Objective A total of 102 ESRD patients undergoing hemodialysis for over 3 months in our dialysis center were asked to complete the SF-36 scales.They were also assessed by Hamilton Depression Scale(HAMD17).Univariate analysis was performed to determine the impact of factors such as age,gender,employment status,education,mental status and dialysis status on their quality of life.Methods The 102 patients with ESRD undergoing hemodialysis for over 3 months in our dialysis center completed the SF-36 scales with self-administration,and they were also assessed by Hamilton Depression Scale (HAMD17).Univariate analysis was performed to determine the impact of variables such as age,gender,employment status,education,mental status and dialysis status on the quality of life in patients.Results The scores of PF,RP,BP,GH,VT,SF,RE and MH in patients were significantly lower than those in the normal controls(P

OBJECTIVETo establish a method for detecting plasma concentration of corn polysaccharide iron complex (CPIC) and investigate its absorption, distribution and elimination in rats.

METHODSUsing radioactivity isotope tracing method, we detected the radioactivity of (59)Fe-CPIC in the plasma of rats at different time points by gavages of 3 doses (28.0, 14.0, and 7.0 mg/kg) (59)Fe-CPIC in SD rats. The pharmacokinetic parameters was obtained using DAS 2.0 program for analysis of tissue distribution and elimination of (59)Fe-CPIC.

RESULTSThe standard curve was linear within the range of 0.14-141 µg/ml (r=0.9999, n=5). The average recovery was 95% with a relative standard deviation no more than 15%. The pharmacokinetic parameters at 3 doses obtained, namely t1/2 and AUC (0-), were 214∓104, 231∓110, and 181∓81 min, and 1986.3∓513.3, 737.0∓467.0, and 315.1∓226.1 mg·min-1·L(-)1, respectively. (59)Fe-CPIC were detected in all the 13 tissues types examined and high radioactivity intensity was found in the gastrointestinal tract, hematogenic organs and other organs rich in blood. (59)Fe-CPIC was eliminated after intragastric administration primarily via the feces in rats.

CONCLUSIONThe method we established is easy and specific, and the pharmacokinetic parameters of (59)Fe-CPIC fit the two- compartment open model.

Administration, Oral ; Animals ; Area Under Curve ; Coordination Complexes ; administration & dosage ; pharmacokinetics ; urine ; Feces ; chemistry ; Female ; Intestinal Absorption ; Iron ; administration & dosage ; pharmacokinetics ; urine ; Iron Radioisotopes ; Male ; Polysaccharides ; administration & dosage ; isolation & purification ; pharmacokinetics ; urine ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tissue Distribution ; Zea mays ; chemistry

Objective .To prove aristolochic (AA) caused vascular endothelial cells (VEC) injury via intracellular calcium overloa-ding and investigate the mechanism of calcium dobesilate antagonism. Methods Human umbilical vein endothelial cells (HUVEC) were cultured in vitro, and randomly divided into three groups: Control group, AA group, intervention group. Microscope and transmission elec-tron microscopy were used to observe changes of cell morphology and ultrastructure. ELISA method were applied to determine thrombomedu-lin (TM) in cell culture supernatant, fluorescent indicator FLuo-3/AM and intracellular calcium concentration ([Ca2+]. Results TM val-ue and average [Ca2+] i of AA group were significantly higher than that of control group (P < 0.05). Compared with the AA group, when the concentration of calcium dobesilate was 25 μM or 50 μM, TM value and average [Caz +] significantly decreased in intervention group (P < 0.05). Compared with control group, endoplasmic reticulum was pool expansion shaped, and mitochondrial cristae was absent in AA group cells. Endoplasmic reticulum and mitochondria patterns in the intervention group cells showed some improvement, compared with AA group. Conclusion AA induced VEC calcium overloading, 'I'M secretion and injury of endothelial ceils, endoplasmic reticulum and mito-chondria destruction. Dabesilate calcium could protect endoplasmic reticulum and mitochondria and reduce AA induced VEC calcium over-loading, and these could protect VEC.

The treatment of late stage hepatocellular carcinoma (HCC) presently remains a great challenge. A very few drugs have been recently approved for clinical use except sorafenib and lenvatinib. After decades of failure and experience with molecular targeted and immunosuppressive therapy, immune checkpoint inhibitors are becoming one of the potentially effective therapies for patients with HCC, whose tumor is in the middle and late stages. Moreover, immune checkpoint is one of the main mechanisms of tumor immune evasion; of which programmed cell death protein 1 and its ligand (PD1/PD-L1) are important immune checkpoint targets, and its related pathway has shown to have an antitumor effect in a variety of solid or hematologic tumors and its inhibitors can effectively exert antitumor immunosuppressive effects. This review summarizes the current role of PD1/PD-L1 inhibitors in the treatment of late stage HCC, and explores the forecasting value of combined therapy strategy for HCC.

Patients with brain injury are often accompanied by emotional disorders, which can cause a variety of mental disorders, and mental disorders will continue to exist after rehabilitation, seriously affecting the ability of patients to adapt and integrate into society, greatly reducing the quality of life.Therefore, the research on the mechanism of emotional disorders after brain injury is of great significance to the clinical prevention and treatment of mental disorders related to emotional disorders.Functional magnetic resonance imaging (fMRI) provides a more intuitive and accurate research method for the study of emotional regulation, so many scholars have conducted in-depth research on emotional disorders after craniocerebral injury from different perspectives.In this paper, the functional MRI studies of emotional disorders were reviewed after craniocerebral injury in the past decade and most of the resting MRI studies showed that the mechanism of emotional disorders after craniocerebral injury is related to the imbalance of interaction among the resting default network, executive network and salience network, while the task MRI studies found that the amygdala, dorsolateral prefrontal lobe and anterior Cingulate gyrus and right inferior frontal gyrus played an important role in attention distribution, cognitive reappraisal, expression inhibition and other emotional regulation strategies, and the damage of these brain regions will cause corresponding emotional regulation disorders.In this paper, the neural mechanism and research progress of emotional disorders after brain injury were systematically reviewed, summarize the existing problems, and propose possible solutions from the perspective of resting and task state functional MRI.

Objective:To systematically evaluate the correlation of high sensitivity C-reactive protein (hs-CRP) with contrast-induced nephropathy (CIN) in patients following coronary angiography (CAG) or percutaneous coronary intervention (PCI).Methods:PubMed, web of science, CBM, CNKI and Wanfang Data were searched for studies on hs-CRP levels in patients undergoing CAG or PCI patients from the incipience of the database to March 7, 2021. Meta-analysis was performed by RevMan 5.3 and Stata 12.0 software.Results:Fourteen related studies were included involving 11 885 patients undergoing CAG or PCI (1 034 cases with CIN and 10 851 cases without CIN). The results of meta-analysis showed that the level of hs-CRP in CIN group was significantly higher than that in non-CIN group (WMD=3.77,95 %CI:2.80—4.74, P<0.001, I2=93%), patients with higher levels of hs-CRP before CAG or PCI were more likely to develop CIN. Sensitivity analysis shows that the results of this study had good stability. The results of subgroup analysis show that the differences in sample size, study population, geographical location and the definition of CIN were statistically significant. Conclusion:Available evidence shows that high hs-CRP level is a risk factor for CIN in patients undergoing CAG or PCI, large sample trials are still needed to support this conclusion.

Objective:To analyze the clinical features, differential diagnosis, treatment and prognosis of complex lymphatic malformations.Methods:The clinical data of patients with complex lymphatic malformation were retrospectively analyzed from April 2010 to April 2022 in the Multidisciplinary Outpatient Department of the Vascular Disease Team of West China Hospital, Sichuan University. All patients were diagnosed with complex lymphatic malformation after consultation with multidisciplinary experts in pediatric surgery, radiology, plastic surgery, pathology, rehabilitation and other departments. The clinical manifestations, blood routine, coagulation function, magnetic resonance imaging and treatment methods of the patients were analyzed. According to the follow-up and disease results, the patients were divided into improvement, stability, progress and death.Results:A total of 18 patients with complex lymphatic malformations were included in the study, including 6 males and 12 females. The age of first diagnosis ranged from 1 month to 29 years old, and the median age was 2.5 years old. Patients were followed up and treated for 0.4 to 12.0 years, with an average follow-up of 3.5 years. Ten patients had pleural and pericardial effusion; 15 patients had visceral involvement which showed multifocal changes in imaging examinations; 9 cases were accompanied by bone destruction, which in Gorham-Stout disease patients broke through the cortex while in generalized lymphatic anomalies it did not; 14 patients had various degrees of coagulation abnormalities, of which 8 patients with severe coagulation dysfunction were all diagnosed as kaposiform lymphangiomatosis. Of the 18 patients, one kaposiform lymphangiomatosis patient died; six patients progressed; eight patients were stable; and three patients improved.Conclusion:The clinical characteristics of patients with complex lymphatic malformations are systemic, diverse and complex. The clinical symptoms of patients with diffuse lymphatic malformation accompanied by involvement of bone and multiple internal organs, chest and abdominal effusion, and coagulation dysfunction should be considered as complex lymphatic malformation. However, due to overlapping clinical characteristics of each subtypes, it is difficult to distinguish patients with complex lymphatic malformation, and the curative effect and prognosis are poor. Precision targeted drugs are the future research direction for the treatment of such diseases.

Objective:To analyze the clinical features, differential diagnosis, treatment and prognosis of complex lymphatic malformations.Methods:The clinical data of patients with complex lymphatic malformation were retrospectively analyzed from April 2010 to April 2022 in the Multidisciplinary Outpatient Department of the Vascular Disease Team of West China Hospital, Sichuan University. All patients were diagnosed with complex lymphatic malformation after consultation with multidisciplinary experts in pediatric surgery, radiology, plastic surgery, pathology, rehabilitation and other departments. The clinical manifestations, blood routine, coagulation function, magnetic resonance imaging and treatment methods of the patients were analyzed. According to the follow-up and disease results, the patients were divided into improvement, stability, progress and death.Results:A total of 18 patients with complex lymphatic malformations were included in the study, including 6 males and 12 females. The age of first diagnosis ranged from 1 month to 29 years old, and the median age was 2.5 years old. Patients were followed up and treated for 0.4 to 12.0 years, with an average follow-up of 3.5 years. Ten patients had pleural and pericardial effusion; 15 patients had visceral involvement which showed multifocal changes in imaging examinations; 9 cases were accompanied by bone destruction, which in Gorham-Stout disease patients broke through the cortex while in generalized lymphatic anomalies it did not; 14 patients had various degrees of coagulation abnormalities, of which 8 patients with severe coagulation dysfunction were all diagnosed as kaposiform lymphangiomatosis. Of the 18 patients, one kaposiform lymphangiomatosis patient died; six patients progressed; eight patients were stable; and three patients improved.Conclusion:The clinical characteristics of patients with complex lymphatic malformations are systemic, diverse and complex. The clinical symptoms of patients with diffuse lymphatic malformation accompanied by involvement of bone and multiple internal organs, chest and abdominal effusion, and coagulation dysfunction should be considered as complex lymphatic malformation. However, due to overlapping clinical characteristics of each subtypes, it is difficult to distinguish patients with complex lymphatic malformation, and the curative effect and prognosis are poor. Precision targeted drugs are the future research direction for the treatment of such diseases.

Objective To investigate the value of interleukin(IL)-6 and kidney injury molecule(Kim)-1 in the early prediction of contrast-induced pnephropathy(CIN)after percutaneous coronary intervention(PCI)in patients with coronary heart disease.Methods A total of 730 patients with coronary heart disease who underwent PCI were retrospectively collected,divided into CIN group(n=46)and non-CIN group(n=684),and the medical records of the two groups were compared,and the relationship between Kim-1 and IL-6 of renal injury and CIN was analyzed by binary regression,and the receiver operating characteristic(ROC)curve was used to explore the predictive value of these two markers on CIN after PCI for coronary heart disease.Results There was no significant difference between two groups in terms of preoperative IL-6(P=0.467)and Kim-1(P=0.643),and 48h and 72h after PCI,IL-6 and Kim-1 in CIN group was higher than that in non-CIN group(P＜0.001),and IL-6 and Kim-1 in CIN group was higher than that in before surgery(P＜0.001).48h postoperative IL-6(OR=1.884,P=0.002),48h postoperative Kim-1(OR=1.409,P＜0.001)and 72h postoperative IL-6(OR=1.377,P＜0.001)and 72 hours postoperative Kim-1(OR=1.092,P=0.004)were independent risk factors for CIN.The ROC curve showed that when used as a diagnostic marker for CIN,the area under the curve(AUC)of IL-6(48h),IL-6(72h)were 0.837,0.782,AUC of 48h Kim-1 and 72h Kim-1 were 0.820 and 0.827,respectively.Conclusion IL-6 and Kim-1 are independent risk factors for CIN after PCI for coronary heart disease.IL-6 and Kim-1 were positively correlated with the occurrence of CIN after PCI for coronary heart disease.IL-6 and Kim-1 have good diagnostic sensitivity and specificity for CIN after PCI for coronary heart disease.

Background::DOK3 (Downstream of kinase 3) is involved primarily with immune cell infiltration. Recent research reported the role of DOK3 in tumor progression, with opposite effects in lung cancer and gliomas; however, its role in prostate cancer (PCa) remains elusive. This study aimed to explore the role of DOK3 in PCa and to determine the mechanisms involved.Methods::To investigate the functions and mechanisms of DOK3 in PCa, we performed bioinformatic and biofunctional analyses. Samples from patients with PCa were collected from West China Hospital, and 46 were selected for the final correlation analysis. A lentivirus-based short hairpin ribonucleic acid (shRNA) carrier was established for silencing DOK3. A series of experiments involving the cell counting kit-8, bromodeoxyuridine, and flow cytometry assays were performed to identify cell proliferation and apoptosis. Changes in biomarkers from the nuclear factor kappa B (NF-κB) signaling pathway were detected to verify the relationship between DOK3 and the NF-κB pathway. A subcutaneous xenograft mouse model was performed to examine phenotypes after knocking down DOK3 in vivo. Rescue experiments with DOK3 knockdown and NF-κB pathway activation were designed to verify regulating effects. Results::DOK3 was up-regulated in PCa cell lines and tissues. In addition, a high level of DOK3 was predictive of higher pathological stages and worse prognoses. Similar results were observed with PCa patient samples. After silencing DOK3 in PCa cell lines 22RV1 and PC3, cell proliferation was significantly inhibited while apoptosis was promoted. Gene set enrichment analysis revealed that DOK3 function was enriched in the NF-κB pathway. Mechanism experiments determined that knockdown of DOK3 suppressed activation of the NF-κB pathway, increased the expressions of B-cell lymphoma-2 like 11 (BIM) and B-cell lymphoma-2 associated X (BAX), and decreased the expression of phosphorylated-P65 and X-linked inhibitor of apoptosis (XIAP). In the rescue experiments, pharmacological activation of NF-κB by tumor necrosis factor-α (TNF-α) partially recovered cell proliferation after the knockdown of DOK3.Conclusion::Our findings suggest that overexpression of DOK3 promotes PCa progression by activating the NF-κB signaling pathway.