31 diabetes-related deaths occurred. Elevated SHR was significantly associated with diabetes-related mortality (HR=3.48, P<0.001) in a dose-response manner. SHR exhibited a U-shaped relationship with both all-cause and cardiovascular mortality (non-linearity P<0.001), indicating increased risk at both low and high SHR levels. Subgroup analyses revealed that sex, BMI, and hyperlipidemia significantly modified the association between SHR and diabetes-related death. ConclusionSHR is an independent predictor of mortality risk in patients with advanced CKM syndrome, particularly for diabetes-related death. These findings support the integration of SHR into risk stratification of high-risk CKM populations and provide a basis for metabolic stress-targeted interventions.