Sphingosine kinase 1 (SK1) is an endothelial

cell (EC) enzyme responsible for generation selleck chemicals llc of sphingosine-1-phosphate (S1P), a lipid molecule implicated in the activation of hepatic stellate cells (HSC). Since binding of fibroblast growth factor (FGF2) to its cognate receptor FGF receptor 1 (FGFR1) leads to EC activation, we hypothesized that that this pathway may stimulate EC to produce SK1 as part of a lipid signaling cascade that regulates HSC activation. Methods/Results: S1P (0.5 μm) increased HSC chemotaxis in Boyden cell migration assay (vehicle: 45.8±26 vs S1P: 1 74.67±68; p<0.05) and stimulated HSC contractility as assessed by increase in phalloidin staining of actin stress fibers. In vivo, mRNA levels of SK1 and FGFR1 were upregulated in human cirrhotic liver tissue

compared to normal liver by qPCR. In isolated liver EC, FGF2 upregulated SK1 based on qPCR (2-fold; p<0.05), Western blot, and ELISA (2-fold; p<0.05). Studies using the 1.9-Kb SK1 promoter and several deletion mutants revealed that the FGF2/FGFR1 pathway regulated the expression of SK1 at the level of transcription. Highest basal and FGF2 stimulated-promoter activity was mapped to two GC-rich regions located within 633 bp from the transcription start site (p<0.05). Sitedirected mutagenesis demonstrated that disruption of these GCrich sites resulted in a 5-7 buy FDA-approved Drug Library fold decrease in basal and selleck screening library FGF2 stimulated promoter activity. Screening for GC-rich binding transcription

factors that could activate this site demonstrated that KLF14, a gene implicated in metabolic syndrome, binds to this region. Congruently, overexpression of KLF14 increased basal and FGF2 stimulated WT SK1 promoter activity by 3-fold (p<0.05), but not upon mutation of the GC-rich sites. In addition, KLF14 siRNA transfection decreased SK1 mRNA levels by 3-fold (p<0.05) and SK1 protein levels in presence andabsence of FGF2 stimulation. Finally, SK1 mRNA and protein levels were decreased in livers from KLF14 knockout (ko) mice compared to wild-type mice (WT: 2.9±0.28 vs KLF14ko: 1.17±0.32 p<0.05). Conclusions: These results show the importance of FGF2 and KLF14 in the activation of the SK1 gene in liver EC and potentially link metabolic syndrome with HSC activation through EC derived S1P. Disclosures: The following people have nothing to disclose: Thiago de Assuncao, Sheng Cao, Gwen Lomberk, Usman Yaqoob, Yan Bi, Angela Mathison, Raul A. Urrutia, Vijay Shah Expression of N-methyl-D-aspartate receptors (NMDARs) is classically associated with excitoxic injury in neuronal tissues, e. g., ischemic or traumatic insults, Alzheimer’s, Parkinson’s, schizophrenia, etc. This spurred wide interest in drugs to suppress NMDAR activity.

001). At the end of the follow-up period, corticosteroids were used in 23 patients (72%), and neither liver-related death nor liver transplantation had been noted. The sensitivity and specificity of the simplified selleck compound AIH scoring system for prediction of patients who required corticosteroids during

clinical course was 92% and 75% in the training set (n = 17), and 91% and 80% in the validation set (n = 16) of overlap. Only 3% of PBC patients were diagnosed as having indication for corticosteroid use. Conclusion:  In PBC-AIH overlap, AIH-like features are dominant in liver histology. The simplified AIH scoring system could predict patients who needed corticosteroids with a higher specificity. “
“Hepatitis C virus (HCV) particles associate viral and lipoprotein moieties to form hybrid lipoviral particles (LVPs). Cell culture–produced HCV (HCVcc) and ex vivo–characterized LVPs primarily differ by their apolipoprotein (apo) B content, which is low for HCVcc, but high for LVPs. Recombinant nucleocapsid-free subviral LVPs are assembled and secreted by apoB-producing cell lines. Selleckchem FK506 To determine whether such

subviral particles circulate in HCV-infected individuals, LVPs complexed with immunoglobulin were precipitated with protein A from low-density plasma fractions of 36 hepatitis C patients, and their lipid content, apolipoprotein profile, and viral composition were determined. HCV RNA in LVPs was quantified and molar ratios of apoB and HCV genome copy number were calculated. LVPs lipidome from four patients was determined via electrospray ionization/tandem mass spectrometry. Protein A–purified LVPs contained at least the envelope glycoprotein E2 and E2-specific antibodies. LVPs were learn more present in every patient and were characterized by high lipid content, presence of apolipoproteins characteristic of triglyceride-rich lipoproteins (TRLs), HCV RNA, and viral glycoprotein. Importantly, save for four

patients, LVPs fractions contained large amounts of apoB, with on average more than 1 × 106 apoB molecules per HCV RNA genome. Because there is one apoB molecule per TRL, this ratio suggested that most LVPs are nucleocapsid-free, envelope glycoprotein-containing subviral particles. LVPs and TRLs had similar composition of triacylglycerol and phospholipid classes. Conclusion: LVPs are a mixed population of particles, comprising predominantly subviral particles that represent a distinct class of modified lipoproteins within the TRL family. (HEPATOLOGY 2012;56:39–48) Hepatitis C virus (HCV) is a member of the Flaviviridae family and a major cause of chronic hepatitis often leading to liver cirrhosis and hepatocellular carcinoma.1 Chronic hepatitis C is a complex disease associated with host metabolic modifications resulting in a unique metabolic syndrome including insulin resistance, liver steatosis, and hypobetalipoproteinemia.

“
“It has long been advocated that patient input in service quality development is essential. We have developed

a model of quality evaluation and improvement within a comprehensive haemophilia service, and describe the issues and improvements that resulted from the process. The project utilized an action research methodology. Seven patients were recruited from the haemophilia service for the initial focus groups. The main themes initially explored were as follows: patient experience of the outpatient, inpatient and weekend services and provision of information. The focus group data were analysed using basic content analysis. The main themes the initial focus group identified were Ipatasertib order the need to optimize the annual review, emergency care and inpatient facilities. Following this, the haemophilia care team worked on improving these issues. At the second focus group the patients contributed Akt inhibitor at a higher level – patient participation. Patients assisted in addressing outstanding issues such as ID alert card content and the algorithm of care for emergency

services. Finally, a patient panel was developed and the relationship became one of direct negotiation and partnership with the haemophilia team to address issues within the service. The expectations and needs of patients attending the haemophilia comprehensive care service are complex. The process of including patients as partners at the highest level of patient involvement evolved and proved an effective method of service evaluation and development, facilitating lateral decision-making, selleck chemicals llc not only improving care directly, but also improving the user experience. “
“The minimum goal of secondary prophylaxis may be to delay the progression of haemarthropathy below a critical level over which it has a great impact on the QoL of haemophilia patients. However, the critical level of haemarthropathy may be different across countries. For these reasons, the impact of haemarthropathy on the QoL in Korean haemophilia A patients was investigated. Depending on observed Pettersson scores

of 27 severe haemophilia A patients, they were divided into three groups, P (Pettersson score) ≤10, P11~19 and P ≥ 20 groups. The QoL of each patient, assessed by the SF36, was compared between the groups. In addition, the changes in the QoL of the patients were observed according to the changes of Pettersson scores to find out the critical level of arthropathy. None of the scores of the SF36 scales were different between the P ≤ 10 and P11~19 groups. In contrast, the scores of PF and MH scales were significantly different between the P11~19 and P ≥ 20 groups. When changes in the scores of each scale in the SF36 were observed according to changes in Pettersson scores, the average P score of 13.0 ± 2.

Scanning was performed Fulvestrant concentration using a 3T MRI Trio (Siemens Medical, Erlangen, Germany). Each fMRI scan was acquired using a standard multislice single-shot gradient echo echo planar imaging (EPI) sequence with the following parameters: TR = 2.2 seconds, TE = 35 ms, 64 × 64 matrix, parallel imaging factor of 2, 3 × 3 × 3 mm voxels, 280 volumes, 36 ascending transverse slices with approximate anterior commissure-posterior commissure (AC-PC) alignment. After each volume was acquired, it was automatically exported in DICOM format from the MRI scanner computer to a separate computer for in-scan

processing. Turbo-BrainVoyager (TBV) 2.0 software (Maastricht, The Netherlands) was used to perform in-scan processing. Real-time prestatistical processing included motion correction and spatial smoothing using a Gaussian kernel of 8.0 mm full width half maximum (FWHM). No feedback motor imagery fMRI scans were acquired using a block design paradigm to provide participant-specific activation, to guide ROI placement for the following RTfMRIf acquisitions. Toward the end of the no feedback motor imagery scan, a 7-slice ROI was selected for activation in the left-hemisphere (using

a t value threshold of 3, with cluster threshold size of 4), visually approximated to be premotor cortex (see Fig 2 and Fig S2). The following settings were used for generating neurofeedback: average feedback values to calculate feedback value = 2 timepoints for continuous feedback paradigm and 6 timepoints for intermittent feedback paradigm, selleck chemicals llc maximum percent signal change (PSC) of feedback bar = 2, general linear model (ROI-GLM) baseline enabled for stable baseline estimation, dynamic ROI enabled using best voxel selection of top 33% (effectively creates a sub-ROI to give better signal extraction from a coarse anatomical ROI selection and with small alignment errors within and between scans). The experimental paradigm and feedback were

presented with a mirrored-projector system, using EPrime 2.0 software learn more (Psychology Software Tools, Pittsburgh, PA). Thermometer bar images were exported from the analysis computer (running TBV software) to the presentation computer (running EPrime software) for the real feedback conditions, or thermometer bar images were taken from a precreated folder on the presentation computer (full-range set of thermometer images selected by fixed randomization) for the false feedback conditions. Data were excluded if motion greater than 3 mm or if no activation was seen in the no feedback ROI localizer scan during post-hoc fMRI analysis. As TBV is an operational software with limited capacity for post-hoc analysis, time series extraction was performed using FSL 4.1.5 (Oxford Centre for Functional MRI of the Brain, Oxford, UK).

Transmission electron microscopy and Xbp1 mRNA splicing analysis were also used for detection of ER stress. Results: 2-APB effectively decreased

HSC viability and total cell count and increased the number of apoptotic cells in both early and late stages. 2-APB also decreased the gene and protein expressions of TRPM7 and α-SMA and increased expressions of pro-apoptotic factor bax and ER stress related factors CHOP, caspase-12, ATF4, ATF6, Xbp1, GRP78 and calnexin in mRNA and/or protein profiles. Meanwhile, morphological ER changes and spliced Xbp1 mRNA were also observed in 2-APB treated cells. Conclusion: Blockage of TRPM7 selleck screening library could inhibit activation and proliferation of primary HSC and induce apoptotic death of activated cells, in which ER stress was identified as one of the possible underlying molecular bases. Key Word(s): 1. HSC; 2. TRPM7; 3. apoptosis; 4. ER stress; Presenting Author: WEI LIU Corresponding Author: WEI LIU Affiliations: Tianjin Second People’s Hospital Objective: To observe the effect

of f segment of complement C3 on expression and secretion of collagen I, III and TGF-β1 in human embryonic lung fibroblast (MRC-5). Methods: Seventeen-peptide f segment of complement C3 was cultured with MRC-5; ELISA was used for determining extracellular levels of collagen I, III and TGF-β1 and immunohistochemistry was employed for detecting intracellular expression of TGF-β1. Results: Compared with check details the control, decreased level of collagen I, III and TGF-β1 companied with the increasing level of f segment of complement C3 in supernatant of the stimulated cell. Also, decreased expression of intracellular TGF-β1 level was observed. Conclusion: F segment of complement C3 may lower the level

of fibrosis according to inhibiting the expression of TGF-β1. Key Word(s): 1. MRC-5; 2. TGF-β1; 3. collagen I, III; 4. Silicosis; Presenting Author: YAN XU Additional Authors: CHANGYU ZHOU, YONGGUI ZHANG, SHANGWEI JI, PING ZHAO, HONGHUA GUO, JIAN JIAO, YAN LI, JIANGBIN WANG Corresponding Author: JIANGBIN WANG Affiliations: china-japan this website union hospital of jilin university Objective: Although the efficacy of entecavir in patients with chronic hepatitis B virus (HBV) infection without cirrhosis is well established, few data are available in patients with cirrhosis. Methods: This prospective study evaluated the clinical outcomes of treatment with entecavir (0.5 mg) for 288 weeks in nucleoside-naive patients with compensated or decompensated cirrhosis. Results: The proportion of patients with Child-Pugh class A disease was significantly increased at Week 288 (98.5%) versus baseline (47.1%; P < 0.0001), the proportion of patients with Child-Pugh class B disease and Child-Pugh class C disease were significantly decreased at Week 288 versus baseline (P < 0.05). The proportion of patients with disease progression in decompensated cirrhosis group was 4.6% during 288 weeks, No patients occurred disease progression in compensated cirrhosis.

By achieving the highest AUC in our study (0.833), the absolute HBsAg level offers the best predictive value of eventual HBsAg seroclearance. From our study, HBsAg <200 IU/mL is already optimal buy Enzalutamide in predicting eventual HBsAg seroclearance (Youden’s index, 5.76), although HBsAg <100 IU/mL also had good predictive value (Youden's index, 5.42). Whether the slightly inferior predictive

value of HBsAg <100 IU/mL (n = 151 in patients with HBsAg seroclearance) to that of <200 IU/mL (n = 170) is a result of the statistical underpower for detection needs further clarification. The second-best method in predicting HBsAg seroclearance would be using the annual log reduction in HBsAg (AUC, 0.803). Serum HBsAg reduction is especially useful in patients with serum HBsAg ≥200 IU/mL (AUC, 0.867), when compared to HBsAg <200 IU/mL (AUC, 0.796). Therefore, adapting an annual 0.5-log reduction of HBsAg levels to predict subsequent HBsAg seroclearance is recommended in patients with baseline HBsAg ≥200 IU/mL. In the control group, annual 1-log reductions in HBsAg levels

were uncommon, accounting for less than 5% for all time points, in contrast to 20.7%-48.7% of 1-log reductions noted in patients eventually clearing HBsAg. Thus, our study provides evidence that serial serum HBsAg measurements can be useful in identifying CHB patients selleck screening library with good immune control and eventual HBsAg seroclearance. From our study, an annual HBsAg reduction of 0.5 log already offers the best predictive value of HBsAg seroclearance, for all patients and also for patients with serum HBsAg ≥200 IU/mL. Serum HBV DNA levels and their reductions were less useful in predicting HBsAg seroclearance. In addition, there

was poor correlation between HBV DNA and HBsAg in both patient groups. It has been previously suggested that the relationship between viral replication and HBsAg production breaks down in HBeAg-negative CHB, probably because viral integration, a nonessential event in the see more life cycle of HBV, produces HBsAg in the absence of viral replication.12, 26 Also, HBsAg is produced in excess by replicating viruses. The significant decrease in HBsAg/HBV DNA ratios over time among patients with HBsAg seroclearance in our study implies a decrease in subviral particle production occurring in the absence of marked changes in viral replication before HBsAg seroclearance. Unlike the identification of inactive carriers,20 the combined analysis of HBV DNA and HBsAg levels in our study did not yield favorable AUCs and is less useful in predicting HBsAg seroclearance. Among patients achieving HBsAg seroclearance, patients developing anti-HBs (n = 63) had a significantly younger age of HBsAg seroclearance (P = 0.013).

[5] Inflammation driven by M1 macrophages is counterbalanced by alternatively polarized M2 macrophages that promote resolution of inflammation and tissue repair.[1, 2] Beneficial properties of alternative M2 macrophages are reported in several inflammatory disorders, including insulin resistance,[6, 7] atherosclerosis,[3] muscle repair,[8] infectious colitis,[4] and chronic glomerulopathies.[9] Altogether, dysregulation of the M1/M2

phenotypic balance is emerging as a central mechanism TGF-beta inhibitor governing the pathogenesis of chronic inflammatory diseases, suggesting that strategies restraining M1 macrophage polarization and/or favoring the M2 macrophage phenotype may protect against exacerbated inflammation and thus limit tissue injury. Alcoholic and nonalcoholic fatty liver disease Talazoparib cost (ALD and NAFLD) are leading causes of liver-related morbidity and mortality in Western countries.[10, 11] Clinical findings and experimental data have demonstrated that activation of Kupffer cells

(KCs) is a central event in the initiation of liver injury.[11-14] The resulting exacerbated release of M1 Kupffer cell-derived mediators contributes to the pathogenesis of several liver lesions, namely, hepatocyte steatosis and apoptosis, inflammatory cell recruitment, and activation of fibrogenesis.[14-17] We have previously shown that limiting M1 KC polarization reduces ALD progression.[6, 7, 14] Here we investigated the impact of M2 KC polarization on alcohol- and high fat-induced liver injury and uncover a novel mechanism limiting M1 KC function, which relies on a proapoptotic effect of M2 KCs for their M1 counterparts. All subjects gave their informed written consent to participate in this research study according to French legislation regarding Ethic and Human Research (Huriet-Serusclat law, the “Comité Consultatif de Protection des Personnes dans la Recherche Biomedicale de Nice” approved this study, Nos. 03.613 and 03.017). The M2 signature was investigated in liver biopsies from 15 heavy alcohol drinkers with similar age and daily this website alcohol intakes, and limited fibrosis, as defined by a fibrosis stage

<2 according to the modified METAVIR scoring system (Table 1). Patients were part of a previously characterized cohort of 109 consecutive alcohol drinkers.[18] Patients were divided into two groups according to serum transaminase levels: group 1 with minimally increased transaminases (10 patients with aspartate aminotransferase [AST], < 2 ULN [(upper limit of normal] and normal alanine aminotransferase [ALT]), and group 2 with elevated transaminases (five patients with AST >2× ULN and ALT >ULN). All patients had ongoing alcohol intoxication until admission. Ultrasound-guided liver biopsy was performed after a mean period of 4 ± 1.9 days of alcohol abstinence, with no difference in duration of abstinence between groups (group 1; 4.5 ± 1.

[5] Inflammation driven by M1 macrophages is counterbalanced by alternatively polarized M2 macrophages that promote resolution of inflammation and tissue repair.[1, 2] Beneficial properties of alternative M2 macrophages are reported in several inflammatory disorders, including insulin resistance,[6, 7] atherosclerosis,[3] muscle repair,[8] infectious colitis,[4] and chronic glomerulopathies.[9] Altogether, dysregulation of the M1/M2

phenotypic balance is emerging as a central mechanism selleck chemicals llc governing the pathogenesis of chronic inflammatory diseases, suggesting that strategies restraining M1 macrophage polarization and/or favoring the M2 macrophage phenotype may protect against exacerbated inflammation and thus limit tissue injury. Alcoholic and nonalcoholic fatty liver disease GSK-3 inhibitor (ALD and NAFLD) are leading causes of liver-related morbidity and mortality in Western countries.[10, 11] Clinical findings and experimental data have demonstrated that activation of Kupffer cells

(KCs) is a central event in the initiation of liver injury.[11-14] The resulting exacerbated release of M1 Kupffer cell-derived mediators contributes to the pathogenesis of several liver lesions, namely, hepatocyte steatosis and apoptosis, inflammatory cell recruitment, and activation of fibrogenesis.[14-17] We have previously shown that limiting M1 KC polarization reduces ALD progression.[6, 7, 14] Here we investigated the impact of M2 KC polarization on alcohol- and high fat-induced liver injury and uncover a novel mechanism limiting M1 KC function, which relies on a proapoptotic effect of M2 KCs for their M1 counterparts. All subjects gave their informed written consent to participate in this research study according to French legislation regarding Ethic and Human Research (Huriet-Serusclat law, the “Comité Consultatif de Protection des Personnes dans la Recherche Biomedicale de Nice” approved this study, Nos. 03.613 and 03.017). The M2 signature was investigated in liver biopsies from 15 heavy alcohol drinkers with similar age and daily learn more alcohol intakes, and limited fibrosis, as defined by a fibrosis stage

<2 according to the modified METAVIR scoring system (Table 1). Patients were part of a previously characterized cohort of 109 consecutive alcohol drinkers.[18] Patients were divided into two groups according to serum transaminase levels: group 1 with minimally increased transaminases (10 patients with aspartate aminotransferase [AST], < 2 ULN [(upper limit of normal] and normal alanine aminotransferase [ALT]), and group 2 with elevated transaminases (five patients with AST >2× ULN and ALT >ULN). All patients had ongoing alcohol intoxication until admission. Ultrasound-guided liver biopsy was performed after a mean period of 4 ± 1.9 days of alcohol abstinence, with no difference in duration of abstinence between groups (group 1; 4.5 ± 1.

Associations with adult ulcerative colitis and biliary/hepatic disease have been described. New insights into the immune response and subsequent pathogenesis associated with infection have also been LY294002 datasheet published. Genomic advances include description of new and unique species and the complete genome description for both Helicobacter felis and Helicobacter suis. Molecular studies have also elucidated the mechanism of action of some functional components of these organisms. Helicobacter species have now been detected in 142 vertebrate species, including animals from every continent and all four nonfish vertebrate taxonomic

classes [1]. Helicobacter colonization has been confirmed for the first time in pancake tortoise, Atlantic spotted dolphins, and brushtail possums along with the more traditional hosts whose repertoire of associated Helicobacter species has been expanded. The Helicobacteraceae family has also been expanded through the description

of Helicobacter magdeburgensis. Stacy and Wellehan [2] reported the identification of a potentially new Helicobacter species in a pancake tortoise (Malacochersus tornieri) diagnosed with septicemia. Spiral-shaped organisms were detected in pathological lesions with partial 16S rDNA sequencing, indicating these were novel Helicobacter. Helicobacter cetorum in stomach and duodenal ampulla in Atlantic spotted dolphin (Stenella frontalis) was detected Buparlisib mw using histology and molecular analyses [3]. Novel Helicobacter organisms were also identified in the gastrointestinal tract of brushtail possums [4]. A study performed with Italian beagle dogs described the colocalization of Helicobacter felis and Helicobacter bizzozeronii learn more in the fundic mucosa of the stomach. H. bizzozeronii was found in the superficial and the basal portions of the fundic glands, whereas

H. felis was only detected in the superficial portions of the glands. Helicobacters were also located free in the cytoplasm or within lysosomes of parietal cells. Additionally, intracytoplasmic Helicobacters were observed in macrophages in the lamina propria [5]. Another study investigated the spatial distribution of Helicobacter species in the GI tract and hepatobiliary system of cats. PCR-based analyses were used to compare Helicobacter spp. presence in fresh and formalin-fixed paraffin-embedded (FFPE) tissues. Helicobacter spp. DNA was detectable in the pancreas, liver, stomach, and duodenum in fresh tissue samples but only in the stomach in FFPE samples. Probably, the most exciting aspect of the study was the detection of Helicobacter spp. DNA in the pancreas, raising the question of how Helicobacter gained access to this organ that traditionally is considered to be sterile [6].

Associations with adult ulcerative colitis and biliary/hepatic disease have been described. New insights into the immune response and subsequent pathogenesis associated with infection have also been AZD8055 nmr published. Genomic advances include description of new and unique species and the complete genome description for both Helicobacter felis and Helicobacter suis. Molecular studies have also elucidated the mechanism of action of some functional components of these organisms. Helicobacter species have now been detected in 142 vertebrate species, including animals from every continent and all four nonfish vertebrate taxonomic

classes [1]. Helicobacter colonization has been confirmed for the first time in pancake tortoise, Atlantic spotted dolphins, and brushtail possums along with the more traditional hosts whose repertoire of associated Helicobacter species has been expanded. The Helicobacteraceae family has also been expanded through the description

of Helicobacter magdeburgensis. Stacy and Wellehan [2] reported the identification of a potentially new Helicobacter species in a pancake tortoise (Malacochersus tornieri) diagnosed with septicemia. Spiral-shaped organisms were detected in pathological lesions with partial 16S rDNA sequencing, indicating these were novel Helicobacter. Helicobacter cetorum in stomach and duodenal ampulla in Atlantic spotted dolphin (Stenella frontalis) was detected Autophagy inhibitor order using histology and molecular analyses [3]. Novel Helicobacter organisms were also identified in the gastrointestinal tract of brushtail possums [4]. A study performed with Italian beagle dogs described the colocalization of Helicobacter felis and Helicobacter bizzozeronii selleck chemical in the fundic mucosa of the stomach. H. bizzozeronii was found in the superficial and the basal portions of the fundic glands, whereas

H. felis was only detected in the superficial portions of the glands. Helicobacters were also located free in the cytoplasm or within lysosomes of parietal cells. Additionally, intracytoplasmic Helicobacters were observed in macrophages in the lamina propria [5]. Another study investigated the spatial distribution of Helicobacter species in the GI tract and hepatobiliary system of cats. PCR-based analyses were used to compare Helicobacter spp. presence in fresh and formalin-fixed paraffin-embedded (FFPE) tissues. Helicobacter spp. DNA was detectable in the pancreas, liver, stomach, and duodenum in fresh tissue samples but only in the stomach in FFPE samples. Probably, the most exciting aspect of the study was the detection of Helicobacter spp. DNA in the pancreas, raising the question of how Helicobacter gained access to this organ that traditionally is considered to be sterile [6].