Confocal fluorescence and immunoelectron microscopy (IEM) of transiently GFP-MdRABE1 overexpressing interphase cells demonstrated that the GFP-MdRABE1 protein was localized selleck inhibitor to the endoplasmic reticulum, dictyosomes, exocytotic vesicles, the cell margin, the membranes of cell organelles, and in the isthmus zone around the nucleus. Although overexpression phenotyping of both N- and C-terminal green fluorescent protein (GFP) fusions failed to indicate

additional functional evidence of the MdRABE1 protein due to mortality of those transgenic cells, its expression profile, bioinformatics, and intracellular localization suggest a role in vesicle trafficking during morphogenesis. “
“Methionine (Met) residues of proteins can be oxidized by reactive oxygen species (ROS) with the formation of two epimers of methionine sulfoxide, S-MetSO and R-MetSO, which are reduced back to methionine by methionine sulfoxide reductase A (MSRA)

and B (MSRB), respectively. UfMSRA and UfMSRB were cloned from the marine macroalga Ulva fasciata Delile, and the role of retrograde signal in gene CHIR-99021 mouse expression was studied. Transcripts of UfMSRA and UfMSRB were increased after light exposure with a peak at 1 h. Treatment of photosynthetic electron transport inhibitors, 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone (DBMIB), or stigmatellin, promoted the light-activated increase in UfMSRA transcripts, and a PSI electron donor, 2,6-dichlorophenolindophenol (DCPIP), reversed their effects. Increase of UfMSRB transcript by light was inhibited by DCMU and DBMIB treatments, and their effects were not reversed by DCPIP. Stigmatellin treatment did not affect UfMSRB transcripts. Thus, a relatively oxidized state of electron transport downstream from the cytochrome b6f (cytb6 f ) complex is involved in the light up-regulation of UfMSRA gene expression, and a more reduced state of Qo of the cytb6 f complex is required for the light activation of gene Avelestat (AZD9668) expression

of UfMSRB. “
“Species of Volvox sect. Volvox (Volvocaceae, Chlorophyceae) are unique because they have thick cytoplasmic bridges between somatic cells and spiny-walled zygotes. This section is taxonomically important because the genus Volvox is polyphyletic. However, taxonomic studies of species in Volvox sect. Volvox have not been carried out on cultured material. Here, we performed a taxonomic study of monoecious species of Volvox sect. Volvox based on the comparative morphology and molecular phylogeny of chloroplast genes and the internal transcribed spacer (ITS) regions of nuclear rDNA using various strains originating from Japan and two preserved strains from the USA. The strains were clearly divided into four species, V. globator L., V. barberi W. Shaw, V. kirkiorum sp. nov., and V. ferrisii sp. nov.

3B). Additionally,

the mRNA levels CP-868596 chemical structure of the genes encoding basolateral bile acid excretion transporters (ATP-binding cassette subfamily C member 1/4/5 [Abcc1/4/5, also known as Mrp1/4/5] and organic solute transporter β [Ostb]) were markedly increased in MCD diet–treated mice (Fig. 3B). The expression of canalicular bile acid excretion transporters (Abcc2 [also known as Mrp2] and ATP-binding cassette subfamily B member 11 [Abcb11, also known as Bsep]) was unchanged (Fig. 3B). Furthermore, mRNA encoding arachidonate 12-lipoxygenase (Alox12), involved in 12-HETE metabolism, was increased by MCD diet treatment (Fig. 3C). All these changes in the mRNA levels were also detected in mice treated with the MCD diet for 2 weeks (Supporting Fig. 2). To further clarify the association between the development of NASH and the changes in serum metabolites and related genes, mice were fed an MCD diet for 3 days, 1 week, and 2 weeks, and the changes in serum metabolites and related gene expression were investigated. Serum ALT levels and hepatic TG contents were increased as early as 3 days after starting MCD treatment and further increased after 2 weeks of treatment (Supporting Fig. 3). The increases

in serum ALP levels followed those in serum ALT levels, and both were correlated with altered hepatic pathologies (Supporting Fig. 3). Although the changes in serum LPC and 12-HETE became greater in a time-dependent manner, serum tauro-β-muricholate AZD8055 solubility dmso and taurocholate Avelestat (AZD9668) were rapidly increased in mice treated with the

MCD diet for 2 weeks (Supporting Fig. 4A). Serum LPC levels were decreased with the increases in hepatic expression of Lpcat1-4 (Supporting Fig. 4). Indeed, serum concentrations of 16:0-, 18:0-, and 18:1-LPC demonstrated a strong negative correlation with hepatic mRNAs encoding Lpcat1-4, especially Lpcat1/2/4 (Supporting Fig. 5A). Increased tauro-β-muricholate and taurocholate levels paralleled the increases in Abcc1/4/5 and Ostb mRNAs and the decreases in mRNAs encoding Slc10a1 and Slco1a1 (Supporting Fig. 4). These bile acid levels were strongly correlated with Abcc1 mRNA levels (Supporting Fig. 5B). However, serum 12-HETE levels did not correlate with hepatic Alox12 mRNA levels (Supporting Fig. 5C). Because LPC is a precursor of PC and PC is known to be an important endogenous compound associated with bile acid excretion and maintenance of choline homeostasis,21, 22 it is reasonable to consider that the decreased LPC and the increased tauro-β-muricholate and taurocholate in serum simply result from dietary choline deficiency. Therefore, supplementation of methionine or choline to the MCD diet was examined. Methionine supplementation to the MCD diet, i.e.

However, it remains impossible at this time to conclusively assess the pathologic role of neutrophils in HILI due to the lack of neutrophil lineage-ablated mice. In conclusion, the work presented

here supports a pathogenic role of eosinophils in a mouse model of HILI. The mechanisms responsible for eosinophil infiltration during the early stages of liver injury and the exact role of eosinophils in mediating toxicity remain unclear and warrant further studies. However, this report begins to connect the prevalence of eosinophilia in clinical CHIR-99021 solubility dmso cases of HILI2 and DILI in general2-5 with hepatotoxicity. Aberrant levels of eosinophils and/or associated chemokines mediated by genetic and other modulators of gene expression may serve as potential risk factors for DILI, as well as potential biomarkers for new or existing drugs in development RAD001 in vivo or on the market. We thank the NHLBI Flow Cytometry core facility, NHLBI Pathology core facility, and Dr. Michael Eckhaus of the NIH Diagnostic and Research Services Branch. We thank Drs. Nancy and James Lee at Mayo Clinic Arizona, Scottsdale,

AZ, for generously providing the anti-MBP antibody. We also thank Tami Graf for reviewing the article and providing helpful suggestions. Additional Supporting Information may be found in the online version of this article. “
“Hepatitis C Virus (HCV) infects 3. 2 million people in the United States and leads to cirrhosis in 20% over 20 years. Although therapy has dramatically improved, difficult to treat populations remain. The immunoregulatory protein Galectin-9 (Gal-9) may be partially responsible for the development and maintenance of persistent infection. In HCV patients, Gal-9 is elevated in the sera and liver, and localizes to Kupffer cells. Gal-9 induces apoptosis of HCV antigen-specific T cells and increases inhibitory regulatory

T-cells via Bay 11-7085 the receptor Tim-3 (PLoS ONE 2010 5(3): e9504). Our current study focuses on elucidating the signals that increase Gal-9 in Kupffer cells. Methods: しsing quantitative real-time PCR, we analyzed Gal-9 mRNA in co-cultures of the Huh7. 5 cell line infected with JFH-1 HCV and either the THP-1 monocyte cell line or human monocytes from healthy donors. Additionally, we examined Gal-9 levels upon phorbol 12-myristate 13-acetate (PMA)-induced maturation of THP-1 cells to macrophages, and in human monocytes matured to proinflammatory macrophages (M1) with GM-CSF, or alternative (M2) with M-CSF. Flow cytometry confirmed protein expression. Results: THP-1 cells upregulate Gal-9 three to five-fold (p<0.001) when exposed to HCV-infected Huh7. 5s. Induction is likely dependent on contact or proximity, as Gal-9 mRNA levels remain constant when THP-1s and infected Huh7. 5s are cultured on opposite sides of a permeable membrane. Furthermore, medium from infected hepatocytes fails to increase Gal-9 in THP-1s. Gal-9 induction by infected Huh7.

8 years (3.5 years plus a 3-month window around the final study milestone) after randomization when patients were being treated actively with peginterferon or followed on no therapy. The remaining 69 deaths

(57%) occurred after the conclusion of the randomized phase when all patients were being followed but no study treatment was offered. More deaths occurred in patients in the cirrhosis stratum (n = 80) MK2206 than the fibrosis stratum (n = 42), and the survival distributions differed significantly (P < 0.0001, Fig. 2). Seven-year cumulative mortality rates were more than two times higher in patients in the cirrhosis stratum than the fibrosis stratum (27% versus 11%), which is equivalent to average annual death rates of 3.9% in the cirrhosis and 1.5% in the fibrosis stratum. Similarly, the distributions of the combined outcome of death or liver transplantation differed significantly in the Alectinib ic50 two strata (P < 0.0001), resulting in a 7-year cumulative rate of 36% (n = 120) in the cirrhosis stratum compared to 16% (n = 66) in the fibrosis stratum. Of the 122 deaths, 76 were categorized as liver-related (62%) and 46 as nonliver-related (38%)

(Table 1). The majority of liver-related deaths were attributable directly to complications of endstage chronic hepatitis C or HCC; however, eight deaths (11%) were attributed to liver disease even though other potentially fatal medical conditions were present (e.g., cancer other than HCC, septicemia, influenza and pneumonia, or accident). The proportion of liver-related deaths was slightly higher among patients in the cirrhosis stratum compared to those in the fibrosis stratum, but this difference was not statistically significant (65% versus 57%, P = 0.39). Overall, as well as within each stratum, the death rate was higher in patients in the treatment group compared to patients in the control group (P = 0.049, Fig. 3). The cumulative 7-year death rate was 20% in treated and 15% in control patients. The mortality rates began to separate after 3 years of therapy and continued to separate during

the 2 to 3 years of follow-up observation G protein-coupled receptor kinase after treatment. The difference in mortality rates between patients in the treatment and control groups was statistically significant in the fibrosis stratum (P = 0.01) but was not significant in the cirrhosis stratum (P = 0.49) (Fig. 4A). In the fibrosis stratum, at the end of the randomized phase (3.8 years) the cumulative mortality rate was 5.0% in patients in the treatment group compared to 1.9% in patients in the control group (P = 0.04).6 By 7 years these rates increased to 14% and 7%, respectively. In the cirrhosis stratum the mortality rates in patients in the treatment and control groups were 9.1% and 8.4% at the end of the randomized phase6 and, during follow-up observation, increased to 28% and 26%. In the fibrosis stratum, as in the group overall, the major separation of mortality rates occurred after 3 years of treatment.

For this, cells were initially stained with calcein AM and ethidium homodimer 1 dye to quantitate live and dead cells (Fig. 5A). The percentage of dead cells (red color) was significantly higher in HCV-infected siBCN1 IHHs (∼70%) versus HCV-infected control IHHs (∼20%). A time-course experiment involving cell

viability after HCV infection was performed. A significant inhibition of cell viability was noted in HCV-infected siBCN1 IHHs versus control IHHs (Fig. 5B). Subsequently, apoptosis as a possible PKC412 mechanism of cell death was examined. HCV-infected control IHHs and siBCN1 IHHs were incubated for 72 hours. Cell lysates were examined for the induction of apoptosis. PARP was significantly cleaved to an 86-kDa signature peptide in HCV-infected siBCN1 IHHs in comparison with HCV-infected control IHHs (Fig. 5C). Our results also demonstrated that BCN1-knockdown IHHs infected with HCV induced caspase-9 and caspase-3 activation. Procaspase-9 and procaspase-3 were cleaved to 37- and 17-kDa protein bands, respectively (Fig. 5C). Similar results were obtained in

HCV-infected siATG7 IHHs (data not shown). Therefore, it is conceivable that autophagy machinery is needed for HCV-infected cell survival, and impairment of this pathway induces apoptosis. Autophagy has recently been identified as a novel component of the innate immune system against viral infection. In this study, we have observed that HCV-infected siBCN1 IHHs do not induce autophagy, and virus growth is reduced. We have further demonstrated that HCV-infected siBCN1 IHHs induce IFN-β, OAS1, IFN-α, ZD1839 mouse and IFI27 mRNA expression and apoptotic cell death. Similar results have also been obtained for HCV-infected ATG7-knockdown IHHs. We propose that HCV induces autophagy to in favor of its own survival; inhibition of autophagic proteins enhances

cell death; and as a result, virus growth is reduced (Fig. 6). This may have potential for future therapeutic modalities. Autophagy plays a key role in recognizing signatures of viral infection and represents a critical effector mechanism for restricting virus production.25 Upon invasion by a pathogen, the host may initiate autophagosome formation as a cellular defense. Autophagy is proposed to serve as a scaffold for intracellular membrane–associated replication for RNA viruses. In rotavirus-infected cells, the NSP4 protein is involved in virus replication and colocalized with LC3 in a double-layered vesicular compartment, a site for nascent viral RNA replication.26 In dengue virus–infected cells, LC3 colocalizes with double-stranded RNA and with the NS1 protein; this suggests the presence of replication complexes in autophagic vesicles.27 We and others have shown that HCV induces autophagy through an accumulation of autophagosomes in infected hepatocytes without colocalization of HCV and autophagy-related proteins.

Total nucleic acid was extracted from leaf tissues and subjected to reverse transcription polymerase chain reaction (RT-PCR) using Hop stunt viroid (HSVd) and Citrus exocortis viroid (CEVd)-specific primers, followed by sequencing of PCR products. RT-PCR with HSVd primers amplified a 302- or 305-bp product from affected samples, but none from healthy plants. CEVd was not detected in affected trees. HSVd was also found in graft- and mechanically

inoculated plants. Sequence analyses showed three variants of HSVd in symptomatic mulberries related to plum and peach variants of this viroid with 94.9% identity, but with only 93% identity to Lebanese and Italian mulberry isolates. This is the first report of HSVd associated with vein clearing in mulberry in Iran. “
“Brown eye spot, Selleck XL765 caused by Cercospora coffeicola, Sunitinib is an important disease of coffee. Both adaxial and abaxial leaf surfaces were inoculated with a conidial suspension of C. coffeicola. Samples were collected from 4 to 168 h after inoculation and then again at 35 days. Germinated conidia showed positive tropism to stomata where attempted penetrations occurred. Appressoria were not observed. After penetration, C. coffeicola colonized the lacunous parenchyma both inter and intracellularly. Sporulation occurred through or

around the stomata. Results from this study provide new insights into the infection process of C. coffeicola on coffee leaf. “
“Alfalfa fields in three western provinces of Iran were surveyed for Peanut stunt virus (PSV) during 2011 and 2012. Forty-seven of 115 samples tested (41%) were infected with PSV. Phylogenetic analysis using coat protein (CP) gene sequences showed that the Iranian isolates belong to the subgroup II of PSV. Pairwise identity analysis revealed four groups representing

four http://www.selleck.co.jp/products/Rapamycin.html phylogenetic subgroups. PSV strains in subgroups III and IV are closely related to each other, as supported by the lowest nucleotide diversity, high pairwise nucleotide identity and high haplotype diversity as evidence of a recent population expansion after a genetic bottleneck. Using the maximum likelihood method, amino acid 86S in the CP gene of the Iranian PSV isolates was found to be under positive selection, although the likelihood ratio test statistics is not significant. This is the first report of the occurrence and phylogenetic relationships of Iranian PSV isolates in west Iran. “
“Gummy stem blight (GSB) is one of the most destructive foliar diseases of cucurbits, worldwide. To identify and characterize the pathogen which causes GSB on watermelon and muskmelon in East China, morphological characteristics, pathogenicity assays as well as sequence characterization of the rDNA internal transcribed spacer (ITS) were performed on 41 isolates collected from Jiangsu, Zhejiang, Anhui and Jiangxi provinces.

e., the loss of income associated with premature death). Thein et al.[6] in the current issue of Hepatology present a population-based study reporting the healthcare costs associated with HCC. The study, based on the Ontario Cancer Registry and linked administrative data, enrolled 2,341 cases of HCC identified in Ontario, Canada, between 2002 and 2008. The authors measured the “direct costs” of care, i.e., the expenditures for medical procedures and services used for the care of the disease. The main limitations of the study are the lack of tumor stage classification and the lack of etiological stratification.

Furthermore, it is worth noting that due to differences in epidemiology, medical practice, physicians selleck compound attitude and culture, patterns of treatment, patients’ preferences, and financial incentives these results cannot be transferred from one healthcare system

to another without proper adjustments. Despite these limitations, this important study provides us with innovative cost analyses, including: Estimates of the 5-year average net cost of a patient with HCC. As shown in Thein et al.’s article, selleck kinase inhibitor the per-patient 5-year net cost of care for HCC is higher than other cancers (about $77,000, range: $60,000 to $94,000). This is not surprising, because HCC usually occurs as a complication of liver cirrhosis. The presence of a chronic disease and of reduced liver function restricts therapeutic approaches and aggravates the costs of the disease. As discussed by the authors, these costs are also higher

than those calculated in prior studies reporting HCC costs in the U.S. and Taiwan.[7, 8] Clearly, several factors come into play, including types of data collected and local regulatory and reimbursement issues. Nevertheless, the methodology described in this article should Ketotifen be useful for further studies evaluating costs for specific healthcare systems. Estimates of the aggregate 5-year net costs of treating all patients with HCC from the perspective of a universal coverage healthcare system based on a whole population, and not on a sample. Thein et al.’s article does not provide estimates of the burden based on a more or less representative sample, but rather on the aggregate economic value of the care provided to the entire population. Should these figures be transferable to the U.S., the cost of managing the 20,000 new U.S. cases per year, not including morbidity and mortality costs, would be around one billion U.S. dollars. Phase-specific estimates of the direct costs of HCC. In Western countries, HCC is most often diagnosed in patients with liver cirrhosis undergoing an ultrasound (US) / alpha-fetoprotein (αFP)-based protocol of oncologic surveillance. The primary tumor is treated following a stage-based approach defined by the American Association for the Study of Liver Diseases (AASLD) guidelines. Patients showing a complete response undergo an intensive follow-up protocol.

When you combine the fact that asymptomatic individuals can have high levels of circulating virus with the fact that B19 is a non-enveloped DNA virus and as such is highly resistance to heat, solvent and detergent treatments, you begin to see the challenges facing the blood banking industry [39]. Solvent detergent

treatment, which is highly effective for inactivating enveloped viruses like HIV, HBV and HCV, does not inactive non-enveloped viruses like B19 and HAV. As a result of this, the industry has had to turn to using more complicated and expensive dry-heat treatment and nano-filtration methods to reduce or eliminate the level of non-enveloped viruses. In most countries, blood is not routinely screened for the presence of B19. Determining whether to screen blood and/or blood products for B19 and at what level, if any, B19 is considered a VX-765 mw minimal or Inhibitor Library concentration low risk for transmission is being actively addressed. As B19 cannot easily replicate in conventional cell or tissue culture methods, nucleic acid amplification testing (NAAT) has been developed and is the recommended method used to screen blood and blood products for the presence of B19 DNA. The Food and Drug Administration does not currently mandate

screening the blood supply for B19, but is proposing that manufactured pools contain plasma B19 DNA levels consistently below 104 geq mL−1 [36]. Similarly, the Health Council for the Netherlands (2002/07; ISBN) considers 104 geq mL−1 the maximum permissible limit. The Health Council for the Netherlands has also recommended that a high-risk group approach be adopted for cellular Calpain blood products containing B19 DNA. In Europe, although there is no official guideline published for plasma pools, and screening of blood donations for B19 DNA is not routine, many manufacturers now voluntarily perform B19 polymerase chain reaction on plasma pools. The basis for the current recommended viral load cutoff came from observations of healthy volunteers. The findings of these studies suggest that

acute B19 infection can occur from administration of blood components containing ≥107 geq mL−1 of B19 DNA. In contrast, patients receiving <104 geq mL−1 have not shown evidence of virus transmission [36,40]. A recent study linking donors and recipients was undertaken to assess the risk of transmission from B19 DNA-positive units containing <106 IU mL−1 into B19 susceptible recipients (B19-specific IgG negative). In this study, 105 B19 DNA-positive donations resulted in the transfusion of 112 B19-positive components into 107 recipients. None of the 24 susceptible cases resulted in a B19 infection [41]. Other investigators found that transmission did not occur in components containing <106 IU mL−1, transmission.

Missing CIT (7%) and CIT less than 2 hours or greater than 20 hours (1.5%) were imputed with the median CIT for the region by share type. The Kaplan-Meier method was used to estimate observed posttransplant graft survival. The log-rank

Selleckchem NVP-AUY922 test compared survival estimates across strata and Bonferroni corrected P values adjusted for multiple comparisons. We used the Cox proportional hazards model to evaluate recipient and donor factors associated with graft loss. Time to graft loss was defined as days from liver transplant to the first of retransplant FK506 ic50 or death. Patients alive or lost to follow-up were censored at the date of last follow-up. When valid Social Security death dates were available

for patients coded as alive or lost to follow-up, posttransplant follow-up status and date were updated with data from the Social Security death certificate master file. Donor factors with a prespecified statistical significance of P < 0.1 were analyzed by multivariate Cox regression models. Backwards elimination with P < 0.05 was used to select the multivariate donor model. The final model was adjusted for recipient age, gender, HCC, blood type match, laboratory MELD and albumin at transplant, and region. A novel donor risk model specific for AA recipients with HCV (AADRI-C) was developed. We investigated the interaction between donor age and donor race.

The adjusted donor 3-oxoacyl-(acyl-carrier-protein) reductase model was stratified by donor race (AA versus non-AA) to quantify and demonstrate differences in the risk of graft failure for the donor age by donor race interaction. Predicted survival estimates for tertiles of AADRI-C (tertile 1, AADRI-C <1.6; tertile 2, AADRI-C 1.6-2.44; and tertile 3, AADRI-C >2.44) and DRI (tertile 1, DRI <1.18; tertile 2, DRI 1.18-1.55; and tertile 3, DRI >1.55) were derived from the Cox proportional hazards model. To compare the AADRI-C to the DRI, we identified a separate cohort of 294 HCV-positive AA patients receiving liver transplants between January 1, 2010 and January, 31, 2011 in the UNOS STAR file (created April 30, 2012) meeting our study selection criteria. These patients were not included in the original development dataset.

Mean patient age was 56 + 14.5 years.

Thirty-nine patients (51.3%) were male. Tujuh puluh enam pasien telah dilakukan tindakan pembedahan oleh divisi PI3K Inhibitor Library cell assay bedah digestive RSCM yang terdiri dari 44 pasien laki-laki dan 32 pasien perempuan dengan usia berkisar antara 40–70 tahunKeluhan utama pasien kanker lambung lanjut adalah perut terasa cepat penuh sebanyak 69 pasien (90.8%) dengan durasi ≤ 1 bulan sebanyak 63 pasien (82.9%) dan median durasi adalah 1 tahun sampai dilakukan tindakan bedaThe main complaint advanced gastric cancer patients is the stomach feel full faster by 60 patients (79%) with a duration of ≤ 1 month were 63 patients (82.9%) and the median duration was 1 year until surgical intervention. Faktor risiko yang paling banyak ditemukan adalah Sosio ekonomi rendah 72 pasien (94,7%), Diet Tinggi garam sebanyak 71 pasien (93.4%), golongan darah A sebanyak 68 pasien (89.5%),makan sayuran dan buah mentah sebanyak 58 pasien (79,3%), makan masakakan DMXAA molecular weight asap/kurang masak sebanyak 45 pasien (59,2%),merokok sebanyak 44 pasien (57,9%), suku Batak 28 pasien (36,7%),suku Jawa 20 pasien (26,3%), suku Padang 11 pasien (14,5% Tindakan operasi yang dilakukan terbanyak adalah

sub total gastrectomi sebanyak 28 pasien (36.8%). Tipe histolopatologi yang sering ditemukan adalah adenokarsinoma tubular sebanyak 73 pasien (96.1%). Angka morbiditas adalah 21.7%. Komplikasi tersering infeksi luka operasi sebanyak 2 pasien (2,6%). Median lama perawatan pasien kanker lambung lanjut adalah 9 hari dengan rentang 7–15 hari. Pada studi ini tidak ditemukan rekurensi dalam 1 tahun pasca operasi maupun hubungan yang bermakna antara karakteristik pasien heptaminol dengan komplikasi pasca operasi. The risk factors most commonly found is the low economic Socio 72 patients (94.7%), High salt diet were 71 patients (93.4%), blood group A were 68 patients (89.5%), eating raw vegetables and fruits as much as 58 patients (79.3%), eating smoke / less cook as many as 45 patients (59.2%), smoking as many as 44 patients (57.9%), Bataknese 24 patients (31,6%), Javanese 20 patients (26.3%), Padang tribe 14 patients (18,4%

Patients were grouped according to surgical procedure: group 1 underwent resection (40 patients), group 2 underwent bypass procedures (10 patients), and group 3 underwent either celiotomy and biopsy alone or jejunostomy placement (26 patients). Twenty patients (26%) developed operative complications, but most were minor. There was no difference in morbidity between surgical groups and no difference according to patient’s age. Operative mortality was 2.6%. Good palliation of symptoms was significantly more common in group 1 patients (82%) than in group 2 patients (60%) (P = 0.0001). Median survival was 8 months (95% confidence interval 4 to 12) for the entire cohort and 13, 5, and 3 months for groups 1, 2, and 3, respectively (P = 0.00001 for group 1 vs groups 2 and 3).