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Arnold-Chiari malformations (ACM) is a rare congenital hindbrain maldevelopment, leading to downward herniation of the cerebellar tonsils. Clinical features relates to cerebrospinal fluid disturbances, manifesting as symptoms of headaches, pseudotumour-like episodes, cranial nerve palsies and cerebellar dysfunction. Ocular manifestations includes varying ophthalmoloplegia and accommodation abnormalities. Papilloedema has been rarely implicated and remains an uncommon feature of ACM. We report a case of ACM who developed papilloedema and visual disturbance, that was successfully treated with suboccipital decompression. The presentation of patients with ACM-I and papilloedema unaccompanied by localising signs may resemble that of IIH. Neuroimaging with special attention to the craniocervical junction in saggital and transverse planes is crucial. Surgical decompression of the posterior fossa seems to improve headache symptoms and clinical signs of papilloedema.

Background Competitive Endogenous RNA (ceRNA) may be closely associated with tumor progression. However, studies on ceRNAs and immune cells in LUAD are scarce. Method The profiles of gene expression and clinical data of LUAD patients were extracted from the TCGA database. Bioinformatics methods were used to evaluate differentially-expressed genes (DEGs) and to form a ceRNA network. Preliminary verification of clinical specimens was utilized to detect the expressions of key biomarkers at the tissues. Cox and Lasso regressions were used to identify key genes, and prognosis prediction nomograms were formed. The mRNA levels of 9 genes in the risk score model in independent clinical LUAD samples were detected by qRT-PCR. The interconnection between the risk of cancer and immune cells was evaluated using the CIBERSORT algorithm, while the conformation of notable tumor-infiltrating immune cells (TIICs) in the LUAD tissues of the high and low risk groups was assessed using the RNA transcript subgroup in order to identify tissue types. Finally, co-expression study was used to examine the interconnection between the key genes in the ceRNA networks and the immune cells. Result A ceRNA network of 115 RNAs was established, and nine key genes were identified to construct a Cox proportional-hazard model and create a prognostic nomogram. This risk-assessment model might serve as an independent factor to forecast the prognosis of LUAD, and it was consistent with the preliminary verification of clinical specimens. Survival analysis of clinical samples further validated the potential value of high risk groups in predicting LUAD prognosis. Five immune cells were identified with significant differences in the LUAD tissues of the high and low risk groups. Besides, two pairs of biomarkers associated with the growth of LUAD were found, i.e., E2F7 and macrophage M1 (R = 0.419, p = 1.4e− 08) and DBF4 and macrophage M1 (R = 0.282, p − 16). Conclusion This study identified several important ceRNAs, i.e. (E2F7 and BNF4) and TIICs (macrophage M1), which might be related to the development and prognosis of LUAD. The established risk-assessment model might be a potential tool in predicting LUAD of prognosis.

Aberrant ERα signaling and altered circadian rhythms are both features of ER-positive breast cancer, however, the molecular interaction between them is still not fully understood. Herein, we analyzed the interplay between the circadian rhythm molecule DEC1 and ERα and its effect on the proliferation of ER-positive breast cancer cells, providing a new clue for clarifying the pathogenesis of breast cancer. In this study, we revealed that DEC1 negatively regulates the proliferation of ER-positive breast cancer MCF-7 cells through interaction with ERα protein. DEC1 co-localized with ERα in the nucleus of MCF7 cells, stabilized ERα protein independently of its transcriptional activity and without affecting by estrogen stimulation and inhibited the degradation of ERα mediated by CHX in a time-dependent manner. Moreover, results from luciferase reporter assay showed that overexpression of DEC1 significantly inhibits ERα-mediated transcriptional activity in a dose-dependent manner. These results together suggested that DEC1 may serve as a co-repressor of ERα in ER-positive breast cancer. Although DEC1 improved the stability of ERα and alleviated protein degradation, DEC1 inhibited the proliferation of MCF7 cells by decreasing ERα-mediated signal transduction.

Sepsis associated encephalopathy (SAE) is a severe disease secondary to sepsis, which is associated with increased mortality and causes long-term cognitive deficits in survivors. Recently, an increasing body of evidence has shown that gut microbiota is closely related to the central nervous system, and could influence brain function via microbiota-gut-brain axis. Therefore, in the occurrence and development of SAE, cholinergic anti-inflammatory pathway is one of the mechanisms by which gut microbiota could improve cognitive function. Efferocytosis, a process of eliminating apoptotic cells in the body, has anti-inflammatory effects and provides organ protection in sepsis. On the other hand, it could be enhanced by some metabolites of gut microbiota, making it another potential mechanism for gut microbiota regulating SAE. This review summarizes the mutual regulation of gut microbiota, efferocytosis and SAE, to explore potential mechanisms and therapeutic targets of SAE.

OBJECTIVE: To assess the effect of transnasal humidified rapid-insufflation ventilatory exchange (THRIVE) on gastric insufflation during general anesthesia induction in obese patients. METHODS: Ninety obese patients (BMI 30-39.9 kg/m(2)) undergoing laparoscopic cholecystectomy under general anesthesia were randomized into 3 groups (n=30) to receive facemask pre- oxygenation followed by face mask ventilation (FMV) after administration of anesthetics (Group M), oxygenation with THRIVE (Group T), or pre-oxygenation with facemask combined with THRIVE followed continuous oxygenation with both FMV and THRIVE after administration of anesthetics (Group M+T). The patients in the latter two groups received continuous oxygen via THRIVE during tracheal intubation. All the patients received real-time ultrasound monitoring of the gastric antrum, and positive gastric insufflation (GI(+)) was defined by the presence of comet-tail artifacts. The cross-sectional area of the gastic antrum (CSA-GA) was measured by ultrasound before and after pre-oxygenation and after intubation. The patients' SpO(2), PaO(2), and PaCO(2) at admission (T(1)), 5 min after pre-oxygenation (T(2)), 5 min after medication (T(3)), and immediately after intubation (T(4)) were recorded, and the incidence of postoperative adverse events was assessed. RESULTS: The incidence of gastric insufflation was significantly higher in Group M and Group M+T than in Group T (P < 0.05). The CSA-GA was significantly greater at T(4) than at T(1) in Group M and Group M+T and in their GI(+)s ubgroups. The GI(+) subgroups in Group M and Group M+ T had significantly larger CSA-GA at T(4) than the GI(-) subgroups (P < 0.05). CSA-GA did not vary significantly during anesthesia induction in Group T (P>0.05). The incidence of grade Ⅰ gastric distension was lower but grade Ⅱ gastric distention was higher in Group M and Group M+T than in Group T (P < 0.05). Group M showed significantly greater variations of PaO(2) at T(3) and T(4) than Group T and Group M+T (P < 0.05). CONCLUSION: Ultrasound monitoring of the comet tail sign and the changes of CSA-GA in the gastric antrum is feasible and reliable for detecting gastrointestinal airflow, and in obese patients, the application of THRIVE for induction of anesthesia can ensure the oxygenation level without further increasing gastric insufflation.

Abnormal protein acetylation and succinylation in lysine residues can cause the initiation and development of numerous different types of tumors. However, to the best of our knowledge, there is currently a lack of systematic investigation in breast cancer. Using proteomic techniques, the present study systematically investigated the two modifications of all proteins in invasive ductal carcinoma tissues to identify potential targets. The results revealed significantly higher modification levels for the majority of proteins in breast cancer tissue when compared with para-carcinomous normal tissue. The bioinformatic analysis demonstrated that either highly acetylated or succinylated proteins were significantly enriched in histone H2A.X (H2A.X) complexes and nucleophosmin (NPM1) may be the key member among them. The results of further analyses revealed that H2A.X complexes were associated with DNA damage response (DDR), and the proteomic results for protein quantification provided further evidence for the abnormal DDR condition in breast cancer tissues. Later, the western blotting results validated the high acetylation and succinylation levels of the majority of proteins, including the modification of NPM1 and its correlation with cell viability. Finally, the upregulation of H2A.X in breast cancer tissues further demonstrated the association between H2A.X complex modification and DDR in breast cancer. Overall, the present study systematically investigated the protein acetylation and succinylation in breast cancer and provided evidence to support H2A.X complexes as potential targets. These results broaden the horizon for breast cancer investigation and link it with epigenetics.

Sepsis is considered to be the most common contributing factor in the development of acute kidney injury (AKI). However, the mechanisms by which sepsis leads to AKI remain unclear. Autophagy is important for a number of fundamental biological activities and plays a key role in numerous different diseases. The present study demonstrated that autophagy is involved in sepsis-induced kidney injury and upregulates ATG7, LC3 and Beclin I. In addition, it was revealed that miR-526b is decreased in sepsis-induced kidney injury, and miR-526b was identified as a direct regulator of ATG7. Furthermore, the present study investigated the biological effects of ATG7 inhibited by miR-526b and demonstrated that miR-526b could promote cell viability by inhibiting autophagy, potentially through targeting ATG7. In conclusion, the present study highlights the role of autophagy in sepsis-induced AKI, and miR-526b in regulating autophagy through targeting ATG7, which suggested that miR-526b may be a molecular therapeutic target for sepsis-induced AKI.

Background: The purpose of this study was to evaluate the effects of adding ketamine to propofol on cognitive functions in patients undergoing sedation for colonoscopy. Methods: In this randomized, double-blinded, and controlled study, 200 patients were randomly allocated to ketamine/propofol admixture group (Group KP, n = 100), and propofol group (Group P, n = 100). Patients in Group KP received 0.25 mg/kg of ketamine and 0.5 mg/kg of propofol. Patients in Group P received 0.5 mg/kg propofol. Cognitive functions were measured using CogState battery before and after the colonoscopy procedure. Ninety five patients in Group KP and 92 patients in Group P had completed the CogStates tests and were included in the data analysis. Results: Compared with before procedure baseline, the performance on detection and identification tasks were significantly impaired after the procedure in both Group KP (P = .004, P = .001) and Group P patients (P = .005, P

Background It has been reported that postoperative cognitive dysfunction (POCD) is correlated with the degeneration of the central nervous system, oxidative stress, inflammation, and endocrine and immune dysfunction. Increased age, predisposed comorbidity, long surgery time, and prolonged stay in the intensive care unit have been reported to be risk factors for developing POCD for cardiac surgery. In the present study, the risk factors of early POCD after colorectal surgery were investigated. Methods Eighty patients, who provided informed consents for their participation in this study, were enrolled and received colorectal surgery under general anesthesia. Neuropsychological tests were performed preoperatively and on postoperative day seven. The risk factors for POCD were analyzed using a multivariate logistic regression model. Results Nineteen patients were diagnosed with POCD (24.7%). Diabetes history (OR = 8.391 [2.208–31.882], P = 0.012), fasting over 3 days after surgery (OR = 5.236 [1.998–13.721], P = 0.001) and an SIRS score of > 3 on the second day after surgery (OR = 6.995 [1.948–25.111], P = 0.003) were risk factors for early POCD in colorectal cancer patients. Conclusion The risk factors for early POCD after colorectal surgery included diabetes history, fasting over 3 days, and an SIRS score of > 3 on the second day.

MicroRNA (miRNA) are emerging as critical regulators of neuropathic pain development. Neuroinflammation contributes to the development of neuropathic pain. miR‑142‑3p has been characterized as an inflammation‑related miRNA in various pathological processes. However, little is known about the role of miR‑142‑3p in neuroinflammation and neuropathic pain. The present study aimed to investigate the function of miR‑142‑3p in neuropathic pain by creating a murine model using spinal nerve ligation (SNL). A significant reduction in miR‑142‑3p expression was observed in the dorsal root ganglion of mice with SNL (P

Currently, advanced glycation end product (RAGE) is receiving much attention in carcinogenesis research due to its involvement in cancer progression and metastasis. We therefore sought to examine the association of circulating soluble RAGE (sRAGE) with all types of cancer by a meta-analysis. The PubMed and EMBASE databases were searched before March 1, 2014. Data and study quality were assessed in duplicate. Effect estimates were expressed as weighted mean difference (WMD) and its 95 % confidence interval (CI). Altogether, nine eligible articles including 1,337 cancer patients and 1,839 controls were analyzed. The overall analysis indicated that circulating sRAGE was remarkably reduced by 222.07 pg/ml in cancer patients compared with controls (95 % CI: −373.77 to −70.37; P = 0.004), with heterogeneity and without publication bias. In subgroup analyses, this reduction was weakened yet still significant in prospective studies (WMD = −87.62; 95 % CI: −138.60 to −36.63; P = 0.001) with improved heterogeneity (I 2 = 56.5 %; P = 0.056). Restricting analyses to the large studies (total number of subjects ≥200) identified significant reduction of circulating sRAGE in cancer patients relative to controls (WMD = −231.34; 95 % CI: −450.10 to −12.58; P = 0.038). Further meta-regression analysis showed that smoking status explained some part of heterogeneity for the association of circulating sRAGE with cancer risk (regression coefficient: −67.02; P = 0.046). Our findings demonstrate a protective role of circulating sRAGE in the development of cancer, especially in patients without diabetes mellitus or with normal renal function.

Background Although photoplethysmography and cerebral state index (CSI) have been used as indices in monitoring vital signs perioperatively, there are only a few reports comparing the performance of photoplethysmography with CSI in monitoring anaesthesia depth. The aim of the present study was to clarify features of photoplethysmography in monitoring balanced general anesthesia compared with CSI. Material/Methods Forty-five patients undergoing elective operation under general anaesthesia were enrolled in this study. Anaesthesia was induced with target-controlled infusion propofol. The photoplethysmogram, CSI, Modified Observer’s Assessment of Alertness/Sedation Scale (MOAAS), and mean arterial pressure (MAP) were continuously monitored and recorded. Finger photoplethysmogram amplitude (PPGA) and pulse beat interval (PBI) were calculated off-line. Results For the period of time from pre-induction to pre-intubation, the coefficient of correlation between MOAAS and CSI was higher than those between MOAAS and PPGA, PBI, and MAP. CSI showed higher prediction probabilities (Pk) to differentiate the levels of MOAAS than did PPGA, PBI, and MAP. PPGA, PBI, and MAP values showed significant differences between before and after intubation, as well as pre- and post-incision (P0.05). Conclusions The present study shows that photoplethysmography-derived parameters appear to be more suitable in monitoring the nociceptive component of balanced general anesthesia, while CSI performs well in detecting the sedation or hypnotic component of balanced general anesthesia.

Background Pain on injection is an acknowledged adverse effect (AE) of propofol administration for the induction of general anesthesia. Flurbiprofen axetil has been reported to reduce the pain of injection. However, results of published papers on the efficacy of flurbiprofen axetil in managing pain on injection of propofol are inconsistent. Material/Methods We conducted a comprehensive meta-analysis of studies to appraise the efficacy and safety of flurbiprofen axetil for controlling pain induced by propofol injection. The pooled risk ratio (RR) with corresponding 95% confidence intervals (CI) was calculated employing fixed- or random-effects models, depending upon the heterogeneity of the included trials. Results Compared with the placebo group, flurbiprofen axetil allows more patients to have no pain (RR 3.51, 95% CI 2.22–5.55, p=0.000), and decreases the cumulative number of patients with mild, moderate, and severe pain on injecting propofol (RR 0.70, 95% CI 0.58–0.86, p=0.000; RR 0.59, 95% CI 0.46–0.75, p=0.000; RR 0.25, 95% CI 0.16–0.38, p=0.000, respectively). In the stratified analysis by the doses, flurbiprofen axetil at a dose of over 50 mg was found to be effective in reducing propofol-induced pain on injection; however, there were no significant differences in relieving pain between treatment and placebo groups with flurbiprofen axetil at a dose of 25 mg. In terms of drug safety, there were no adverse effects (AEs) reported between flurbiprofen axetil-based regimens and placebo regimens. Conclusions Flurbiprofen axetil, an injectable prodrug of flurbiprofen, can significantly prevent or relieve the pain induced by propofol injection. More studies are required to assess its adverse effects.

Background SESN2 plays important roles in the regulation of cell survival, cell protection, and tumor suppression. However, the relationship between SESN2 expression and the clinicopathological attributes of hepatocellular carcinoma (HCC) is barely investigated. Methods One-step quantitative reverse transcription PCR, Western blotting analysis in 15 fresh HCC tissues, and immunohistochemistry (IHC) analysis in a tissue microarray (TMA) containing 100 HCC cases were performed to examine SESN2 expression. Survival analyses by Cox regression method and Kaplan-Meier curve were performed to describe the overall survival of 100 HCC patients. Results The SESN2 expression in HCC tissues declined dramatically compared with the corresponding noncancerous tissues, and SESN2 expression was remarkably associated with HBV infection (p = 0.019), HCV infection (p = 0.001), and lymph node metastasis (p = 0.033). Survival analysis further demonstrated that SESN2 expression could serve as an independent prognostic biomarker for overall survival in univariate (p = 0.001) and multivariate analyses (p = 0.003). Conclusion The data are the first to indicate that SESN2 might be a novel prognostic marker for HCC and that elevated SESN2 expression predicts advantageous outcomes in HCC patients.

To observe the effects of ultrasound-guided stellate ganglion block (SGB) on cerebral oxygen metabolism and postoperative cognitive dysfunction (POCD) of elderly patients, we collected 80 elderly patients undergoing selective coronary artery bypass graft under cardiopulmonary bypass. The Mini Mental State Examination (MMSE) was applied to test the cognitive function. The SjvO2, Da-jvO2 and CEO2 were used for the analysis of the cerebral oxygen metabolism. We found that POCD was related to disequilibrium of cerebral oxygen metabolism. Ultrasound-guided SGB before surgery reduced the incidence of POCD because of the improvement of cerebral oxygen metabolism.

To evaluate the serum levels of cytokines in postoperative cognitive dysfunction (POCD) patients having received colorectal surgery.Eighty patients who had received colorectal surgery were enrolled in the study based on the defined inclusion and exclusion criteria. Cognitive function was assessed on day 1 before operation and day 7 after operation using a battery of neuropsychological tests. Serum levels of 120 cytokines were measured at two time points (day 1 before surgery and 4 hours after surgery) using high-throughput cytokine screening. Serum interleukin 6 (IL-6), IL-11, IL-17, Fas, methyl-accepting chemotaxis protein 3 (MCP3), myeloid progenitor inhibitory factor-1 (MPIF-1), macrophage inflammatory protein 3 alpha (MIP-3α), brain-derived neurotrophic factor (BDNF) were determined by ELISA.Seventy-seven patients completed both neurocognitive tests and blood samples collection. Nineteen cases were diagnosed with POCD at 7 days after surgery. The age, ASA classification and diabetes incidence of POCD patients were significantly higher and the education level was lower than those in patients without POCD. Serum IL-17, Fas, MIP-3α levels were higher and leptin was lower when compared with non-POCD patients at 1 day before surgery. Serum IL-6, IL-11, IL-17, MCP3, MPIF-1, MIP-3α levels were higher and BDNF was lower when compared with non-POCD group at 4 hours after surgery. In POCD group, serum IL-6, IL-17, MCP3 and MPIF-1 levels at 4 hours postoperatively were higher when compared with ones at 1 day preoperatively. In non-POCD group, serum IL-6 and IL-17 at 4 hours postoperatively were higher while Fas and BDNF were lower when compared with ones at 1 day preoperatively.Serum cytokines IL-6, IL-11, IL-17, Fas, MPIF-1, MIP-3α, MCP3, leptin, BDNF were found to display differential expressions in POCD patients after colorectal surgery.

The proposition that white adipose tissue is involved in the inflammatory response and metabolic dysregulation of endotoxaemia has been examined. Mice were injected with lipopolysaccharide (LPS; 25 mg/kg) and epididymal, perirenal and subcutaneous adipose tissue removed 4 or 24 h later. The expression of genes encoding key inflammation-related adipokines was measured by real-time polymerase chain reaction. At 24 h after the administration of LPS, there was no change in leptin mRNA level, and adiponectin mRNA fell. However, major increases in TNFalpha, MCP-1 (up to 40-fold) and IL-6 (up to 250-fold) mRNA levels were evident; a substantial elevation in these mRNAs occurred by 4 h, and adipose tissue IL-6 protein also increased (three- to eightfold). At 24 h, the responses in the subcutaneous depot were much lower than in epididymal and perirenal adipose tissue, but at 4 h, the subcutaneous tissue showed major increases in IL-6, MCP-1 and TNFalpha gene expression. In contrast to the inflammatory adipokines, the mRNA level of two macrophage markers, F4/80 and MAC-1, was unaltered in adipose tissue during endotoxaemia. Expression of the hypoxia-sensitive transcription factor, HIF-1alpha, gene was increased at both 4 and 24 h, and HIF-1alpha protein was elevated at 4 h, suggesting that the tissue was hypoxic. It is concluded that white adipose tissue may play an important role in the production of inflammatory mediators in endotoxaemia.

To study the epidemiological, pathological, clinical features and therapy of collision carcinoma.Seven patients were studied retrospectively against the background of the literature from 1980 to 2001, including the incidence, age of onset, sex ratio, predilection sites, clinical signs, pathological features and therapies.Collision carcinoma is rare, but more common in males than in females. The peak onset age is more than 65 years. It is found frequently in the stomach, liver, uterine, esophagogastric junction, and lung. Without special clinical features, it is difficult to diagnose. Pathological findings are the only way to make a correct diagnosis before operation. Operation is the major therapy, assisted by chemotherapy or/and radiotherapy when necessary. Collision carcinoma represents a coexistence of two adjacent but histologically different malignant neoplasmas without histological admixture in an organ.Collision carcinoma is rare but composed of mosaics of two malignant tumours. The clinical features of collision carcinoma need further investigation.