[2] However, an increasing variety of therapeutic options are available for patients

with HCC.[3] Many of these options have survival benefit, so it is conceivable that these patients with HCC with longer survival will have greater chances of developing complications of end-stage liver disease (ESLD). Variceal bleeding (VB) is one of the complications that characterize decompensated cirrhosis. In the last 30 years, there has been a substantial improvement selleck chemical in the survival of patients with VB as a result of the use of vasoactive drugs, the introduction of endoscopic band ligation, and the use of antibiotic prophylaxis.[4, 5] Presently, further efforts are targeted at developing individualized therapeutic strategies to adjust the approach to the risk the patient has.[6, 7] Several prognostic studies have identified the presence of HCC as a negative prognostic factor in VB.[5, 8, 9] However, many studies in the context of VB were performed at times when the incidence of HCC was much lower.[10, CHIR-99021 molecular weight 11] Furthermore, most observational and experimental studies in the setting of secondary prophylaxis excluded patients with HCC,[12-25] whereas other studies have excluded only patients with advanced HCC[26-28] or HCC outside of the Milan criteria.[6, 29] Therefore, it is unclear whether or not secondary prophylaxis

is useful in these patients. A recent study in patients admitted because of VB demonstrated greater in-hospital mortality this website in

those patients with HCC, compared to patients without HCC.[9] However, this study was performed on a large database, based on International Classification of Diseases, Ninth Revision (ICD-9), diagnosis, with the limitations these studies have. Given the lack of information, the management of the acute VB (AVB) episode and then the use of secondary prophylaxis in these patients is most likely very heterogeneous across different centers. This gap in knowledge is becoming increasingly relevant, given the rising incidence of HCC, mainly associated with viral cirrhosis, which is expected to peak within the next 10 years.[30] Therefore, the aim of this study was to evaluate the management and long-term outcomes, as defined by rebleeding and death, of patients with HCC and esophageal VB (EVB) in comparison to patients without HCC. This retrospective observational study was performed in 10 centers in Spain (Hospital Vall d’Hebron [Barcelona], Hospital Clinic [Barcelona], Hospital Santa Creu i Sant Pau [Barcelona], Hospital del Mar [Barcelona], Hospital Germans Trías i Pujol [Badalona], Hospital Arnau de Vilanova [Lleida], Hospital Puerta de Hierro [Madrid], Hospital Ramón y Cajal [Madrid], Hospital Gregorio Marañón [Madrid], and Hospital Universitario de Canarias [Tenerife]).

4, 5 Thus, the hepatoprotective function of IL-22 likely plays an important role in inhibiting liver fibrosis in these models. It has been reported that hepatic IL-22 PF-02341066 price levels are elevated in viral

hepatitis patients; but, the effect of IL-22 on liver injury and fibrosis in these patients remains obscure. We have previously shown that the number of IL-22+ lymphocytes positively correlates with the grade of inflammation and serum ALT or aspartate aminotransferase levels in viral hepatitis patients.13 Interestingly, a recent study has shown that hepatic IL-22 expression inversely correlates with the histological activity index and fibrosis stage in hepatitis B virus patients.14 These findings suggest that elevated hepatic IL-22 levels may play a compensatory role in preventing liver injury and fibrosis in viral hepatitis patients. The authors thank Dr. Michitaka Ozaki (Hokkaido University, Sapporo, Japan) for providing the caSTAT3 adenovirus and also Drs. Mingquan Zheng and Jay K.

Kolls (Louisiana State University, New Orleans, LA) for providing IL-22 adenovirus; and also thank Dr. Scott Friedman (Mount Sinai School selleck screening library of Medicine, New York) for providing the LX2 cells. They thank Dr. Howard Young (National Cancer Institute at Frederick, National Institutes of Health) for editing the manuscript for this article. Additional Supporting Information may be found in the online version of this article. “
“Lactase non-persistence is common in India. We evaluated: (i) frequency of lactase gene (C/T-13910 and G/A-22018) polymorphisms in irritable bowel syndrome (IBS) and healthy controls (HC), (ii) association between these polymorphisms and IBS-subtypes and symptoms. A total of 150 IBS patients (Rome-III criteria) and 252 age and gender-matched HC were evaluated for C/T-13910 and G/A-22018 genotypes using polymerase chain reaction-restriction

fragment length polymorphism (PCR-RFLP). Totals of 79 (52%), 52 (35%) and 19 (13%) patients had diarrhea-predominant IBS (D-IBS), constipation predominant IBS (C-IBS) and alternating diarrhea and constipation IBS (A-IBS), respectively (Rome-III). Frequency of C/T-13910 [genotypes: CC 102 (68%), CT 43 (29%), TT 5 (3%) vs CC 155 (61%), CT 83 (33%), TT 14 (6%), P > 0.05] learn more and G/A-22018 [GG 97 (65%), GA 41 (27%), AA 12 (8%) vs GG 154 (61%), GA 78 (31%), AA 20 (8%), P > 0.05] were similar among IBS and HC. Patients with D-IBS more often had C/T-13910 and G/A-22018 genotypes than C-IBS (CC 71 [90%], CT 6 [8%], TT 2 [2%]) versus (24 [46%], 25 [48%], 3 [6%]), A-IBS (7 [39%], 12 [63%], 0, [0%]) and HC (155 [61%], 83 [33%], 14 [6%]), P < 0.0001 and (GG 69 [87%], GA 6 [8%], AA 4 [5%]) vs (22 [42%], 24 [46%], 6 [12%]) vs (6 [32%], 11 [58%], 2 [10%]), P < 0.0001. IBS with CC and GG genotypes more often had abdominal pain (P = 0.005), distension (P = 0.031) and higher stool frequency (P = 0.003) and reported symptoms following dairy products than non-CC (P < 0.0001).

The observation

group was given 20 mg of leucogen before radiotherapy, three times a day, until the end of radiotherapy. The control group was given Midostaurin supplier 2∼5 μg/kg of recombinant human granulocyte colony-stimulating factor unless bone marrow suppression, once a day. The efficacy, incidence rate and occurrence time of bone marrow suppression and, the levels of white blood cells and platelets were compared. Results: There was no significant difference of response rate and disease control rate between the two groups (P > 0.05). The incidence rate of bone marrow suppression of observation group was 16.7 %, which was significantly lower than that of the control group (60.0 %, P < 0.05). No significant differences of the levels of white blood cells and platelets was found between before and after treatment in the observation group, but they were significantly decreased Selleck CCI-779 in the control group after

treatment (P < 0.05), which was significantly lower than those of the observation group after treatment (P < 0.05). Conclusion: Leucogen was effective in the prevention and treatment of bone marrow suppression induced by radiotherapy in patients with malignant tumor, it was worthy of being popularized in clinic. Key Word(s): 1. Leucogen; 2. Radiotherapy; 3. Bone marrow; 4. Malignant tumor; Presenting Author: DONG UK KIM Additional Authors: GWAN HA KIM, GEUN AM SONG, TAE KYUN KIM, see more JUNG HO BAE, HONG RYEOL CHEONG, JOON HYUNG JHI Corresponding Author: DONG UK KIM Affiliations: PNU Hospital Objective: To evaluate the usefulness of the argon plasma coagulation (APC) for microscopic remnant tissues after endoscopic resection of ampullary neoplasms. Methods: Endoscopic snare papillectomy was performed in 34 patients with ampullary neoplasms (32 ampullary adenomas and 2 ampullary adenocarcinomas).

Thirteen patients had the microscopic remnant tissues (all adenomas) in the pathologic report after endoscopic en bloc resection. Eight patients were additionally treated by the APC at 5–7 days after endoscopic resection. In 5 patients, follow-up endoscopy with biopsies was performed after 3 months and then, in the presence of remnant tissues, the APC was introduced. All patients were followed by endoscopy with biopsies at 3 and 6 months and then, in the absence of recurrence, at yearly intervals. Results: There were no local recurrence in 8 patients received the immediate APC. Three of 5 follow-up patients experienced the local recurrence, which was successfully treated with repeated APC. Median follow-up periods was 13.4 months (reange: 3–37 months). Early complications occurred in 5 of 13 patients (38.5%, major bleeding, 1; perforation, 0; pancreatitis 3; cholecystitis, 1). Late complications occurred in 4 of 13 patients (30.8%, ampullary stricture, 1; bile duct stone, 2; pancreatitis, 1).

Conclusions:  Chronic GM treatment does not have a major effect on hepatic encephalopathy in rats with TAA-induced acute liver failure and rats with chronic liver failure induced by common bile duct ligation. “
“We investigated hepatitis B virus (HBV) and hepatitis C virus (HCV) infections among adults in Siem Reap, Cambodia, to consider the prevention strategy

in cooperation with the Ministry of Health in Cambodia. Serological tests for determining HBV and HCV infections and questionnaires were performed from 2010 to 2012 among the general population in the province of Siem Reap. Multivariate logistic regression analysis was conducted to clarify the factors related to HBV and HCV infections. There were 483 participants, comprising 194 men and 289 women (age range, 18–89 years). The prevalence of click here hepatitis B surface antigen was not very high at 4.6%, while anti-hepatitis B core (anti-HBc) was high at 38.5%. All HBV DNA samples were classified as genotype C. Anti-HBc showed Selleck Napabucasin the trend that the older the age, the higher the positive rate (P = 0.0002). The prevalence of HCV RNA

and anti-HCV were 2.3% and 5.8%, respectively. HCV RNA was detected in 39.3% of anti-HCV positive samples and most of them were classified as genotype 6 (54.5%) and 1 (27.3%). Remarkably, in multivariate logistic regression analysis, history of operation and blood transfusion were significantly associated with the positivity for HBV infection and HCV RNA, respectively. Our results showed that operation and blood transfusion were potential risk factors for HBV and HCV infection, respectively, and supposed that horizontal HBV transmission may be frequent in adults in Cambodia. Hence, for reducing HBV and HCV infections, it is necessary to improve

the safety of blood and medical treatment. “
“25-Hydroxyvitamin D (25[OH]D) can potentially interfere with inflammatory response and fibrogenesis. Its role in selleck chemical disease progression in chronic hepatitis C (CHC) and its relation with histological and sustained virological response (SVR) to therapy are unknown. One hundred ninety-seven patients with biopsy-proven genotype 1 (G1) CHC and 49 healthy subjects matched by age and sex were consecutively evaluated. One hundred sixty-seven patients underwent antiviral therapy with pegylated interferon plus ribavirin. The 25(OH)D serum levels were measured by high-pressure liquid chromatography. Tissue expression of cytochrome (CY) P27A1 and CYP2R1, liver 25-hydroxylating enzymes, were assessed by immunochemistry in 34 patients with CHC, and in eight controls. The 25(OH)D serum levels were significantly lower in CHC than in controls (25.07 ± 9.92 μg/L versus 43.06 ± 10.19; P < 0.001). Lower levels of 25(OH)D were independently linked to female sex (P = 0.007) and necroinflammation (P = 0.04) by linear regression analysis. CYP27A1, but not CYP2R1, was directly related to 25(OH)D levels (P = 0.01), and inversely to necroinflammation (P = 0.01).

Knowledge of regulatory elements will point us toward new therapeutic approaches and expand the “druggable genome.” A specific example is the use of Farnesoid X receptor (FXR) agonists to augment the transcription of FXR-responsive genes such as

dimethylarginine dimethylaminohydrolase in portal hypertension, a target with no alternative pharmacological agonist.18 However, ENCODE also opens the door for targeted therapies to regulatory elements. Functional elements, including DNA sequences, transcription factors, and noncoding RNAs, have been widely considered “undruggable” targets, mostly because of the incomplete molecular understanding of these complex systems. However, as an example, microRNAs Sunitinib supplier (miRs) are ABT-263 cell line key RNA molecules regulating gene expression. Anti-miR oligonucleotide therapies directed to the liver have been shown to modulate cholesterol metabolism and hepatitis C viral kinetics, and phase 2 clinical studies are in progress.19 Thus, the paradigm shift in genomic data provided by ENCODE, along with improved chemistry for the

delivery of nucleic acid based therapies to the liver, has provided the opportunity for novel genome and epigenome targeted therapies. As William Ford Gibson famously said, “the future already exists, it’s just not very evenly distributed. “
“Chronic hepatitis C virus (HCV) infection can cause liver damage, ranging from mild to more severe conditions, such as fibrosis and cirrhosis.

Hepatic stellate cell (HSC) activation is a key event in HCV-induced liver fibrosis. HSCs express several HCV coreceptors that interact with HCV proteins, promoting liver fibrogenesis. In addition, HSCs have the ability to engulf apoptotic bodies of hepatocytes find more induced by HCV and trigger a profibrogenic response. Recent studies have suggested that HSCs may play a novel role in the liver innate immunity. HSCs enhanced differentiation and accumulation of regulatory T cells. HSCs-activated natural killer cells could produce γ-interferon that inhibits HCV replication. Importantly, HSCs possess functional Toll-like receptor-3 and retinoic acid-inducible gene I that can be activated by their ligands (poly I : C, 5′ppp-dsRNA), leading to the induction of interferon and inhibition of HCV replication in hepatocytes. These new observations highlight the importance of HSCs in liver immunity against HCV, which is the focus of this review paper. Because of the chronic nature of hepatitis C virus (HCV) infection and its high prevalence and significant morbidity of the resulting diseases, HCV is and will continue to be a serious global health threat for many years to come.[1] As a hepatitis virus, HCV infects human liver where the interactions between HCV and innate immunity play a key role in the immunopathogenesis of HCV disease. Unfortunately, the majority of HCV-infected subjects develop chronic infection that can result in liver fibrosis and cirrhosis.

This see more study showed that the area under the receiver operating characteristic curve for the total CK-18 prediction of a liver fibrosis stage ≥ F2 was 0.73, which is similar to the values reported for various assays based on multiple putative fibrosis biomarkers.9 This proves that a single good biomarker of liver epithelial

death (total CK-18) provides a fairly robust readout of liver fibrosis, which is a complex injury response presumably captured by the other assays. This suggests that an active liver injury (often subclinical) is the main force perpetuating liver fibrosis in most individuals and provides a reason for optimism because it supports the dynamic nature of fibrogenesis/fibrinolysis and the inherent reversibility of liver fibrosis. Like more complex assays, the total CK-18

ELISA reliably differentiates advanced fibrosis from no fibrosis, but it is less discriminating at lower fibrosis stages; this reflects the dynamic nature of fibrosis and the fact that no available assay captures both sides of the fibrosis equation. Total CK-18 assays measure the predominant liver fibrosis stimulus (i.e., liver epithelial cell death), whereas other assays largely reflect Akt inhibitor various aspects of the resultant wound-healing response. The use of both stimulus and response assays might provide complementary/additive information that could perfect the noninvasive staging of fibrosis. In other words, combining an assessment of the strength of the fibrosis stimulus (CK-18) with an estimate of the intensity of the fibrogenic response (fibrosis markers or elastography) might permit individuals with given levels of liver cell death to be stratified into groups of hyporesponders, normoresponders, and hyperresponders with respect to wound healing. Additional power might be obtained by

the serial acquisition of such information from given individuals. Further research is needed to test and refine these concepts. Success offers exciting opportunities for personalizing liver disease management and facilitating the discovery of effective antifibrotic therapies. “
“Background and Aim: Endoscopic forceps biopsy (EFB) as the primary histological this website diagnosis of gastric epithelial neoplasia (GEN) is debated in the era of endoscopic resection (ER). Our aim was to investigate the diagnostic reliability of EFB in patients with GEN compared to ER specimens as the reference standard for the final diagnosis in a large consecutive series. Methods: This was a cross-sectional retrospective study at a tertiary-referral center. A total of 354 consecutive patients with 397 GENs underwent ER (endoscopic mucosal resection or endoscopic submucosal dissection).

This RXDX-106 solubility dmso study showed that the area under the receiver operating characteristic curve for the total CK-18 prediction of a liver fibrosis stage ≥ F2 was 0.73, which is similar to the values reported for various assays based on multiple putative fibrosis biomarkers.9 This proves that a single good biomarker of liver epithelial

death (total CK-18) provides a fairly robust readout of liver fibrosis, which is a complex injury response presumably captured by the other assays. This suggests that an active liver injury (often subclinical) is the main force perpetuating liver fibrosis in most individuals and provides a reason for optimism because it supports the dynamic nature of fibrogenesis/fibrinolysis and the inherent reversibility of liver fibrosis. Like more complex assays, the total CK-18

ELISA reliably differentiates advanced fibrosis from no fibrosis, but it is less discriminating at lower fibrosis stages; this reflects the dynamic nature of fibrosis and the fact that no available assay captures both sides of the fibrosis equation. Total CK-18 assays measure the predominant liver fibrosis stimulus (i.e., liver epithelial cell death), whereas other assays largely reflect Metformin purchase various aspects of the resultant wound-healing response. The use of both stimulus and response assays might provide complementary/additive information that could perfect the noninvasive staging of fibrosis. In other words, combining an assessment of the strength of the fibrosis stimulus (CK-18) with an estimate of the intensity of the fibrogenic response (fibrosis markers or elastography) might permit individuals with given levels of liver cell death to be stratified into groups of hyporesponders, normoresponders, and hyperresponders with respect to wound healing. Additional power might be obtained by

the serial acquisition of such information from given individuals. Further research is needed to test and refine these concepts. Success offers exciting opportunities for personalizing liver disease management and facilitating the discovery of effective antifibrotic therapies. “
“Background and Aim: Endoscopic forceps biopsy (EFB) as the primary histological this website diagnosis of gastric epithelial neoplasia (GEN) is debated in the era of endoscopic resection (ER). Our aim was to investigate the diagnostic reliability of EFB in patients with GEN compared to ER specimens as the reference standard for the final diagnosis in a large consecutive series. Methods: This was a cross-sectional retrospective study at a tertiary-referral center. A total of 354 consecutive patients with 397 GENs underwent ER (endoscopic mucosal resection or endoscopic submucosal dissection).

7, 8 In addition to being the envelope of infectious HBV particles, HBsAg is also found in the form of noninfectious spheres or filaments, which exceed infectious virions in number by 102 to 105.9 Serum HBsAg appears to correlate with transcriptionally active cccDNA and is considered a surrogate Sorafenib manufacturer marker of infected cells.10-14 Although cccDNA is the most accurate reflection of the number of infected

hepatocytes, it can be assessed in tissue only with complex techniques that are restricted to specialized research centers. This excludes the analysis of cccDNA levels from general clinical applications. The quantitation of HBV DNA by polymerase chain

reaction is now a standard part of the diagnostic workup for CHB. A serum HBV DNA decline reflects a reduction in viral replication. In contrast, a serum HBsAg decline represents a reduction in the translation of messenger RNAs produced from transcriptionally active cccDNA or integrated sequences.14 Thus, HBsAg quantitation provides different but complementary information that may aid us in the characterization of an individual’s infection status. Several cross-sectional studies have compared HBsAg and HBV DNA levels during different phases of CHB (Table BGB324 mouse 1). The results are encouragingly similar, even though the studies were conducted in different patient populations and, therefore, with different genotypes. Both HBsAg and HBV DNA levels vary during the natural course of the infection, and they are highest in the initial immune tolerance phase when the serum alanine aminotransferase (ALT) level is normal with no or minimal hepatitis activity. HBsAg levels become lower during the immune clearance phase and decrease slowly and progressively in those who maintain persistently normal ALT levels after hepatitis B e antigen (HBeAg) seroconversion.10 All groups have observed the lowest levels of HBsAg and HBV

DNA during this check details inactive phase, which is also characterized by the highest HBsAg/HBV DNA ratio.7, 10, 15 A Hong Kong follow-up study of 68 HBeAg-negative patients over a median period of 8 years showed a slow overall decrease in HBsAg levels, and a >1 log10 IU/mL HBsAg decline between the initial and last visits reflected improved immune control, which was associated with a higher HBsAg seroclearance rate and stronger viral suppression.10 Two European studies of inactive HBsAg carriers showed that those with subsequent HBsAg seroclearance had a significantly greater HBsAg decline than those who remained HBsAg-seropositive (0.28-0.29 versus 0.054-0.058 log10 IU/mL/year).

05) and returned to normal values with renal recovery post-LT. In the validation set (n = 46), a number of proteins were significantly higher in both rAKI and iAKI versus nAKI. However, only pre-LT plasma OPN (P = 0.009) and TIMP-1 (P = 0.019) levels were significantly higher in rAKI versus iAKI. Logistic regression modeling was used to correlate the probability of post-LT rAKI, factoring in both pre-LT protein markers and clinical variables. A combined model including

elevated OPN and TIMP-1 levels, age <57, and absence of diabetes had the highest area under the curve of 0.82, compared to protein-only and clinical variable–only models. Conclusion: These data suggest that plasma protein profiles might improve the prediction of pre-LT kidney injury recovery after LT. However, multicenter, prospective studies FK506 cell line are needed to validate these findings and Atezolizumab ic50 ultimately test the value of such protein panels in perioperative management

and decision making. (Hepatology 2014;60:2016–2025) “
“A significance number of autoantibodies have been reported in patients with Non Alcoholic Fatty Liver Disease (NAFLD) patients. In the present study, our aim was to assess the role of disease and cell-specific antibodies, namely anti-adipocyte antibodies (anti-AdAb) in patients with NAFLD and Non Alcoholic Steatohepatitis (NASH). Flow Cytometry was used to detect the presence of anti-AdAb (IgM and IgG) in sera from patients with biopsy-proven NAFLD (n=98) and in controls (n=49) without liver disease. Uni- and multivariate analysis was performed to draw associations between anti-AdAb IgM and IgG levels see more and

the different clinical variables. Patients with NAFLD had significantly higher levels of anti-AdAb IgM and significantly lower levels of AdAb IgG when compared to controls (p=0.002 and p<0.001, respectively). Patients with NASH had significantly higher levels of anti-AdAb IgM when compared to Non NASH NAFLD patients, p=0.04. In multivariate analysis, anti-AdAb IgM was independently associated with a higher risk for NASH [OR: 2.90(CI 1.18-7.16), p=0.02)]. Anti-AdAb IgM was also found to be independently associated with portal inflammation in patients with NAFLD [OR: 3.01(CI 1.15-7.90 p=0.02)]. Anti-AdAb IgM was independently associated with NAFLD and NASH while Anti-AdAb IgG was found to be protective against NAFLD. Anti-AdAb IgM was found specifically to be associated with the inflammatory processes in NAFLD. These findings indicate that the Anti-AdAb IgM and IgG may play an immunomodulatory role in the pathogenesis of NAFLD and NASH. "
“Stem cells have potential for therapy of liver diseases, but may also be involved in the formation of liver cancer.

Silymarin is known for its hepatoprotective activity whereas propolis and OPC are strong antioxidants with vascular dilating effects. This study provides a possible molecular mechanism for the beneficial effects attributed to these natural drugs including the upregulation of detoxifying UGT1A enzymes by activation of XRE and ARE binding elements in the respective promoters. selleck inhibitor However, the intake of these

drugs could influence the clearance of other drugs and therefore result in adverse effects when combined with other medications undergoing glucuronidation. Furthermore, the UGT1A mediated antioxidant effects of silymarin, propolis and OPC are affected by frequently occurring genetic variants of UGT1A promoters. Small molecule library molecular weight Disclosures: Michael P. Manns – Consulting: Roche, BMS,

Gilead, Boehringer Ingelheim, Novartis, Idenix, Achillion, GSK, Merck/MSD, Janssen, Medgenics; Grant/Research Support: Merck/MSD, Roche, Gilead, Novartis, Boehringer Ingelheim, BMS; Speaking and Teaching: Merck/MSD, Roche, BMS, Gilead, Janssen, GSK, Novartis The following people have nothing to disclose: Sandra Kalthoff, Anja Winkler, Christian P. Strassburg Purpose: Occupational vinyl chloride (VC) exposures have been linked to toxicant associated steatohepatitis (TASH), although the modes of action are largely unknown. Circulating levels of oxidized metabolites of linoleic acid (OXLAMs) were elevated in previous studies of alcoholic (ASH) and nonalcoholic steatohepatitis (NASH), although the potential pathologic role of OXLAMS in steatohepatitis is unknown. The aim of the present study was to determine whether VC exposure is associated with increased plasma OXLAMs, and learn more to evaluate potential mechanisms of OXLAM hepatotoxicity. Methods: Human Study:

Archived serum samples from highly exposed male VC workers with high-level VC exposures (n=17) and unexposed healthy volunteers (n=27) were obtained from the UofL Occupational Toxicology Specimen Bank. Plasma metabolomic analyses were performed by GC/MS (Thermo-Finnigan Trace DSQ fast-scanning single-quadrupole mass spectrometer) and LC/MS/MS (Waters ACQUITY UPLC, Thermo-Finnigan LTQ mass spectrometer) following metabolite extraction. In-vitro Experiments: HepG2 cells were exposed to linoleic acid and multiple OXLAM isoforms overnight. Seahorse and Cellomics analysis were performed to evaluate effects of treatments on mitochondria function, ER stress, and cell survival. Results: 613 unique named metabolites were identified in plasma of the VC workers. Of these, 189 metabolites were significantly increased in the VC exposure group while 94 metabolites were significantly decreased. Essential (7 of 7) and long chain free fatty acids (19 of 19) were significantly increased with VC exposure.