Interplay of sleep patterns and oxidative balance score on total cardiovascular disease risk: Insights from the National Health and Nutrition Examination Survey 2005-2018.

Background: Unhealthy lifestyle and diet may contribute to the development of cardiovascular disease (CVD), but limited evidence exists regarding the association between sleep patterns, oxidative stress-related exposures to diet and lifestyle, and CVD risk. Methods: We analysed data from 10 212 adults in the National Health and Nutrition Examination Survey (NHANES) database (2005-2018). Self-report questionnaires were used to collect data on sleep duration, sleepiness, and trouble sleeping, classified into three categories: healthy, intermediate, and poor sleep patterns. Healthy sleep was defined as sleeping seven to nine hours per night with no self-reported sleepiness or trouble sleeping, while intermediate and poor sleep patterns indicated one and two to three sleep problems, respectively. The oxidative balance score (OBS) was calculated based on twenty oxidative stress-related exposures to dietary and lifestyle factors, with a higher score indicating greater antioxidant exposure. Survey-based multivariable-adjusted regression analysis was conducted to examine the association of sleep patterns or OBS alone and combined with the total and specific CVD risk. Results: Participants with poor sleep patterns had a higher likelihood of developing CVD (odds ratio (OR) = 1.76; 95% confidence interval (CI) = 1.26-2.45, P < 0.05), while an inverse association was found between OBS and CVD risk (quartile (Q) 4 vs Q1: OR = 0.67; 95% CI = 0.47-0.94, P = 0.02, P for trend <0.05). There was an interaction between sleep patterns and OBS (P for interaction = 0.03). Participants with unhealthy (intermediate and poor) sleep patterns and pro-oxidant OBS (Q1 and Q2) were significantly associated with increased risk of total CVD (OR = 2.31; 95% CI = 1.42-3.74, P < 0.05), as well as angina and congestive heart failure, but not coronary heart disease (CHD). Stratified analysis showed that among individuals without hyperlipidaemia, participants with both unhealthy sleep patterns and pro-oxidant OBS exhibited a higher risk of CHD compared to those with healthy sleep patterns and antioxidative OBS. Conclusions: Unhealthy sleep patterns and reduced oxidative balance are positively associated with an increased risk of overall and specific CVD. Interventions that target healthy sleep habits and antioxidant-rich diets and lifestyles may be important for reducing the risk of CVD.

Identification of the key immune-related genes and immune cell infiltration changes in renal interstitial fibrosis.

Background: Chronic kidney disease (CKD) is the third-leading cause of premature mortality worldwide. It is characterized by rapid deterioration due to renal interstitial fibrosis (RIF) via excessive inflammatory infiltration. The aim of this study was to discover key immune-related genes (IRGs) to provide valuable insights and therapeutic targets for RIF in CKD. Materials and methods: We screened differentially expressed genes (DEGs) between RIF samples from CKD patients and healthy controls from a public database. Least absolute shrinkage and selection operator regression analysis and receiver operating characteristic curve analysis were applied to identify significant key biomarkers. The single-sample Gene Set Enrichment Analysis (ssGSEA) algorithm was used to analyze the infiltration of immune cells between the RIF and control samples. The correlation between biomarkers and immune cell composition was assessed. Results: A total of 928 DEGs between CKD and control samples from six microarray datasets were found, 17 overlapping immune-correlated DEGs were identified by integration with the ImmPort database, and six IRGs were finally identified in the model: apolipoprotein H (APOH), epidermal growth factor (EGF), lactotransferrin (LTF), lysozyme (LYZ), phospholipid transfer protein (PLTP), and secretory leukocyte peptidase inhibitor (SLPI). Two additional datasets and in vivo experiments indicated that the expression levels of APOH and EGF in the fibrosis group were significantly lower than those in the control group, while the expression levels of LTF, LYZ, PLTP, and SLPI were higher (all P < 0.05). These IRGs also showed a significant correlation with renal function impairment. Moreover, four upregulated IRGs were positively associated with various T cell populations, which were enriched in RIF tissues, whereas two downregulated IRGs had opposite results. Several signaling pathways, such as the "T cell receptor signaling pathway" and "positive regulation of NF-κB signaling pathway", were discovered to be associated not only with immune cell infiltration, but also with the expression levels of six IRGs. Conclusion: In summary, six IRGs were identified as key biomarkers for RIF, and exhibited a strong correlation with various T cells and with the NF-κB signaling pathway. All these IRGs and their signaling pathways may evolve as valuable therapeutic targets for RIF in CKD.

Phosphorus-rich biochar modified with Alcaligenes faecalis to promote U(VI) removal from wastewater: Interfacial adsorption behavior and mechanism.

Phosphorus-rich biochar (PBC) has been extensively studied due to its significant adsorption effect on U(VI). However, the release of phosphorus from PBC into solution decreases its adsorption performance and reusability and causes phosphorus pollution of water. In this study, Alcaligenes faecalis (A. faecalis) was loaded on PBC to produce a novel biocomposite (A/PBC). After adsorption equilibrium, phosphorus released into solution from PBC was 2.32 mg/L, while it decreased to 0.34 mg/L from A/PBC (p < 0.05). The U(VI) removal ratio of A/PBC reached nearly 100%, which is 13.08% higher than that of PBC (p < 0.05), and it decreased only by 1.98% after 5 cycles. When preparing A/PBC, A. faecalis converted soluble phosphate into insoluble metaphosphate minerals and extracellular polymeric substances (EPS). And A. faecalis cells accumulated through these metabolites and formed biofilm attached to the PBC surface. The adsorption of metal cations on phosphate further contributed to phosphorus fixation in the biofilm. During U(VI) adsorption by A/PBC, A. faecalis synthesize EPS and metaphosphate minerals by using the internal components of PBC, thus increasing the abundance of acidic functional groups and promoting U(VI) adsorption. Hence, A/PBC can be a green and sustainable material for U(VI) removal from wastewater.

The surgical outcomes and risk factors of giant hepatic haemangiomas: a single centre experience.

OBJECTIVE: To evaluate the safety of performing surgery on cavernous haemangiomas in the liver larger than 10 cm and establish preoperative predictors of intraoperative blood transfusion and morbidity. METHODS: A total of 373 patients with haemangiomas larger than 10 cm who underwent surgery in our hospital were retrospectively analysed. According to tumour diameter, the patients were divided into a giant haemangioma (GH) group (241 cases) (10 cm ≤ diameter < 15 cm) and an enormous haemangioma (EH) group (132 cases) (diameter ≥ 15 cm). Clinical parameters were then compared between the two groups. RESULTS: Compared with the GH group, the EH group had higher rates of leukopenia (10.6% vs. 4.5%), anaemia (26.5% vs. 15.7%), and thrombocytopenia (13.6% vs. 6.2%). The occlusion time in the EH group was longer than that in the GH group (26.33 ± 14.10 min vs. 31.85 ± 20.09 min, P < 0.01). The blood loss and blood transfusion in the EH group were greater than those in the GH group (P < 0.05). Moreover, the morbidity in the EH group was higher than that in the GH group (17.4% vs. 9.13%, P < 0.05). According to the results of the multivariable analysis, the operation time and size of the haemangioma may be independent risk factors for blood transfusion (P < 0.05). Additionally, the size of the haemangioma may be an independent risk factor associated with complications (P < 0.05). CONCLUSION: Enormous haemangioma is more likely to cause haematologic abnormalities than giant hepatic haemangioma. The risks of the operation and postoperative complications of enormous haemangioma are higher than those of giant hepatic haemangioma.

miR-214-5p targeted by LncRNA DANCR mediates TGF-ß signaling pathway to accelerate proliferation, migration and inhibit apoptosis of prostate cancer cells.

OBJECTIVE: This research was designed to probe into the regulatory mechanism of long non-coding RNA (LncRNA) differentiation antagonizing non-protein coding RNA (DANCR) in potential applications and molecular mechanisms of prostate carcinoma (PC). METHODS: The DANCR and miR-214-5p levels in PC tissues and cell lines were tested via real-time PCR, and those of transforming growth factor-ß (TGF-ß) signaling pathway related proteins were evaluated via Western Blot (WB). Cell proliferation, migration, apoptosis and the regulatory relationship between target genes were assessed via MTT method, scratch test, flow cytometry, dual-luciferase report, RNA co-immunoprecipitation and RNA pull-down test, respectively. RESULTS: DANCR was up-regulated in PC patients' serum and cell lines, while miR-214-5p was opposite, showing negative correlation. Besides, DANCR was significantly correlated with PSA, Gleason score and T stage in PC patients. The area under the curve (AUC) of DANCR and miR-214-5p for diagnosing PC was not less than 0.850, while the AUC for predicting poor prognosis was more than 0.800. Cox analysis results also revealed that the two might be prognostic indicators of PC patients. We found that DANCR high levels or miR-214-5p low levels were related to PC patients' poor prognosis. Up-regulating DANCR or down-regulating miR-214-5p could promote PC cells' malignant proliferation and migration, prevent apoptosis, and activate TGF-ß signaling pathway, while reverse treatment of DANCR or miR-214-5p can reverse the above results. DANCR regulates miR-214-5p in a targeted manner, and DANCR over-expression can reduce the cancer inhibitory effect of miR-214-5p on PC cells. CONCLUSION: DANCR-miR-214-5p-TGF-ß axis regulatory network plays a key regulatory part in PC progression. It may provide new strategies for the screening and treatment of patients.

[Silencing ERp29 promotes the invasiveness of human PCa cells in vitro: Molecular mechanisms].

OBJECTIVE: To analyz the correlation of the expression of ERp29 with the clinicopathological characteristics of PCa and investigate the effect of small interfering RNA (siRNA) silencing the ERp29 gene on the biological behavior of PCa LNCaP cells. METHODS: The expression of the ERp29 gene in the BPH and PCa tissues was detected by immunohistochemistry and that of the ERp29 protein in the PCa and adjacent normal tissues of 6 PCa patients determined by Western blot. Human LNCaP cells were transfected with siRNA using LipofectamineTM 2000, and the expressions of ERp29 mRNA and protein in the LNCaP cells detected by quantitative real-time PCR (qRT-PCR) and Western blot, respectively. The proliferation of the LNCaP cells was measured by MTT assay, their in vitro migration and invasiveness evaluated by the Transwell method, and the expressions of E-cadherin and Vimentin determined by qRT-PCR. RESULTS: The expression of ERp29 was significantly lower in the PCa than in the adjacent normal tissue (73.9% vs 91.9%， P < 0.05), with a significant correlation between the down-regulated ERp29 expression and metastasis (M) staging (P < 0.05). After transfection with siRNA, the LNCaP cells showed dramatically increased proliferation, migration and invasiveness (P < 0.05), and the expression of E-cadherin was markedly down-regulated while that of Vimentin up-regulated as compared with those in the normal control group (P < 0.05). CONCLUSIONS: The ERp29 gene may be a novel repressor of tumor metastasis. Silencing ERp29 can promote the invasiveness of human PCa cells in vitro by down-regulating the expression of E-cadherin and increasing epithelial-mesenchymal transition.

circFN1 Mediates Sorafenib Resistance of Hepatocellular Carcinoma Cells by Sponging miR-1205 and Regulating E2F1 Expression.

In recent years, circular RNAs (circRNAs) have been shown to have critical regulatory roles in the resistance to anti-cancer drugs. However, the contributions of circRNAs to sorafenib resistance in hepatocellular carcinoma (HCC) remain largely unknown. The present study aims to explore the involvement of circFN1 in sorafenib resistance and how circFN1 is associated with the miR-1205/E2F1 pathway, which have been demonstrated to mediate this resistance in HCC cells. We investigated the expression of circRNAs in five paired sorafenib-sensitive HepG2 cells and sorafenib-resistant (SR)-HepG2 cells by microarray analysis. The quantitative real-time PCR analysis was used to investigate the expression pattern of circFN1 in HCC patient tissues and cell lines. Then, the effects of circFN1 on sorafenib resistance, cell proliferation, and apoptosis were assessed in HCC in vitro and in vivo. In this study, circFN1 was observed to be upregulated in HCC patient tissues and cell lines. Overexpression of circFN1 in HCC was significantly correlated with aggressive characteristics and served as an independent risk factor for overall survival in patients with HCC. Our in vivo and in vitro data indicated that inhibition of circFN1 enhances the sorafenib sensitivity of HCC cells. Mechanistically, we found that circFN1 could promote the expression of E2F1 by sponging miR-1205. In summary, our study demonstrated that circFN1 contributes to sorafenib resistance by regulating the miR-1205/E2F1 signaling pathway. These results indicate that circFN1 may represent a potentially valuable target for overcoming sorafenib resistance for HCC.

iTRAQ-Based Comparative Proteomics Analysis of Urolithiasis Rats Induced by Ethylene Glycol.

Nephrolithiasis is a frequent chronic urological condition with a high prevalence and recurrence rate. Proteomics studies on urolithiasis rat models are highly important in characterizing the pathophysiology of kidney stones and identifying potential approaches for preventing and treating kidney stones. The isobaric tags for relative and absolute quantification (iTRAQ) were performed to identify differentially expressed proteins (DEPs) in the kidney between urolithiasis rats and control rats. The results showed that 127 DEPs (85 upregulated and 42 downregulated) were identified in urolithiasis and control rats. The functions of DEPs were predicted by Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and protein-protein interaction (PPI) network analysis. The expression of four upregulated proteins (Tagln, Akr1c9, Spp1, and Fbn1) and four downregulated proteins (Hbb, Epb42, Hmgcs2, and Ca1) were validated by parallel reaction monitoring (PRM). Proteomics studies of ethylene glycol-induced urolithiasis rat models using iTRAQ and PRM helped to elucidate the molecular mechanism governing nephrolithiasis and to identify candidate proteins for the treatment of kidney stones.

A retrospective cohort analysis for the risk factors of intraoperative hypotension.

AIM OF THE STUDY: To reveal the risk factors of intraoperative hypotension (IH) and investigate whether IH was corrected in time. METHODS USED TO CONDUCT THE STUDY: This retrospective cohort study included patients undergoing surgeries in one medical centre. We divided all patients into two groups, the IH group and non-IH group. The clinical features of these two groups were compared and the independent risk factors for IH were analysed. RESULTS OF THE STUDY: A total of 5864 non-cardiac surgery patients were included, of which 931 patients had IH diagnose. The independent risk factors of IH include older age, high grade American Society of Anaesthesiologists (ASA) physical status, intrathecal anaesthesia, emergency surgery and medical history of hypertension (P < .01). Among the patients with IH, 44.5% had hypotension lasting between 30 and 120 minutes, and 25.2% had hypotension lasting >120 minutes. Patients with IH are more likely to develop major post-operative complications after surgery (P < .01). CONCLUSIONS: The independent risk factors of IH include older age, high grade ASA physical status, intrathecal anaesthesia, emergency surgery and history of hypertension. Hypotension during surgery is not always effectively treated.

The role of activated NLRP3 inflammatory body in acute kidney injury in rats caused by sepsis and NLRP3-TXNIP signaling pathway.

OBJECTIVE: The model of acute renal injury (AKI) induced by sepsis in rats was established by abdominal resection through surgical suture. The activation mechanism of nod-like receptor with pyrin domain containing 3 (NLRP3) inflammatory corpuscle in AKI induced by sepsis was analyzed. METHODS: Here, 60 male rats were selected and divided into two groups, including sham-operated group (NO-OPs group, n = 15) and sepsis group (CELP group, n = 45). In order to examine each index of CELP group, four time points (10, 20, 30, and 40 h) were set as control. In NO-OPs group, only abdominal resection through surgical suture was carried out. The expression levels of NLRP3, apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), caspase-1, and the expression level of NLRP3-TXNIP signaling pathway were measured by immunohistochemistry, Western blotting, immunoprecipitation, and mito-TEMPO (a mitochondria-targeted antioxidant) 40 h after operation and 10, 20, 30, and 40 h post-operation in CELP group. Herein, 40 h post-operation in NO-OPs group and 10, 20, 30, and 40 h post-operation in CELP group, peripheral blood samples were collected. RESULTS: Compared with NO-OPs group, the levels of serum creatinine (Scr) and blood urea nitrogen (BUN) in CELP group were increased (P < 0.05). Compared with NO-OPs group, the expression levels of interleukin-1ß (IL-1ß), NLRP3, ASC, and caspase-1 in CELP group were increased (P < 0.05). The expression level of TXNIP in renal tubular epithelial cells in rats was up-regulated. There was a positive correlation between TXNIP and NLRP3. The binding of NLRP3-TXNIP signaling pathway could be inhibited by siRNA transfection or mito-TMPO, and the activity of NLRP3 inflammatory bodies could be inhibited as well. CONCLUSION: Activation of NLRP3 inflammatory corpuscles could promote AKI induced by sepsis. Simultaneously, renal injury may lead to the production of mitochondrial reactive oxygen species (mROS), which may induce the binding of TXNIP to NLRP3.

Expression of Programmed Death Ligand 1 Is Associated with the Prognosis of Intrahepatic Cholangiocarcinoma.

BACKGROUND: Programmed death ligand 1 (PD-L1) is expressed in many malignancies and plays a critical role in escape from immune surveillance through inhibition of its receptor programmed death 1. The role of PD-L1 in intrahepatic cholangiocarcinoma (ICC) and mechanisms of its regulation, however, remain largely unknown. AIMS: To analyze the expression and prognostic significance of PD-L1 in ICC and to study the regulatory mechanisms of PD-L1. METHODS: Samples were obtained from 125 patients diagnosed with ICC in the Eastern Hepatobiliary Surgery Hospital from January 2012 to January 2013. The records of each patient were analyzed to examine the relationship between PD-L1 and clinical data. In vitro experiments were performed to investigate the relationship between PD-L1 and the IL-6/mTOR signaling pathway and the feedback mechanism pathway of PD-L1. RESULTS: Expression of PD-L1 is closely related to tumor vascular invasion, lymphatic metastasis and TNM staging. High PD-L1 expression is closely related to poor prognosis in ICC. Mechanically, IL-6 induces PD-L1 expression through mTOR signaling in ICC cells. In addition, PD-L1 has a negative feedback inhibition effect on AKT signaling. CONCLUSIONS: In summary, high PD-L1 expression was found to be associated with poor prognosis. The IL-6/mTOR pathway upregulates expression of PD-L1, thus promoting tumor invasion, and PD-L1 negatively inhibits the AKT pathway.

Anatomic resection and wide resection margin play an important role in hepatectomy for hepatocellular carcinoma with peritumoural micrometastasis.

BACKGROUND: Anatomic hepatectomy and wide resection margin may improve surgical outcome of patients with hepatocellular carcinoma (HCC), but not everyone gain survival benefit. It remains unclear what kind of patients would benefit from those surgical methods. We investigated the factors affecting survival of patients with HCC, with special attention paid to the surgical methods and pathological factors. METHODS: A retrospective analysis was conducted on 231 patients with hepatitis B-related HCC who underwent surgery from August 2011 to November 2013 in authors' institute. The survival analysis included the following variables: gender, age, viral load, alpha-fetoprotein, des-γ-carboxy prothrombin, tumour size, cirrhosis, blood transfusion, complications, resection method, resection margin, microvascular invasion (mVI), peritumoural satellite nodule, recurrence time and recurrent burden. RESULTS: The median follow-up time was 59 months. A total of 196 patients (84.9%) recurred and 151 patients (65.4%) deceased due to the disease. Multivariate analysis showed that cirrhosis, mVI and periturmoral satellite nodules were independent risk factors affecting overall survival after operation. The comparison between anatomic resection and local resection, and wide resection margin and narrow resection margin showed no significant differences for recurrence-free survival and overall survival, respectively (P = 0.089 and 0.068, 0.108 and 0.122). Stratified analysis revealed that anatomic resection and wide resection margin surgery improved survival when mVI or peritumoural satellite existed. CONCLUSION: Anatomic resection and wide resection margin are effective methods to improve the surgical outcome of HCC with periturmoral micrometastasis, although tumour characteristics affect patients' survival more than surgical techniques.

STAT gene family mRNA expression and prognostic value in hepatocellular carcinoma.

BACKGROUND: Signal transducer and activator of transcription (STAT) proteins are well-known transcription factors that play an important role in the progression of cancer. However, the association between STAT family genes and hepatocellular carcinoma (HCC) remains unclear. This study investigates the expression level, the prognostic value and the potential mechanism of STAT family genes in HCC. METHODS: Data from 365 HCC patients in The Cancer Genome Atlas (TCGA) database and 241 HCC patients in the Gene Expression Omnibus (GEO) database were used to investigate the diagnostic and prognostic values of STAT genes by survival analysis and nomogram. Gene set enrichment analysis (GSEA) was used to investigate the potential mechanism of the STAT genes in the development of HCC. RESULTS: Our results showed that STAT4/5B mRNA expression levels in HCC tissues were lower than those in normal tissues. Importantly, our results indicated that high expression of STAT5A, STAT5B and STAT6 was associated with better overall survival in HCC patients. Joint effects analysis of STAT5A, STAT5B and STAT6 suggested that the prognosis difference for any combination of genes was more significant than that for any individual gene. Then, we developed a risk score model could predict HCC prognosis and the nomogram visualized gene expression and clinical factors of probability for HCC prognosis. The ROC and calibration curves showed good performance in survival prediction in both the TCGA and the GEO databases. GSEA suggested that high expression of STAT5A, STAT5B and STAT6 were involved in immune-related biological processes, drug metabolism cytochrome P450, JAK-STAT signalling pathway, and PPAR signalling pathways. CONCLUSION: Our data suggest that STAT5A, STAT5B and STAT6 expression may be potential prognostic markers of HCC and, in combination, have a better predictive value for HCC prognosis.

LncRNA FOXD2-AS1 as a competitive endogenous RNA against miR-150-5p reverses resistance to sorafenib in hepatocellular carcinoma.

The current study elucidated the role of a long non-coding RNA (lncRNA), FOXD2-AS1, in the pathogenesis of hepatocellular carcinoma (HCC) and the regulatory mechanism underlying FOXD2-AS1/miR-150-5p/transmembrane protein 9 (TMEM9) signalling in HCC. Microarray analysis was used for preliminary screening of candidate lncRNAs in HCC tissues. qRT-PCR and Western blot analyses were used to detect the expression of FOXD2-AS1. Cell proliferation assays, luciferase assay and RNA immunoprecipitation were performed to examine the mechanism by which FOXD2-AS1 mediates sorafenib resistance in HCC cells. FOXD2-AS1 and TMEM9 were significantly decreased and miR-150-5p was increased in SR-HepG2 and SR-HUH7 cells compared with control parental cells. Overexpression of FOXD2-AS1 increased TMEM9 expression and overcame the resistance of SR-HepG2 and SR-HUH7 cells. Conversely, knockdown of FOXD2-AS1 decreased TMEM9 expression and increased the sensitivity of HepG2 and Huh7 cells to sorafenib. Our data also demonstrated that FOXD2-AS1 functioned as a sponge for miR-150-5p to modulate TMEM9 expression. Taken together, our findings revealed that FOXD2-AS1 is an important regulator of TMEM9 and contributed to sorafenib resistance. Thus, FOXD2-AS1 may serve as a therapeutic target against sorafenib resistance in HCC.

lncARSR promotes liver cancer stem cells expansion via STAT3 pathway.

Liver cancer stem cells (CSCs) have important functions in tumorigenesis, progression, recurrence and drug resistance of hepatocellular carcinoma (HCC). lncARSR has been reported to play an important role in the maintenance and self-renewal of renal cancer stem cells, but its role in liver cancer stem cells (CSCs) remains obscure. Herein, we observed high expression of lncARSR in chemoresistant hepatocellular carcinomas (HCCs). A remarkable increase of lncARSR expression in EpCAM or CD133-positive liver CSCs as well as in CSC-enriched hepatoma spheres. Interference lncARSR suppressed liver CSC expansion by inhibiting the dedifferentiation of hepatoma cells and decreasing the self-renewal ability of liver CSCs. Mechanistically, we found STAT3 as the downstream of lncARSR in HCC cells. The special STAT3 inhibitor S3I-201 abolished the discrepancy in liver CSC proportion and the self-renewal capacity between lncARSR knockdown hepatoma cells and control cells, which further confirmed that STAT3 was required in lncARSR promoted liver CSCs expansion. More importantly, interference lncARSR HCC cells were more sensitive to sorafenib or cisplatin treatment. This maybe means that patients with low lncARSR levels benefited from cisplatin or sorafenib treatment, but patients with high lncARSR expression did not. Conclusion: lncARSR was upregulated in liver CSCs and could promote HCC cells dedifferentiation and liver CSCs expansion by targeting STAT3 signaling.

Changing expression profiles of long non-coding RNAs, mRNAs and circular RNAs in ethylene glycol-induced kidney calculi rats.

BACKGROUND: To explore long non-coding RNA (lncRNA), mRNA and circular RNA (circRNA) expression profiles and their biological functions in the pathogenesis of kidney stones in ethylene glycol-induced urolithiasis rats. RESULTS: The expression of 1440 lncRNAs, 2455 mRNAs and 145 circRNAs was altered in the kidneys of urolithiasis rats. GO and KEGG biological pathway analysis were performed to predict the functions of differentially expressed lncRNAs, circRNAs and co-expressed potential targeting genes. Co-expression networks of lncRNA-mRNA and circRNA-miRNA were constructed based on correlation analysis between differentially expressed RNAs. mRNAs coexpressed with lncRNAs were involved in many kidney diseases, e.g., Ephb6 was associated with the reabsorption ability of the kidney. Arl5b was associated with the dynamic changes in the podocyte foot process in podocyte injury. miRNAs co-expressed with circRNAs, such as rno-miR-138-5p and rno-miR-672-5p, have been proven to be functional in hypercalciuria urolithiasis. CONCLUSION: The expression profile provided a systematic perspective on the potential functions of lncRNAs and circRNAs in the pathogenesis of kidney stones. Differentially expressed lncRNAs and circRNAs might serve as treatment targets for kidney stones.

Treatment of gallbladder stone with common bile duct stones in the laparoscopic era.

BACKGROUND: Laparoscopic common bile duct exploration (LCBDE) for stone can be carried out by either laparoscopic transcystic stone extraction (LTSE) or laparoscopic choledochotomy (LC). It remains unknown as to which approach is optimal for management of gallbladder stone with common bile duct stones (CBDS) in Chinese patients. METHODS: From May 2000 to February 2009, we prospective treated 346 consecutive patients with gallbladder stones and CBDS with laparoscopic cholecystectomy and LCBDE. Intraoperative findings, postoperative complications, postoperative hospital stay and costs were analyzed. RESULTS: Because of LCBDE failure,16 cases (4.6%) required open surgery. Of 330 successful LCBDE-treated patients, 237 underwent LTSE and 93 required LC. No mortality occurred in either group. The bile duct stone clearance rate was similar in both groups. Patients in the LTSE group were significantly younger and had fewer complications with smaller, fewer stones, shorter operative time and postoperative hospital stays, and lower costs, compared to those in the LC group. Compared with patients with T-tube insertion, patients in the LC group with primary closure had shorter operative time, shorter postoperative hospital stay, and lower costs. CONCLUSIONS: In cases requiring LCBDE, LTSE should be the first choice, whereas LC may be restricted to large, multiple stones. LC with primary closure without external drainage of the CBDS is as effective and safe as the T-tube insertion approach.

MiR-223-3p targeting SEPT6 promotes the biological behavior of prostate cancer.

MicroRNAs (miRNAs) present frequently altered expression in urologic cancers including prostate, bladder, and kidney cancer. The altered expression of miR-223 has been reported in cancers and other diseases in recent researches. MiR-223 is up-regulated in systemic lupus erythematosus and rheumatoid arthritis. In neoplastic diseases, miR-223 is proved to be up-expressed in plasma or serum and cancer tissues compared with normal tissues in pancreatic cancer, gastric cancer, et al. However, whether altered expression of miR-223 is associated with prostate cancer (PCa) and what it is potential functions in PCa remained unveiled. In this study, we firstly found miR-223-3p were up-regulated in prostate cancer tissues and then we study functional role of miR-223-3p in PCa using DU145, PC3 and LNCaP cell lines. Our data suggested that miR-223-3p might target gene SEPT6 and promoted the biological behavior of prostate cancer. Notably, we found increasing SEPT6 expression might reverse the biological activity induced by miR-223-3p, which might be a potential therapeutic target for PCa.

Primary closure after laparoscopic common bile duct exploration versus T-tube.

BACKGROUND: Laparoscopic common bile duct exploration (LCBDE) is now one of the main methods for treating choledocholithiasis accompanied with cholelithiasis. The objective of our study was to assess the safety and effectiveness of laparoscopic primary closure for the treatment of common bile duct (CBD) stones compared with T-tube drainage. METHODS: Patients who underwent CBD stones were studied prospectively from 2002-2012 in a single center. A total of 194 patients were randomly assigned to group A (LCBDE with primary closure) with 101 cases and group B (LCBDE with T-tube drainage) with 93 cases. Intraoperative cholangiography and choledochoscopy were performed in all patients. Patient demographics, intraoperative findings, postoperative stay, complications, and hospital expenses were recorded and analyzed. RESULTS: There was no mortality in the two groups. Four patients (3.96%) of group A were converted to open surgery, and three patients (3.23%) in group B. The mean operating time was much shorter in group A than in group B (102.6 ± 15.2 min versus 128.6 ± 20.4 min, P < 0.05). The length of postoperative hospital stay was longer in group B (4.9 ± 3.2 d) than in group A (3.2 ± 2.1 d). The hospital expenses were significantly lower in group A. Three patients experienced postoperative complications, which were related to the usage of the T-tube in group B. The incidences of overall postoperative complications were insignificantly lower in group A. CONCLUSIONS: Laparoscopic primary closure of CBD is safe and effective for the management of CBD stones, and can be performed routinely as an alternative to T-tube drainage.

Role of elevated liver transaminase levels in the diagnosis of liver injury after blunt abdominal trauma.

The liver is the second most commonly injured organ following blunt abdominal trauma. The stable patient with minimal physical findings with a history of blunt abdominal trauma presents a challenge for diagnosis of liver injury. This study was conducted to determine the usefulness of hepatic transaminases in predicting the presence of liver injury and its severity following blunt abdominal trauma. In this retrospective study, we included all patients who had sustained blunt abdominal injury and were treated at our institution between January 2008 and December 2010. The grading of the liver injury was verified using CT scans or surgical findings. One hundred and eighty-two patients with blunt abdominal trauma underwent the required blood tests and were included in the study. Using receiver operating characteristic (ROC) curve assessment, optimum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and γ-glutamyl transpeptidase (GGT) thresholds were determined to be >57 U/l, 113 U/l, 595 U/l and 50 U/l. ALT >57 U/l (OR, 66.1; P<0.001) and AST >113 U/l (OR, 30.6; P<0.001) were strongly associated with the presence of liver injuries. This association was also observed in patients with elevated LDH >595 U/l (OR, 3.8; P<0.001) and GGT >50 U/l (OR, 3.0; P<0.05). None of the laboratory tests were related to the severity of the liver injuries. In patients with blunt abdominal trauma, abnormal hepatic transaminase levels are associated with liver injuries. Patients with ALT >57 U/l and AST >113 U/l are strongly associated with liver injury and require further imaging studies and close management.