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.
ObjectiveTo systematically review the associations of cognitive frailty with mortality and hospitalization in the elderly. MethodsThe VIP, PubMed, CNKI, WanFang Data, CBM, Embase, Cochrane Library and Web of Science databases were electronically searched to collect cohort studies on the association of cognitive frailty with mortality or hospitalization in the elderly from inception to May, 2023. Two reviewers independently screened the literature, extracted data and assessed risk of bias of the included studies. Meta-analysis was performed by R 4.2.2 software. ResultsA total of 19 cohort studies involving 63 624 elderly were included. The results of meta-analysis showed that compared with healthy elder, the elder with cognitive frailty had a higher mortality (OR=2.75, 95%CI 2.10 to 3.59, P<0.01) and hospitalization (OR=1.67, 95%CI 1.40 to 2.00, P<0.01). Subgroup analysis showed that cognitive frailty was related to the risk of death in different status of frailty and cognitive function, different assessment tools, different countries of development, different follow-up time and research sites. At the same time, different status of frailty and cognitive function and different levels of development of countries were related to the risk of hospitalization. ConclusionCurrent evidence shows that cognitive frailty can increase the risk of hospitalization and mortality in the elderly. It is suggested that early screening and intervention of cognitive frailty should be carried out to effectively reduce the risk of adverse consequences, so as to achieve healthy aging.
Pyroptosis is a newly discovered form of cell death. Through the activation of inflammasome complexes, pyroptosis induces the production of interleukin (IL) -1β and IL-18, and the osmotic swelling of cells, thus induces cellular rupture and death. It plays a role in the pathological process of a variety of human diseases. The death of retinal cells including photoreceptor cells and retinal pigment epithelium (RPE) cells is the main reason leading to visual dysfunction in the pathogenesis in ocular fundus diseases. Researches have demonstrated that pyroptosis is closely related to the onset and progression of various retinal diseases. In age-related macular degeneration, pyroptosis directly causes apoptosis of RPE cells and upregulation of pro-inflammatory factors, enhancing toxic effect of lipofuscin. For retinitis pigmentosa, pyroptosis is the leading manner of death of secondary cone photoreceptor cells. In cytomegalovirus retinitis, pyroptosis is the main responding way to infection. This review presented the molecular mechanism of pyroptosis and its role in age-related macular degeneration, retinitis pigmentosa and cytomegalovirus retinitis and other retinal diseases.
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)。643%(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。
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.
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)
Risk stratifications are valuable aids for stratifying patients by disease severity, driving informed clinical decisions, because they allow the selection of the most appropriate strategy of treatment based on the patient's individual characteristics. The clinical algorithms help patients and their families to get a better understanding of issues relevant to treatment strategies and subsequent risks as part of the process to obtain informed consent. The current risk stratifications of coronary artery bypass grafting included the Society of Thoracic Surgeons Score, the European System for Cardiac Operative Risk Evaluation, SinoSystem for Coronary Operative Risk Evaluation. This review focuses on the progress of risk stratifications of coronary artery bypass grafting for patients undergoing cardiac surgery.
Objctive To explore the relationship between the expression of Fas/FasL and the apoptosis occurs in retinal ischemia/reperfusion injury of rats , as well as the therapeutic effects of bFGF on the ischemic retina.Methods Th emodels of retinal ischemia/reperfusion injury was made by transient elevating introcular pressure. A total of 28 rats were divided into normal and operation group.The latter were subdivided into 1 hour, 6, 12, 24, 48 and 72 hours after reperfusion group, in which the left eyes of the rats were in the ischemia/reper fusion groups and the right ones were in the treatment groups (bFGF intracameral injection). Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) method, and the expression of Fas and Fas ligand was studied by strept avidin-biotin complex （SABC）immunohistochemistry. Results No positive cells were observed in the normal rats′retinae, but there was a significant number of TUNEL positive cells in 6-24 hours after transient ischemia followed by a decrease at the 48th hour. The number of TUNEL positive cells reached a maximum at the 24th hour after ischemia. The expression of Fas gradually increased as early as when it was at the 6th hour, reached a peak at the 24th hour, and then decreased at the 48th hour. Similarly, the expression of Fas ligand was at peak in 24-48 hours in GCL and INL of retina. Conclusions Retinal ischemia-reperfusion after transient elevated IOP induced apoptosis of cells in the retina. Fas/FasL may play an important role in the early events of the apoptotic pathways. bFGF can rescue RGCs from retinal ischemia/reperfusion injury through downregulation of the expression of Fas/FasL and may represent an important mechanism for therapeutic neuroprotection. (Chin J Ocul Fundus Dis，2003，19：160-163)