Immune response to hepatitis B vaccination and factors associated with poor immune response among healthcare workers.

BACKGROUND: Hepatitis B virus (HBV) infection is a major global health problem, and healthcare workers (HCWs) are at high risk for HBV infection. Current guidelines strongly recommend immunization and screening for high-risk groups. AIMS: We evaluated immunization and screening for HBV vaccination, assessed post-vaccination immune status of HCW's and characterized potential risk factors associated with poor immune response. MATERIALS AND METHODS: From January 2010 to December 2018, we retrospectively analyzed comprehensive health checkup data for a total of 303 HCWs who received an HBV vaccination. After vaccination, HBV surface antibody (anti-HBs) titers were collected and the distribution of immune response types was determined. Risk factors for poor immune responses were identified using logistic regression. RESULTS: A total of 213 HCWs were analyzed after exclusion based on the exclusion criteria. In total, 28 (13.2%) HCWs had anti-HBs titers <100 mIU/mL (hyporesponsive/nonresponsive groups), and 185 (86.8%) had anti-HBs titers ≥100 mIU/mL (hyperresponsive group). Follow-up observations found that 75% (21/28) of the hyporesponsive/nonresponsive groups did not have increased anti-HBs titers or did not maintain an increased response. A multivariate analysis showed that HBV antibody titers at the time of employment were a significant risk factor (OR, 6.12; CI, 1.34-27.93; P = 0.019). CONCLUSIONS: More attention should be paid to groups that are hyporesponsive/nonresponsive after vaccination and to those with low anti-HBs titers at the beginning of employment. HCWs can be further protected from HBV if their results are discussed at postvaccination follow-ups.

Visceral obesity, but not central obesity, is associated with cardiac remodeling in subjects with suspected metabolic syndrome.

BACKGROUND AND AIMS: Metabolic syndrome (MetS) is a cluster of multiple risk factors including central obesity that may lead to cardiac damage and cardiovascular events. We investigated whether visceral obesity induces cardiac structural and functional remodeling independently from central obesity and other risk factors in subjects with suspected MetS. METHODS AND RESULTS: We studied 229 participants with suspected MetS. Visceral fat area (VFA) was measured by bioelectrical impedance analysis. Left ventricular (LV) mass index, early diastolic velocity of mitral annulus (e'), and LV global longitudinal strain (GLS) were measured by echocardiography. Subjects were categorized into high and low VFA group (VFAh and VFAl). MetS was more prevalent in the VFAh than in the VFAl (p = 0.004). The VFAh had a higher waist circumference (WC) than the VFAl (p < 0.001). LV mass index was higher, but e' and GLS were lower in the VFAh than in VFAl (all p < 0.05). VFA was well correlated with blood pressure, fasting blood glucose, triglyceride, high-sensitivity C-reactive protein and adiponectin (all p < 0.05). VFA was correlated to LV mass index, e', and GLS (all p < 0.05) and was independently associated with GLS after adjustment for other risk factors, including WC (p = 0.005). CONCLUSIONS: Visceral obesity assessed by VFA was well correlated with parameters of MetS. Visceral obesity, but not central obesity measured by WC, was independently associated with structural and functional cardiac remodeling in subjects with suspected MetS. It suggests that visceral obesity should be considered as an important risk factor for cardiac damage in dysmetabolic subjects. TRIAL REGISTRATION: NCT02077530 (date of registration: November 1, 2013).

Plasma neutrophil gelatinase-associated lipocalin levels are positively associated with diabetic retinopathy in patients with Type 2 diabetes.

AIM: To assess the relationship between plasma neutrophil gelatinase-associated lipocalin (NGAL) levels and diabetic retinopathy in patients with Type 2 diabetes. METHODS: In total, 204 patients with Type 2 diabetes were investigated in this cross-sectional study. They were classified as having no diabetic retinopathy, non-proliferative diabetic retinopathy (NPDR) or proliferative retinopathy (PDR), according to the degree of diabetic retinopathy. Thus, diabetic retinopathy in the patients in this study was either NPDR or PDR. RESULTS: Plasma NGAL concentrations were significantly higher in patients with diabetic retinopathy than in those without. The mean plasma NGAL levels differed significantly according to the severity of diabetic retinopathy (no diabetic retinopathy, 120.8 ng/ml; NPDR, 217.8 ng/ml; PDR, 372.4 ng/ml; P for trend = 0.002) after adjustment for other covariates. In multivariable analysis, plasma NGAL levels were significantly associated with diabetic retinopathy (odds ratio for each standard deviation increase in the logarithmic value, 7.75; 95% confidence interval, 2.04-29.41, P = 0.003). CONCLUSION: Plasma NGAL levels were positively associated with diabetic retinopathy in patients with Type 2 diabetes.

Serum Cystatin C Levels are Positively Associated with Cardiovascular Autonomic Neuropathy in Patients with Type 2 Diabetes.

AIMS: Previous studies have reported that cystatin C is associated with degenerative disorder in the nervous system. However, the relationship between serum cystatin C concentrations and cardiovascular autonomic neuropathy (CAN) in patients with type 2 diabetes is currently unknown. The aim of this study was to assess the relationships between serum cystatin C levels and CAN in patients with type 2 diabetes. METHODS: A total of 357 patients with type 2 diabetes were studied in this cross-sectional study. CAN was diagnosed by a cardiovascular autonomic reflex test. According to the American Diabetes Association criteria, the degree of cardiovascular autonomic dysfunction was graded as normal, early, definite, or severe. CAN was either definite or severe in the subjects of the present study. RESULTS: Serum cystatin C concentrations were significantly higher in patients with CAN than in those without CAN. The mean cystatin C levels differed significantly according to the degree of cardiovascular autonomic dysfunction (normal, 0.78 mg/l; early, 0.79 mg/l; definite, 0.87 mg/l; severe, 0.90 mg/l; P for trend=0.021) after adjustment for other covariates. In multivariate analysis, serum cystatin C levels were significantly associated with CAN (odds ratio [OR] of each standard deviation increase in the logarithmic value, 5.25; 95% confidence interval [CI], 1.17-23.70, P=0.025). CONCLUSIONS: Serum cystatin C levels are positively associated with CAN in patients with type 2 diabetes.

Serum bilirubin concentrations are positively associated with serum C-peptide levels in patients with Type 2 diabetes.

AIMS: To investigate the relationship between physiological serum total bilirubin concentrations and serum C-peptide levels in Korean patients with Type 2 diabetes. METHODS: A total of 588 patients with Type 2 diabetes were investigated in this cross-sectional study. Fasting C-peptide level, 2-h postprandial C-peptide level and ΔC-peptide (postprandial C-peptide minus fasting C-peptide) level were measured in all patients. RESULTS: Fasting C-peptide level, postprandial C-peptide level and ΔC-peptide level tended to be higher in patients with higher bilirubin concentrations. Partial correlation analysis showed that serum bilirubin levels were significantly correlated with fasting C-peptide level (r = 0.159, P < 0.001), postprandial C-peptide level (r = 0.209, P < 0.001) and ΔC-peptide level (r = 0.186, P < 0.001) after adjustment for other covariates. In the multivariate model, the association between serum bilirubin concentrations and serum C-peptide levels remained significant after adjustment for confounding factors including age, gender, familial diabetes, hypertension, hyperlipidaemia, BMI, HbA1c , duration of diabetes and associated liver function tests (fasting C-peptide level: ß = 0.083, P = 0.041; postprandial C-peptide level: ß = 0.106, P = 0.005; ΔC-peptide level: ß = 0.096, P = 0.015, respectively). CONCLUSIONS: Serum bilirubin concentrations within the physiological range were positively associated with serum C-peptide levels in patients with Type 2 diabetes.

Physiological serum bilirubin concentrations are inversely associated with the prevalence of cardiovascular autonomic neuropathy in patients with Type 2 diabetes.

AIMS: Although severe hyperbilirubinaemia causes kernicterus in neonates, normal to modestly elevated bilirubin concentrations have been reported to be neuroprotective. However, the relationship between serum bilirubin concentrations and cardiovascular autonomic neuropathy in patients with Type 2 diabetes is currently unknown. This study assessed the relationships between physiological serum total bilirubin concentrations and cardiovascular autonomic neuropathy in patients with Type 2 diabetes. METHODS: A total of 2991 patients with Type 2 diabetes were investigated in this cross-sectional study. Cardiovascular autonomic neuropathy was diagnosed by a cardiovascular reflex test. According to the American Diabetes Association criteria, the degree of cardiovascular autonomic dysfunction was graded into normal, early, definite and severe. Cardiovascular autonomic neuropathy was either definite or severe in the present study. An analysis of covariance after adjustment for other covariates was performed. A logistic regression model was used to assess an association of cardiovascular autonomic neuropathy with serum total bilirubin tertiles. RESULTS: Serum total bilirubin concentrations were significantly lower in subjects with cardiovascular autonomic neuropathy. The mean total bilirubin values differed significantly according to the severity of cardiovascular autonomic dysfunction (normal 13.0 µmol/l; early 12.3 µmol/l; definite 11.8 µmol/l; severe 10.1 µmol/l; P for trend < 0.001) after adjustment for other covariates. In multivariate analysis, serum total bilirubin levels were significantly associated with cardiovascular autonomic neuropathy (odds ratio 0.36; 95% CI 0.21-0.63 for the highest vs. the lowest bilirubin tertile, P < 0.001). CONCLUSIONS: Serum total bilirubin concentrations within the physiologic range are inversely associated with the prevalence of cardiovascular autonomic neuropathy in patients with Type 2 diabetes.

Feasibility of proposed single-nucleotide polymorphisms as predictive markers for targeted regimens in metastatic colorectal cancer.

BACKGROUND: Surrogate biomarkers for metastatic colorectal cancer (mCRC) are urgently needed to achieve the best outcomes for targeted therapy. METHODS: A clinical association analysis was performed to examine the three single-nucleotide polymorphisms (SNPs) that were previously proposed as markers of chemosensitivity to the cetuximab (124 patients) and bevacizumab regimens (100 patients) in mCRC patients. In addition, biological correlations were examined for the candidate SNPs in terms of their regulatory pathway. RESULTS: For cetuximab regimens, patients homozygous for the wild-type alleles (GG) of LIFR rs3729740 exhibited a 1.9 times greater overall response rate (ORR) and 1.4 months longer progression-free survival (PFS) than those homozygous or heterozygous for the mutant allele (GA and AA; P=0.022 and 0.027, respectively). For bevacizumab regimens, patients homozygous for the minor alleles (TT) of ANXA11 rs1049550 exhibited an ORR twice as high as those homozygous or heterozygous for the ancestral allele (CC and CT; P=0.031). Overall response rate gain was achieved up to 10% in patients with wild-type LIFR rs3729740 patients either with wild-type KRAS or skin toxicity (P=0.001) respectively. Specifically in clones treated with cetuximab and bevacizumab regimens, active p-ERK and MMP-9 expressions were significantly reduced in clones expressing wild-type LIFR rs3729740 (P=0.044) and in those expressing minor-type ANXA11 rs1049550 (P=0.007), respectively. CONCLUSION: LIFR rs3729740 and possibly ANXA11 rs1049550 may be useful as biomarkers for predicting whether mCRC patients are sensitive to relevant target regimens, although further validation in large cohorts is needed.

Interleukin-18 system plays an important role in keloid pathogenesis via epithelial-mesenchymal interactions.

BACKGROUND: Keloid scarring is a dermal fibroproliferative disorder characterized by increased fibroblast proliferation and excessive production of collagen and extracellular matrix (ECM) components. To date, the role of cytokines in keloid pathogenesis has not been completely unravelled. Interleukin (IL)-18 is a pro-inflammatory cytokine that plays important roles in wound healing, fibrogenesis and carcinogenesis. OBJECTIVES: Our aim was to study the role of the IL-18 system in keloid pathogenesis. MATERIALS AND METHODS: Expression and localization of IL-18 and its receptor (IL-18R) were investigated in normal skin and keloid tissues using Western blot and immunohistochemistry. We further studied the expression of the IL-18 system in normal and keloid-derived cell lines in a coculture model. RESULTS: Results from Western blot and immunohistochemistry revealed that IL-18, IL-18Rα and IL-18Rß expression was elevated in keloid tissue compared with normal skin tissue. Studies on the expression of IL-18 and its antagonist, IL-18 binding protein (IL-18BP), using a coculture model demonstrated severe IL-18/IL-18BP imbalance in keloid keratinocyte/keloid fibroblast (KK/KF) cocultures with significant elevation of bioactive IL-18 whereas IL-18BP levels remained the same. This overproduction of bioactive IL-18 in keloid cocultures could be due to increased caspase-1 and decreased caspase-3 expression in keloid tissue, as well as decreased soluble IL-10 levels observed in keloid cocultures. The important inductive effects of IL-18 on KFs were further underscored by the observation that exposure of KF to IL-18 resulted in increased collagen and ECM component synthesis, and increased secretion of profibrotic cytokines such as IL-6 and IL-8. Finally, the addition of phosphatidylinositol 3-kinase (PI3K), mitogen activation protein kinase (MAPK), specificity protein 1 (Sp1) and mammalian target of rapamycin (mTOR) inhibitors inhibited IL-18 secretion in keloid cocultures. CONCLUSIONS: The present study has proven that the IL-18 system plays an important role in keloid pathogenesis via epithelial-mesenchymal interactions. It also suggests a therapeutic potential of PI3K, MAPK, Sp1 and mTOR inhibitors in the treatment of keloid scarring.

A case of xanthoma disseminatum with spontaneous resolution over 10 years: review of the literature on long-term follow-up.

Xanthoma disseminatum (XD) is a rare and potentially progressive non-Langerhans-cell histiocytosis. To date, a few cases of XD with spontaneous complete resolution have been described. The present report describes a 16-year-old girl who presented with yellow to red-brown papules and nodules on her eyelids, cheeks, axillae, back and buttocks. Indirect laryngoscopy showed multiple xanthomatous plaques on the larynx, posterior pharynx, epiglottis, and vocal cords. Additional findings were polyuria, polydipsia, and amenorrhea. Skin biopsy and electron microscopy results confirmed the diagnosis of XD. The patient was treated with fenofibrate, simvastatin, desmopressin, and sex-hormone replacement therapy. Her skin lesions began to slowly fade 6 years after disease onset, eventually resolving spontaneously and completely, but leaving an atrophic scar, frank anetoderma, and persisting diabetes insipidus. This case report together with a review of the English-language literature on the long-term follow-up of XD patients provides additional information on the natural history of this disease.

Comparison of the technical and clinical performance of the Elecsys HBsAg II assay with the Architect, AxSym, and Advia Centaur HBsAg screening assays.

South East Asia has some of the highest prevalence rates of hepatitis B virus (HBV) infection (>or=8%) in the world, and the emergence of hepatitis B surface antigen (HBsAg) mutant strains is a growing problem. Assays with the highest levels of sensitivity, including mutant detection, should be used for routine HBsAg screening. In this large multicenter study, the clinical and technical performance of the fully automated Elecsys HBsAg II assay was compared with the Architect, AxSYM, and Advia Centaur HBsAg assays for HBsAg screening. Nine laboratories (three each from Thailand, Korea, and Singapore) compared the Elecsys HBsAg II assay with their routine HBsAg screening assay against a range of stored and routine clinical samples, including recombinant mutants. The Elecsys HBsAg II assay demonstrated equivalent sensitivity and specificity to the Architect HBsAg assay. However, the Elecsys HBsAg II assay recognized a native mutant sample (L94S, L97V, L98V, T123A) that the Architect HBsAg assay failed to detect. The AxSYM and Advia Centaur HBsAg assays appeared less sensitive for the detection of early HBV infection and also failed to detect some of the recombinant mutant strains. There was almost complete agreement between the Elecsys HBsAg II assay and comparator assays with respect to routine serum samples. The results of this study demonstrate that the Elecsys HBsAg II assay is a highly sensitive and specific screening assay for HBsAg and detects reliably the most important and clinically relevant HBV mutants and genotypes. It is suitable for routine HBsAg screening in Asia.

Transcatheter embolisation of intrahepatic arteriovenous shunts in patients with hepatocellular carcinoma.

This paper assesses the feasibility of transcatheter embolisation of arteriovenous shunts in patients with hepatocellular carcinoma, and reviews available embolic agents, based on our experience and a literature review. From 2001 to 2007, 11 patients with unresectable hepatocellular carcinoma and significant arteriovenous shunts underwent transcatheter embolisation of liver arteriovenous shunts. The age range was 36 to 80 years. A total of 17 embolisations were performed using different embolic agents including absolute ethanol (n=11), histoacryl (n=1), coils (n=2), and polyvinyl alcohol particles (n=1). We reviewed the degree of shunt occlusion and the clinical outcomes. There were 15 arteriovenous shunts. Nine (60%) were arterioportal venous shunts and six were arteriohepatic venous shunts. Two were classified as 'simple' types, according to our protocol, and 13 were 'complex' types. More than 80% occlusion was achieved in 80% of the shunts. In the simple shunts, coil embolisation achieved complete occlusion. In complex shunts with multiple feeders and draining veins, liquid or particulate agents were required to achieve satisfactory occlusion. Managing arteriovenous shunts with embolisation was feasible. The choice of embolic agent should be based on good understanding of the underlying mechanism of the shunts and their angio-architecture.

Outbreak of brucellosis in domestic elk in Korea.

Seven of 18 elk on a deer farm were found by the official Rose-Bengal agglutination test (RBT) and tube agglutination test to be brucellosis reactors/suspects. Evaluation with the competitive ELISA (C-ELISA) and the fluorescence polarization assay (FPA) tests revealed that six and five sera were positive respectively. The seven reactors/ suspects were slaughtered and their blood and tissues were collected. Brucella species could be isolated from three of the slaughtered animals, with nine isolates being obtained from the popliteal, supramammary and submandibular lymph nodes, vaginal discharge, mammary tissue and spleen. Brucella genus-specific PCR based on 16S rRNA and AMOS-PCR, which is specific for differential Brucella species, revealed that all nine isolates were Brucella abortus. These nine were further confirmed to be B. abortus biovar 1 by classical biotyping scheme assays. This is the first report of an outbreak of brucellosis in domestic elk in Korea. Our observations suggest that deer should be included in the routine Brucella surveillance programme for the effective control and prevention of brucellosis in Korea.

Suppression of hypoxic cell death by APIP-induced sustained activation of AKT and ERK1/2.

Apaf-1-interacting protein (APIP) was previously isolated as an inhibitor of mitochondrial cell death interacting with Apaf-1. Here, we report a hypoxia-selective antiapoptotic activity of APIP that induces the activation of AKT and extracellular signal-regulated kinase (ERK)1/2. Stable expression of APIP in C2C12 (C2C12/APIP) cells suppressed cell death induced by hypoxia and etoposide. Unlike etoposide, however, APIP induces the sustained activation of AKT and ERK1/2 and the phosphorylation of caspase-9 during hypoxia. Inhibition of AKT and ERK1/2 activation by the treatments with phosphatidylinositol 3'-kinase and mitogen-activated protein kinase kinase (MEK)1/2 inhibitors sensitized C2C12/APIP cells to hypoxic cell death and abolished the hypoxia-induced phosphorylation of caspase-9. Further, overexpression of phosphorylation-mimic caspase-9 mutants (caspase-9-T125E and caspase-9-S196D), but not phosphorylation-defective caspase-9 mutants (caspase-9-T125A and caspase-9-S196A), effectively suppressed hypoxia-induced death of C2C12 cells. These results elucidate a novel Apaf-1-independent antiapoptotic activity of APIP during hypoxic cell death, inducing the sustained activation of AKT and ERK1/2 and leading to caspase-9 phosphorylation.

Interleukin-18 is a critical factor for vascular endothelial growth factor-enhanced migration in human gastric cancer cell lines.

Cell migration and angiogenesis are key steps in tumor metastasis. However, the mechanism of migration regulated by vascular endothelial growth factor (VEGF), a potent regulator of angiogenesis, is not completely understood. This study examined the relationship between VEGF and migration, along with the mechanism involved in the VEGF-regulated migration of human gastric cancer cells. The level of cell migration was increased by recombinant human (rh)VEGF-165 in the VEGF receptor-2-expressing SNU-601 cells. Interleukin (IL)-18 is associated with the malignant progression of tumors. Accordingly, this study examined the effect of IL-18 on the migration of cancer cells in order to identify the factors involved in VEGF-enhanced migration. Inhibiting IL-18 markedly reduced the level of VEGF-enhanced migration, and IL-18 increased cell migration directly through filamentous-actin polymerization and tensin downregulation. It was confirmed that rhVEGF-165 increased IL-18 production significantly. An antioxidant and an extracellular signal-regulated kinase (ERK)1/2-specific inhibitor blocked rhVEGF-165-enhanced IL-18 production. Accordingly, rhVEGF-165 increased the generation of region of interest (ROI) and activated the ERK1/2 pathway. These results suggest that rhVEGF-165 enhances IL-18 production via the generation of ROI and ERK1/2 phosphorylation, which results in the increased migration of gastric cancer cells.

Relationship between inspiratory muscle strength and cough capacity in cervical spinal cord injured patients.

STUDY DESIGN: Prospective single centre study. OBJECTIVES: Pulmonary rehabilitation focuses on improving the expiratory muscle function in order to increase the reduced cough capacity in patients with cervical spinal cord injuries (SCI). However, an improvement in the inspiratory function is also important for coughing effectively. Therefore, this study was to examine the significance of the inspiratory muscle strength on the cough capacity in the patients with a cervical SCI. SETTING: SCI unit, Yonsei Rehabilitation Hospital, Seoul, Korea. METHODS: The vital capacity (VC), maximum inspiratory pressure (MIP), and maximum expiratory pressure (MEP) were measured. Moreover, the unassisted peak cough flow (PCF) and assisted PCF under three conditions were evaluated. RESULTS: All three assisted cough methods showed a significantly higher value than the unassisted method (P < 0.001). The VC correlated with the voluntary cough capacity and the MIP (R = 0.749) correlated more significantly with the VC than the MEP (R = 0.438) (P < 0.01). The MIP showed a higher correlation with both the unassisted PCF and all three assisted PCFs than the MEP (P < 0.001). CONCLUSIONS: The management of the inspiratory muscle strength should be considered in the pulmonary rehabilitation at cervical SCI patients.

Effect of glycolic acid on UVB-induced skin damage and inflammation in guinea pigs.

OBJECTIVES: Recently the use of glycolic-acid-containing cosmetics has received increased public interest in their supposed ability to reduce wrinkles, roughness, age spots and other skin damage. However, the safety of such products when used excessively or chronically, especially by photosensitive people, is being questioned. The purpose of this study was to examine the effects of glycolic acid alone or in combination with UVB on skin damage and inflammatory response. METHOD: Guinea pigs were treated with glycolic acid (from 1 to 7 mg/cm(2)) alone or in combination with UVB (0.4 or 3 J/cm(2)) for 14 days. Skin damage was evaluated by scoring the skin irritation value by the method of Draize and by histopathological observations. Cyclooxygenase 2 (COX-2) expression and prostaglandin E(2) (PGE(2)) production were also assessed. RESULTS: Glycolic acid caused an increase in the level of skin damage in a dose- and time-dependent manner. Lower doses (1 and 3 mg/cm(2)) of glycolic acid mostly caused erythema and eschar, and these consequently formed scales, whereas higher doses (5 and 7 mg/cm(2)) of glycolic acid caused redness, edema and necrotic ulceration. Glycolic acid also increased the thickness of the epidermal layer, reduced the organization of the stratum corneum and eventually destroyed some parts of the epidermal layer at 7 mg/cm(2). UVB (0.4 and 3 J/cm(2)) caused redness and edema as well as reduced the integrity of the stratum corneum. Glycolic acid enhanced the UVB-induced skin damage. The magnitude of the damage caused by combined UVB and glycolic acid treatment was much greater than that caused by glycolic acid or UVB alone. Moreover, partial destruction of the epidermal layer was observed in skin treated with 3 J/cm(2) UVB and 3 mg/cm(2) glycolic acid. However, glycolic acid did not change the basal and UVB-induced PGE(2) production and COX-2 protein expression. CONCLUSION: These results show that glycolic acid causes skin damage in a dose- and time-dependent manner and that it enhances UVB-induced skin damage without accompanying PGE(2) production or COX-2 protein expression. Therefore, caution should be exercised by those using glycolic acid on a chronic basis or excessively. Moreover, those with photosensitive skins and those more exposed to the sun should be particularly careful.

Synthesis and characterization of a novel extracellular polysaccharide by Rhodotorula glutinis.

The aim of this work was to characterize an exopolysaccharide by Rhodotorula glutinis KCTC 7989 and to investigate the effect of the culture conditions on the production of this polymer. The extracellular polysaccharide (EPS) produced from this strain was a novel acidic heteropolysaccharide composed of neutral sugars (85%) and uronic acid (15%). The neutral sugar composition was identified by gas chromatography as mannose, fucose, glucose, and galactose in a 6.7:0.2:0.1:0.1 ratio. The molecular weight of purified EPS was estimated to be 1.0-3.8 x 10(5) Dalton, and the distribution of the molecular weight was very homogeneous (polydispersity index = 1.32). The EPS solution showed a characteristic of pseudoplastic non-Newtonian fluid at a concentration >2.0% in distilled water. The maximum EPS production was obtained when the strain was grown on glucose (30 g/L). Ammonium sulfate was the best suitable nitrogen source for EPS production. The highest yield of EPS was obtained at a carbon to nitrogen ratio of 15. The EPS synthesis was activated at the acidic range of pH 3.0-5.0 and increased when the pH of the culture broth decreased naturally to <2.0 during the fermentation. When the yeast was grown on glucose (30 g/L) and ammonium sulfate (2 g/L) at 22 degrees C at an initial pH of 4.0, EPS production was maximized (4.0 g/L), and the glucose-based production yield coefficient and carbon-based production yield coefficient were 0.30 g of EPS/g of glucose and 0.34 g (carbon of EPS)/g (carbon of glucose), respectively.

The behavior of a poly(aniline) solid contact pH selective electrode based on N,N,N',N'-tetrabenzylethanediamine ionophore.

A hydrogen ion-selective solid-contact electrode based on N,N,N',N'-tetrabenzylethanediamine has shown the best Nernstian slope and selectivity and the widest response range in a Tris buffered pH sample solution. Its linear dynamic range was pH 3.50-11.94, and the Nernstian slope showed 52.1 mV/pH (at 20 +/- 0.2 degrees C). When it was directly applied to human whole blood (in pH range 6.0-8.5) we could obtain the same satisfying results. This electrode continuously contacted a Tris 7.47 buffered solution, human whole blood and a hydrofluoric acid solution for one month without any loss of performance. Also, hydrofluoric acid did not influence the surface of this electrode, and thus it was maintained without showing any changes in potentials after being used in a hydrofluoric acid solution. The standard deviation in the determined e.m.f. differences was 1.5 mV (N = 5) for Tris buffer solutions of pH 6.5 and 1.1 mV at a Tris buffer solutions of pH 8.5. The 90% response time of the electrodes obtained by injecting of hydrochloric acid into the Tris buffer sample solution was less than 10 s. Especially, in the this paper, with these potential response characteristics of hydrogen ion selective poly(aniline) solid contact electrode, we have also presented the pH response mechanism of this electrode and the role of poly(aniline) and a doped anion in a poly(aniline) layer.