Development and validation of a nomogram for 30-day readmission after hip fracture surgery in geriatric patients.

OBJECTIVE: 30-day readmission after hip fracture surgery in the elderly is common and costly. A predictive tool to identify high-risk patients could significantly improve outcomes. This study aims to develop and validate a risk nomogram for 30-day readmission after hip fracture surgery in geriatric patients. PATIENTS AND METHODS: We retrospectively analyzed 1,249 geriatric hip fracture patients (≥60 years) undergoing surgery at Dandong Central Hospital from October 2011 to October 2023. Using a 7:3 ratio, patients were randomly divided into training (n=877) and validation (n=372) sets. Independent risk factors for 30-day readmission were identified using LASSO regression and logistic regression in the training set. A nomogram was constructed using the identified predictors. Finally, the C-index, ROC curve, calibration curve, and decision curve analysis were used to validate the model in the training and validation sets respectively. RESULTS: The nomogram was developed based on the 8 predictors of age, prior stroke, chronic liver disease, treatment, uric acid (UA), total protein (TP), albumin (ALB), and pneumonia that were found to be independently associated with 30-day readmission. The nomogram showed good discrimination with a C-index of 0.88 in the training set and 0.84 in the validation set. Calibration curves exhibited good agreement between predicted and observed outcomes. Decision curve analysis demonstrated clinical utility. CONCLUSIONS: We developed and validated a nomogram incorporating eight clinical variables to accurately predict the individualized risk of 30-day readmission after hip fracture surgery in elderly patients. The model demonstrated favorable discrimination, calibration, and clinical utility. It can help to identify high-risk patients needing additional interventions to prevent avoidable hospital readmissions.

Development and validation of a nomogram for urinary tract infection in geriatric patients with hip fracture: a retrospective study.

OBJECTIVE: This study aims to develop and validate a risk nomogram for urinary tract infections (UTIs) in geriatric patients with hip fractures. PATIENTS AND METHODS: A total of 900 geriatric patients who underwent hip fracture surgery at Dandong Central Hospital between June 2017 and June 2023 were systematically collected. The cohort was randomly divided into a training set (70%, n=632) and a validation set (30%, n=268) for model development and validation, respectively. Univariate and multivariate logistic regression analyses were conducted to identify the independent risk factors associated with UTIs. Based on the results of the multivariate analysis, a UTI nomogram prediction model was developed and evaluated in the training and validation sets using the C-index, ROC curve, calibration curve, and decision curve analysis to assess discrimination, calibration, and clinical utility, respectively. RESULTS: Out of the 900 participants, 24.6% were diagnosed with UTIs. The nomogram was developed based on 9 predictors that were found to be independently associated with UTI. The area under the curve (AUC) for predicting UTI in geriatric patients with hip fractures was 0.829 in the training set and 0.803 in the validation set. Following internal verification, the modified C-index remained at 0.829. Furthermore, the nomogram's calibration plot and decision curve analysis demonstrated good performance in both the training and validation sets. CONCLUSIONS: The established and validated nomogram provides a reliable and convenient tool for predicting UTI risk in geriatric patients with hip fractures. This model facilitates the early identification of high-risk patients and offers guidance for implementing targeted preventive interventions.

Development and validation of preoperative proximal and distal lower limb deep vein thrombosis nomograms in geriatric hip fracture patients.

OBJECTIVE: This study aimed to develop and validate a risk nomogram for preoperative proximal and distal deep vein thrombosis (DVT) in geriatric patients with hip fractures. PATIENTS AND METHODS: The 970 collected geriatric hip fracture patients were randomly divided into a training set (70%, n=682) and a validation set (30%, n=288). Multivariate logistic regression analyses were used to optimize the predictive risk variables for proximal and distal preoperative lower extremity DVT in the training set, respectively, and the selected variables were finally incorporated to establish preoperative DVT nomogram prediction models. Receiver operating characteristic curves (ROC), calibration plots, and decision curve analysis (DCA) were performed to validate the nomograms in the training and validation sets, respectively. RESULTS: Among the 970 patients, 125 (12.88%) were diagnosed with preoperative DVT. The area under the curve (AUC) for predicting preoperative proximal DVT was 0.888 in the training and 0.792 in the validation sets. The AUC for predicting preoperative distal DVT was 0.907 in the training and 0.790 in the validation sets. The calibration plots and decision curve analysis for preoperative proximal DVT performed well in the training set and slightly worse in the validation set. The calibration plots and decision curve analysis for preoperative distal DVT performed well in both the training and validation sets. CONCLUSIONS: To construct nomograms for predicting the risk of proximal and distal preoperative lower extremity DVT in geriatric hip fracture patients. For patients at high risk, as assessed by this model, clinicians should intervene and treat them promptly before surgery.

High-Brilliance Ultranarrow-Band X Rays via Electron Radiation in Colliding Laser Pulses.

A setup of a unique x-ray source is put forward employing a relativistic electron beam interacting with two counterpropagating laser pulses in the nonlinear few-photon regime. In contrast to Compton scattering sources, the envisaged x-ray source exhibits an extremely narrow relative bandwidth of the order of 10^{-4}, comparable with an x-ray free-electron laser. The brilliance of the x rays can be an order of magnitude higher than that of a state-of-the-art Compton source. By tuning the laser intensities and the electron energy, one can realize either a single peak or a comblike x-ray source of around keV energy. The laser intensity and the electron energy in the suggested setup are rather moderate, rendering this scheme compact and tabletop size, as opposed to x-ray free-electron laser and synchrotron infrastructures.

The possible effect of different types of ventilation on reducing operation theatre infections: a meta-analysis.

INTRODUCTION: The relation between type of ventilation used in the operating theatre and surgical site infection has drawn considerable attention. It has been reported that there is a possible relationship between the type of ventilation used in the operation theatre and surgical site infection. This meta-analysis was performed to evaluate this relationship. METHODS: Through a systematic literature search up to May 2020, 14 studies describing 590,121 operations, 328,183 were performed under laminar airflow ventilation and 2,611,938 were performed under conventional ventilation. Studies were identified that reported relationships between type of ventilation with its different categories and surgical site infection (10 studies were related to surgical site infection in total hip replacement, 7 in total knee arthroplasties and 3 in different abdominal and open vascular surgery). Odds ratios with 95% confidence intervals were calculated comparing surgical site infection prevalence and type of theatre ventilation using the dichotomous method with a random or fixed-effect model. FINDINGS: No significant difference was found between surgery performed under laminar airflow ventilation and conventional ventilation in total hip replacement (OR 1.23; 95% CI 0.97-1.56, p = 0.09), total knee arthroplasties (OR 1.14; 95% CI 0.62-2.09, p = 0.67) or different abdominal and open vascular surgery (OR 0.75; 95% CI 0.43-1.33, p = 0.33). The impact of the type of theatre ventilation may have no influence on surgical site infection as a tool for decreasing its occurrence. CONCLUSIONS: Based on this meta-analysis, operating under laminar airflow or conventional ventilation may have no independent relationship with the risk of surgical site infection. This relationship forces us not to recommend the use of laminar airflow ventilation since it has a much higher cost compared with conventional ventilation.

Hypoxia-mediated down-regulation of miRNAs' biogenesis promotes tumor immune escape in bladder cancer.

BACKGROUND: The study examines the function of hypoxia-mediated down-regulation of microRNAs (miRNAs) (mir-30c, mir-135a, and mir-27a) in the process of bladder cancer immune escape. METHODS: Quantitative Real-time PCR (qRT-PCR) was carried out to determine gene expression levels of Drosha and Dicer under hypoxia treatment, while western blotting and flow cytometry were used to determine protein expression. Seven reported miRNAs were identified via qRT-PCR assay. Flow cytometry detection of CD3/CD4/CD8-positive expression and statistics. Enzyme-linked immunosorbent assay (ELISA) detected cellular immune factors content. Cell apoptosis was checked via flow cytometry assay. Luciferase report assay and western blot assays were both used to verify the relationship between miRNAs and Casitas B-lineage lymphoma proto-oncogene b (Cbl-b). The animal model was established and Hematoxylin-eosin (HE) staining, TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, and immunohistochemistry (IHC) assays were separately used to verify the conclusions. RESULTS: The CD3 + /CD4 + expression was increased in the hypoxia group, while CD3 + /CD8 + expression, the cellular immune factors content Interleukin-2 (IL-2) and Tumor Necrosis Factor-α (TNFα) along with the cell apoptosis were suppressed. The protein expression of Cbl-b was found to be up-regulated in the hypoxia group. After constructing the overexpression/ knockdown of Cbl-b in peripheral blood mononuclear cell (PBMC), Cbl-b has been found to promote tumor immune escape in bladder cancer. Furthermore, Cbl-b had been identified as the co-targets of mir-30c, mir-135a, and mir-27a and down-regulation of miRNA biogenesis promotes Cbl-b expression and deactivating T cells in vitro/in vivo. CONCLUSION: Hypoxia-mediated down-regulation of miRNAs' biogenesis promotes tumor immune escape in bladder cancer, which could bring much more advance to the medical research on tumors.

Comparison of MESA of and Framingham risk scores in the prediction of coronary artery disease severity.

BACKGROUND: The correlation between cardiovascular risk scoring systems and the severity of coronary artery diseases (CAD) is not clear. The present research aimed to evaluate the Multi-Ethnic Study of Atherosclerosis (MESA) risk score and Framingham risk score (FRS), using the Gensini score (GS) system as reference, so as to determine which model is better for the prediction of CAD severity. METHODS: This research was a single-center and cross-sectional observational study. In total, 1423 patients were included in our study. Three different groups were formed according to GS: 0 < GS ≤ 22 (low GS group, n = 484); 22 < GS ≤ 42 (intermediate GS group, n = 468); GS > 42 (high GS group, n = 471). Logistic and linear regression analyses were carried out to explore the relationship between the risk score models and the GS. The performance of the risk models was determined by receiver operating characteristic curve (ROC) analysis. RESULTS: The MESA risk score and the FRS both had a statistically significant power for the prediction of CAD severity (MESA area under curve: 0.630; FRS area under curve: 0.613). Furthermore, the MESA had a better performance in predicting the severity (p < 0.05) of CAD compared with the FRS. In the subgroup analysis, the MESA showed a better performance in the male (p < 0.05), diabetes mellitus (p < 0.05), and smoking subgroups (p < 0.05) compared with the FRS. CONCLUSION: The MESA and FRS predicted the severity of CAD in the Chinese population of this study. Moreover, the MESA had a better performance than the FRS model in predicting the severity of CAD in the overall population as well as in the male, smoking, diabetes, and non-diabetes subgroups.

MicroRNA-26b-5p promotes development of neonatal respiratory distress syndrome by inhibiting differentiation of mesenchymal stem cells to type II of alveolar epithelial cells via regulating Wnt5a.

OBJECTIVE: The aim was to investigate the role of microRNA-26b-5p in regulating mesenchymal stem cells (MSCs) differentiation to type II of alveolar epithelial cells (AECII) in the disease course of neonatal respiratory distress syndrome (NRDS). MATERIALS AND METHODS: MSCs were first derived from rat bone marrow. In vitro induction of MSCs differentiation to AECII was conducted by SAGM. The mRNA levels of microRNA-26b-5p, Wnt5a, and AECII-related genes (Occludin, KGF, CK18, SpA, SpB, and SpC) during the process of cell differentiation were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Enzyme-linked immunosorbent assay (ELISA) was conducted for detecting levels of inflammatory factors tumor necrosis factor-α (TNF-α), interferon-α (INF-α), and interleukin-1 (IL-1) in cell supernatant. Dual-luciferase reporter gene assay was then carried out to verify the regulatory effect of microRNA-26b-5p on Wnt5a. MicroRNA-26b-5p expression in serum samples of NRDS neonates and healthy neonates was detected by qRT-PCR as well. RESULTS: MicroRNA-26b-5p was overexpressed in NRDS neonates than those of healthy neonates. Besides, microRNA-26b-5p was highly expressed in the process of MSCs differentiation to AECII. MicroRNA-26b-5p overexpression remarkably inhibited AECII differentiation and Wnt5a expression. Levels of TNF-α, INF-α, and IL-1 in cell supernatant during differentiation induction were elevated. The regulatory effects of microRNA-26b-5p on AECII differentiation, Wnt5a expression, and inflammatory response were reversed by Wnt5a overexpression. CONCLUSIONS: MicroRNA-26b-5p inhibits MSCs differentiation to AECII via inhibiting Wnt5a expression through the Wnt pathway.

Association of VDR and OPG gene polymorphism with osteoporosis risk in Chinese postmenopausal women.

AIMS: The underlying mechanisms of vitamin D receptor (VDR) and osteoprotegerin (OPG) genetic variation associated with bone mineral density and osteoporosis remain uncertain. This study aimed to investigate the association of VDR and OPG gene polymorphism as well as gene-gene interaction and their haplotype combination with the risk of osteoporosis. METHODS: Polymerase chain reaction restriction fragment length polymorphism was carried out for single nucleotide polymorphism (SNP) detection. Generalized multifactor dimension reduction (GMDR) is used to identify the interaction. SHEsis software evaluated the haplotype and logistic regression was performed to assess the association between the SNPs within the VDR and OPG genes and osteoporosis. RESULTS: The risk of osteoporosis in the VDR-rs2228570 polymorphism T-allele carriers was significantly higher than that in CC (CT/TT versus CC) individuals (adjusted odds ratio [OR] [95% confidence interval (CI)] = 1.76 [1.33-2.22]). The risk of osteoporosis was also higher in the G-allele carrier of the OPG-rs3102735 polymorphism than in individuals with the AA genotype (AG/GG vs. AA) (adjusted OR [95% CI] = 1.65 [1.27-2.14]). However, after adjusting for sex, age, and waist circumference covariates, no significant association of VDR-rs17879735 and OPG-rs2073618 with the osteoporosis risk was revealed. The GMDR method identified that gene-gene interactions were significant, but not for gene/AO interaction. Haplotypes were analyzed with SHEsis software. We did not detect a high-risk haplotype combination associated with osteoporosis. CONCLUSIONS: Both VDR-rs2228570-T and OPG-rs3102735-G and their interactions are related to the increased risk of osteoporosis.

MicroRNA-200a promotes proliferation and invasion of ovarian cancer cells by targeting PTEN.

OBJECTIVE: We investigate whether microRNA-200a could regulate proliferation and invasion of ovarian cancer cells, thereby participating in the occurrence and development of ovarian cancer. We also explore the specific mechanism of microRNA-200a in regulating ovarian cancer. PATIENTS AND METHODS: Expression level of microRNA-200a in ovarian cancer tissues and paracancerous tissues were detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The regulatory effects of microRNA-200a on proliferation and invasion of ovarian cancer cells were examined by Cell counting kit-8 (CCK-8) and cell invasion assay, respectively. Dual-luciferase reporter gene assay was performed to confirm the binding relationship between microRNA-200a and PTEN (phosphatase and tensin homolog deleted on chromosome ten). The regulatory role of microRNA-200a in PTEN expression was accessed by Western blot. Rescue experiments were conducted to assess whether microRNA-200a regulated proliferation and invasion of ovarian cancer cells by inhibiting PTEN expression. RESULTS: MicroRNA-200a expression in ovarian cancer tissues was significantly higher than that of paracancerous tissues. Besides, microRNA-200a was also overexpressed in ovarian cancer cell lines than that of normal ovarian cells. Overexpression of microRNA-200a promoted the proliferative and invasive abilities of SKOV3 and OVCAR3 cells. Dual-luciferase reporter gene assay showed that microRNA-200a could directly degrade PTEN. Overexpression of PTEN in SKOV3 and OVCAR3 cells partially reversed the increased cell proliferation and invasion induced by overexpressed microRNA-200a. CONCLUSIONS: Overexpressed microRNA-200a promoted the proliferative and invasive abilities of ovarian cancer cells, which might be related to the targeted regulation of PTEN expression.

Expression of sodium/iodide transporters and thyroid stimulating hormone receptors in thyroid cancer patients and its correlation with iodine nutrition status and pathology.

OBJECTIVE: To investigate the relationship between the expression of sodium/iodide transporter (NIS) and thyroid stimulating hormone receptor (TSHR) and iodine nutritional status in patients with thyroid carcinoma. PATIENTS AND METHODS: 146 cases of thyroid cancer in Shanghai Gongli Hospital, the Second Military Medical University between February and December 2014 were selected as thyroid cancer group, 120 cases of normal thyroid morphology examined by thyroid ultrasound at the same period were selected as normal group. General information and thyroid function of two groups were recorded and analyzed. H&E staining was used to perform histopathological study on both normal group and thyroid cancer group, and immunohistochemistry was used to detect NIS and TSHR protein expression and position. Reverse transcriptase polymerase chain reaction (RT-PCR) was used for quantitative detection of NIS and TSHR mRNA in the two groups, and the relationship between iodine nutrition and NIS and TSHR expression in thyroid cancer patients was studied. The expression of NIS and TSHR in each group was detected by Western blotting, and the difference in NIS and TSHR expression was analyzed by SPSS 17.0 statistical software. RESULTS: The difference of serum total triiodothyronine (TT3), total thyroxine (TT4), and thyroid stimulating hormone (TSH) levels between the normal group and the thyroid cancer group was statistically significant (p < 0.05). H&E staining showed that the histopathology of the thyroid cancer group was significantly different from that of the normal group. Immunohistochemistry showed the positive expression of NIS and TSHR in thyroid cancer group. The expression of NIS and TSHR mRNA and protein in thyroid cancer patients was significantly lower than that in normal group detected by RT-PCR and Western blotting. Analysis of variance showed that the difference of NIS and TSHR expression between the two groups was statistically significant (p < 0.05). CONCLUSIONS: These findings indicated that the expression of NIS and TSHR in thyroid cancer is closely related to iodine nutritional status, which has important research value.

Downregulation of SASH1 correlates with poor prognosis in cervical cancer.

OBJECTIVE: The aim of this study was to analyze the association of SASH1 expression with clinicopathological features and prognosis in patients suffering cervical cancer. PATIENTS AND METHODS: The expressions of SASH1 mRNA and protein in cervical cancer tissues and matched normal cervical tissues were detected by Real-time PCR and Immunohistochemistry. Based on the above findings, the association among SASH1 expression and clinicopathological features was analyzed. Overall survival was evaluated using the Kaplan-Meier method. The variables were used in univariate and multivariate analysis by the Cox proportional hazards model. RESULTS: The results demonstrated that both SASH1 mRNA and proteins were downregulated in cervical cancer tissues compared with those in matched normal tissues (both p < 0.05). Also, decreased SASH1 expression in cervical cancer was found to be significantly associated with high FIGO Stage (p = 0.001), lymph nodes metastasis (p = 0.003) and differentiation (p = 0.018). Furthermore, Kaplan-Meier analysis demonstrated that low SASH1 expression level was associated with poorer overall survival (p < 0.01). Univariate and multivariate analyses indicated that status of SASH1 was an independent prognostic factor for patients with cervical cancer. CONCLUSIONS: These findings suggested that SASH1 can be useful as a new prognostic marker and therapeutic target in cervical cancer patients.

Enhancement or inhibition of PLCγ2 expression in rat hepatocytes by recombinant adenoviral vectors that contain full-length gene or siRNA.

We investigated the effects of recombinant adenovirus vectors that overexpress or silence PLCγ2 on the expression of this gene during hepatocyte proliferation. Hepatocytes were isolated, identified by immunofluorescent cytochemical staining and infected by previously constructed Ad-PLCγ2 and Ad-PLCγ2 siRNA1, siRNA2 and siRNA3. Green fluorescent protein (GFP) expression was observed by fluorescence microscopy. Infection percentage was calculated by flow cytometry. mRNA and protein levels of PLCγ2 were detected by quantitative reverse transcription-PCR (qRT-PCR) and western blotting, respectively. The viability of the infected hepatocytes was measured by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. We found that nearly 97% of cells were positive for the hepatocyte marker, CK18. After infection of Ad-PLCγ2 and Ad-PLCγ2 siRNA, more than 99% of hepatocytes expressed GFP significantly, and mRNA and protein expression of PLCγ2 was up-regulated significantly in Ad-PLCγ2 infected hepatocytes, but down-regulated in Ad-PLCγ2 siRNA2 infected cells. The cell proliferation rate decreased in PLCγ2-overexpressing cells, while the rate increased in PLCγ2-silencing cells. We verified that recombinant Ad-PLCγ2 and Ad-PLCγ2 siRNA2 were constructed successfully. These two recombinant vectors promoted or decreased the expression of PLCγ2 in rat hepatocytes and affected the cell proliferation rate, which provides a useful tool for further investigation of the role of PLCγ2 in hepatocyte apoptosis.

Construction of recombinant adenovirus Ad-rat PLCγ2 and its effects on apoptosis of rat liver cell BRL-3A in vitro.

Although the role of PLCγ2 in apoptotic response has been reported, too little is known about whether PLCγ2 induces liver cell apoptosis during liver regeneration. Therefore, this study firstly packaged Ad-PLCγ2 recombinant adenovirus and primarily evaluated its effect on apoptosis of rat liver cell BRL-3A in vitro. Following ten days of co-transfection of pHBAd-MCMV-GFP-PLCγ2 and pHBAd-BHG into HEK293 cells, viral cytopathic effect (CPE) was apparent. Following three rounds of amplification, tissue culture infectious dose 50 (TCID50) assay showed that the titer value reached 1×1010 PFU/mL. After 24 h of transfection of recombinant adenovirus into BRL-3A cells, transfection efficiency of adenovirus into BRL-3A cells was above 90% when obsereved under fluorescent microscopy. qRT-PCR and Western blot assays showed mRNA and protein levels of PLCγ2 were significantly elevated in the transfected BRL-3A cells. Flow cytometric analysis showed that, compared with the control and Ad-GFP groups, cell apoptosis rate of Ad-PLCγ2 group were significantly increased (P<0.01), and the cell cycle in Ad-PLCγ2 group was arrested at G1 phase which was manifested by a marked increase (P<0.01) in the percentage of G1 phase cells and a great decrease (P<0.01) in the percentage of S and G2/M phase cells. It was concluded from above results that recombinant adenovirus Ad-PLCγ2 was packaged successfully, and could promote cell apoptosis by arresting the transition from G1 to S phase of BRL-3A cells.

Construction of recombinant adenovirus Ad-rat PLCg2-shRNA and successful suppression of PLCg2 expression in BRL-3A cells.

Phospholipase Cg2 (PLCg2) induces apoptosis of immune and tumor cells; however, it remains unclear whether PLCg2 promotes hepatocyte apoptosis during liver regeneration (LR). Therefore, to establish a framework for further exploring the function of PLCg2, we generated recombinant adenoviruses carrying a template encoding short hairpin (sh)-RNA targeting PLCg2 (Ad-PLCg2-shRNA), which were used to silence the expression of PLCg2 in BRL-3A cells. First, three pairs of PLCg2-shRNAs were designed, synthesized, and cloned into a shuttle vector, pHBAd-U6-GFP, after annealing. The recombinant shuttle plasmids were co-transfected with the backbone vector pHBAd-BHG into HK293 cells to package the recombinant Ad-PLCg2-shRNAs used to infect BRL-3A cells. Infection efficiency was monitored by observing the number of GFP-positive cells under a fluorescent microscope. To determine the recombinant adenoviruses with the highest silencing efficiency, levels of PLCg2 mRNA were evaluated by qRT-PCR. DNA sequencing confirmed that the correct shRNA coding sequences were inserted into the shuttle vectors and adenoviral plasmids. The titers of three recombinant adenoviruses were at least 1 x 10(10) PFU/mL. The most effective adenoviral construct, with interference efficiency of 77%, was determined by qRT-PCR. These results show that a recombinant adenovirus, Ad-PLCg2-shRNA, was developed and was effective at silencing the rat PLCg2 gene. This construct may contribute to the study of PLCg2 in hepatocyte apoptosis during LR.

Improved systolic function of rat cardiocytes during heart failure by overexpression of SERCA2a.

OBJECTIVE: This study shows that overexpression of SERCA2a can improve the systolic function and reduce the occurr-ence of arrhythmias in cardiocytes isolated from the heart of a rat model of heart failure. MATERIALS AND METHODS: An animal model of rats experiencing heart failure was established by a surgical procedure producing abdominal aortic coarctation. Cardiocytes from sacrificed rats were isolated by a collagenase digestion method. The SERCA2a adenovirus vector was transfected into the cells after 48h of culture. Overexpression of SERCA2a in cardiocytes was verified by Western Blot. Measurements were taken using a single cell dynamic edge detection system to evaluate the effects on the myocardiocyte function and calcium homeostasis. RESULTS: Cardiocytes overexpressing SERCA2a displayed a stronger systolic function and lower occurrence rate of abnormal systolic rhythm than mock-transfected cardiocytes. The contraction rhythm abnormality rate percentage was 5.270 ± 1.566% vs. 3.955 ± 1.684% (p < 0.01). The time at which they reached the maximum contraction (TTP) was 0.095 ± 0.009s vs. 0.114 ± 0.008s (p < 0.01). The time at which they reached 50% of the diastolic amplitude (R50) was 0.039 ± 0.008s vs. 0.057 ± 0.010s (p < 0.01). Finally, the occurrence rate of abnormal systolic rhythm during maximal contraction was 58% vs. 81% (p < 0.01). These results show that all data were significantly improved in the SERCA2a overexpressing group, and that parameters achieved were similar to those in the sham-operated non-heart failure group. CONCLUSIONS: The overexpression of SERCA2a in cardiocytes during heart failure significantly improves cell function and arrhythmia occurrence.

Construction of polycythemia vera protein interaction network and prediction of related biological functions.

Here, polycythemia vera (PV)-related genes were screened by the Online Mendelian Inheritance in Man (OMIM), and literature pertaining to the identified genes was extracted and a protein-protein interaction network was constructed using various Cytoscape plugins. Various molecular complexes were detected using the Clustervize plugin and a gene ontology-enrichment analysis of the biological pathways, molecular functions, and cellular components of the selected molecular complexes were identified using the BiNGo plugin. Fifty-four PV-related genes were identified in OMIM. The protein-protein interaction network contains 5 molecular complexes with correlation integral values >4. These complexes regulated various biological processes (peptide tyrosinase acidification, cell metabolism, and macromolecular biosynthesis), molecular functions (kinase activity, receptor binding, and cytokine activity), and the cellular components were mainly concentrated in the nucleus, intracellular membrane-bounded organelles, and extracellular region. These complexes were associated with the JAK-STAT signal transduction pathway, neurotrophic factor signaling pathway, and Wnt signaling pathway, which were correlated with chronic myeloid leukemia and acute myeloid leukemia.

Prognostic value of circulating tumor cells in metastatic breast cancer: a systemic review and meta-analysis.

OBJECTIVE: Metastatic breast cancer (MBC) remains the main cause of cancer-related death, and the clinical significance and prognostic role of circulating tumor cells (CTCs) in metastatic breast cancer are still controversial. Here, we conducted a meta-analysis to clarify the correlation between CTCs and the clinicopathological features and prognosis of MBC. METHODS: We performed a comprehensive search of Pubmed and the ISI Web of Science through December 2014. Only articles that focused on MBC patients and detected CTCs using the CellSearch system were included. The associations between CTCs and survival rate and clinicopathological parameters, including molecular pattern, metastatic region and treatment response, were evaluated. RESULTS: This meta-analysis included 24 studies (3701 MBC patients), 13 prospective studies and 11 retrospective studies. We found that CTCs were more frequently detected with HER2 + primary tumors (pooled RR = 0.73, 95 % CI = 0.63-0.84). Additionally, higher CTC numbers indicated a worse treatment response (RR = 0.56, 95 % CI = 0.40-0.79), poorer PFS (RR = 0.64, 95 % CI = 0.56-0.73) and poorer OS (RR = 0.69, 95 % CI = 0.64-0.75) in MBC patients. CONCLUSION: Based on these results, we propose that HER2 positivity could be a significant risk factor for the presence of CTCs. Additionally, CTCs have a significant prognostic value for MBC patients. Therefore, CTCs should be continually monitored to guide the treatment of MBC patients, especially those with HER2 + primary tumors.

Effect of specific silencing of EMMPRIN on the growth and cell cycle distribution of MCF-7 breast cancer cells.

The extracellular matrix metalloproteinase inducer (EMMPRIN, CD147) is a member of the immunoglobulin family and shows increased expression in tumor cells. We examined the effect of RNAi-mediated EMMPRIN gene silencing induced by lentiviral on the growth and cycle distribution of MCF-7 breast cancer cells. Lentiviral expressing EMMPRIN-short hairpin RNA were packaged to infect MCF-7 cells. The inhibition efficiency of EMMPRIN was validated by real-time fluorescent quantitation polymerase chain reaction and western blotting. The effect of EMMPRIN on cell proliferation ability was detected using the MTT assay and clone formation experiments. Changes in cell cycle were detected by flow cytometry. EMMPRIN-short hairpin RNA-packaged lentiviral significantly down-regulated EMMPRIN mRNA and protein expression, significantly inhibited cell proliferation and in vitro tumorigenicity, and induced cell cycle abnormalities. Cells in the G0/G1 and G2/M phases were increased, while cells in the S phase were decreased after infection of MCF-7 cells for 3 days. The EMMPRIN gene facilitates breast cancer cell malignant proliferation by regulating cell cycle distribution and may be a molecular target for breast cancer gene therapy.