Role of tumour location and surgical extent on prognosis in T2 gallbladder cancer: an international multicentre study.

BACKGROUND: In gallbladder cancer, stage T2 is subdivided by tumour location into lesions on the peritoneal side (T2a) or hepatic side (T2b). For tumours on the peritoneal side (T2a), it has been suggested that liver resection may be omitted without compromising the prognosis. However, data to validate this argument are lacking. This study aimed to investigate the prognostic value of tumour location in T2 gallbladder cancer, and to clarify the adequate extent of surgical resection. METHODS: Clinical data from patients who underwent surgery for gallbladder cancer were collected from 14 hospitals in Korea, Japan, Chile and the USA. Survival and risk factor analyses were conducted. RESULTS: Data from 937 patients were available for evaluation. The overall 5-year disease-free survival rate was 70·6 per cent, 74·5 per cent for those with T2a and 65·5 per cent among those with T2b tumours (P = 0·028). Regarding liver resection, extended cholecystectomy was associated with a better 5-year disease-free survival rate than simple cholecystectomy (73·0 versus 61·5 per cent; P = 0·012). The 5-year disease-free survival rate was marginally better for extended than simple cholecystectomy in both T2a (76·5 versus 66·1 per cent; P = 0·094) and T2b (68·2 versus 56·2 per cent; P = 0·084) disease. Five-year disease-free survival rates were similar for extended cholecystectomies including liver wedge resection versus segment IVb/V segmentectomy (74·1 versus 71·5 per cent; P = 0·720). In multivariable analysis, independent risk factors for recurrence were presence of symptoms (hazard ratio (HR) 1·52; P = 0·002), R1 resection (HR 1·96; P = 0·004) and N1/N2 status (N1: HR 3·40, P < 0·001; N2: HR 9·56, P < 0·001). Among recurrences, 70·8 per cent were metastatic. CONCLUSION: Tumour location was not an independent prognostic factor in T2 gallbladder cancer. Extended cholecystectomy was marginally superior to simple cholecystectomy. A radical operation should include liver resection and adequate node dissection.

ANTECEDENTES: En el cáncer de vesícula biliar, la ubicación del tumor subdivide el estadio T2 en tumores con invasión del lado peritoneal y del lado del hígado (T2a y T2b). Para los tumores que invaden el lado peritoneal (T2a) se sugiere que se puede obviar la resección hepática sin que ello comprometa el pronóstico. Sin embargo, este argumento no ha sido validado. El estudio tuvo como objetivo investigar el valor pronóstico de la localización del tumor en el cáncer de vesícula biliar T2 y establecer la extensión adecuada de la resección quirúrgica. MÉTODOS: Se recogieron los datos clínicos de pacientes que se sometieron a cirugía por cáncer de vesícula biliar en 14 hospitales de Corea, Japón, Chile y Estados Unidos. Se realizaron análisis de la supervivencia y de los factores de riesgo. RESULTADOS: Se dispuso de datos de 937 pacientes para ser evaluados. La tasa de supervivencia global libre de enfermedad a los 5 años fue del 70,6%, y las de T2a y T2b del 74,5% y 65,5% (P = 0,028). Con respecto a la resección hepática, la colecistectomía extendida presentó una tasa mejor de supervivencia libre de enfermedad a los 5 años que la colecistectomía simple (73,0% versus 61,5%, P = 0,012). La tasa de supervivencia libre de enfermedad a los 5 años fue marginalmente mejor para la colecistectomía extendida que para la colecistectomía simple tanto en T2a (76,5% versus 66,1%, P = 0,094) como en T2b (68,2% versus 56,2%, P = 0,084). Las tasas de supervivencia libre de enfermedad a los 5 años no fueron diferentes entre la resección hepática en cuña y la segmentectomía S4b+S5 (74,1% versus 71,5%, P = 0,720). En el análisis multivariable, los factores de riesgo independientes para la recidiva fueron la presencia de síntomas (cociente de riesgos instantáneos, hazard ratio, HR 1,52, P = 0,002), la resección R1 (HR 1,96, P = 0,004) y el estadio N1/N2 (N1 HR 3,40, P < 0,001; N2 HR 9,56, P < 0,001). El 70,8% de las recidivas eran metastásicas. CONCLUSIÓN: La localización del tumor no fue un factor pronóstico independiente en el cáncer de vesícula biliar T2. La colecistectomía extendida fue marginalmente superior que la colecistectomía simple. La cirugía radical debe incluir una resección hepática y una linfadenectomía adecuada.

Reversibility of atrophic gastritis and intestinal metaplasia after Helicobacter pylori eradication - a prospective study for up to 10 years.

BACKGROUND: Atrophic gastritis and intestinal metaplasia are premalignant conditions for gastric cancer. Their reversibility by Helicobacter pylori eradication remains controversial. AIM: To evaluate the reversibility of atrophic gastritis and intestinal metaplasia by H. pylori eradication with long-term follow-up. METHODS: 598 subjects were prospectively enrolled and followed for up to 10 years. They were categorised as H. pylori-negative (n = 65), H. pylori non-eradicated (n = 91), and H. pylori-eradicated (n = 442). Histological assessment was performed for antrum and corpus by Sydney classification. RESULTS: Histological follow-up was performed regularly at 1, 2, 3-4 and ≥5 years, with mean follow-up of 1.07 ± 0.21, 2.29 ± 0.83, 3.93 ± 1.02, and 6.45 ± 1.28 years, respectively. Atrophic gastritis in antrum and corpus gradually and significantly (both P < .05 for all timepoints) improved only in the H. pylori-eradicated group compared to that at baseline. Significant difference in atrophic gastritis between H. pylori-eradicated and H. pylori-negative groups disappeared from 1-year follow-up. Similarly, intestinal metaplasia in antrum and corpus improved significantly (both P < .05 for all timepoints) only in the H. pylori-eradicated group in comparison with that at baseline. Significant difference in intestinal metaplasia between H. pylori-eradicated and H. pylori-negative groups disappeared from ≥5 years of follow-up in the antrum and from 3 years of follow-up in the corpus. CONCLUSION: H. pylori eradication may be a preventative strategy for intestinal-type gastric cancer by regression of atrophic gastritis and intestinal metaplasia.

Intrahepatic Artery Pseudoaneurysm-induced Hemobilia Caused by a Plastic Biliary Stent After ABO-incompatible Living-donor Liver Transplantation: A Case Report.

Bile leakage after duct-to-duct anastomosis in living-donor liver transplantation (LDLT) can mostly be managed by therapeutic endoscopic retrograde cholangiopancreatography. Following this, various complications such as biliary infection, pancreatitis, perforation, and bleeding can occur, and endoscopic sphincterotomy is primarily associated with post- endoscopic retrograde cholangiopancreatography bleeding; other causes have been published in case reports. In the present case, a plastic biliary stent used for treating liver abscesses and leakage at the bile duct anastomosis site after ABO-incompatible LDLT resulted in an intrahepatic artery pseudoaneurysm and hemobilia, which were managed by angiography and coil embolization. Although the complex postoperative course after LDLT can obscure the prompt diagnosis of an intrahepatic artery pseudoaneurysm and hemobilia, biliary stenting should be considered as a possible cause.

Anti-inflammaging effects of Lactobacillus brevis OW38 in aged mice.

In the present study, lactic acid bacteria (LAB) strains were collected from kimchi and were screened to isolate strains that inhibit lipopolysaccharide (LPS) production by Escherichia coli and p16 expression and nuclear factor-kappa B (NF-κB) activation in LPS-stimulated macrophages. Oral administration of Lactobacillus brevis OW38 (1×109 cfu/mouse) to aged mice (male, 18 months old) for 8 weeks reduced the LPS level in colon fluid and blood. In addition, OW38 treatment also reduced the ratio of Firmicutes or Proteobacteria to Bacteroidetes, which was significantly higher in aged mice than in young mice. Treatment with OW38 in aged mice inhibited the expression of inflammatory markers, such as myeloperoxidase, tumour necrosis factor (TNF), and interleukin (IL)-1ß, and inhibited NF-κB activation. Furthermore, it induced the expression of colonic tight junction proteins zonula occludens-1, occludin, and claudin-1. OW38 treatment also suppressed the expression of senescence markers p16, p53, and SAMHD1 in the colon and the hippocampus of aged mice. In addition, it significantly restored spontaneous alternation as well as the expression of brain-derived neurotrophic factor and doublecortin in aged mice compared to that in young mice (P<0.05). Based on these findings, we conclude that OW38 treatment may ameliorate aging-associated colitis and memory impairment by inhibiting gut microbiota LPS production, NF-κB activation, and p16 expression.

CR6-interacting factor 1 is a key regulator in Aß-induced mitochondrial disruption and pathogenesis of Alzheimer's disease.

Mitochondrial dysfunction, often characterized by massive fission and other morphological abnormalities, is a well-known risk factor for Alzheimer's disease (AD). One causative mechanism underlying AD-associated mitochondrial dysfunction is thought to be amyloid-ß (Aß), yet the pathways between Aß and mitochondrial dysfunction remain elusive. In this study, we report that CR6-interacting factor 1 (Crif1), a mitochondrial inner membrane protein, is a key player in Aß-induced mitochondrial dysfunction. Specifically, we found that Crif1 levels were downregulated in the pathological regions of Tg6799 mice brains, wherein overexpressed Aß undergoes self-aggregation. Downregulation of Crif1 was similarly observed in human AD brains as well as in SH-SY5Y cells treated with Aß. In addition, knockdown of Crif1, using RNA interference, induced mitochondrial dysfunction with phenotypes similar to those observed in Aß-treated cells. Conversely, Crif1 overexpression prevented Aß-induced mitochondrial dysfunction and cell death. Finally, we show that Aß-induced downregulation of Crif1 is mediated by enhanced reactive oxygen species (ROS) and ROS-dependent sumoylation of the transcription factor specificity protein 1 (Sp1). These results identify the ROS-Sp1-Crif1 pathway to be a new mechanism underlying Aß-induced mitochondrial dysfunction and suggest that ROS-mediated downregulation of Crif1 is a crucial event in AD pathology. We propose that Crif1 may serve as a novel therapeutic target in the treatment of AD.

A multifunctional protein EWS regulates the expression of Drosha and microRNAs.

EWS (Ewing's Sarcoma) gene encodes an RNA/DNA-binding protein that is ubiquitously expressed and involved in various cellular processes. EWS deficiency leads to impaired development and early senescence through unknown mechanisms. We found that EWS regulates the expression of Drosha and microRNAs (miRNAs). EWS deficiency resulted in increased expression of Drosha, a well-known microprocessor, and increased levels of miR-29b and miR-18b. Importantly, miR-29b and miR-18b were directly involved in the post-transcriptional regulation of collagen IV alpha 1 (Col4a1) and connective tissue growth factor (CTGF) in EWS knock-out (KO) mouse embryonic fibroblast cells. The upregulation of Drosha, miR-29b and miR-18b and the sequential downregulation of Col4a1 and CTGF contributed to the deregulation of dermal development in EWS KO mice. Otherwise, knockdown of Drosha rescued miRNA-dependent downregulation of Col4a1 and CTGF proteins. Taken together, our data indicate that EWS is involved in post-transcriptional regulation of Col4a1 and CTGF via a Drosha-miRNA-dependent pathway. This finding suggests that EWS has a novel role in dermal morphogenesis through the modulation of miRNA biogenesis.

A comparison of serum inflammatory cytokines according to phenotype in patients with psoriasis.

BACKGROUND: Plaque-type psoriasis manifests with various morphological phenotypes and different clinical activity over time in the same individual or from one patient to another. Circulating cytokines, especially T-helper (Th) 1- and Th17-related, have been suggested to reflect the inflammatory nature of psoriasis. However, studies regarding cytokine profile according to morphological phenotypes are quite scarce. OBJECTIVES: We sought to analyse the circulating Th1 and Th17 cytokines according to clinical phenotype and investigated the correlation between disease severity [Psoriasis Area and Severity Index (PASI)] and the serum level of inflammatory cytokines. METHODS: Seventy-one patients with psoriasis were divided into two groups according to clinical phenotype: chronic stable (CS) and eruptive inflammatory (EI). Th1- and Th17-derived cytokines were measured using multiplex cytokine assay. RESULTS: It was noted that interleukin (IL)-1 receptor antagonist and IL-17A were elevated in the EI group compared with the CS group. We also noticed that the PASI is relatively well correlated with serum cytokine level in the CS state but not as well in the EI counterpart. CONCLUSIONS: The level of serum inflammatory cytokines differs according to morphological phenotype. Also, the PASI does not seem to be a suitable tool to assess disease severity in patients with psoriasis with EI characteristics.

ATRX induction by mutant huntingtin via Cdx2 modulates heterochromatin condensation and pathology in Huntington's disease.

Aberrant chromatin remodeling is involved in the pathogenesis of Huntington's disease (HD) but the mechanism is not known. Herein, we report that mutant huntingtin (mtHtt) induces the transcription of alpha thalassemia/mental retardation X linked (ATRX), an ATPase/helicase and SWI/SNF-like chromatin remodeling protein via Cdx-2 activation. ATRX expression was elevated in both a cell line model and transgenic model of HD, and Cdx-2 occupancy of the ATRX promoter was increased in HD. Induction of ATRX expanded the size of promyelocytic leukemia nuclear body (PML-NB) and increased trimethylation of H3K9 (H3K9me3) and condensation of pericentromeric heterochromatin, while knockdown of ATRX decreased PML-NB and H3K9me3 levels. Knockdown of ATRX/dXNP improved the hatch rate of fly embryos expressing mtHtt (Q127). ATRX/dXNP overexpression exacerbated eye degeneration of eye-specific mtHtt (Q127) expressing flies. Our findings suggest that transcriptional alteration of ATRX by mtHtt is involved in pericentromeric heterochromatin condensation and contributes to the pathogenesis of HD.

Radiosurgery for metastatic spinal tumors: follow-up MR findings.

BACKGROUND AND PURPOSE: MR imaging is the primary tool for evaluation and monitoring of spinal tumors. We retrospectively analyzed the MR imaging findings before and after SRS for metastatic spinal tumors. MATERIALS AND METHODS: We reviewed MR imaging findings on 79 metastatic spinal tumor lesions in 44 patients (29 male and 15 female)who had undergone radiosurgery between November 2003 and April 2008. Posttreatment MR imaging was evaluated retrospectively for 3 aspects: 1) changes in tumor volume; 2) changes in T2 signal intensity;and 3) changes in contrast enhancement patterns. RESULTS: With regard to tumor volume on MR images, 32 lesions(40.5%) decreased in volume (group 1), 39 (49.4%) showed no change (group 2), and 8 (10.1%) increased in volume (group 3). T2 signal intensities were unchanged in 4 lesions (type 1), homogeneously increased in 3 (type 2), and changed to a homogeneously dark signal in 4 (type 4). The T2 signal intensity was increased and inter mixed with dark signal intensity (type 3) in 68 lesions. A decrease in contrast enhancement with or without non-enhancing foci was seen in 73 lesions. A persistent homogeneous enhancement pattern was seen in all 4 of the type 1 lesions, in 1 of the 3 type 2 lesions, and in 1 of the 68 type 3 lesions. CONCLUSIONS: Main MR imaging features of locally controlled metastatic spinal tumors included no increase in tumor volume, increased T2 signal intensity with intermixed T2 dark signal intensity,and decreased contrast enhancement. Follow-up MR imaging also provided several patterns of tumor recurrence [corrected].

Dysregulation of upstream binding factor-1 acetylation at K352 is linked to impaired ribosomal DNA transcription in Huntington's disease.

Huntington's disease (HD) is an autosomal-dominant neurological disorder caused by expanded CAG repeats in the Huntingtin (Htt) gene, but it is not known how this mutation causes neurodegeneration. Herein, we found that dysfunction of upstream binding factor-1 (UBF-1) is linked to reduced ribosomal DNA (rDNA) transcription in HD. We identified that UBF1 acetylation at Lys (K) 352 by CREB binding protein (CBP) is crucial for the transcriptional activity of rDNA. UBF1 mutation (K352A, K352Q, and K352R) decreased rDNA transcriptional activity. Moreover, both CBP-dHAT mutant and knockdown of CBP by siRNA reduced acetylation of UBF1 and resulted in the decreased transcription of rDNA into rRNA. ChIP analysis showed a significant reduction of UBF1 occupancy in the promoter of rDNA in STHdh(Q111) cell line model of HD. These results demonstrate that abnormal activity of UBF1 and its acetylation by CBP are linked to impaired rDNA transcription in HD. This novel mechanism suggests that modulation of UBF-mediated rDNA synthesis by CBP may be a therapeutic target for improving neuronal rDNA transcription in HD.

Immediate pigment darkening and persistent pigment darkening as means of measuring the ultraviolet A protection factor in vivo: a comparative study.

BACKGROUND: Persistent pigment darkening (PPD) is a widely used in vivo method for measurement of ultraviolet (UV) A protection factor (UVAPF). However, with increased emphasis on UVA protection and sunscreen products with higher UVAPF gaining popularity, the immediate pigment darkening (IPD) method is drawing attention again. Furthermore, only about a quarter of the recommended quantity of sunscreen is used during daily activities. However, there is as yet no clearly defined relationship between the UVAPF and the amount of sunscreen applied. OBJECTIVES: To analyse the differences between the IPD and PPD methods, and to establish a relationship between the quantity of sunscreen application and the UVAPF. METHODS: Different doses of sunscreen were applied on the back of 15 healthy volunteers, and the UVAPF was measured using both the IPD and the PPD methods. RESULTS: Both methods proved to be effective for measuring the UVAPF. However, all the UVAPF values determined by the PPD method were lower than those determined by the IPD method. Additionally, an exponential relationship between the amount of sunscreen applied and the UVAPF was observed. CONCLUSIONS: The IPD method can also be used as an appropriate endpoint in the determination of UVA protection. It is time saving, and thus considerably lowers the risk of UV exposure, particularly when testing sunscreen products with higher UVAPF. We further state that in order to achieve the desired protective effect of the sunscreen, the quantity of application is also very important.

Living donor liver transplantation for acute hepatic failure caused by reactivation of hepatitis B virus infection after chemotherapy for hematologic malignancy: case reports.

Cancer chemotherapy in chronic hepatitis B virus (HBV) carriers occasionally leads to acute hepatic failure (AHF) from viral reactivation resulting in an high mortality rate. In this situation, living donor liver transplantation (LDLT) can be life saving. Herein we have reported 2 cases of successful LDLT performed for AHF caused by reactivation of HBV infection during chemotherapy for hematologic malignancies. In case 1, a 38-year-old male HBV carrier with a neck mass was hisopathologically diagnosed as Hodgkin's lymphoma. During 4 cycles of chemotherapy he developed right upper quadrant pain and jaundice. Laboratory data (alanine amino transferase, 701 U/L, total bilirubin: 7.92 mg/dL, positive hepatitis B e antigen showed that he had experienced an acute exacerbation of chronic hepatitis. Soon, he developed grade IV hepatic encephalopathy with a total bilirubin level of 50.56 mg/dL and a model for End-Stage Liver Disease score of 40. After LDLT, he has been free of relapse for 52 months so far. In case 2, a 49-year-old male HBV carrier was diagnosed in the chronic phase of chronic myeloid leukemia. The patient had been under Imatinib treatment for 1 year until he was admitted for AHF. He developed grade II encephalopathy with a total bilirubin of 50.8 mg/dL. We performed LDLT; the patient has been free of relapse for 17 months. LDLT was a life-saving procedure for AHF caused by reactivation of HBV during chemotherapy for hematologic malignancy. It can provide long-term survival if the coexistent hematologic malignancy has been controlled.

First Report of Pyricularia grisea Causing Gray Leaf Spot on Lily in Korea.

Lily is an economically important ornamental crop in Korea. In August 2008, severe leaf spot symptoms were observed on an oriental Lily 'Action' in a plant nursery in Daegu, Korea. Disease incidence was 20 to 30%. Initial symptoms were olive green-to-brown lesions on the leaf that developed into tan, elliptical, necrotic lesions. On severely infected leaves, lesions coalesced and killed the entire leaf blade. Infected leaves were surface disinfested with 70% ethanol for 30 s and 2% chlorox for 15 min before plating 1 cm2 sections onto potato dextrose agar. Hyphae appeared 5 days after inoculation and pure culture. Conidia were hyaline, transversely septate with one to three septa; most had two. Conidia were obpyriform and measured 29 to 46 µm long and 7 to 17 µm wide. Mycelia morphology and conidia production were consistent with that described previously for Pyricularia grisea (1). Koch's postulates were fulfilled by spraying five, healthy, vegetative-stage plants with 2 × 105 conidia per ml of sterile distilled water plus 0.05% Tween 20. As a control, five similar plants were sprayed with sterile water plus 0.05% Tween 20 only. Plants were placed inside plastic bags to maintain high relative humidity and incubated in a growth chamber at 25°C under fluorescent light for 14 h and at 20°C in darkness for 10 h. After 3 days, the plastic bags were removed and plants were maintained under the same conditions. Initial symptoms were observed 7 days after inoculation. Ten days after inoculation, disease symptoms on inoculated plants were similar to those previously described in the nursery. Control plants did not show any symptoms. Fungi isolated from these lesions had the same morphological characteristics as the ones isolated previously from plants in the nursery. To our knowledge, this is the first report of gray leaf spot on lily caused by P. grisea in Korea. References: (1) M. B. Ellis. Dematiaceous Hyphomycetes. CMI, Kew, Surrey, UK, 1971.

Annihilation of photochemical reactivity of photo-alignment layer.

The gas-polymer and liquid-polymer interfacial reactions of photosensitive polyimide can annihilate photo-reactive carbon-carbon double bonds, which remain after photo-alignment process. The annihilation processes dramatically affect voltage holding ratio and reorientation of photo-active functional groups. Photochemical dimerizations were identified using UV-visible and FT-IR spectroscopy. Polyimide films containing cinnamate groups were irradiated by linear polarized ultra violet (LPUV) light. Schadt et al. claims that the photo-alignment results from the anisotropy depletion of the cinnamate side chains as a consequence of the (2+2) cycloaddition reactions. The photo-aligned polyimide induces the orientation of nematic liquid crystals perpendicular to the polarization axis. However, the un-reacted photo-sensitive functional groups generate problems such as image sticking and reduced contrast ratio. Voltage holding ratio and photo-fading observed from photo-alignment layer can be dramatically improved by annihilation process of remnant photoreactive groups.

Intracranial xanthoma: long-term follow-up MR findings.

SUMMARY: We report the serial MR findings and histologic features of intracerebral xanthoma in a patient with hyperlipidemia. MR imaging revealed nodule formations with variable degrees of edema and enhancement in the perivascular spaces. In some lesions, high-signal-intensity foci were observed on unenhanced T1-weighted images, which suggest lipid contents of the lesion.

Percutaneous insertion of Zilver stent in malignant biliary obstruction.

BACKGROUND: We evaluated the clinical efficacy and technical feasibility of the percutaneously inserted self-expandable nitinol stent (Zilver stent) for palliation of malignant biliary obstruction. METHODS: Seventeen patients with malignant tumors involving the intra- or extrahepatic bile duct who presented with obstructive jaundice underwent percutaneous insertion of a self-expandable nitinol stent. We retrospectively reviewed the hospital records of patients and evaluated the technical feasibility on stent placement, complications, patient survival, and duration of stent patency. RESULTS: Percutaneous biliary stenting with 27 Zilver stents was performed in 17 patients with malignant biliary obstruction. Technical success was 95%. Malposition of the stent was encountered in one patient. Minor technical problems were encountered in two patients: the introducer tip was broken during stent insertion, so endoscopic removal was done. Mean follow-up period for the 17 patients was 182 days (range 29-485 days): nine patients died of progressive disease at a mean follow-up of 151 days (range 61-371days) after stent insertion and eight patients remained alive at the final follow-up of 216 days (range 29-485 days). The median survival period for all patients was 277 days. The stent occlusion rate was 26% and the mean patency period was 280 days. In five patients, seven stents were obstructed by tumor ingrowth and overgrowth. Stent patency rates were 100%, 100%, 75%, 61%, and 41% at 1, 2, 3, 6, and 12 months, respectively. A late complication, erosive bleeding of the hepatic artery by the stent, developed in one patient. CONCLUSION: Percutaneous biliary stenting using the nitinol stent is technically feasible and safe and clinically efficacious treatment for malignant biliary obstruction, even with a minor technical problem during stent insertion.

Size removal on polyester fabrics by plasma source ion implantation device.

Plasma treatment was evaluated as an alternative clean desizing technology in this work. As indicated by weight loss, O2 plasma treatment efficiently removed sizing agents such as polyvintyl alcohol (PVA), polyacrylic acid esters and their mixture (MIX) on polyethylene terephthalate (PET) fabrics. SEM pictures of the plasma treated samples directly proved the disappearance of the sizing agents. XPS analysis showed apparent changes in chemical composition and functional groups of the PET surface after O2 plasma treatment. Carbon content decreased due to the removal of sizing agents while oxygen content increased. O2 plasma treatment also increased hydrophilic functional groups of sizing agents, which is confirmed by C1s and O1s deconvolution analyses. After O2 plasma treatment, the PET fabric was subjected to conventional desizing process at different temperatures. Except for the PET fabric sized with PVA, plasma-treated fabrics showed more efficient desizing results when compared with untreated fabrics. Furthermore, the desizing effluent from the treated fabric gave lower TOC, COD and BOD values.

Functional and genetic assessment of IFN-gamma receptor in patients with clinical tuberculosis.

OBJECTIVE: The molecular basis of the genetic vulnerability underlying the most common form of clinical tuberculosis (TB) remains largely unknown. We speculated that mild genetic defects in the interferon-gamma (IFN-gamma) signalling pathway caused a subtle functional impairment of IFN-gamma which would explain susceptibility to Mycobacterium tuberculosis in clinical TB. DESIGN: A case-control study. RESULTS: We evaluated functional responsiveness to IFN-gamma in monocytes from patients with clinical TB (n = 10), and analysed the genetic sequences of the IFN-gamma receptor 1 (IFN-gammaR1) and STAT1 genes in patients with disseminated TB (n = 18). IFN-gamma stimulated an increase in the expression of HLA-DR and CD64 on monocytes of both controls and patients; the rate of increase in expression was the same in both groups. Treatment with IFN-gamma before lipopolysaccharide (LPS) stimulation further increased tumour necrosis factor-alpha (TNF-alpha) production as compared to TNF-alpha production with LPS stimulation alone; the rate of increase in TNF-alpha production was the same in both groups. The known mutations in the coding sequences of the IFN-gammaR1 and STAT1 genes were not found in the patients with disseminated tuberculosis. CONCLUSION: These results suggest that impairment of the IFN-gamma signalling pathway did not account for cases of clinical TB in this study.

Diffusion-weighted magnetic resonance imaging in Wernicke's encephalopathy.

OBJECTIVE: To report diffusion-weighted imaging (DWI) findings and postulate the pathogenic mechanism of Wernicke's encephalopathy (WE). PATIENT: A 47-year-old-woman presented with altered consciousness, ophthalmoplegia, and ataxia. DWI revealed the abnormal signal changes in periaqueductal gray matter, mamillary bodies and bilateral medial thalami. Apparent diffusion coefficient (ADC) map revealed the high signal intensity lesions in bilateral medial thalami, suggestive of vasogenic edema. The abnormal signal intensity lesions disappeared on follow-up imaging with clinical improvement. CONCLUSIONS: Vasogenic edema plays an important role in the pathogenesis of WE and can be reversed by proper management. DWI findings in the early stage of WE may provide useful information about the prognosis.