The purpose of this study was to determine the incidence and risk factors of symptomatic adjacent segment disease (ASD) following single-lever anterior cervical discectomy and fusion (ACDF) for cervical degenerative diseases.From January 2000 to December 2010, a total of 582 patients with cervical radiculopathy and myelopathy who had undergone single-lever ACDF surgery in the authors’ institution were reviewed retrospectively. Patients who had a revision surgery for symptomatic ASD were selected for this study. The authors analyzed the incidence for ASD after single-lever ACDF. And univariate analysis and logistic regression analysis were performed to identify the risk factors of ASD.Among the 582 patients, 36 patients received subsequent surgical management for ASD after initial single-lever ACDF for an overall prevalence of 6.2%. The average onset time of ASD was 8.5 (2–15) years. The univariate analysis showed that there were no significant differences in sex, duration of disease, BMI, DM, smoking, operative levels, and follow-up period (P > .05) between the 2 groups with and without ASD. There were statistically significant differences in age at the time of operation (χ2 = 4.361, P = .037), and developmental canal stenosis (χ2 = 4.181, P = .041) between patients with and without ASD. The variables of age at the time of operation and developmental canal stenosis were included in a logistic regression model. The logistic regression analysis revealed that age at the time of operation ≤50 years (P = .045, OR = 3.015, 95% CI = 1.024–8.882) and developmental canal stenosis (P = .042, OR = 2.797, 95% CI = 1.039–7.527) were the risk factors for ASD after single-lever ACDF.In the present study, the incidence of symptomatic ASD after single-lever ACDF was 6.2%. And the age at the time of operation ≤50 years and developmental canal stenosis were the risk factors for ASD. The patients ≤50 years old at the time of operation or with developmental canal stenosis are more likely to develop ASD after surgery, and the risk of reoperation will increase.

Objective:To investigate the effect of berberine (BBR) on intestinal barrier function in nonalcoholic fat liver disease (NAFLD) in rats.Materials and Methods:Rats were divided into three groups: normal diet group (control group [CON group]), high-fat diet feeding group (HFD group), and HFD with BBR group. After 8 weeks of HFD feeding, rats in the BBR group were given BBR intragastrically at a dose of 150 mg/kg daily for 4 weeks. The same volume of normal saline was given to the CON and HFD groups. Liver index was detected, and Sudan black B staining was used to study fatty degeneration, also the expression level of occluding and intestinal flora was analyzed.Results:BBR administration significantly reduced HFD-induced increase in body weight (CON group: 379.83 ± 61.51 g, HFD group: 485.24 ± 50.15 g, and BBR group: 428.60 ± 37.37 g). It obviously alleviated the HFD-induced liver fatty degeneration and histopathological changes of intestinal mucosa according to liver index low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and total cholesterol (P < 0.05). The triglyceride, alanine transaminase, and aspartate aminotransferase levels were greatly elevated after BBR treatment (P < 0.05); while endotoxin, intestinal fatty acid-binding protein, and tumor necrosis factor-α were significantly reduced (P < 0.05). Moreover, we found that BBR could obviously elevate the level of occludin and decrease the level of Faecalibacterium prausnitzii and upregulate the level of bacteroides.Conclusion:BBR provides significant protection in NAFLD through ameliorating intestinal barrier function.SUMMARY Berberine (BBR), an alkaloid that can be isolated from many plants, has been medically used for its wide range of antimicrobial and anti-inflammatory effectsThis is a study of BBR on liver function and intestinal barrier function in nonalcoholic fat liver disease (NAFLD)BBR treatment for NAFLD could significantly restore the liver function and provide significant protection in NAFLD through ameliorating intestinal barrier function. Abbreviations used: BBR: Berberine, NAFLD: Nonalcoholic fat liver disease, ALT: Alanine transaminase, AST: Aspartate aminotransferase, TG: Triglyceride, I-FABP: Intestinal-fatty acid-binding protein, IBD: Inflammatory bowel disease.

AIMTo investigate potential effects of poly I:C on mucosal injury and epithelial barrier disruption in dextran sulfate sodium (DSS)-induced acute colitis.METHODSThirty C57BL/6 mice were given either regular drinking water (control group) or 2% (w/v) DSS drinking water (model and poly I:C groups) ad libitum for 7 d. Poly I:C was administrated subcutaneously (20 μg/mouse) 2 h prior to DSS induction in mice of the poly I:C group. Severity of colitis was evaluated by disease activity index, body weight, colon length, histology and myeloperoxidase (MPO) activity, as well as the production of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin 17 (IL-17) and interferon-γ (IFN-γ). Intestinal permeability was analyzed by the fluorescein isothiocyanate labeled-dextran (FITC-D) method. Ultrastructural features of the colon tissue were observed under electron microscopy. Expressions of tight junction (TJ) proteins, including zo-1, occludin and claudin-1, were measured by immunohistochemistry/immunofluorescence, Western blot and real-time quantitative polymerase chain reaction (RT-qPCR).RESULTSDSS caused significant damage to the colon tissue in the model group. Administration of poly I:C dramatically protected against DSS-induced colitis, as demonstrated by less body weight loss, lower disease activity index score, longer colon length, colonic MPO activity, and improved macroscopic and histological scores. It also ameliorated DSS-induced ultrastructural changes of the colon epithelium, as observed under scanning electron microscopy, as well as FITC-D permeability. The mRNA and protein expressions of TJ protein, zo-1, occludin and claudin-1 were also found to be significantly enhanced in the poly I:C group, as determined by immunohistochemistry/immunofluorescence, Western blot and RT-qPCR. By contrast, poly I:C pretreatment markedly reversed the DSS-induced up-regulated expressions of the inflammatory cytokines TNF-α, IL-17 and IFN-γ.CONCLUSIONOur study suggested that poly I:C may protect against DSS-induced colitis through maintaining integrity of the epithelial barrier and regulating innate immune responses, which may shed light on the therapeutic potential of poly I:C in human colitis.

No abstract

Abstract. Acute intermittent porphyria (AIP) is a rare inherited disorder of heme metabolism. It has the ability to trigger posterior reversible encephalopathy syndrome (PRES), a rare acute neurologic condition that is characterized by acute neurological symptoms. Pregnancy may induce AIP attacks. The present report describes the case of a pregnant woman with AIP. The patient was treated with heme-arginate during pregnancy and successfully delivered a healthy baby. Following delivery, the patient presented with PRES and experienced generalized seizures. Treatment including arginine hemoglobin, calcium gluconate and sodium chloride was administered. The symptoms of epilepsy did not recur. Magnetic resonance imaging of the head demonstrated that the bilateral occipital lobe lesions were significantly reduced in size following the treatment. In the present report, it was demonstrated that administration of heme-arginate for AIP during pregnancy is safe. Timely administration of arginine hemoglobin, calcium gluconate and sodium chloride may more efficiently improve the clinical status in AIP patients diagnosed with PRES who experience generalized seizures.