Extended approach or usage of nasoseptal flap is a risk factor for olfactory dysfunction after endoscopic anterior skullbase surgery: results from 928 patients in a single tertiary center.

BACKGROUND: The aim of this study was to compare olfactory function change in patients who underwent endoscopic skull-base surgery. METHODOLOGY: A total of 928 patients were included in this retrospective study. Olfactory function was measured using the non- validated Likert scale (0â€"100), the Cross-Cultural Smell Identification Test (CC-SIT) and the butanol threshold test (BTT). Patients were divided into two groups: an endoscopic trans-sellar approach group (ETA, n = 768) and an extended endoscopic endonasal approach group (EEEA, n = 160). The ETA group was sub-divided into Nasoseptal flap (NSF) and no NSF groups. RESULTS: Non-validated olfactory function significantly worsened in the EEEA and ETA-NSF groups compared with that in the ETA- no NSF group for at least 6 months post-operatively. Validated olfactory impairment (BTT and CC-SIT) was also significantly worse in the EEEA and NSF groups compared with that in the ETA-no NSF group 3 months post-operatively. Additionally, the degrees of non-validated and validated olfactory deterioration were not significantly different between the EEEA and ETA-NSF groups. We also found that CC-SIT score changes were significantly impaired in tuberculum sellae meningioma patients than in craniopharyn- gioma patients. CONCLUSIONS: We conclude that NSF was the key factor that led to olfactory impairment after endoscopic skull-base surgery.

Inflammatory response of a prostate stromal cell line induced by Trichomonas vaginalis.

While Trichomonas vaginalis, a cause of sexually transmitted infection, is known as a surface-dwelling protozoa, trichomonads have been detected in prostatic tissue from benign prostatic hyperplasia and prostatitis by immunoperoxidase assay or PCR. However, the immune response of prostate stromal cells infected with T. vaginalis has not been investigated. Our objective was to investigate whether T. vaginalis could induce an inflammatory response in prostate stromal cells. Incubation of a human prostate stromal myofibroblast cells (WPMY-1) with live T. vaginalis T016 increased expression of the inflammatory chemokines CXCL8 and CCL2. In addition, TLR4, ROS, MAPK and NF-κB expression increased, while inhibitors of TLR4, ROS, MAPKs and NF-κB reduced CXCL8 and CCL2 production. Medium conditioned by incubation of WPMY-1 cells with T. vaginalis stimulated the migration of human neutrophils and monocytes (THP-1 cells). We conclude that T. vaginalis increases CXCL8 and CCL2 production by human prostate stromal cells by activating TLR4, ROS, MAPKs and NF-κB, and this in turn attracts neutrophils and monocytes and leads to an inflammatory response. This study is the first attempt to demonstrate an inflammatory reaction in prostate stromal cells caused by T. vaginalis.

Urine liver-type fatty acid-binding protein predicts graft outcome up to 2 years after kidney transplantation.

BACKGROUND: Several new biomarkers for the detection of early tubular injury have been investigated in kidney transplant recipients. We recently identified day 2 urinary neutrophil gelatinase-associated lipocalin (NGAL) as a predictor of slow graft function and adverse 1-year outcome. In the present study, we further investigated the value of urinary NGAL and liver-type fatty acid binding protein (L-FABP) for predicting long-term graft outcomes up to 2 years. METHODS: This study was a single-center, prospective observational study. Serial urinary NGAL and L-FABP levels at 0 hours, 2 days, and 6 days after kidney transplantation (KT) were measured, and the clinical data were assessed during the 2-year period after KT. RESULTS: During the 2-year follow-up period, 13 (18.8%), 5 (7.2%), and 4 (5.8%) patients were diagnosed with acute T-cell-mediated rejection, acute antibody-mediated rejection (AMR) and chronic AMR, respectively. In addition, 10 patients (14.3%) developed calcineurin inhibitor toxicity and 6 (8.7%) developed BK viremia. The mean estimated glomerular filtration rates (eGFR) at 1 and 2 years after KT were 65.1 ± 19.1 and 58.5 ± 22.6 mL/min/1.73 m(2), respectively, When poor long-term graft function was defined as eGFR of less than 50 mL/min/1.73 m(2) at 2 years, elderly donors, acute rejection, and high 0-hour urinary L-FABP levels were significant risk factors. Furthermore, in rejection-free patients, L-FABP was strongly associated with poor long-term graft function (P = .006). Multivariate logistic regression analysis showed that high 0-hour L-FABP (P = .015) and acute rejection (P = .006) were independent factors predicting poor long-term graft function. Receiver operating characteristic analysis showed that the area under the curve for urinary L-FABP was 0.692 (P = .036). CONCLUSIONS: Our results suggest that urinary L-FABP may be a useful predictor of adverse long-term outcomes in KT patients.

CAG repeats of CTG18.1 and KCNN3 in Korean patients with bipolar affective disorder.

BACKGROUND: Trinucleotide repetition combined with variable penetrance of expression could be responsible for the complex transmission pattern observed in bipolar affective disorder (BPAD). The purpose of this study was to investigate the association of excess longer allele of KCNN3 and CTG18.1 in the patients with BPAD. METHODS: CAG/CTG repeat distribution in KCNN3, CTG 18.1 and ERDA1 was examined and the copy number of ligation product in repeat expansion detection (RED) was measured in Korean bipolar patients in comparison to ethnically matched healthy controls. RESULTS: No significant difference was found in the allele distribution of those repeats between bipolar patients and controls. Ligation product size in RED was not increased in bipolar patients. However, the copy number of ligation product in RED was highly correlated with CAG/CTG copies of ERDA1 (P=0.0001), partly with CTG 18.1 (P=0.04), but not with KCNN3. CONCLUSIONS: A longer CAG repeat alleles of KCNN3 or CTG 18.1 may not be a risk factor for BPAD in Korean population and the copy number of ligation product in RED in the patients with BPAD is influenced by the longer allele of CAG/CTG of ERDA1 or CTG 18.1.

Serum melanotransferrin, p97 as a biochemical marker of Alzheimer's disease.

The protein melanotransferrin (p97) is associated with the brain lesions of Alzheimer's disease (AD) and is a potential marker of the disorder. We measured serum p97 concentrations in 211 subjects: 71 patients with AD, 56 patients with non-AD-type dementia, and 84 normal control subjects. Serum p97 concentrations were elevated 3- to 4-fold in AD (median 15.00 pg/microl, interquartile range 10.20-17.00 pg/microl) as compared to non AD dementia (2.85 pg/microl, 1.93-7.15 pg/microl) and normal controls (3.20 pg/microl, 2.55-3.95 pg/microl). The mean elevation was significant at 13.54 +/- 3.72 pg/microl, even in the 38 subjects with mild AD (CDR stage 0.5-1). Receiver operating characteristic analyses confirmed an optimal diagnostic threshold of 10.0 pg/microl, which yielded over-all accuracy of 0.882 to 0.915. Serum p97 is a candidate marker of AD, even in the early stage when clinical diagnosis is most uncertain.