ObjectiveTo explore the morbidity rate and risk factors of proliferative diabetic retinopathy (PDR) in type 2 diabetes.MethodsThe clinical data of patients, with PDR in 2739 consecutive cases of type 2 diabetes diagnosed in this hospital from 1994 to 2001 were analyed retospectively. The diagnosis of diabetic retinopathy (DR) was confirmed by ophthalmoscopy and fundus fluorescein angiography (FFA). Blood pressure, fasting and postprandial blood sugar, glycosylated haemoglobin（HbA1c）, total serum cholesterol, triglyceride, creatinine, and albumin excretion rate were measured.ResultsThe morbidity rate of type 2 DR was 27.8%（761/2739）, and the morbidity rate of PDR was 4.2%（114/2 739） occupying 15% of the patients with DR. The duration, fasting blood sugar, glycosylated haemoglobin, blood pressure and albumin excretion rate were much higher than those in the control（P＜0.01, glycosylated haemoglobin P＜0.05）. The independent risk factors of PDR were duration of the disease （r=0.15, P＜0.01） and albumin excretion rate （r=0.08, P＜0.05）. The risk factors of PDR were albumin excretion rate and fasting blood sugar (r=0.13, P＜0.05) in patients with longer duration(≥5 years). The morbidity rate of PDR was 2.3%, 5.9% and 12.4% in patients with duration less than 5 years, 5 to 10 years and over 10 years groups, respectively. The morbidity of PDR of the patients in normal albuminuria, microalbuminuria and overt albuminuria group was 2.1%、5.3% and 18.8% respectively.ConclusionsType 2 diabetes accompanied with PDR is relative to the duration of the diabetes, albumin excretion rate, fasting blood sugar, blood pressure, and glycosylated haemoglobin, in which the duration of the disease, albuminuria and fasting blood sugar are the risk factors of occurance of PDR. (Chin J Ocul Fundus Dis, 2003,19:338-340)
ObjectiveTo analyze the expression and clinical significance of cyclin-dependent kinase 1 (CDK1) in lung adenocarcinoma by bioinformatics.MethodsBased on the gene expression data of lung adenocarcinoma patients in The Cancer Genome Atlas (TCGA), the differential expression of CDK1 in lung adenocarcinoma tissues and normal lung tissues was analyzed. The expression of CDK1 gene in lung adenocarcinoma was analyzed by UALCAN at different angles. Survival analysis of different levels of CDK1 gene expression in lung adenocarcinoma was performed using Kaplan-Meier Plotter. Correlation Cox analysis of CDK1 expression and overall survival was based on clinical data of lung adenocarcinoma in TCGA. Gene set enrichment analysis was performed on gene sequences related to CDK1 expression in clinical cases. The protein interaction network of CDK1 from Homo sapiens was obtained by STRING. CDK1-related gene proteins were obtained and analyzed by the web server Gene Expression Profiling Interactive Analysis (GEPIA).ResultsBased on the analysis of TCGA gene expression data, CDK1 expression in lung adenocarcinoma was higher than that in normal lung tissues. UALCAN analysis showed that high CDK1 expression may be associated with smoking. Survival analysis indicated that when CDK1 gene was highly expressed, patients with lung adenocarcinoma had a poor prognosis. Univariate and multivariate Cox regression analysis of CDK1 expression and overall survival showed that high CDK1 expression was an independent risk factor for survival of patients with lung adenocarcinoma. Gene set enrichment analysis revealed that high CDK1 expression was closely related to DNA replication, cell cycle, cancer pathway and p53 signaling pathway.ConclusionCDK1 may be a potential molecular marker for prognosis of lung adenocarcinoma. In addition, CDK1 regulation may play an important role in DNA replication, cell cycle, cancer pathway and p53 signaling pathway in lung adenocarcinoma.
OBJECTIVE: To explore the mechanism of microvascular spasm after limb ischemia-reperfusion. METHODS: The rabbit hindlimb normothermic tourniquet ischemia model was employed. The tendon on the dorsum of the foot was exposed for observation of microvessels. The responses of arterioles on tendon surface to topical application of 10(-6) mol/L noradrenaline (NE) (a vasoconstrictor), 10(-6) mol/l acetylcholine(Ach) (an endothelium-dependent vasodilator) and 10(-4) mol/L nitroglycerin(NTG) (an endothelium-independent vasodilator) were observed at the period of ischemia and following 30 minutes of reperfusion after 2 hours and 5 hours of ischemia by use of intravital microscopy. RESULTS: No significant changes in the responses of arterioles to NE, Ach and NTG were noted following 30 minutes of reperfusion after 2 hours of ischemia compared with pre-ischemia. The constrictor responses of arterioles to NE were still not significantly altered following 30 minutes of reperfusion after 5 hours of ischemia, however, the dilation responses to Ach and NTG were significantly decreased (to Ach P lt; 0.01; to NTG, P lt; 0.05). CONCLUSION: Reperfusion after 5 hours of ischemia significantly impairs both the endothelium-dependent and endothelium-independent vasodilation, meanwhile preserves constrictor responses to NE, these may contribute to the genesis of the vasospasm in ischemia reperfusion.
ObjectiveTo explore therapeutic mechanisms and clinical application prospects of novel weight-loss medications in patients with obesity complicated by cardiovascular-kidney-metabolic (CKM) syndrome, aiming to provide theoretical support and therapeutic strategies for personalized precision management of CKM syndrome. MethodsRecent domestic and international studies were retrospectively reviewed, focusing on the mechanisms of action, clinical research outcomes, and application progress of novel weight-loss medications, including glucagon-like peptide 1 (GLP-1) receptor agonists, dual glucose-dependent insulinotropic peptide (GIP)/GLP-1 receptor agonists, triple GIP/GLP-1/glucagon receptor agonists, and amylin analogues. Special emphasis was placed on their comprehensive effects on cardiovascular, renal, and metabolic parameters. ResultsNovel weight-loss medications had demonstrated significant weight reduction and multisystem benefits through precise regulation of central appetite pathways, insulin sensitivity, and lipid metabolism. Among these medications, GLP-1 receptor agonists (e.g., semaglutide) and dual agonists (e.g., tirzepatide) had been confirmed in phase Ⅲ clinical trials (STEP and SURMOUNT studies) to effectively reduce cardiovascular event risks, slow renal function deterioration, and markedly improve glycemic control in obese patients with CKM syndrome. Triple agonists (e.g., retatrutide) and combination therapies (e.g., cagrisema) have further enhanced weight-loss efficacy, providing novel therapeutic avenues for obesity-related diseases. Additionally, these medications usually require combined application with traditional chronic disease medications, such as sodium-glucose linked transporter 2 inhibitors and renin-angiotensin-aldosterone system blockers, to achieve comprehensive therapeutic outcomes in CKM syndrome patients. However, further studies are needed to address long-term safety in real-world settings, optimization of drug formulations, and application in precision medicine. ConclusionsNovel weight-loss medications offer promising strategies for personalized precision treatment of obesity with CKM syndrome due to their significant weight-loss efficacy and multisystem synergistic effects. Although current clinical trials demonstrate substantial therapeutic potential, the complexity of CKM syndrome and individual patient variability necessitate additional in-depth research to facilitate broader clinical adoption and optimization of these medications.
Objective To explore the role and clinical significance of cell-cycle dependent kinase 1 (CDK1) and its upstream and downstream molecules in the development of malignant peripheral nerve sheath tumor (MPNST) through the analysis of clinical tissue samples. Methods A total of 56 tumor samples from MPNST patients (“Tianjin” dataset) who underwent surgical resection, confirmed by histology and pathology between September 2011 and March 2020, along with 17 normal tissue samples, were selected as the research subjects. MPNST-related hub genes were identified through transcriptome sequencing, bioinformatics analysis, immunohistochemistry staining, and survival analysis, and their expression levels and prognostic associations were analyzed. Results Transcriptome sequencing and bioinformatics analysis revealed that upregulated genes in MPNST were predominantly enriched in cell cycle-related pathways, with CDK1 occupying a central position among all differentially expressed genes. Further differential analysis demonstrated that CDK1 mRNA expression in sarcoma tissues was significantly higher than in normal tissues [based on searching the cancer genome atlas (TCGA) dataset, P<0.05]. In MPNST tissues, CDK1 mRNA expression was not only significantly higher than in normal tissues (based on Tianjin, GSE141438 datasets, P<0.05), but also significantly higher than in neurofibromatosis (NF) and plexiform neurofibromas (PNF) (based on GSE66743 and GSE145064 datasets, P<0.05). Immunohistochemical staining results indicated that the expression rate of CDK1 protein in MPNST tissues was 40.31%. Survival analysis results demonstrated that CDK1 expression was associated with poor prognosis. The survival time of MPNST patients with high CDK1 mRNA expression was significantly lower than that of the low expression group (P<0.05), and the overall survival trend of patients with positive CDK1 protein expression was worse than that of patients with negative CDK1 expression. Additionally, differential analysis of CDK family genes (CDK1-8) revealed that only CDK1 was significantly upregulated in MPNST, NF, and PNF. Conclusion Increased expression of CDK1 is associated with poor prognosis in MPNST patients. Compared to other CDK family members, CDK1 exhibits a unique expression pattern, suggesting its potential as a therapeutic target for MPNST.
Objective To investigate the effect of the synthetic bone morphogenetic protein 2 (BMP-2)derived peptide on the osteogenic induction in the marrow mesenchymal stem cells (MSCs）and to evaluate the osteoinductivity and dosedependence of the BMP-2 derived peptide in vitro. Methods MSCs of 4-week old Wistar rats were separated and cultured. In the 3rd passage, the conditional culture medium was changed, in which the BMP-2-derived peptide in the following doses was added: 300,200, 100, 50, and 0 μg/ml, respectively (Groups A-E). The activity of alkaline phosphatase (ALP）and the amount of calciumdeposition were meassured at 5，10，15 and 20 days during the culture with the conditional culture medium. The real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) was performed to measure the mRNA expressions of collagen type Ⅰ, osteopontin (OPN), and osteocalcin（OCN）and to measure the osteoinductivity of the BMP-2-derived peptide in the different concentrations.Results Under the inverted phase contrast microscope, MSCs cultured in the conditional culture medium for 3-4 days were changed in shape, from long fusiform to short fusiform or polygon. As the concentration of the BMP-2-derived peptide increased, the time for MSCs to change into the osteoblasts decreased. There was a significantly greater level of the ALP activity and amount of the calcium deposition in Groups A and B than in the other groups（Plt;0.05）. However,there was no significant difference between Group A and Group B （Pgt;0.05）. Theresult of FQPCR showed that after MSCs were cultured in the different doses of theconditional culture medium for 14 days, the mRNA expressions of collagen type Ⅰ, OPN andOCN were at higher levels. An increasing order in the level of the cycle threshold (Ct) was found in the following groups: Agt;Bgt;Cgt;D. Almost no expression was found in Group E. The Ct levels were significantly greater in Groups A and B thanin Groups C and D（Plt;0.05）. However, there was no significant difference between Group A and Group B （Pgt;0.05）.ConclusionThe BMP-2-derived peptide can greatly promote differentiation of MSCs into the osteoblasts, the promotion of osteogenesis has a dosedependent pattern, and the best inducing dosage is 200 μg/ml.
ObjectiveTo review the recent progress in the role of thrombospondins (TSPs) in synapse formation in the central nervous system (CNS).MethodsA wide range of domestic and foreign literature on the role of TSPs in the synapse formation of the CNS was reviewed. The role of TSPs in structural features, molecules, and related diseases was reviewed.ResultsAs an oligosaccharide protein, TSPs play important roles in angiogenesis, inflammation, osteogenesis, cell proliferation, and apoptosis. In the nervous system, they bind to voltage-dependent calcium channels, neuronectin, and other extracellular matrix proteins and cell surface receptors, and participate in and regulate multiple processes such as synapse formation, maturation, and function in the CNS.ConclusionTSPs as an oligomeric extracellular matrix protein play an important role in the formation of synapses and the repair of synapses after CNS injury.
Objective To observe macular vascular density and structural characteristics in children with transfusion-dependent β-thalassemia (TDT). MethodsA retrospective clinical study. From October 2022 to December 2023, 29 TDT children (58 eyes) diagnosed and examined at the Department of Hematology, Affiliated Hospital of Guangdong Medical University were included in the TDT group, along with 29 age- and gender-matched healthy children (58 eyes) as the control group. All participants underwent optical coherence tomography and angiography. Measurements included central macular thickness (CMT), subretinal choroidal thickness (SFCT), choroidal thickness (ChT), choroidal vascularity index, blood flow density in the superficial capillary plexus (SCP), deep capillary plexus (DCP), choriocapillaris layer (CC), and choroidal layer of the macular region, as well as the foveal avascular zone (FAZ) area of the SCP and DCP. A generalized estimating equation was used to compare differences in the above parameters between the two groups. Pearson correlation analysis was employed to examine the relationships between fundus structural parameters, blood flow density, and blood indices. ResultsCompared with the control group, the TDT group showed significantly thinner CMT (χ2=6.044) and ChT at 3.0 mm nasal (χ2=4.451) and temporal (χ2=4.767) to the fovea (P＜0.05). The TDT group also demonstrated reduced blood flow density in the inferior DCP (χ2=5.254), whole CC (χ2=3.996), and superior CC (χ2=5.094), as well as enlarged FAZ area in DCP (χ2=4.286) (P＜0.05). Correlation analysis revealed a negative correlation between SFCT and disease duration (r=−0.357, P=0.006). ConclusionsIn children with TDT, CMT and ChT become thinner and the area of FAZ expands. The blood flow densities of DCP and CC in the macular area decreased.
The temperature dependence of relative permittivity and conductivity of ex-vivo pig liver, lung and heart at 2 450 MHz was studied. The relative permittivity and conductivity of three kinds of biological tissues were measured by the open-end coaxial line method. The dielectric model was fitted according to the principle of least square method. The results showed that the relative permittivity and conductivity of pig liver, pig lung and pig heart decreased with the increase of tissue temperature from 20 to 80 ℃. The relative permittivity and conductivity models of pig liver, pig lung and pig heart were established to reflect the law of dielectric properties of biological tissue changing with temperature and provide a reference for the parameters setting of thermal ablation temperature field.
ObjectiveThe re-hospitalization and death events of patients heart failure caused by coronary heart disease are characterized by non-independence, heterogeneity, and censored data. A joint frailty model is established to jointly model the events, explore the risk factors affecting the prognosis of patients, and reduce the re-hospitalization rate and mortality of patients. MethodsThe sample included 4 682 patients with heart failure caused by coronary heart disease in two tertiary hospitals from January 2014 and June 2019. The electronic medical record information of patients during hospitalization and their follow-up information were collected. The Cox model, conditional frailty model and joint frailty model were used to analyze patient re-hospitalization and death. ResultsThe joint frailty model identified patients with a higher risk of both relapse and death (θ=0.209, P<0.001). Risk factors for re-hospitalization were advanced age, grade 3 hypertension, mental work, no medical insurance, high cystatin C, low ejection fraction, and low free thyroxine-3 and thyroxine-4. Antiplatelet drugs and statins significantly reduced the risk of re-hospitalization. Risk factors for death were advanced age, New York Heart Association classification Ⅲ to Ⅳ, no medical insurance, mental work, high cystatin C level, high troponin-I level, low free thyroxine-3, and low ejection fraction. Percutaneous coronary intervention, and taking antiplatelet drugs and statins significantly reduced the risk of death. ConclusionThe joint frailty model can simultaneously model recurring and terminal events, and accurately predict them. Our results suggest that thyroid hormone levels and cystatin C levels of patients should be considered more carefully. People with mental jobs should change bad working habits to reduce adverse outcomes.