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OBJECTIVE: Osteoporosis (OP), a persistent metabolic bone disorder linked with inflammation, has an undetermined cause. In our research, we employed bidirectional Mendelian randomization (MR) to investigate the interplay between OP and inflammation agents. MATERIALS AND METHODS: We performed two-way pooled-level MR analyses to characterize the causal relationship between 41 circulating inflammatory modulators and OP. Genetic variation data for the 41 regulatory factors associated with inflammation were obtained from genome- wide association studies (GWASs) of human cytokines. Bone mineral density (BMD) was utilized as a phenotype for OP in our approach. The BMD dataset, sourced from the GEFOS consortium, a large GWAS meta-analysis study and UK Biobank, was classified based on varied sections [whole body (TB), lumbar spine (LS), femoral neck (FN), forearm (FA), and heel] and age brackets (0-15 years, 15-30 years, 30-45 years, 45-60 years, and above 60 years). Primary MR analyses were executed using the inverse variance weighting (IVW) method, and sensitivity analyses were performed using the MR-Egger, weighted median, simple model, and weighted model. Cochran's Q test was utilized to evaluate the existence of heterogeneity. We used MREgger regression and MR multiplicity of residuals and outliers (MR-PRESSO) to assess pleiotropy. RESULTS: After false discovery rate (FDR) correction, elevated levels of circulating interleukin-8 (IL-8) [β = 0.072 (0.031-0.114), p < 0.01], macrophage inflammatory protein-1b (MIP-1β) [β = 0.008 (0.003-0.013), p < 0.01; β = 0.026 (0.009-0.042), p < 0 .01], a nd c utaneous T -cell a ttracting chemokine (CTACK) [β = 0.037 (0.017-0.056), p < 0.01] was associated with a reduced risk of OP. Reduced levels of hepatocyte growth factor (HGF), IL-1ra, IL-10, macrophage colony-stimulating factor (MCSF), and MIP-1α were associated with a reduced risk of OP [β = -0.030 (-0.047 - -0.013), p < 0.01; β = -0.025 (-0.041 - -0.010), p < 0.01; β = -0.018 (-0.029 - -0.007), p < 0.01; β = -0.060 (-0.097 - -0.024), p < 0 .01; β = - 0.118 (-0.190 - -0.047), p < 0.01]. We observed a significant causal correlation between FN-BMD and MCP-3 (FDR < 0.05). The occurrence of OP may also lead to elevated levels of MCP3 [β = -0.466 (-0.714 - -0.217), p < 0.01]. The reliability of the results was confirmed by sensitivity analyses. CONCLUSIONS: This study demonstrated the pathogenic role of circulating inflammatory modulators in OP using bidirectional MR analysis. This further deepens the understanding of OP pathogenesis and provides new ideas for therapeutic intervention in OP. [ABSTRACT FROM AUTHOR]

OBJECTIVE: In this study, we investigated the internal relationship between the pathogenesis of diabetic kidney disease (DKD) and abnormal glucose and lipid metabolism to identify potential biomarkers for diagnosis and treatment and investigated the role of the immune microenvironment of glucose and lipid metabolism disorders in the occurrence and progression of DKD. MATERIALS AND METHODS: The chip datasets GSE104948 and GSE96804 from the Gene Expression Common Database (GEO) were merged using the "lima" and "sva" software packages in R Software (4.2.3), and the merged dataset was used as the validation set. The intersection between the differential genes of DKD and the glucose and lipid metabolism genes in the MSigDB database was identified, and a nomogram of the incidence risk of DKD was built using three machine learning methods, namely LASSO regression, support vector machine (SVM), and random forest (RF), to validate the accuracy of the prediction model. Immune scores were conducted using the unsupervised clustering method, and patients were divided into two subgroups. The two subgroups were screened for differential genes for enrichment analysis. The differential genes of patients diagnosed with DKD were clustered into two gene subgroups for co-expression analysis. In this study, we utilized the Cytoscape software to construct a network of interactions among key genes. RESULTS: Using machine learning, a diagnostic model was developed with G6PC and HSD17B14 as key factors. Enrichment analysis and immune scoring demonstrated that the development of DKD was related to the imbalance in the microenvironment brought about by glucose lipid metabolism disorders. CONCLUSIONS: G6PC and HSD17B14 may be potential biomarkers for DKD, and the established predictive model is more helpful in predicting the incidence of DKD. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study aimed to investigate the relationship between common clinical immune indicators, disability degree, and cognitive impairment in patients with neuromyelitis optica spectrum disorder (NMOSD). PATIENTS AND METHODS: We retrospectively analyzed lymphocyte subsets and routine parameters in the peripheral blood of 55 patients with NMOSD. We assessed the degree of disability using the Extended Disability Status Scale (EDSS). The Montreal Cognitive Assessment (Mo-CA) scores were used to assess cognitive function. In addition, we also determined the cytokine levels in 33 patients with NMOSD. The relationships of these immunological indicators with disability and cognitive impairment were assessed using correlation and multiple linear regression analyses. RESULTS: The results of the multiple linear regression analysis suggested that for patients with NMOSD, the neutrophil-lymphocyte ratio (NLR) (ß=0.072, p=0.034) and number of attacks (ß=0.131, p=0.03) were positively correlated with EDSS scores, whereas the number of attacks was positively correlated with MoCA scores. In addition, we also collected cytokine levels in 33 of these patients. The results of the study showed a positive correlation between IL-10 and EDSS scores and a negative correlation between IL-6 and MoCA scores. CONCLUSIONS: Our results show that these immune cells and cytokines are, to some extent, associated with the degree of disability and cognitive impairment in patients with NMOSD. Closely monitoring these indicators may allow detecting changes in patients' disease courses and predicting the severity of their disease. In clinical practice, this may facilitate early intervention and appropriate treatment decisions, which may improve the management of patient prognosis. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Ulcerative colitis (UC), a chronic inflammatory disease of the colon with unknown etiology, is characterized by remission and recurrence. At present, a considerable number of UC cases are misdiagnosed or delayed in diagnosis and treatment. We aimed to identify UC-related genes to aid the development of drugs for this condition. PATIENTS AND METHODS: Transcriptome data of 362 patients with UC and 126 control subjects were obtained from the Gene Expression Omnibus. The 362 patients with UC were subgrouped using unsupervised machine learning. R software was used to analyze the clinical characteristics of the subgroups, screen subgroup-specific genes, assess the relationships between gene modules and clinical characteristics using weighted gene co-expression network analysis, and perform Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the subgroups. RESULTS: Patients w ith UC were c lassified into two subgroups. Genes specific to subgroup I included IL21R, ATP8B2, and PLEKHO1. Severe disease tended to be associated with immune cell infiltration; anti-tumor necrosis factor (TNF)-a antibodies and ustekinumab may have been effective in this subgroup. Subgroup II-specific genes included SLC4A4, EPB41L4B, and PLCE1. Patients in this subgroup had mild clinical conditions; however, their disease was more likely to progress to colorectal cancer. Thus, 5-aminosalicylic acid-based drugs may be effective for the treatment of UC in these patients. CONCLUSIONS: We divided UC into two molecular subgroups based on transcriptome data, providing molecular evidence for the development of diagnostic methods and individualized treatment strategies for UC. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of the study was to investigate the clinical effectiveness and safety of sclerotonyxis in acute angle-closure glaucoma (ACG) with persistent high intraocular pressure (IOP). PATIENTS AND METHODS: The clinical data of 50 eyes from 50 patients (mean age: 68.9±7.19 years) with acute ACG and persistently high IOP who were admitted to our department between January 2012 and January 2022 were retrospectively analyzed. Patients who were administered the maximum dose of systemic and topical anti-glaucoma drugs and still had an IOP of >40 mmHg 24 hours after admission underwent sclerotonyxis. After the IOP control, an individualized phase II treatment plan was designed according to the patient's ocular condition. RESULTS: Forty-eight patients showed improvement in their visual acuity 6 months postoperatively compared to their preoperative values. The mean IOPs were 54.84±7.82 mmHg and 21.34±7.81 mmHg 24 hours pre and postoperatively, respectively. The mean anterior chamber depth showed statistically significant differences pre and postoperatively (1.75±0.16 mm and 1.84±0.17 mm, respectively) (p<0.05). After IOP stabilized, four patients underwent YAG laser peripheral iridectomy, 18 underwent simple cataract phacoemulsification combined with intraocular lens (IOL) implantation, 21 underwent cataract phacoemulsification combined with IOL implantation and goniosynechialysis under a gonioscope, and 7 patients underwent combined surgery of glaucoma and cataract. The mean IOPs were 15.94±3.3 mmHg and 15.64±2.99 mmHg 1 week and 6 months after stage II surgery, respectively. Moreover, 42 eyes (84%) attained complete success and 8 eyes (16%) attained conditional success 6 months postoperatively. No serious complications, such as corneal endothelial decompensation, malignant glaucoma, vitreous or eruptive choroidal hemorrhage, and retinal detachment, were observed intraoperatively or postoperatively in both procedures. CONCLUSIONS: Sclerotonyxis can rapidly lower IOP, release the pupillary blockage, reconstruct the anterior chamber, and reduce systemic complications caused by long-term highdose antiglaucoma drugs. Thus, it normalizes the IOP and provides a safe operating space for stage II surgery, effectively reducing complications in patients in a persistent high IOP state. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Osteoarthritis (OA) is a high-incidence disease of the orthopedic system. However, studies on the molecular mechanisms of OA and pyroptosis, apoptosis, and necroptosis (PANoptosis) at the transcriptome level remain scarce. Therefore, this study purposed to detect biomarkers in OA and explore their relationship to the immune microenvironment. MATERIALS AND METHODS: OA-related expression data was sourced from the Gene Expression Omnibus (GEO) database. Subsequently, differentially expressed analysis and a Venn diagram were performed to obtain differentially expressed PANoptosis-related genes (DEPGs). Furthermore, the least absolute shrinkage and selection operator (LASSO), Support Vector Machine-Recursive Feature Elimination (SVMRFE), and random forest (RF) were implemented to screen diagnostic genes. Receiver operating characteristic (ROC) curves were performed to verify the diagnostic ability of the diagnostic genes. Next, immune infiltration analysis was performed to find the relationships between differential immune cells (OA vs. normal) and diagnostic genes. Finally, drug prediction analysis was also carried out, and the expression of diagnostic genes was verified in external datasets. RESULTS: A total of 62 DEPGs were identified, which were enriched for regulating apoptotic signaling pathways, tumor necrosis factor (TNF) signaling pathways, and other related pathways. Three feature genes, nuclear factor-kappa-B inhibitor-alpha (NFKBIA), RING finger protein 34 (RNF34), and serine incorporator 3 (SERINC3) were obtained by intersecting genes obtained by the LASSO regression algorithm, SVM algorithm, and RF algorithm and showed excellent diagnostic efficacy with the Area under the curve (AUC) values of individual genes were all greater than 0.7, indicating that the model was more effective. Immuno-infiltration analysis showed that RNF34 was positively correlated with CD56dim natural killer cells, type 17 helper T cells, and NFKBIA was positively correlated with plasmacytoid dendritic cells. Additionally, 12 drugs were predicted by NFKBIA, such as gambogic acid and dioscin. In addition, NFKBIA and SERINC3 were significantly downregulated, and RNF34 was upregulated in OA samples. CONCLUSIONS: Three genes (NFKBIA, RNF34, and SERINC3) related to PANoptosis, were obtained by bioinformatics analysis, which would provide a new direction for the diagnosis and treatment of OA. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Autism is a disorder that manifests itself in early childhood. Early diagnosis of autism may not only help the affected children themselves, but also affect family well-being and social stability. The natural drug Albizia bark has been reported to have some effect in the prevention and treatment of autism in children. Therefore, we used network pharmacology and molecular docking to explore the possible mechanism. MATERIALS AND METHODS: TCMID and BATMAN-TCM was used to retrieve the chemical constituents of Albizia bark, and then obtained the relevant targets about autism by TTD, Gene Cards and OMIM. The resulting ingredients and targets were predicted, then a protein interaction network was constructed, and finally bioinformatics analysis was performed. Finally, molecular docking was used to verify the effective ingredients and targets obtained from the screening. RESULTS: Leucaena saponin B, luteolin, 3’, 4’, 7-trihydroxyflavone, which may be the key compounds for the treatment of autism. BP mainly involving signal transduction, G protein coupled receptor signal pathway, protein phosphorylation. CC, mainly involving plasma membrane, integral component of plasma membrane, MF, including protein binding, adenosine triphosphate binding, protein kinase activity. Molecular docking showed that AKT1, HRAS, PIK3CA, PIK3R1 and SRC, five potential targets, had good binding ability to Leucaena saponin B. CONCLUSIONS: The natural drug Albizia bark exerts pharmacological effects in a multi-component, multi-target and multi-channel manner, including neural regulation, inflammatory response and immune regulation. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Intestinal acute graftversus-host disease (aGVHD) is a serious complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Abnormal autophagy levels in intestinal aGVHD have been confirmed in many studies. LncRNAs exert coregulatory functions and participate in a variety of intracellular regulatory processes. In this study, we investigated how lnc-AC145676.2.1-6-3 regulates dysregulated STX3-related autophagy in aGVHD. MATERIALS AND METHODS: First, we established a mouse model of aGVHD by transplanting a mononuclear cell suspension from Balb/c donor mice treated with 60Co X-rays into CB6F1 recipient mice. STX3-related indicators were analyzed by Western blotting (WB) and immunohistochemistry which confirmed that STX3 plays an important role in dysregulating autophagy in intestinal aGVHD. TNF-ainduced Caco-2 cells, which is an in vitro model of intestinal barrier dysfunction, were established to verify the effect of STX3. The direct interaction between the partners of lnc-AC145676.2.1-6-3-mediated hsa-miR-1292-3p and STX3 axis was evaluated by the Dual-Luciferase activity assay. We performed PCR, WB, and immunofluorescence in Caco-2 cells to determine whether the abnormal autophagy levels were influenced by lnc-AC145676.2.1-6-3. RESULTS: The results showed that lnc-AC145676.2.1-6-3 could significantly suppress the number of autophagic vacuoles, the LC3-II/I ratio, and beclin1 levels by increasing STX3 levels. CONCLUSIONS: Lnc-AC145676.2.1-6-3 may play an important role in intestinal aGVHD by targeting STX3. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate key points for the differential diagnosis of immunoglobulin G4-related sialadenitis (IgG4-RS) and Kimura's disease (KD) involving the salivary glands. The clinical, serological, radiological, histological, and immunohistochemical features of 85 IgG4-RS cases and 52 KD cases were evaluated comparatively. Seventy-two IgG4-RS cases had enlargement of multiple salivary and/or lacrimal glands; 67 patients had bilateral submandibular gland (SMG) involvement. Unilateral parotid gland involvement (59.6%) and comorbid skin lesions (61.5%) were common in KD. Serum IgG4 was elevated in 94.1% of IgG4-RS cases versus 19.0% of KD cases (cut-off value = 266.5 mg/dl). KD was more commonly associated with elevated eosinophil counts (86% vs 23.1%) and elevated IgE concentrations (95.5% vs 76.6%). Storiform fibrosis, irregular lymphoid follicles, and increased IgG4-positive cells (112.9 ± 37.6/high-power field (HPF)) were common in IgG4-RS. Acellular fibrosis, regular lymphoid follicles, IgE-positive reticular networks, increased IgE-positive cells (43.4 ± 26.7/HPF), and tryptase-positive mast cells (29.7 ± 13.3/HPF) were usually detected in KD. Computed tomography showed that 85.7% of KD cases involved subcutaneous fat tissue. A superficial hypoechoic and reticular pattern with multiple hypoechoic foci were the sonographic features of the SMG in IgG4-RS. Despite numerous overlapping manifestations, histopathological examination showed meaningful differences in the types of fibrosis, eosinophils, and IgG4-positive cell counts. Comprehensive evaluation of clinical, serological, radiological, and histopathological features are crucial for the differential diagnosis. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The incidence of acute myocardial infarction (AMI) has increased significantly in recent years, seriously threatening human life and health. This paper focused on the role of microRNA-802-5p (miR-802-5p) in myocardial infarction (MI) and its underlying mechanisms. MATERIALS AND METHODS: Quantitative Real-Time Polymerase Chain Reaction (RT-PCR) was employed to detect miR-802-5p expression. Western blot was performed to detect protein expression. Flow cytometry and terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining were performed to observe myocardial apoptosis. Hematoxylin-eosin (HE) staining was used to observe the morphology of myocardial tissue. The cardiac function of rats was detected using echocardiography. RESULTS: The expression of miR-802-5p was increased in hypoxic-treated H9c2 cells and infarcted myocardium in MI rats. Hypoxia treatment reduced the viability of cardiomyocytes and increased the level of lactate dehydrogenase (LDH) in the cell supernatant. Hypoxia treatment increased Bax expression in myocardial cells while Bcl-2 expression decreased, and the number of apoptotic cells increased. MiR-802-5p silencing reversed these effects. Moreover, miR-802-5p silencing reduced myocardial damage in MI rats, and significantly improved cardiac function. Through the Luciferase activity assay, we proved that miR-802-5p could directly target PTCH1. The knockdown of PTCH1 reversed the protective effect of miR-802-5p silencing on hypoxic myocardium. CONCLUSIONS: MiR-802-5p expression was increased in hypoxia-treated H9c2 cells and infarcted myocardium in MI rats. MiR-802-5p silencing could inhibit apoptosis after MI via activating Sonic Hedgehog signaling pathway by targeting PTCH1, thereby reducing myocardial injury and improving cardiac function of MI rats. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Renal injury caused by sepsis is a difficult point in the field of critical care medicine today, which seriously endangers the health of patients. The aim of our paper was to study the role of irisin in the inflammation and apoptosis of renal injury caused by sepsis and its potential mechanism of action. MATERIALS AND METHODS: Lipopolysaccharide (LPS) was utilized to establish an acute kidney injury model. HK-2 cells were divided into 3 groups: control group, LPS group, LPS+irisin group. The expression of TNF-α, IL-1β, Bcl- 2, and Bax were detected using Western blot. Commercial enzyme-linked immunosorbent assay (ELISA) kits were used to detect the levels of TNF-α, IL-6, and IL-1β in the cell supernatant. The LDH content was detected to observe cell damage. TUNEL staining and flow cytometry were to investigate the apoptosis in three groups. The viability of HK-2 cells was detected using Cell Counting Kit-8 (CCK-8) assay. RESULTS: After HK-2 cells were treated with LPS, the LDH content in the cell supernatant was greatly increased, and the expression of TNF-α, IL-6, and IL-1β was also significantly increased. However, after treatment with irisin, LDH content and expression of inflammatory factors were significantly suppressed. Similarly, LPS treatment greatly elevated the levels of TNF-α, IL-1β, Bax, p65 and IĸKα, as well as inhibited the expression of Bcl-2 and IĸB-α. However, irisin treatment reversed these situations. In addition, the number of TUNEL-positive cells and the apoptotic rate were also greatly decreased in LPS+irisin group compared with those in LPS group. CONCLUSIONS: Irisin could inhibit inflammation and apoptosis of HK-2 cells treated with LPS via the NF-ĸB pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Diabetic nephropathy (DN) is one of the most representative diabetic microangiopathy complications. So far, there have been no satisfactory therapeutic strategies, and the injection of stem cells provides a target for DN therapy. PATIENTS AND METHODS: Urine-derived stem cells (USCs) were obtained from 9 healthy men. 24 mice were randomly and equally divided into control group, DN model group, DN+hUSC group (treated with USCs for 3 times). Hematoxylin-eosin (HE) and Masson staining were used to detect histological changes of kidney injury. Creatinine and blood urea nitrogen (BUN) were measured to assess renal function. Besides, myofibroblast accumulation, macrophage infiltration, cell proliferation, and oxidative stress were detected by immunohistochemical analysis. RESULTS: Compared with DN model group, DN+hUSC group showed lower function loss, cell infiltration, and oxidative stress, as well as less renal fibrosis, histological damage, and cell proliferation. CONCLUSIONS: USC can alleviate inflammation and oxidative stress, reduce renal interstitial fibrosis, improve renal tissue structure and protect renal function through paracrine effect. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the influences of micro ribonucleic acid (miR)-205 on renal injury in sepsis rats through the high-mobility group box 1 (HMGB1)-phosphatase and tensin homolog deleted on chromosome ten (PTEN) signaling pathway. MATERIALS AND METHODS: A rat model of sepsis-induced renal injury was established by cecal ligation and perforation. The rats were randomly divided into 3 groups, namely the Sham group, the Model group, and the miR-205 group. Hematoxylin and eosin (HE) staining was applied to examine the pathological renal morphology. The enzyme-linked immunosorbent assay (ELISA) was adopted to measure the serum levels of Caspase-3 and Bcl-2-associated X protein (Bax) in rats. Cell apoptosis rate in the renal tissues was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Finally, the protein levels of phosphorylate-HMGB1 (p-HMGB1) and p-PTEN in the renal tissues were determined using the Western blotting (WB) assay. RESULTS: Compared with those in the Sham group, the pathological morphology of the renal tissues was poor in Model group. The serum levels of Caspase-3 and Bax, the apoptosis rate, and the protein levels of p-HMGB1 and p-PTEN were remarkably enhanced in the Model group compared to the Sham group. In comparison with those in Model group, the pathological changes in renal morphology, apoptosis-related indexes, and protein levels of p-HMGB1 and p-PTEN were alleviated in the miR-205 group. CONCLUSIONS: MiR-205 agonist can improve the pathological morphology in the sepsis rats with renal injury, improve renal cell apoptosis, and inhibit the protein levels of HMGB1 and PTEN in renal tissues. MiR-205 alleviates sepsis-induced renal injury through the HMGB1-PTEN signaling pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The long non-coding ribonucleic acid (lncRNA)-myocardial infarction associated transcript (MIAT) has been demonstrated to serve as a key regulator in various physiological and pathological processes. This study aims to explore whether lncRNA-MIAT regulates the expression of micro RNA (miR)-29a to affect kidney’s injury in sepsis rats. MATERIALS AND METHODS: A total of 30 healthy male Sprague-Dawley (SD) rats were randomly divided into experimental group and control group. Rats in the experimental group were injected with lipopolysaccharide (LPS) through the tail vein to prepare the model of sepsis-induced kidney injury, while those in the control group with the equal volume of normal saline. After the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) in rats were determined to ascertain successful modeling, fluorescence quantitative Real- time polymerase chain reaction (qRT-PCR) was performed to measure the expression levels of the lncRNA-MIAT and miR-29a messenger RNAs (mRNAs) in renal tissues. The normal rat kidney epithelial (NRK-52E) cell line was cultured in vitro, and the model was established in vitro via LPS to study the influences of lncRNA-MIAT and miR-29a on the kidney injury in sepsis rats. Moreover, cell apoptosis was detected using Western blotting. RESULTS: According to the results of the rat in vivo experiment and NRK-52E cell line in vitro experiment, the model of kidney injury was established successfully, and compared with the control group, experiment group had significantly raised SCr and BUN levels (p<0.01) and a remarkably increased lincRNA-MIAT gene expression level (p<0.01), but a substantially decreased miR-29a gene expression level (p<0.01). Additionally, when the expression of lncRNA-MIAT was up-regulated, the expression of miR-29a was prominently decreased (p<0.01), but that of the cell apoptosis gene cysteine-aspartic proteases (Caspase)-8 protein was remarkably increased (p<0.01). However, the expression of Caspase-8 protein was significantly lowered (p<0.01) once the expression of miR-29a was up-regulated. CONCLUSIONS: LncRNA-MIAT may bind to miR-29a to participate in sepsis-related kidney injury. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This paper aims to investigate the clinical efficacy of B-ultrasound- guided puncture in the treatment of incision infection after total abdominal hysterectomy (TAH) and to provide references for the clinical treatment. PATIENTS AND METHODS: 116 patients with uterine incision infection after TAH were selected and randomly divided into the observation group and the control group, with 58 cases in each group. The patients in the control group received an intravenous drip of ceftazidime and tinidazole to prevent infection, and the patients in the observation group received B-ultrasound- guided puncture treatment on the basis of the treatment plan of the control group. The clinical therapeutic effects between the two groups were compared. RESULTS: The cure rate of excellence in the observation group was 84.48%, and the cure rate in the control group was 53.45%, while the difference between the two groups was statistically significant (p<0.05). The total effective rate in the observation group was 98.28%, and that in the control group was 87.93%, but there was no statistically significant difference between the two groups. The hospital stay was (9.5±1.6) days in the observation group and (12.3±2.1) days in the control group, and the mean hospital stay in the observation group was significantly shorter than that in the control group; the difference between the two groups was statistically significant (p<0.05). CONCLUSIONS: TAH should be performed on patients when they are in the best physical condition, and strictly according to the operation steps to reduce the duration of surgery. The application of B-ultrasound-guided puncture can effectively improve the excellent recovery rate of the incision infection after TAH and shorten the hospitalization time. It is worth popularizing in clinical practice. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the effect of dexmedetomidine (DEX) on kidney injury in sepsis rats through the Toll-like receptor 4 (TLR4)/myeloid differential protein-88 (MyD88)/nuclear factor-κB (NF-κB)/inducible nitric oxide synthase (iNOS) signaling pathway. MATERIALS AND METHODS: A total of 30 Sprague-Dawley (SD) rats were randomly divided into three groups, including the control group (n=10), lipopolysaccharide (LPS)-induced acute kidney injury (AKI) group (model group, n=10) and DEX treatment group (DEX group, n=10). The model of sepsis was successfully established in rats. The levels of serum creatinine (Cr), blood urea nitrogen (BUN), serum interleukin-6 (IL-6), IL-1β, IL-10 and tumor necrosis factor-α (TNF-α) were detected via enzyme-linked immunosorbent assay (ELISA). The pathological changes in kidney tissues were detected via hematoxylin-eosin (HE) staining. Furthermore, the mRNA and protein expressions of TLR4, MyD88, NF-κB, and iNOS in the kidney were detected via fluorescence quantitative Polymerase Chain Reaction (PCR) and Western blotting, respectively. RESULTS: Compared with the control group, rats in the model group showed significant kidney injury, markedly increased levels of serum Cr, BUN and pro-inflammatory cytokines, remarkably decreased the level of IL-10 (p<0.05), and significantly increased mRNA and protein expressions of TLR4, MyD88, NF-κB, and iNOS. In the DEX group, AKI was markedly improved, while the expressions of inflammatory cytokines were remarkably declined. Furthermore, the mRNA and protein expressions of TLR4, MyD88, NF-κB, and iNOS decreased significantly. CONCLUSIONS: DEX has a protective effect on LPS-induced AKI, whose mechanism may be related to the inhibition of the TLR4/MyD88/NF-κB/iNOS pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Numerous studies have proved that long non-coding RNAs (lncRNAs) have an important role in malignant tumors, including non-small cell lung cancer (NSCLC). LncRNA olfactory receptor family 3 subfamily A member 4 (OR3A4) was explored to identify how it functions in resistance of NSCLC patients to cisplatin. MATERIALS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect OR3A4 expression in NSCLC patients. Then, we conducted Cell Counting Kit-8 (CCK-8) assay and flow cytometric analysis to detect the function of OR3A4 on the resistance of NSCLC cells to cisplatin. Furthermore, the potential mechanism was explored by mechanism assays. RESULTS: Compared with OR3A4 expression of paired A549 cells, OR3A4 expression of A549/DDP cells was higher. Moreover, the functional assay showed that after OR3A4 was silenced in A549/DDP cells, cell cycle arrest and cell apoptosis was induced, and resistance to cisplatin was reversed. Furthermore, it was found that CDK1 expression was suppressed in A549/DDP cells by knockdown of OR3A4. CONCLUSIONS: The present work suggests that OR3A4 participates in regulating cell cycle, cell apoptosis of NSCLC cells and the resistance to cisplatin via upregulating CDK1, indicating that OR3A4 could be identified as a potential therapeutic target for NSCLC patients. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To elucidate the function of long non-coding RNA (lncRNA) SNHG5 in cisplatin-resistant gastric cancer (GC), and its potential mechanism. PATIENTS AND METHODS: We detected the expressions of SNHG5, apoptosis-specific genes (Bax and Bcl-2) and drug resistance-specific genes (MDR1 and MRP1) in cisplatin-sensitive and cisplatin-resistant GC patients. The expression levels were also detected in cisplatin-resistant GC cell lines (BGC823/DDP, SGC7901/DDP) and GC cell lines (BGC823 and SGC7901). Through the liposome transfection, the regulatory effects of SNHG5 on proliferative potential and apoptosis were examined by cytotoxicity assay and flow cytometry assay, respectively. The protein levels of apoptosis-related genes and drug resistance-related genes influenced by SNHG5 were detected by Western blot. RESULTS: Compared with cisplatin-sensitive GC patients, SNHG5 expression was remarkably higher in cisplatin-resistant GC patients. Besides, higher SNHG5 expression was observed in BGC823/DDP and SGC7901/DDP cells relative to that of their parental cells. Proliferative rate (OD450) and IC50 decreased, but the apoptotic rate increased in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown. It is found that SNHG5 overexpression reduced cisplatin sensitivity in BGC823 and SGC7901 cells. Decreased cisplatin cytotoxicity, elevated IC50 and inhibited apoptotic rate were observed in GC cells overexpressing SNHG5. Moreover, the expression levels of Bax, MDR1 and MRP1 were upregulated, while Bcl-2 downregulated in BGC823 and SGC7901 cells overexpressing SNHG5. CONCLUSIONS: SNHG5 is highly expressed in cisplatin-resistant GC. SNHG5 promotes cisplatin resistance in GC by regulating apoptosis-related genes and drug resistance-related genes. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Phosphatase and tensin homologue deleted on chromosome ten (PTEN) regulates cell proliferation and apoptosis by inhibiting phosphatidylinositol-3 kinase (PI3K) and protein kinase (AKT) signaling. High expression of miR-21 was associated with ovarian cancer. This study aims to investigate whether miR-21 regulates PTEN/PI3K/AKT signaling as well as its role in the proliferation and apoptosis of ovarian cancer cells. MATERIALS AND METHODS: Bioinformatics analysis was used to identify the binding site between miR-21 and the 3'-UTR of PTEN mRNA. A dual-luciferase reporter gene assay was performed to confirm the relationship between miR-21 and PTEN. The expression of miR-21, PTEN, and p-AKT was measured in normal ovarian cell IOSE80, ovarian cancer cell lines A2780, and SKOV3. miR-NC or miR-21 inhibitor was transfected into A2780 or SKOV3 cells followed by the analysis of the expression of miR-21, PTEN, p-AKT, cell apoptosis by flow cytometry, and proliferation by EdU assay. RESULTS: There was a targeted relationship between miR-21 and PTEN. Compared with IOSE80 cell, levels of miR-21 and p-AKT were significantly elevated in A2780 and SKOV3 cells, with the statistical reduction of PTEN expression (p<0.05). The inhibition of miR-21 significantly reduced the expressions of miR-21 and p-AKT and induced PTEN level in A2780 and SKOV3 cells, which also restricted cell proliferation and promoted cell apoptosis. CONCLUSIONS: The miR-21 expression is found elevated in ovarian cancer cells. The suppression of miR-21 increases PTEN expression, inhibits PI3K/AKT activity, promotes cell apoptosis, and reduces cell proliferation. This finding provides new leads to the future treatment of ovarian cancer. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to explore the role of long non-coding RNA (LncRNA) small nucleolar RNA host gene 14 (SNHG14) in cervical cancer, and to further understand the possible underlying mechanism. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of SNHG14 in cervical cancer. The relationship between SNHG14 expression with clinic-pathological features and prognosis of patients was analyzed. Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and flow cytometry were used to evaluate the proliferation and apoptosis of cells. At the same time, the changes in the expression of apoptosis-related proteins after SNHG14 knockdown were detected. RESULTS: Compared with normal cervical tissues, the expression of SNHG14 was significantly higher in cervical cancer tissues. The prognosis of patients with higher expression of SNHG14 was worse than those with a lower level. The relationship between the expression of SNHG14 and clinicopathological features of patients with cervical cancer was further analyzed. The results demonstrated that a higher expression level of SNHG14 indicated later tumor stage and higher incidence of lymph node metastasis. Compared with normal cervical epithelial cell line End1/E6E7, the level of SNHG14 in cervical cancer cell lines (including SW756, SiHa and HeLa) was markedly up-regulated. Among them, SW756 and SiHa cells exhibited the highest level of SNHG14. After knocking down SNHG14, the viability and proliferation ability of SW756 and SiHa cells were remarkably decreased, while cell apoptosis was increased. Subsequently, we investigated the possible underlying mechanism. The results found that the knockdown of SNHG14 enhanced the activation of caspases-3, and increased the protein expression of Bax, JAK2 and STAT3, whereas decreased the expression of Bal-2 and Bid. CONCLUSIONS: LncRNA SNHG14 was highly expressed in cervical tumor tissues or cells, which could promote the progression of cervical cancer. Furthermore, SNHG14 might be associated with the activation of the JAK-STAT pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To detect the expression pattern of LINC01308 in ovarian cancer (OC), and further clarify whether LINC01308 could promote the malignant progression of OC by mediating microRNA-506 (miRNA-506). PATIENTS AND METHODS: Relative level of LINC01308 in 28 pairs of OC tissues and paracancerous tissues was determined by quantitative Real-time polymerase chain reaction (qRT-PCR). We analyzed the correlation between LINC01308 level and the prognosis of OC patients. Subsequently, LINC01308 level in OC cell lines was determined as well. By transfection of sh-LINC01308 in 3AO and CAOV3 cell lines, we evaluated the influence of LINC01308 on cellular behaviors of OC through cell counting kit-8 (CCK-8), transwell and wound healing assay. Target downstream of LINC01308 was verified by dual-luciferase reporter gene assay. Finally, the regulatory effect of LINC01308/miRNA-506 on OC cell behaviors was examined through a series of rescue experiments. RESULTS: LINC01308 was highly expressed in OC tissues relative to controls. OC patients with high-level LINC01308 had higher rates of lymph node metastasis and distant metastasis, and lower survival rate compared with those with low level. By transfection of sh-LINC01308 in OC cells, the migratory and invasive abilities were markedly weakened. MiRNA-506 was found to be the target gene of LINC01308, and its level was negatively regulated by LINC01308 in OC tissues. Finally, we found that miRNA-506 knockdown reversed the regulatory effect of LINC01308 on the migratory and invasive abilities of OC cells. CONCLUSIONS: LINC01308 is highly expressed in OC and correlated to metastasis and poor prognosis. LINC01308 enhances OC cells to migrate and invade by targeting miRNA-506. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The development of multidrug resistance (MDR) is a key issue for tumor recurrence and metastasis, leading to treatment failure of gastric cancer (GC). Long non-coding RNA (lncRNA) DANCR has been shown to be highly expressed in GC patients, which accelerates growth and metastasis of GC cells. This study aims to elucidate the role of DANCR in regulating MDR of GC. PATIENTS AND METHODS: The mRNA level of DANCR in GC patients with or without DDP-resistance was determined by quantitative Real- time polymerase chain reaction (qRT-PCR). DANCR expression in GC cell lines (SGC7901, BGC823) and cisplatin (DDP)-resistant cell lines (SGC7901/DDP, BGC823/DDP) was determined as well. Knockdown or overexpression of DANCR in GC cells with or without DDP-resistance was achieved by siRNA interference technology or stable transfection of lentivirus, respectively. The regulatory effects of DANCR on cytotoxicity and apoptosis were examined by cytotoxicity assay and flow cytometry method (FCM), respectively. In addition, we detected the expressions of MDR1, MRP1, mechanistic target of rapamycin (mTOR) and hypoxia inducible factor-1a (HIF-1a) in GC cells overexpressing DANCR by qRT-PCR and Western blot. RESULTS: DANCR expression remained high in DDP-resistant GC tissues or cells. SGC7901/DDP and BGC823/DDP cells transfected with si-DANCR presented decreased survival and increased apoptosis. On the contrary, SGC7901/DDP and BGC823/DDP cells overexpressing DANCR showed increased survival and decreased apoptosis. In addition, DANCR overexpression could upregulate expressions of MDR1 and MRP1 in DDP-induced SGC901 and BGC823 cells. CONCLUSIONS: Upregulation of DANCR can accelerate the MDR development of GC, which may become a potential target for treating GC with MDR. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Researchers have discovered the important role of long noncoding RNA (lncRNAs) in tumorigenesis recently. In this work, we aimed to explore whether lncRNA linc- ITGB1 affected the development of clear cell renal cell carcinoma (ccRCC), and to elucidate the possible underlying mechanism. PATIENTS AND METHODS: Linc-ITGB1 expression in both ccRCC cells and tissue samples was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the association between linc-ITGB1 expression level and patients' disease-free survival rate was explored. Then, wound healing and transwell assays were conducted. Furthermore, the underlying mechanism was explored through RT-qPCR and Western blot assay. RESULTS: Linc-ITGB1 expression level in ccRCC samples was markedly higher than that of the adjacent ones. The expression of linc- ITGB1 was closely related to the disease-free survival time of ccRCC patients. Moreover, the migration and invasion of ccRCC cells were remarkably enhanced after linc-ITGB1 upregulation in vitro. In addition, the mRNA and protein expression of Mcl-1 were significantly downregulated after linc-ITGB1 overexpression. Furthermore, the expression level of Mcl-1 was negatively correlated with the linc-ITGB1 expression in ccRCC tissues. CONCLUSIONS: Our findings suggested that linc-ITGB1 could enhance ccRCC cell migration and invasion via downregulating Mcl-1. In addition, linc-ITGB1 might be a potential therapeutic target for ccRCC. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Rho-associated kinases (ROCKs) are recognized to be involved in many pathophysiological processes caused by hyperglycemia. We performed experiments to evaluate the effects of fasudil, the Rho/ROCK inhibitor, on preventing hepatic fibrosis in type 1 diabetic rats and to elucidate the underlying mechanisms. MATERIALS AND METHODS: Sprague-Dawley (SD) rats were randomly divided into five groups: normal control (NC), untreated diabetic (DM), low-dose fasudil-treated (L-Fas), high-dose fasudil-treated (H-Fas) and captopril-treated (Cap) groups. Streptozotocin was injected to establish the diabetes model. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), were analyzed. Hematoxylin and eosin (HE) and Masson's trichrome staining were used for histological observations. The expression of transforming growth factor-β (TGF-β1), metalloproteinase-9 (MMP-9)/tissue inhibitor of metalloproteinase-1 (TIMP-1), collagen type Iα (Coll α1), nuclear factor-kappa B (NF-κB) and ROCK-1 were measured to investigate the mechanisms involved in fibrosis. RESULTS: The DM group exhibited hepatic fibrosis with remarkable liver damage and inflammation reaction by the activation of the NF-κB pathway. Treatment with fasudil or captopril suppressed not only the inflammation reaction but also the accumulation of the extracellular matrix due to the downregulation of TGF-β1 and MMP-9/TIMP-1, which induces the amelioration of the liver fibrosis with diabetes. Furthermore, fasudil significantly attenuated the activation of ROCK-1 and NF-κB in the livers of diabetic rats. CONCLUSIONS: These results suggest that fasudil exert anti-inflammation actions and markedly decrease the accumulation of extracellular matrix. Fasudil is a good candidate agent for treating hepatic fibrosis in diabetes. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We investigated the effects of BMSCs, which was modified by programmed death ligand-1 immunoglobulin (PD- L1 Ig) gene, on the immunological rejection of orthotopic liver transplantation (OLT) in rats. MATERIALS AND METHODS: Rat BMSCs were cultured and modified by recombinant adenovirus pAdEasy-1/PDL1Ig for 72h. The total protein was extracted, and the protein expression of PDL1 Ig after transfection was detected by Western blotting. Mixed lymphocyte reaction was applied to detect the inhibitory effect of BM- SCs, including pre-transfection and post-transfection, on the cell activity of T lymphocytes in peripheral blood. The male Wistar rats were used as donors, and the male Sprague-Dawley (SD) rats were used as recipients. The improved cuff method was computed in OLT to establish the rat orthotopic liver transplantation model of acute rejection. The rats were randomly divided into 4 groups, including a control group (10 pairs), BMSCs treatment group (10 pairs), BM- SCs/GFP (green fluorescent protein) treatment group (10 pairs), and BMSCs/PDL1Ig treatment group (10 pairs). 5 rats in each group were randomly collected and euthanized at day 7 after the operation. The peripheral blood was gathered to detect levels of 3 types of cytokines, including interferon gamma (IFN-γ), interleukin-4 (IL-4), and IL-2. In addition, the liver function of rats was checked, and the pathological changes of liver transplantation were observed under the optical microscope. The remaining five rats in every group were used for measuring the survival situation and survival time. RESULTS: After BMSCs were modified by a recombinant adenovirus pAdEasy-1/PDL1Ig for 72h, the expression of PDL1Ig in the BMSCs was detected. The inhibitory effects of BMSCs/ PDL1Ig on the cell activity of lymphocytes were stronger than that of BMSCs/GFP. The levels of IL-4 in BMSCs/PDL1Ig group were significantly higher than those in the other 3 groups, and the levels of IFN-γ and IL-2 were significantly decreased (p<0.05). The liver function of 4 groups was measured at day 7 after transplantation. Our results showed that the liver function in BMSCs/PDL1Ig group was most significantly improved, and the levels of ALT, AST, and TBil almost recovered to normal. The differences were statistically significant compared to the control group, BMSCs treatment group, and BMSCs/ GFP treatment group. Results of pathological examination of liver tissue showed that the control group underwent severe rejection of liver transplantation. The BMSCs treatment group and BMSCs/GFP treatment group also rejected the liver transplantation, but the degree was lighter when compared to the control group. In addition, there was almost no rejection of liver transplantation in the BMSCs/PDL1Ig group. The recipient survival time of most rats was more than 100d, which was significantly longer than the other 3 groups (p<0.05). CONCLUSIONS: PDL1Ig-modified BMSCs can inhibit the rejection of liver transplantation in rats, induce the formation of the immune tolerance of liver transplantation, and the effect was more significant than that of BMSCs alone. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Wilms' tumor is the most common malignant tumor in children worldwide. Considering the poor therapeutic effect on Wilms' tumor, we determined the effects of microRNA-613 on cell proliferation and metastasis in vitro, providing therapeutic targets for the treatment of Wilms' tumor. PATIENTS AND METHODS: Quantitative real-time PCR (qRT-PCR) was employed to identify the expression level of miR-613. CCK8 and colony formation assays were incorporated to assess cell viability and proliferation capacity. Cell migration and invasion assays were performed to investigate the metastasis capacity of Wilms' tumor cells. Flow cytometry was used to detect cell cycle distribution and cell apoptosis. Protein levels were assessed by western blotting assay. The target gene was predicted and verified by bioinformatics analysis and luciferase assay. RESULTS: The expression of miR-613 was downregulated in Wilms' tumor tissues compared with adjacent normal tissues (n=32). Overexpression of miR-613 could attenuate Wilms' tumor cell viability, proliferation, invasion, and migration capacity, as well as induce cell cycle arrest at the G0/G1 phase. FRS2 was chosen as the target of miR-613 by bioinformatics analysis and a luciferase reporter assay. MiR-613 expression was inversely correlated with FRS2 in Wilms' tumor tissues. Moreover, restoration of FRS2 rescued the tumor suppressive role of miR-613 in Wilms' tumor cell growth and metastasis. CONCLUSIONS: MiR-613 had a tumor-suppressive effect on Wilms' tumor progression and metastasis via targeting FRS2 in vitro, which provided an innovative and candidate target for the diagnosis and treatment of Wilms' tumor. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study is to investigate the expression and biological function of miRNA-106b in osteosarcoma. PATIENTS AND METHODS: Freshly resected osteosarcoma tissues and the corresponding para-carcinoma tissues were collected from 54 patients. Then miR-106b level in the carcinoma tissues was detected by real-time PCR. To test the function of miR-106b, osteosarcoma cell line U2-OS was transfected with miR-106b inhibitor in vitro. Then, the proliferation, cell cycle, invasion and metastasis of U2-OS cells were detected by CCK-8 assay, flow cytometry, and transwell respectively. The PI3K/AKT signaling pathway activity after treatment was detected by Western blot. RESULTS: miR-106b level was significantly higher in osteosarcoma, and its expression was positively correlated with the lung metastasis and the clinical stages. In vitro experiments showed that the proliferation, invasion, and migration of U2-OS osteosarcoma cells were inhibited after miR-106b inhibition. The transition from G1 to S phase of U2-OS osteosarcoma cells was inhibited after miR-106b inhibition. The Western blot analysis demonstrated that both the AKT phosphorylation in PI3K/AKT pathway and the PI3Kp100 expression were significantly reduced when the expression of miR-106b was down-regulated. CONCLUSIONS: miR-106b level was significantly up-regulated in osteosarcoma, which was positively correlated with the lung metastasis and clinical stages. The down-regulation of miR-16b inhibited the proliferation, invasion, and migration of osteosarcoma cells; thus, it may function as an oncogene to promote osteosarcoma proliferation and invasion through the PI3K/AKT signaling pathway. [ABSTRACT FROM AUTHOR]

Our aim was to differentiate IgG4-related sialadenitis, primary Sjögren syndrome, and chronic obstructive submandibular sialadenitis by analysing clinical, radiographic, and pathological features. Fifty-five patients, 50, and 50 were enrolled, respectively and their baseline characteristics and serological, sialographic, and pathological findings compared. The male:female ratio for IgG4-related sialadenitis was 1:1.2 for primary Sjögren syndrome 1:15.7, and for chronic obstructive submandibular sialadenitis1:0.92. Numbers with enlarged salivary glands were 55, 16, and 50; with xerostomia 26, 48, and 0; with a history of allergy 26, 4, and 6, and with coexisting systemic disease 12, 19, and 0 (p = 0.14). Mean (SD) serum IgG4 concentrations were 109.1 (97.9), 4.9. (1.9) g/L, and 5.3 (1.6) g/L, p < 0.001 in all cases. Sialography showed enlargement of the gland, dilatation of the duct, and slightly decreased secretory function in IgG4-related disease; obvious sialectasia and decreased secretory function in Sjögren syndrome; and dilatation of Wharton’s duct and filling defects in obstructive sialadenitis. Histopathological examination showed lymphoplasmacytic infiltration with storiform fibrosis, lymphoplasmacytic inflammation and lymphoepithelial lesions, and dilatation of the duct with epithelial metaplasia in the three groups, respectively. The number of IgG4-positive plasma cells was 123 (45)/HPF, 8 (3)/HPF, and 5 (4)/HPF, while the IgG4-/IgG-positive cell ratio was 71.7 (13.9)%, 4.6 (2.5)%, 18.9 (19.7)%, respectively (p < 0.001). The three conditions have different clinical, radiographic, and pathological features that provide important clues to the differential diagnosis. Serological and histological tests are important, and comprehensive consideration is necessary. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We studied the effect of non-occupational exposure to lead and cadmium on homocysteine level in plasma. Homocysteine is a marker for plasma folate folic acid metabolism in urban populations. PATIENTS AND METHODS: 159 individuals from Beijing, Guangzhou, Shenzhen and Shanghai with no history of close exposure to heavy metals and no history of metabolic diseases were enrolled to participate in this study. Blood lead and cadmium levels were detected using ICP-MS method and the level of homocysteine was also measured using enzyme method. Our results showed that blood lead and cadmium levels in males were significantly higher than those in females. Also, blood lead and cadmium levels in smokers were higher than those in non-smokers; homocysteine level was significantly higher in smokers as well. According to blood lead and cadmium levels, cases were divided into four groups. RESULTS: Our results showed that a surge in blood lead and cadmium levels could result in an increase in homocysteine level. We concluded that in the Chinese population, smoking and gender might be the risk factors for elevated levels of lead and cadmium. Meanwhile, blood lead and cadmium levels may influence the homocysteine levels in the body. CONCLUSIONS: It is possible to speculate that non-occupational exposure to lead and cadmium, by increasing the homocysteine levels, negatively affect the cardiovascular and nervous system. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore the correlation between plasma β2-microglobulin (β2-MG) as senescence factor with age, heart, liver and kidney function as well as the predictive value of β2-MG in human metabolism function and senescence. PATIENTS AND METHODS: 387 cases of healthy people of different ages were selected and the automatic biochemical analyzer was used to test β2-MG in plasma based on immunoturbidimetry and also all biochemical indexes. The correlation between β2-MG and age, gender and all biochemical indexes was analyzed. RESULTS: β2-MG was positively correlated to age, r = 0.373; and the difference was of statistical significance (p < 0.010). It was significantly negative correlated to HDL-C but positively correlated to LP (a), BUN, CREA, UA, CYS-C, LDH, CK-MB, HBDH, AST, GLB and HCY. CONCLUSIONS: β2-MG was closely correlated to age, heart, kidney and liver biochemical indexes, which can be taken as an important biomarker for human body function and anti-senescence and have significant basic research and clinical guidance values. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The present study aimed to investigate the effectiveness of atosiban in treating women with threatened preterm labor who had become pregnant through assisted reproductive technology (ART) and the corresponding pregnancy outcomes. PATIENTS AND METHODS: Seventy pregnant women with threatened preterm labor after ART were randomly divided into two groups, with 35 cases in the atosiban group and 35 in the ritodrine group. The post-treatment effects and the corresponding pregnancy outcomes were observed. RESULTS: The efficacy of extending gestational age by 48 hours was significantly higher in the atosiban group than in the ritodrine group (p<0.05), whereas the efficacy of extending gestational age by seven days was the same in the two groups (p>0.05). There was no significant difference between the atosiban and ritodrine groups in the average gestational age at birth (p<0.05). The occurrence of side effects in the pregnant women was higher in the ritodrine group than in the atosiban group (p<0.05), although the prevalence of abnormal fetal heart rate was not significantly different (p>0.05). Both the perinatal mortality rate and the prevalence of neonatal asphyxia were significantly lower in the atosiban group than in the ritodrine group (p<0.05). When the medication was applied at a gestational age of fewer than 28 weeks, the perinatal mortality rate and the prevalence of neonatal pneumonia were significantly lower in the atosiban group compared with the ritodrine group (p<0.05). When the first drug administration was at a gestational age of 28 weeks or later, the need for neonatal pediatric treatment was significantly reduced in the atosiban group relative to the ritodrine group. Independent of when the drug administration was initiated, there were no significant differences between the atosiban and ritodrine groups in the occurrences of neonatal asphyxia, acute respiratory distress syndrome (ARDS), neonatal brain injury, or neonatal sepsis (p>0.05). CONCLUSIONS: Administration of atosiban has a comparatively better effect than that of ritodrine on pregnant women who underwent ART and is safe and effective at preventing immediate preterm birth. Atosiban is significantly better than ritodrine at reducing the rates of perinatal mortality and neonatal pneumonia, and the perinatal outcomes for those who began to use atosiban at a gestational age of fewer than 28 weeks were even better. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The study aims to compare the effects of urethane and ketamine anesthesia on kindling-induced after discharges (AD). MATERIALS AND METHODS: We divided forty 4-6 week old female C57BL/6J mice into two groups: one group was anesthetized with urethane (n = 20) and the other with ketamine (n = 20). Kindling was with an electrical stimulation (ES) consisting of a 1-s pulse train of 60 1-ms biphasic pulses at an initial intensity of 700 µA, delivered to the pre-frontal cortex every minute. Ten to fifteen minutes after the first AD was induced, identical electrical stimuli were delivered every 10 minutes for 200 minutes. EEG was continuously recorded from 15 minutes before the first ES until 10 minutes after the last ES. The EEG wave spectrum was analyzed by Fast Fourier Transform and the power spectrum densities (PSDs) of the δ, θ, α, β and γ bands were calculated. EEG wave amplitude was assessed using the root mean square value (RMS). RESULTS: In the urethane group, an initial AD was induced in 70% of mice following 39 ES. In the ketamine group, an initial AD was induced in 60% of mice following 74 ES. The changes in EEG spectra were similar in both groups. Pre- AD, EEG waves predominantly consisted of δ and θ components. During AD, γ and β components increased significantly (p < 0.05). Post-AD, β and γ components decreased and the δ: θ ratio increased to pre-AD levels. CONCLUSIONS: Our data suggest that AD can be induced by kindling stimulation of the prefrontal cortex in mice under either urethane or ketamine anesthesia. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Our objective was to examine the association between single nucleotide polymorphisms of interleukin (IL)-8 (rs4073 and rs2227306) and IL-10 (rs1800871 and rs1800872) genes, and clinical effects of transcatheter arterial chemoembolization (TACE) and subsequent prognosis in patients with liver cancer. PATIENTS AND METHODS: 115 patients with liver cancer underwent TACE. Venous blood specimens were collected for genomic DNA extraction. The restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) analysis was used to detect the above variants of IL-8 and IL-10 genes. In addition, blood levels of alpha fetal protein (AFP) were quantified by radioimmunoassay. Patients were followed up to uncover the association of the above genotypes with treatment efficacy and survival. RESULTS: Patients with the homozygous genotype AA or homozygous genotype TT (respectively, -251 and +781 sites) of IL-8 gene, and wild-type genotype TT or homozygous genotype AA (respectively, -819 and -592 sites) of IL-10 gene showed the best effectiveness of TACE. Furthermore, these patients also exhibited the lowest AFP levels and the longest survival after the treatment. CONCLUSIONS: Clinical efficacy of TACE and patient survival in liver cancer are associated with specific variants of IL-8 and IL-10 genes. [ABSTRACT FROM AUTHOR]

OBJECTIVE: This study examined the usefulness of nasal Duo positive airway pressure (DuoPAP) in the treatment of very low birth weight preterm infants with neonatal respiratory distress syndrome (NRDS). PATIENTS AND METHODS: Eighty-five very low birth weight preterm infants with NRDS were randomly divided into two groups. Forty-five infants were treated with DuoPAP, while 40 infants were treated using nasal continuous positive airway pressure (nCPAP). The study outcomes were pH, PaCO2, PaO2, oxygenation index (PaCO2, FiO2), and the number of failure cases at 1, 12, and 24 hours after non-invasive respiratory support. RESULTS: At all studied time points, after noninvasive respiratory support, PaCO2, PaO2 and oxygenation index were significantly (p < 0.05) better in the nasal DuoPAP group compared with nasal CPAP group. In addition, rates of failure of assisted ventilation (respectively, 4.44% vs. 22.50%) and the occurrence of apnea (13.33% vs. 32.50%) were significantly (p < 0.05) better in the nasal DuoPAP group. Other parameters (such as duration of noninvasive ventilation, number of retinopathies of premature children, intraventricular hemorrhages, or periventricular leukomalacias) were comparable between both non-invasive regimen. CONCLUSIONS: Nasal DuoPAP better improves oxygenation, reduces CO2 retention, and diminishes the need for invasive mechanical ventilation and complications in the treatment of NRDS. [ABSTRACT FROM AUTHOR]

Tissue plasminogen activator (tPA) is the only treatment approved by the USA FDA for acute ischemic stroke. There are many obstacles, however, when it is widely used in clinical setting, such as narrow therapeutic window, cytotoxicity and neurotoxicity. In recent years, many neuroprotective agents aiming to different molecular targets in ischemic cascade have been rapidly developed. Although these agents showed remarkable effects in experimental stroke, they failed to be translated to clinical use for many reasons. As the concept of "neurovascular unit" (NVU) is mentioned, combination of thrombolytic agents such as tPA with neuroprotectants gets more and more attention. Evidences supporting the combination therapy have been obtained from a variety of studies in many kinds of animal models, even though clinical evidences are inadequate. Combination of thrombolysis and neuroprotection has been considered as a promising approach for treatment of acute ischemic stroke. There are many advantages for the combination therapy. In this context, we review the sound rationales and researching achievements to support the therapy. [ABSTRACT FROM AUTHOR]

Anthropogenic influence and natural processes exert important effects on the aquatic ecosystem of Sanya Bay in the northern part of the South China Sea. These effects result to the temporal and spatial differences of water quality in the bay. In this study, four-way principal component analysis is employed to identify the natural characteristics of the water in this bay, as well as the anthropogenic effects on its water quality. The results indicate that anthropogenic influence (nutrients as indicator) is the dominant factor that affects the water quality at the mouth of Sanya River (S1). This region exhibits the maximum effects of the discharge from Saya River, which is indicated by higher nutrient levels and Chl a than in outer bay. Both upwelling and mixing caused by monsoons are the dominant factors that affect water quality in the central and outer bays. The water exchange between the bay and open oceanic water exercises an important effect on the water quality in Sanya Bay. The information on the spatial and temporal variations of the water quality in Sanya Bay may be valuable for the socioeconomic development and human health in this area. [ABSTRACT FROM AUTHOR]