Application effect of multidisciplinary collaborative nursing process in emergency care of patients with hypertensive cerebral hemorrhage.

OBJECTIVE: The aim of the study was to analyze the effect of applying multidisciplinary collaborative nursing process (MCNP) in the emergency care of patients with hypertensive cerebral hemorrhage. PATIENTS AND METHODS: A total of 124 patients with hypertensive cerebral hemorrhage admitted to Qinghai University Affiliated Hospital from January 2020 to January 2021 was divided into control group (treated with regular emergency care, n=64) and study group (treated with MNCP, n=58). The effect of emergency treatment was compared between the two groups. RESULTS: Compared to the control group, initial treatment time, time of opening peripheral veins, first blood drawing time, time of imaging examination, emergency room treatment time, and hospital stay time were lower in MCNP group, the difference was significant (p<0.05). There were significant differences in Functional Independence Assessment (FIM) and National Institutes of Health Stroke Scale (NIHSS) scale scores between the control group and the MCNP group in treatment for 1 week in hospital (p<0.05). The level of total bile acid (TBA) and activated partial thromboplastin time (APTT) in the MCNP group were significantly lower than in the control group (p<0.05). The nursing satisfaction in MCNP was also improved compared to that in the control group (p<0.05). CONCLUSIONS: MCNP enhances the rational improvement of patients' awareness, improves the comprehensive quality of emergency treatments and optimizes prognosis; therefore, it is worthy of clinical promotion and application.

A novel nomogram associated with regulatory T cells infiltration by weighted gene co-expression network analysis for predicting survival in patients with colon cancer.

OBJECTIVE: Traditional diagnostic strategies are unable to accurately discriminate between patients with poor and satisfied prognosis in colon cancer. Therefore, it is urgently recommended to identify new biomarkers in favor of better selection of patients at higher risk of recurrence or poor outcomes, with the aim of early intervention or avoiding overtreatment. MATERIALS AND METHODS: The weighted gene correlation network analysis (WGCNA), together with the proportion of tumor infiltrating immune cells, were employed to screen the key module related to immune infiltration. Using these genes among the key module, a predictive signature was generated via LASSO and multi-Cox regression method. Moreover, a novel nomogram was further developed by combining important clinical parameters and the predictive signature. RESULTS: Genes among the green module, indicating the highest correlation with regulatory T cells (Tregs), were incorporated into the establishment of predictive model. Then, a Tregs-related risk signature (TRRS) consisting of four genes (NRG1, TEX11, OVOL3 and FCRL2) was established, which performed well in predicting the mortality risk of colon cancer in both internal and external validation groups (p=0.004 for TCGA training set, p=0.016 for TCGA testing set and p=0.03 for GSE39582 dataset). Combining TNM stage and age, we developed a nomogram for 1-, 3-, 5-year OS, presenting a more reliable predictive performance in survival based on the receiver operating characteristic (ROC) curves and calibration curves (3-year AUC: 0.83 and 0.74 in the TCGA and GEO database, respectively). CONCLUSIONS: We constructed a four-gene signature for predicting the prognosis of patients with colon cancer, and further developed the nomogram together with TNM stage and age to improve the predictive efficacy.

The detection of SAS1B in serum provides clues for early diagnosis of thyroid cancer.

OBJECTIVE: The incidence of thyroid cancer is rising globally. Most patients progress slowly, but some patients develop lymph node and distant metastasis earlier, and their prognosis is poor. Therefore, early diagnosis and warning of malignancy are very meaningful for such patients. SAS1B gene is a newly discovered protein expressed on the surface of mature egg cells and has metalloendopeptidase activity. We aimed at exploring whether SAS1B is involved in the occurrence of thyroid cancer, and at providing evidence for early diagnosis and targeted therapy of thyroid cancer. PATIENTS AND METHODS: In this study, a rabbit anti-human SAS1B polyclonal antibody was prepared by gene recombination technology. The indirect ELISA method was used to detect the SAS1B protein expression in the serum of 69 patients with thyroid cancer and 55 normal controls, and the relevant pathological factors were analyzed. Immunohistochemistry and PCR technology were used to investigate the expression levels of SAS1B protein and mRNA in 30 thyroid cancer tissues and 23 control thyroid tissues. RESULTS: The titer of SAS1B recombinant antibody was 1:51200. The expression of SAS1B in the serum of patients with thyroid cancer was higher than that in the normal control group (p<0.01). The antibody had a good sensitivity in serum detection of cancer patients (p=0.008<0.01), the linear regression analysis result was that the expression of SAS1B gene was related to tumor envelope invasion and lymph node metastasis (p=0.003<0.01, p=0.003<0.01), and it was irrelevant to the patient's gender, age, tumor mass size, number of cancer foci, pathological stage, etc. (p>0.05). The results of immunohistochemistry showed that SAS1B protein was mainly located in the cytoplasm and membrane of thyroid cancer cells. The expression intensity in thyroid cancer tissues was higher than that in control tissues (p<0.05), but it was not expressed in normal thyroid tissues. Antibodies showed a good sensitivity that was used to detect thyroid cancer tissues (p=0.000<0.01). The results of ordinary PCR detection using thyroid cancer tissue and control thyroid tissue showed that the amplification products of the three domains (N-terminal, C-terminal and catalytic domain) of the SAS1B gene showed high expression in thyroid cancer tissue. q-PCR results showed that the expression of SAS1B gene in thyroid cancer and control thyroid tissue was higher than that in control group (p<0.05), and the genes of Aurora A and BARD1 related to centrosome replication and DNA replication forks protection during the proliferation were highly expressed in thyroid cancer tissue. The study results suggested that SAS1B was involved in the carcinogenesis of thyroid cancer. The Hum_mPLoc.2.0 software, PSORT Ⅱ software and UniProt software were used to predict that SAS1B protein had secretory protein properties. CONCLUSIONS: The above data indicate that the SAS1B gene is closely related to the process of thyroid cancer and can serve as a good tumor marker that can be used for early diagnosis and early warning of thyroid malignancy.

LncRNA ZFPM2-AS1 aggravates the malignant development of breast cancer via upregulating JMJD6.

OBJECTIVE: The purpose of this study was to explore the expression pattern of long non-coding RNA (lncRNA) ZFPM2-AS1 in breast cancer (BC) tissues, and its biological influence on clinical features and prognosis in BC patients. PATIENTS AND METHODS: ZFPM2-AS1 levels in 52 paired BC tissues and adjacent normal ones were detected. Then, the relationship between ZFPM2-AS1 level and clinical features in BC patients was analyzed. Regulatory effects of ZFPM2-AS1 on proliferative and migratory abilities in MCF-7 and SKBR3 cells were assessed. In addition, in vivo regulation of ZFPM2-AS1 in nude mice bearing BC was evaluated. Finally, the interaction between ZFPM2-AS1 and JMJD6 and the involvement of ZFPM2-AS1 in the development of BC were illustrated. RESULTS: The results showed that ZFPM2-AS1 was upregulated in BC tissues, and its high level was linked to advanced tumor stage, high rates of lymphatic metastasis, and distant metastasis, as well as poor prognosis in BC. The knockdown of ZFPM2-AS1 suppressed proliferative and migratory abilities in BC cells. In addition, JMJD6 was verified to be the downstream gene binding to ZFPM2-AS1, which was highly expressed in BC tissues and positively regulated by ZFPM2-AS1. In vivo knockdown of ZFPM2-AS1 in nude mice bearing BC showed a smaller tumor volume and lower tumor weight than controls. In addition, JMJD6 was downregulated in BC tumors extracted from mice with silenced ZFPM2-AS1. CONCLUSIONS: LncRNA ZFPM2-AS1 is upregulated in BC and linked to tumor stage, metastasis, and prognosis in BC patients. It aggravates the malignant development of BC via upregulating JMJD6.

MiR-942-5p alleviates septic acute kidney injury by targeting FOXO3.

OBJECTIVE: Sepsis refers to the systemic inflammatory response caused by infection. Acute kidney injury (AKI) in sepsis is very common, and there are many complicated mechanisms for the occurrence of septic AKI. This article aimed to study the role of miR-942-5p in inflammation and apoptosis of septic AKI and its potential mechanism. MATERIALS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to detect the expression of RNAs. The protein expression was detected using Western blot. The contents of inflammatory factors in the cell supernatant were detected using commercial enzyme-linked immunosorbent assay (ELISA) kits. Cell Counting Kit-8 (CCK-8) assay was utilized to compare the cell viability of each group. Terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining and flow cytometry were used to observe cell apoptosis. RESULTS: MiR-942-5p expression was reduced in lipopolysaccharide (LPS)-treated HK-2 cells. MiR-942-5p mimic could observably increase miR-942-5p expression. The overexpression of miR-942-5p dramatically inhibits the expression of inflammatory factors and Bax, but increase Bcl-2 expression. MiR-942-5p overexpression greatly reversed the LPS-induced decrease in viability of HK-2 cells. In addition, we observed that LPS can markedly increase the number of apoptosis, while miR-942-5p mimic can reduce it. CONCLUSIONS: Taken together, our results demonstrated that miR-942-5p expression was reduced in the LPS-treated HK-2 cells, and miR-942-5p overexpression can inhibit LPS-induced inflammation and apoptosis of HK-2 cells via targeting FOXO3.

LncRNA NBR2 inhibits EMT progression by regulating Notch1 pathway in NSCLC.

OBJECTIVE: The aim of this study was to identify the role of long non-coding RNA (lncRNA) NBR2 in non-small-cell lung cancer (NSCLC) and its possible molecular mechanisms. PATIENTS AND METHODS: The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to explore lncRNA NBR2 expression in NSCLC cells and tissues. The chi-square test was used to analyze the relationship between lncRNA NBR2 expression and the clinical features of NSCLC patients. The pcDNA3.1 and pcDNA3.1-NBR2 vectors were transfected into NSCLC cells, and the proliferation and migration ability of NSCLC cells were detected using cell counting kit-8 (CCK-8) and transwell assay. The epithelial-mesenchymal transition (EMT)-related genes expression was detected by an EMT RT2 PCR array. QRT-PCR and Western blot was used to analyze the mRNA and protein levels of Notch1, Vimentin, N-cadherin, E-cadherin, HEY1, HEY2, and HEYL. RESULTS: The expression of lncRNA NBR2 was decreased in NSCLC patients tissues, and the NSCLC patients in the NBR2 low expression group showed a poor prognosis. Meanwhile, the expression of NBR2 in patients with NSCLC was correlated with tumor size. Overexpression of NBR2 suppressed the viability and migration of NSCLC cells and the expression of Notch1 and EMT-related genes in AsPC-1 cells. Simultaneous overexpression of NBR2 and Notch1 could reverse the inhibitory effect of NBR2 on proliferation and migration of NSCLC cells. CONCLUSIONS: LncRNA NBR2 inhibited the progression of EMT in NSCLC by regulating the Notch1 pathway.

MicroRNA-494-3p alleviates inflammatory response in sepsis by targeting TLR6.

OBJECTIVE: To clarify whether microRNA-494-3p could exert an anti-inflammation effect by suppressing the expression of toll-like receptor 6 (TLR6), thus inhibiting the development of sepsis. PATIENTS AND METHODS: Plasma levels of microRNA-494-3p and TLR6 in sepsis patients and healthy controls were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Diagnostic potential of microRNA-494-3p in sepsis was evaluated by receiver operating characteristic (ROC) curve. In vitro macrophage inflammation model was established by lipopolysaccharides (LPS) induction in RAW264.7 cells. Expression levels of microRNA-494-3p, TLR6 and tumor necrosis factor-α (TNF-α) in LPS-induced RAW264.7 cells were observed. After transfection of microRNA-494-3p mimics in LPS-induced RAW264.7 cells, mRNA and protein levels of TNF-α were determined by qRT-PCR and Western blot, respectively. Meanwhile, cytoplasmic and nuclear fractions of nuclear factor-kappa B (NF-κB) p65 were respectively extracted for evaluating nuclear translocation of NF-κB p65 by Western blot analysis. Dual-luciferase reporter gene assay was performed to verify the binding between microRNA-494-3p and TLR6. Finally, rescue experiments were carried out to elucidate whether microRNA-494-3p attenuated sepsis-induced inflammation through degrading TLR6. RESULTS: Plasma level of microRNA-494-3p in sepsis patients was markedly lower than healthy controls, while plasma level of TLR6 was conversely higher in sepsis patients. With the prolongation of LPS induction in RAW264.7 cells, expression levels of TLR6 and TNF-α gradually increased, whereas microRNA-494-3p expression decreased. Transfection of microRNA-494-3p mimics in RAW264.7 cells reduced TNF-α level, and inhibited nuclear translocation of NF-κB p65. TLR6 was found to be a target gene of microRNA-494-3p, and its expression was markedly downregulated by microRNA-494-3p overexpression. Finally, we proved that the inhibitory effects of microRNA-494-3p on TNF-α level and nuclear translocation of NF-κB p65 were reversed by TLR6. CONCLUSIONS: High expression of microRNA-494-3p attenuated sepsis-induced inflammatory response by degrading TLR6.

High expression of lncRNA MEG3 participates in non-small cell lung cancer by regulating microRNA-7-5p.

OBJECTIVE: This study was made to investigate whether long noncoding RNA (lncRNA) MEG3 could participate in the occurrence and development of non-small cell lung cancer (NSCLC) by regulating the expression of BRCA1 through competitive binding to microRNA-7-5p. PATIENTS AND METHODS: We used quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) to explore the expression of lncRNA MEG3 and BRCA1 in NSCLC tissues and adjacent normal tissues, as well as NSCLC cell lines. The dual luciferase reporter gene assay was used to detect the binding of microRNA-7-5p to lncRNA MEG3 and BRCA1. Meanwhile, the expression of BRCA1, B-cell lymphoma-2 (Bcl-2) and BCL2-associated X (Bax) was detected by Western blot after the cells were overexpressed or knocked down of lncRNA MEG3. All these experiments were designed to investigate whether lncRNA MEG3 participated in the pathogenesis of NSCLC through inhibiting the expression of BRCA1 and Bcl-2 and promoting Bax expression. RESULTS: The expressions of lncRNA MEG3 and BRCA1 in NSCLC tissues and A549 and HCC823 cell lines were significantly lower than those in the normal group. Overexpression of lncRNA MEG3 and BRCA1 in A549 and HCC823 cell lines resulted in increased apoptosis of lung cancer cells. Dual luciferase reporter assay demonstrated that lncRNA MEG3 can regulate the expression of BRCA1 through competitively binding to microRNA-7-5p to form the lncRNA MEG3/microRNA-7-5p/BRCA1 regulatory network. Besides, lncRNA MEG3 could inhibit the apoptosis inhibitory protein Bcl-2 and promote the expression of apoptosis-promoting factor Bax. CONCLUSIONS: LncRNA MEG3 was significantly downregulated in NSCLC, and it could regulate the BRCA1 expression by competitive binding to microRNA-7-5p.

Propofol compared with sevoflurane general anaesthesia is associated with decreased delayed neurocognitive recovery in older adults.

BACKGROUND: The choice of general anaesthetics may affect postoperative cognitive outcomes. This study was designed to compare the potential impact of propofol-based vs sevoflurane-based general anaesthesia on the development of delayed neurocognitive recovery in older adults early after major cancer surgery. METHODS: Older adults (aged ≥65 and <90 yr) who were scheduled to undergo major cancer surgery (≥2 h) were randomised to receive either propofol- or sevoflurane-based general anaesthesia. Cognitive function was assessed before and 1 week after surgery with a battery of neuropsychological tests. Age- and education-matched non-surgical controls were recruited, and their cognitive functions were tested at comparable time intervals in order to adjust for learning effects from repeated tests. Delayed neurocognitive recovery was diagnosed according to the International Study of Postoperative Cognitive Dysfunction 1 definition. RESULTS: From April 1, 2015 to October 15, 2016, 392 patients were enrolled and randomised. Of these patients, 387 completed the intervention and 30-day follow-up, and 379 completed 1-week neuropsychological tests. Fifty-nine control subjects were enrolled and completed repeated neuropsychological tests. The incidence of delayed neurocognitive recovery at 1 week was significantly lower in the propofol group [14.8% (28/189)] than in the sevoflurane group [23.2% (44/190); odds ratio=0.577; 95% confidence interval, 0.342-0.975; P=0.038]. Safety outcomes did not differ between the two groups. CONCLUSIONS: When compared with sevoflurane-based general anaesthesia, propofol-based general anaesthesia might decrease the incidence of delayed neurocognitive recovery in older adults after major cancer surgery. CLINICAL TRIALS REGISTRATION: NCT02662257; Chinese Clinical Trial Registry (identifier: ChiCTR-IPR-15006209).

Comparative study between mini-open TLIF via Wiltse's approach and conventional open TLIF in lumbar degenerative diseases.

OBJECTIVE: To compare the clinical effects, operation safety and radiation exposure of mini-open TLIF via Wiltse's approach (MOTLIF) and conventional open TLIF (COTLIF) in the treatment of single-segment lumbar degenerative disease via the prospective control study. PATIENTS AND METHODS: A total of 77 patients were enrolled from November 2012 to July 2014, including 42 patients in the mini-open group (MOTLIF) and 35 patients in the COTLIF group. Oswestry Disability Index (ODI) and Visual Analogue Scale (VAS) scores before operation, operation time, intraoperative blood loss, postoperative drainage volume, blood transfusion rates, postoperative bedridden time, postoperative hospital stays, intraoperative fluoroscopic time, levels of serum creatine phosphokinase (CPK) before operation, 3 days and 1 week after operation, VAS scores before operation, 3 days and 1 week after operation, and ODI and VAS scores in the last follow-up between the two groups were compared. RESULTS: There were significant differences between the two groups in the operation time, intraoperative blood loss, postoperative drainage, blood transfusion rates, postoperative bedridden time, postoperative hospital stays and intraoperative fluoroscopic time; all indicators in MOTLIF group were superior to those in COTLIF group (p<0.05). There were no significant differences between the two groups in levels of serum CPK before operation and 1 week after operation (p>0.05). However, 3 days after operation, the level of serum CPK in COTLIF group was increased more significantly than that in MOTLIF group (647.4±178.6 vs. 467.4±189.4). There were no differences between the two groups in ODI and VAS scores before operation; ODI score in MOTLIF group in the last follow-up was significantly superior to that in COTLIF group (p>0.05). And VAS scores at 3 days and 1 week after operation and the last follow-up in MOTLIF group were superior to those in COTLIF group (p<0.05). CONCLUSIONS: Compared with the conventional open TLIF, mini-open TLIF via Wiltse's approach using the self-designed operating apparatus is characterized by the convenient operation, small trauma and quick recovery after operation. At the same time, the radiation exposure is lower and long-term follow-up effect is superior. Its short-term and long-term effects in the treatment of lower lumbar degenerative disease are also superior.

A multi-level drill guide template improves the accuracy of pedicle screw placement in lumbar spine.

OBJECTIVE: Free-hand technique is widely used in pedicle screw placement for lumbar spine and generally safe; however, screw malposition still occurs. To develop a novel multi-level drill guide template for pedicle screw placement in lumbar spine and evaluate its accuracy. MATERIALS AND METHODS: Twelve lumbar cadaveric specimens were randomly allocated into guide template group (n=6) and free-hand group (n=6). Computed tomography (CT) scans were obtained for reconstruction of three-dimensional (3D) model of each lumbar vertebra, and further an individual guide template was designed. Then the templates and their corresponding vertebra were developed by rapid prototyping (RP) technology. With the guide of the templates, screws were inserted via mini-open Wiltse approach. The positions of the screws were assessed based on postoperative CT images. RESULTS: In total, 120 pedicle screws inserted (guide template group: n=60 vs. free-hand group: n=60). For all 30 vertebras in the guide template group, all pre-designed personalized drill guide templates can be fitted into the facet joints of each vertebra well. Furthermore, our results revealed a significant improvement for the guide template group in the accuracy rate (p=0.026). CONCLUSIONS: Armed with advantages of minimal invasion, enhanced accuracy and safety, the novel technique of multi-level drill guide template can be properly applied in pedicle screw placement for lumbar spine and promises to be a potential option in clinical application.

Preoperative vitamin D deficiency increases the risk of postoperative cognitive dysfunction: a predefined exploratory sub-analysis.

BACKGROUND: Vitamin D is important for maintaining physiological functions including cognition and its deficiency is associated with the occurrence of cognitive impairment. This study was to explore the association between preoperative vitamin D status and the occurrence of postoperative cognitive dysfunction (POCD) in elderly patients undergoing major surgery. METHODS: This was a predefined exploratory sub-analysis of one-centre data from a randomized controlled trial. In all, 123 elderly (≥ 65 years) patients who were scheduled to undergo major cancer surgery were recruited. Serum 25-hydroxyvitamin D concentration was measured before surgery. In total, 59 nonsurgical control subjects with comparable age and education level were also enrolled. A battery of neuropsychological tests was administered the day before and the 7th day after surgery in patients or at the same time interval in control subjects. POCD was diagnosed according to the ISPOCD1 definition. RESULTS: 71.5% (88/123) of elderly patients had vitamin D deficiency (serum 25-hydroxyvitamin D concentration < 12 ng/ml) before surgery; 24.4% (30/123) of them developed cognitive dysfunction at 1 week after surgery. After adjusting for confounding factors, high preoperative serum 25-hydroxyvitamine D concentration was related to a decreased risk of POCD (odds ratio [OR]: 0.829, 95% confidence interval [CI]: 0.708-0.971; P = 0.020), whereas preoperative vitamin D deficiency was associated with an increased risk of POCD (OR: 8.427, 95% CI: 1.595-44.511; P = 0.012). CONCLUSIONS: Vitamin D deficiency is prevalent in elderly patients undergoing major cancer surgery and increases the risk of early POCD development. Whether prophylactic vitamin D supplementation can reduce POCD in the elderly deserves further study.

Investigating and analyzing three cohorts of mushroom poisoning caused by Amanita exitialis in Yunnan, China.

Amanita exitialis is a lethal mushroom found in China. Knowledge regarding taxonomic characterization, toxin detection, general poisoning conditions, clinical manifestations, laboratory examinations, and clinical treatments for this species is currently lacking. We investigated three A. exitialis mushroom poisoning cohorts in Yunnan Province in 2014 and 2015, involving 10 patients. Mushroom samples were identified by morphological and molecular studies. Ultra performance liquid chromatography-electrospray ionization tandem mass spectrometry was used to detect the peptide toxins in the mushroom samples. Epidemiological information, clinical data, and results of laboratory examinations were collected and analyzed. The mushroom samples were all identified as A. exitialis. The average toxin concentration decreased from the cap to the stipe to the volva, and the average concentration of the peptide toxins decreased in the order of α-amanitin > phallacidin > ß-amanitin > γ-amanitin. The latency period between ingestion and the onset of symptoms was 13.9 ± 2.1 h, and the time from ingestion to hospitalization was 49.6 ± 8.5 h. The most common symptoms were nausea and vomiting (100%). Four patients died from fulminant hepatic failure. Laboratory examinations showed that the alanine transaminase, aspartate transaminase, prothrombin time, and activated partial thromboplastin time levels peaked on the third day post-ingestion. Total bilirubin and direct bilirubin values peaked on day 7. The death group and the survival group had a similar variation trend of serological indexes, but the death group had a greater change. A. exitialis is an extremely dangerous mushroom and there is a need to educate the public to avoid picking and eating wild mushrooms that have not been definitively identified.

Wnt11 overexpression promote adipose-derived stem cells differentiating to the nucleus pulposus-like phenotype.

OBJECTIVE: Our present study aimed to evaluate the effects of Wnt11 overexpression on the adipose-derived stem (ADSCs) cells differentiation to the nucleus pulposus (NP) cells and its function in the ADSCs cells growth, proliferation and induction of the NP cells markers. MATERIALS AND METHODS: The cell growth was detected using the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) (MTT) assay and the cell cycle was assessed by the flow cytometry. The cells morphology was evaluated using the transmission electron microscopy. The transfection efficiencies of Wnt11 lentivirus were observed under fluorescence microscope. Besides, Quantitative Real-time PCR and Western blot analysis were applied to detect the relative mRNA and protein levels. RESULTS: Wnt11 lentivirus treatment could inhibit the ADSCs cells growth and arrest the cell cycle progression at the G0/G1 phase. Besides, the overexpression of Wnt11in ADSCs cells could induce the expression of the NP cells markers. Levels of SOX-9, aggrecan, and collagen type II were significantly increased in the ADSCs cells transfected with the Wnt11 lentivirus, in comparison with the untreated cells or the vector controls. CONCLUSIONS: The Wnt11 overexpression may provide some experimental evidence for the possible opportunity of the Wnt11 to promote the ADSCs cells differentiating to the NP cells. Therefore, the Wnt11 overexpression may have a potential utility for the treatment of the intervertebral disc degeneration.

4-Methylcatechol inhibits cell growth and testosterone production in TM3 Leydig cells by reducing mitochondrial activity.

4-Methylcatechol (4-MC) is a potential neuroprotective drug because it stimulates the synthesis of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in neurons. The present study explored the effect of 4-MC on cell growth and testosterone synthesis in the TM3 Leydig cells of mice. 4-MC did not enhance expression of both BDNF and NGF in these cells. However, this compound significantly inhibited cell proliferation and increased the number of apoptotic cells in a dose-dependent manner. The expression profile of Bax/Bcl-2 gene was altered considerably, and mitochondrial activity was significantly decreased in cells. 4-Methylcatechol also inhibited testosterone synthesis in TM3 Leydig cells. The inhibitory roles of this compound in relation to growth and testosterone synthesis in TM3 Leydig cells maybe associated with increased Bax gene expression and decreased mitochondrial activity. As a result, caspase cascade is activated.

Diagnostic and prognostic value of procalcitonin for early intracranial infection after craniotomy

Intracranial infection is a common clinical complication after craniotomy. We aimed to explore the diagnostic and prognostic value of dynamic changing procalcitonin (PCT) in early intracranial infection after craniotomy. A prospective study was performed on 93 patients suspected of intracranial infection after craniotomy. Routine peripheral venous blood was collected on the day of admission, and C reactive protein (CRP) and PCT levels were measured. Cerebrospinal fluid (CSF) was collected for routine biochemical, PCT and culture assessment. Serum and CSF analysis continued on days 1, 2, 3, 5, 7, 9, and 11. The patients were divided into intracranial infection group and non-intracranial infection group; intracranial infection group was further divided into infection controlled group and infection uncontrolled group. Thirty-five patients were confirmed with intracranial infection after craniotomy according to the diagnostic criteria. The serum and cerebrospinal fluid PCT levels in the infected group were significantly higher than the non-infected group on day 1 (P<0.05, P<0.01). The area under curve of receiver operating characteristics was 0.803 for CSF PCT in diagnosing intracranial infection. The diagnostic sensitivity and specificity of CSF PCT was superior to other indicators. The serum and CSF PCT levels have potential value in the early diagnosis of intracranial infection after craniotomy. Since CSF PCT levels have higher sensitivity and specificity, dynamic changes in this parameter could be used for early detection of intracranial infection after craniotomy, combined with other biochemical indicators.

NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial-mesenchymal transition.

The transcription factor NKX6.1 (NK6 homeobox 1) is important in the development of pancreatic ß-cells and neurons. Although recent publications show that NKX6.1 is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the metastasis suppressor function of human NKX6.1 using cell, animal and clinical analyses. Our data show that NKX6.1 represses tumor formation and metastatic ability both in vitro and in vivo. Mechanistically, NKX6.1 suppresses cell invasion by inhibiting the epithelial-to-mesenchymal transition (EMT). NKX6.1 directly enhances the mRNA level of E-cadherin by recruiting BAF155 coactivator and represses that of vimentin and N-cadherin by recruiting RBBP7 (retinoblastoma binding protein 7) corepressor. Clinical cancer tumors with metastasis show low NKX6.1 protein expression coinciding with low E-cadherin and high vimentin expression. Our results demonstrate that NKX6.1 functions as an EMT suppressor by interacting with different epigenetic modifiers, making it a potential novel therapeutic option.

Gli1 expression in pancreatic ductal adenocarcinoma and its clinical significance.

The aim of this study was to explore the correlation between the expression levels of Gli1 and p53 in pancreatic ductal adenocarcinoma (PDAC) and its pathological significance. Immunohistochemistry (IHC) was employed to measure the expression level of Gli1 and p53 in 85 sets of paraffin-embedded PDAC and corresponding para-carcinoma tissue specimens. The relationship between these results and the respective patients' clinicopathologic parameters was analyzed. IHC staining revealed that the expression levels of Gli1 and p53 in cancer tissues were evidently higher than that of para-carcinoma tissues (P < 0.05); while Gli1 expression levels correlated with the corresponding TNM stage and tumor infiltration depth, p53 expression level correlated with the respective TNM stage (P < 0.05). Taken together, this study demonstrates increased expression of Gli1 and p53 in PDAC, and proves that Gli1 could be apotential biomarker for prognostic judgment.

Relationship between zinc finger protein 36 (ZFP36) gene polymorphisms and obstructive sleep apnea.

Recent data have indicated that inflammation may have an important correlation with obstructive sleep apnea (OSA). Studies have indicated a relationship between OSA and TNF-α gene polymorphisms. Zinc finger protein 36 (ZFP36) regulates TNF-α mRNAs. However, ZFP36 gene polymorphisms have not been investigated in OSA. Therefore, we conducted the present case-control study to assess whether variances in ZFP36 gene polymorphisms account for differences in TNF-α levels in patients with moderate-to-severe OSA. This case-control study aims to investigate the relationship between genetic variations in the ZFP36 gene and moderate-to-severe OSA. Three common single nucleotide polymorphisms of the ZFP36 gene (rs251864, rs3746083, and rs17879933) were evaluated in a group of patients with moderate-to-severe OSA (N = 408) and in a control group (N = 394) by using TaqMan polymerase chain reaction analysis. The moderate-to-severe OSA group and the control group exhibited significant differences in the distributions of rs251864 and rs17879933 genotypes and alleles (P < 0.05). TNF-α levels were significantly different not only among the three rs251864 genotypes but also between the II genotype and the DD + ID genotypes of rs17879933. However, no significant differences in sleep apnea parameters in the three ZFP36 gene polymorphisms were observed. Logistic regression analyses demonstrated that TNF-α and the three ZFP36 gene polymorphisms were not independently associated with OSA. ZFP36 might be involved in TNF-α regulation. However, ZFP36 gene variants were not independent risk factors for moderate-to-severe OSA.

Local-to-remote cortical connectivity in early- and adulthood-onset schizophrenia.

Schizophrenia is increasingly thought of as a brain network or connectome disorder and is associated with neurodevelopmental processes. Previous studies have suggested the important role of anatomical distance in developing a connectome with optimized performance regarding both the cost and efficiency of information processing. Distance-related disturbances during development have not been investigated in schizophrenia. To test the distance-related miswiring profiles of connectomes in schizophrenia, we acquired resting-state images from 20 adulthood-onset (AOS) and 26 early-onset schizophrenia (EOS) patients, as well as age-matched healthy controls. All patients were drug naive and had experienced their first psychotic episode. A novel threshold-free surface-based analytic framework was developed to examine local-to-remote functional connectivity profiles in both AOS and EOS patients. We observed consistent increases of local connectivity across both EOS and AOS patients in the right superior frontal gyrus, where the connectivity strength was correlated with a positive syndrome score in AOS patients. In contrast, EOS but not AOS patients exhibited reduced local connectivity within the right postcentral gyrus and the left middle occipital cortex. These regions' remote connectivity with their interhemispheric areas and brain network hubs was altered. Diagnosis-age interactions were detectable for both local and remote connectivity profiles. The functional covariance between local and remote homotopic connectivity was present in typically developing controls, but was absent in EOS patients. These findings suggest that a distance-dependent miswiring pattern may be one of the key neurodevelopmental features of the abnormal connectome organization in schizophrenia.