Plasma IP-10 levels ≥150 pg/mL occurred more often in non-Aboriginals (51% versus 20%, P = 0.014), those with HCV RNA >6 log IU/mL (76% versus 41% in those <4 log IU/mL, P

= 0.002) and those with HIV infection (70% versus 42%, P = 0.002). No differences were observed in the proportions with plasma IP-10 level ≥150 pg/mL by sex, age, or estimated duration of HCV infection. In adjusted logistic regression 20s Proteasome activity analyses (Table 2), HCV RNA >6 log IU/mL (versus <4 log adjusted odds ratio [AOR] 6.11; 95% CI: 2.11, 17.69) and HIV infection (AOR 2.11; 95% CI: 0.96, 4.61) were independently associated with plasma IP-10 levels ≥150 pg/mL, while individuals of Aboriginal ethnicity were less likely to have plasma IP-10 levels ≥150 pg/mL at the time of acute HCV detection (AOR 0.17; 95% CI: 0.05, 0.58). No difference was observed in the frequency of IL28B rs12979860 CC genotype among Cytoskeletal Signaling inhibitor Aboriginals and non-Aboriginals (39% versus 53%, P = 0.254). Plasma IP-10 levels were monitored longitudinally in 20 untreated individuals with acute HCV (eight with clearance, Fig. 3; Supporting Fig. 2). Although

IP-10 levels generally mirrored HCV RNA levels, there was no clear pattern that could predict clearance or persistence. Among the 245 participants who were positive for HCV RNA at the time of acute HCV detection, 214 were either untreated (n = 137) or had chronic infection (persistent HCV RNA and estimated duration of infection ≥26 weeks) at the time of treatment initiation (n = 77) and formed the study population for assessment of spontaneous clearance (Fig. 1). In this group who were HCV RNA-positive at acute HCV detection (n = 214), spontaneous clearance occurred in 14% (29 of 214) of individuals. Among those with available plasma IP-10 levels at acute HCV

detection (n = 187), individuals who failed to clear HCV spontaneously had significantly higher mean plasma IP-10 levels at acute HCV detection than those with spontaneous viral clearance (248 ± 32 versus 142 ± 22 pg/mL, P = 0.008; Fig. 4A); however, the median plasma IP-10 levels did not differ (133 versus 103 pg/mL, P = 0.430). Although one individual had a very high IP-10 value (3,071 pg/mL), mean IP-10 levels remained significantly higher in those without clearance excluding this individual (230 ± 27 versus 上海皓元医药股份有限公司 142 ± 21, P = 0.010). ROC curve analysis identified an IP-10 level of 380 pg/mL as the most useful threshold associated with spontaneous clearance. No patients with a baseline IP-10 ≥380 pg/mL (0 of 22) achieved spontaneous clearance, compared to 16% (27 of 165) of those with IP-10 levels <380 pg/mL (P = 0.048; Fig. 4B). There was no significant difference in the proportion with spontaneous clearance stratified by plasma IP-10 levels above and below 150 pg/mL (15%, <150 pg/mL, versus 13%, ≥150 pg/mL; P = 0.835). Other factors associated with spontaneous viral clearance were also examined (Table 3).

Although FasL is shown to induce Bid-independent apoptosis in hepatocytes cultured on collagen, the sensitizing effect of TNFα is clearly dependent on Selleckchem PARP inhibitor Bid. Moreover, both c-Jun N-terminal kinase activation and Bim, another B cell lymphoma 2 homology domain 3 (BH3)–only protein, are crucial mediators of TNFα-induced apoptosis sensitization. Bim and Bid activate the mitochondrial amplification loop and induce cytochrome c release, a hallmark of type II apoptosis. The mechanism of TNFα-induced sensitization is supported by a mathematical model that correctly reproduces the biological

findings. Finally, our results are physiologically relevant because TNFα also induces sensitivity to agonistic anti-Fas–induced liver damage. Conclusion: Our data suggest that TNFα can cooperate with FasL to induce hepatocyte apoptosis by activating the BH3-only proteins Bim and Bid. (HEPATOLOGY 2011.) Enhanced apoptosis is critically involved in many acute and chronic liver diseases, and hepatocytes are the main cell type undergoing massive cell death during liver injury. This process is regulated by a complex network of soluble and cell-associated apoptotic and inflammatory signals.1 It is therefore increasingly important to obtain insight into the mechanistic interplay of these signals to define new therapeutic strategies.

In the liver, apoptosis www.selleckchem.com/products/azd-1208.html is mainly initiated by the death receptor ligands Fas ligand (FasL; CD95L) and tumor necrosis factor α (TNFα).2 After

ligand binding, death receptors recruit the adaptor Fas-associated death domain (FADD) and procaspase-8 to their intracellular face, and this forms the death-inducing signaling complex (DISC).3 By this assembly, procaspase-8 is autoprocessed and activated, and it can then trigger two different apoptotic signaling pathways. In so-called type I cells, such as lymphocytes, active caspase-8 directly cleaves and activates procaspase-3 to induce efficient cell death execution.4 In type II cells, such as hepatocytes, apoptosis induction first requires caspase-8–mediated cleavage of Bid into its truncated form [truncated Bid (tBid)]. tBid belongs to the subclass of B cell lymphoma 2 homology domain 3 (BH3)–only B MCE cell lymphoma 2 (Bcl2) family members (e.g., Bim, p53–up-regulated modulator of apoptosis, and Noxa), which sense apoptotic stimuli and convey the death signals for B cell lymphoma 2–associated X protein (Bax) and B cell lymphoma 2 homologous antagonist/killer (Bak) activation on mitochondria. Although it is still unclear how this activation occurs,5 it has become well accepted that Bax and Bak are essential for mitochondrial membrane permeabilization (MOMP) and the release of apoptogenic factors such as cytochrome c and second mitochondria-derived activator of caspases (Smac)/diablo homolog (Diablo).

32 Although this study was not designed to clarify the pathogenetic link between adipose-related features, VAI score in particular, and

viral load in G1 CHC, a few hypotheses would agree with the data in the literature. Experimental and clinical studies have shown a direct relationship between viral load and IR in CHC.27 We could not confirm this association in our study, probably due to the demographic, metabolic, and histological characteristics of the patients. However, it is possible to speculate that because HCV is able to induce hepatic and peripheral IR,33, 34 it could similarly HIF inhibitor interfere with adipose tissue function. HCV could interfere with adipocyte function indirectly, by favoring proinflammatory cytokine production35 and by prompting macrophage fat infiltration, and directly, by theoretical infection of adipose tissue, and by interfering with peroxisome proliferator-activated receptor gamma expression,36 a well-known modulator of adipose tissue homeostasis. In addition, we cannot rule out the possibility that the proinflammatory status, as well as the higher availability of fatty substrates due to adipose dysfunction, are able to stimulate HCV RNA replication. Figure 4 displays

the putative mechanistic relationship linking HCV, host metabolism, and VAI. Finally, we have shown that both Cobimetinib datasheet IR and VAI score had a nonsignificant trend for predicting failure of SVR achievement after standard antiviral therapy, and that after correction for steatosis, only the latter was significantly associated with a lower likelihood of virological clearance, suggesting an indirect role of both VAI score and IR on SVR achievement by steatosis induction. The main limitation of this study lies in its cross-sectional nature, making it impossible to dissect the temporal relationship 上海皓元医药股份有限公司 between IR, VAI score, and steatosis, and between VAI score and viral load in G1 CHC patients. A further methodological question is the potentially limited external validity of the results for different populations

and settings. Our study included a cohort of European patients, largely overweight, who were enrolled in a tertiary referral center for liver disease, limiting the broad application of the results. Another limitation lies in the interobserver variability of the evaluation of hepatic necroinflammatory activity, which could affect the reproducibility of our results.37 Lack of data on the serum levels and on adipose expression of proinflammatory cytokines and adipocytokines may also have affected our interpretation of the results. In conclusion, VAI, a new index of both fat function and distribution, appears to be independently associated with steatosis and necroinflammatory activity in G1 CHC patients and has a direct correlation with HCV viral load. These data suggest a direct role of adipose tissue in liver damage and a possible interference of HCV with adipocyte function.

All pneumatic dilations were performed under fluoroscopic guidance in the supine position. All patients were given topical anesthesia of the pharynx with 2% lidocaine. After a 260 cm-long stiff exchanged wire (Terumo, Tokyo, Japan) was passed through the cardia and into the gastral cavity, the balloon catheter was advanced

over the guide wire and positioned across the diaphragmatic hiatus using the radiopaque markers as guides. The balloon was then inflated for 30–60 s at 9–15 psi until obliteration of the waist. A gastrografin swallow was performed immediately after dilation to exclude any esophageal perforation. If necessary, a repeat dilation was performed. (Fig. 1) Patients were instructed to ingest cold fluid foods for the first 3 days, followed by semisolid or normal foods after the procedure. Routinely, anti-inflammatory agents or stypticum Ku-0059436 nmr were not used to prevent complications. The stent we used in this study (Zhiye Medical Instruments, Guangzhou, China and Youyan Yijin Advanced Materials, Beijing, China) is knitted from a 0.25-mm diameter, non-magnetic memory Ni–Ti alloy wire with a 25–33°C recovery temperature. This stent

consists of a self-expanding, cross-linked, stainless cylindrical mesh body with a 35-mm diameter cydariform and tubaeform at its head and tail, and only the stent body and the tubaeform tail were covered with a silica gel membrane. The diameter of the main stent body was 30 mm, and the total stent length was 80 mm when fully expanded. A trisected antireflux valve was added at the conjunction of the stent body and the tail. Stent wires selleck chemicals were processed and coated with an anti-erosion layer to prevent gastric acid corrosion. Each stent was compressed and deployed by an 8-mm (∼24 Fr) delivery system, and the whole stent body was radiopaqued under the fluoroscope to facilitate accurate positioning. Preparation before stent insertion was the same as pneumatic dilation. After topical anesthesia of the pharynx, the 260-cm long, stiff exchanged wire was inserted through the mouth

into 上海皓元 the stomach under the guidance of fluoroscopy. Along with the guide wire, the stent delivery system was introduced through the guide wire to pass through the cardia. After the stent was positioned according to the osseous anatomy, based on the previous esophagography images under fluoroscopic guidance, the support catheter was held and the sheath was withdrawn to release the stent. After the stent expansion, a repeated barium meal examination was performed to confirm the stent expansion degree and to exclude any esophageal perforation. (Fig. 1) The patients were instructed to ingest thermal semisolid or fluid foods for the first 3 days to prompt full expansion of the stent. Routinely, anti-inflammatory agents and stypticum were used to prevent complications. The inserted stent was removed 3–7 days after the procedure via endoscope.

The lifetime risk of HBV carriers to develop cirrhosis, liver failure, or HCC may be as high as 15% to 40%.[1-3] The identification of risk factors for the development of advanced liver disease, including cirrhosis and HCC, in HBV carriers is important for implementing effective Rucaparib treatment. Recently, several qualitative and quantitative hepatitis B viral factors affecting the prognosis of HBV carriers have been identified.[3, 4] Among these viral factors, baseline serum HBV-DNA level is the main driving force for cirrhosis and HCC development in adult HBV

carriers.[5, 6] Recently, quantitative HBsAg (qHBsAg) has been increasingly recognized to be a promising biomarker to predict both favorable and adverse outcomes of HBV carriers. Based on the weight of each risk factor associated with HBV-related HCC and through a stratification process, it is possible to identify HBV carriers who are at an increased risk of disease progression and HCC development (Table 1). In this article, hepatitis B viral factors

leading to disease progression Fulvestrant and the risk stratification for HBV-related HCC will be reviewed and discussed. Low serum level of HBV-DNA Low serum level of HBsAg HBV genotype C/D BCP A1762T/G1764A mutation Pre-S deletion High serum level of HBV-DNA High serum level of HBsAg According to the divergence in the entire HBV genomic sequences, at least 10 HBV genotypes (A to J) have been defined.[7-9] Several studies suggested that HBV genotype can influence the long-term outcomes of HBV infection. For

example, HBV genotype C and D patients, compared with genotype A and B patients, have late or absent HBeAg seroconversion after multiple hepatitis flares that accelerate the progression of chronic hepatitis.[10-12] Most case–control medchemexpress studies and community-based prospective cohort study indicated that patients with genotype C HBV infection have a higher risk of cirrhosis and HCC than those with genotype B infection.[13-17] In addition, several reports have also shown that HBV genotype B was associated with HCC development in young non-cirrhotic patients. Whereas genotype C was associated with HCC development in old cirrhotic patients.[13, 18, 19] Due to the spontaneous error of viral reverse transcription, HBV mutant strains occur during the natural course of infection as well as with antiviral therapy. Mutations in precore, core promoter, and deletion mutation in pre-S/S genes have been reported to be associated with the progression of liver disease, including cirrhosis and HCC. Previous studies revealed that dual mutations in basal core promoter (BCP) A1762T/G1764A were strongly associated with the risk of HCC development.

Several target genes of miR-21 were

previously reported.20 However, to potentially identify new targets of miR-21 involved in liver regeneration, we chose an unbiased Doxorubicin order approach. We first used the TargetScan algorithm to identify genes targeted by miR-21 in both mice and humans.23 Focusing on conserved miR-21 targets not only increased the probability of target gene prediction but also assured that our results could be extended to human liver regeneration. We then used the PicTar algorithm to scan the 3′UTR of the conserved miR-21 target genes and eliminate genes with a lower score or free energy (Supporting Information Table 2).24 Our findings of impaired G1 to S phase progression in miRNA-deficient hepatocytes and induction of miR-21 at a time when entry into S phase is negotiated suggested that miR-21 acts to promote liver regeneration. Therefore, among the 63 genes meeting the selection criteria, we focused on 17

genes PD-0332991 manufacturer with established negative effects on proliferation (Supporting Information Table 2). Among these genes were the previously reported miR-21 targets Timp3, Reck, and Pdcd4.20 Potential new miR-21 targets included Tgfbi and Smad7, components of the transforming growth factor β (TGFβ) signaling pathway, which is known to restrict liver regeneration.25 Most interestingly, however, our search retrieved Btg2, a gene restraining G1 to S phase transition that, paradoxically, is induced by 2/3 PH.18 Because Btg2 also had the highest score and free energy of the predicted conserved miR-21 target genes with established proliferation-inhibiting function, we investigated whether it is directly targeted by miR-21 (Supporting Information Fig. 4A, Supporting Information MCE公司 Table 2). BTG2 inhibits proliferation

by interfering with activating phosphorylation of FoxM1.26 FoxM1 is activated after 2/3 PH and its deficiency impairs DNA synthesis and Ccnb1 gene expression in regenerating mouse hepatocytes.26, 27Btg2 was previously reported to be immediately induced and peak at 4 hours after 2/3 PH.18 When we investigated the expression of Btg2 at later stages, we found that it returns to baseline levels between 6 and 18 hours after 2/3 PH. Thus, the expression pattern of Btg2 is the mirror opposite of that of miR-21 (Fig. 3A). Analysis of Dgcr8del/fl, Alb-Cre+/− mice lacking oval cells showed that miR-21 is mainly expressed in hepatocytes in the liver (Fig. 3B). Taken together with the similar nature of the cell cycle defect in hepatocytes with FoxM1 or global miRNA deficiency (Fig. 1A,B), our findings suggested that miR-21 antagonizes Btg2 in regenerating hepatocytes to facilitate efficient cell cycle progression. Indeed, Btg2 messenger RNA (mRNA) levels and activity of a reporter gene linked to its 3′UTR readily responded to miR-21 mimic or inhibitor transfection into well-differentiated mouse hepatoma cells (Fig. 3C). These manipulations also caused induction or suppression of the FoxM1 target gene Ccnb1, respectively (Fig. 3D).

However, adverse effects of this therapy that Depression or neuropsychiatric symptoms make it difficult to be completed. The aim of study

is to evaluate neuropsychiatric symptoms with antiviral therapy and its correlation of effects on cerebral glucose metabolism (CMRglu) in chronic hepatitis C patients. Methods: Seven patients with chronic hepatitis C undergoing antiviral therapy (Interferon and Ribavirin) were prospectively evaluated neuropsychiatric symptoms by neuropsychiatric test such as Digit symbol test(DST), Block design test (BDT), and Self-rating Depression Scale(SDS).We assessed cerebral glucose metabolism (CMRglu) using [18F] deoxyglucose positron emission tomography (FDG-PET) before and the 8th weeks of treatment and after the therapy. Results: Compare to before and 8th weeks of treatment, SDS of all patients were worsened. FAK inhibitor CMRglu of six patients were 1-24% decreased in whole of the brain region. CMRglu of one patient was increased in the all of brain regions. There were no trend of result that DST and BDT before and 8th weeks of treatment. Compare to before and after the therapy,

SDS of all three patients after the treatment were recovered within normal range. CMRglu of all of patients were 2-106% increased from 8th week of treatment in learn more whole of the brain. CMRglu of all of three patients were recovered and increased -8~73%from MCE before the treatment. Conclusion: These results suggest that antiviral therapy affects on cerebral glucose metabolism and Depression or neuropsychiatric symptoms in chronic hepatitis C patients. This depression or neuropsychiatric symptoms should be reversible. We believe that Cerebral glucose metabolism is affected by antiviral therapy and that might be reversible. It might be associated with depression or neuropsychiatric symptoms. Key Word(s): 1. antiviral therapy; 2. cerebral metabolism; 3. psychiatric symptoms; 4. FDG-PET; Presenting Author: JING LAI Additional Authors: HAI-XIA SUN, KA ZHANG, FAN ZHANG,

HONG DENG Corresponding Author: JING LAI Affiliations: Department of Infectious Diseases, The Third Affiliated Hospital,Sun Yat-Sen University; Department of Infectious Diseases, The People’s Hospital of Yangshan City Objective: HBV related acute-on-chronic liver failure (ACLF) is a clinical syndrome where acute hepatic insult manifesting as jaundice (serum total bilirubin (TBil) ≥ 5 mg/dL and coagulopathy (international normalized ratio (INR) ≥1.5), complicated within 4 weeks by ascites and/or encephalopathy in a patient with chronic HBV infection. But the correlation of hepatitis B surface antigen (HBsAg) level with HBV DNA, ill severity in hepatitis B e antigen (HBeAg) negative ACLF has been scarcely investigated.

46, 47 This study undoubtedly has some limitations. In the current version of the ITA.LI.CA database, data regarding tumor recurrence after treatment are not

available, and therefore in this study the influence of alpha-fetoprotein levels on some important composite find more endpoints such as recurrence plus death could not be assessed. Furthermore, as expected in our country, hepatitis virus infection was the cause of cirrhosis in most cases, and therefore it remains to be established whether these results can be generalized to HCC patients with other etiologies.48, 49 Lastly, although the ITA.LI.CA database includes more than 3,000 HCC patients, the selection OTX015 price criteria for this study were very strict, and therefore the study population was limited to 205 patients. A post-hoc analysis shows that this sample size had a statistical power of 22% to detect a difference between the observed 5-year survival rates of patients with alpha-fetoprotein below (61%) and above (55%) 20 ng/mL. With such survival rates, a sample size

of 2,118 patients with compensated cirrhosis and single, small HCC treated with curative intent, derived from a population of more than 30,000 patients with HCC, would have been needed to achieve a power of 80%. All in all, we feel that even these figures, if framed in the context of clinical practice, confirm the bland prognostic potential of alpha-fetoprotein in the subset of patients we selected. In conclusion, we found that serum alpha-fetoprotein has no prognostic role in compensated cirrhosis patients with a single, small HCC diagnosed during surveillance and treated with curative intent. These findings emphasize the futility of serum alpha-fetoprotein determination in a clinical setting where surveillance for HCC may provide its maximal benefit in terms of amenability to curative treatment and patients survival. New, more accurate markers are therefore needed to improve our current ability

to predict the outcome of patients diagnosed with early HCC. Other members of the ITA.LI.CA group: Dipartimento di Medicina Clinica, Alma Mater Studiorum, MCE Università di Bologna, Italy: Mauro Bernardi, Maurizio Biselli, Romina Cassini, Paolo Caraceni, Marco Domenicali, Virginia Erroi, Marta Frigerio, Annagiulia Gramenzi, Barbara Lenzi. Dipartimento di Medicina Interna, dell’Invecchiamento e Malattie Nefrologiche, Azienda Ospedaliero-Universitaria di Bologna, Italy: Donatella Magalotti. Divisione di Medicina, Azienda Ospedaliera Bolognini, Seriate, Italy: Claudia Balsamo, Maria Di Marco, Elena Vavassori. Divisione di Medicina, Ospedale Treviglio-Caravaggio, Treviglio, Italy: Lodovico Gilardoni, Mario Mattiello.

46, 47 This study undoubtedly has some limitations. In the current version of the ITA.LI.CA database, data regarding tumor recurrence after treatment are not

available, and therefore in this study the influence of alpha-fetoprotein levels on some important composite Ferroptosis phosphorylation endpoints such as recurrence plus death could not be assessed. Furthermore, as expected in our country, hepatitis virus infection was the cause of cirrhosis in most cases, and therefore it remains to be established whether these results can be generalized to HCC patients with other etiologies.48, 49 Lastly, although the ITA.LI.CA database includes more than 3,000 HCC patients, the selection http://www.selleckchem.com/products/torin-1.html criteria for this study were very strict, and therefore the study population was limited to 205 patients. A post-hoc analysis shows that this sample size had a statistical power of 22% to detect a difference between the observed 5-year survival rates of patients with alpha-fetoprotein below (61%) and above (55%) 20 ng/mL. With such survival rates, a sample size

of 2,118 patients with compensated cirrhosis and single, small HCC treated with curative intent, derived from a population of more than 30,000 patients with HCC, would have been needed to achieve a power of 80%. All in all, we feel that even these figures, if framed in the context of clinical practice, confirm the bland prognostic potential of alpha-fetoprotein in the subset of patients we selected. In conclusion, we found that serum alpha-fetoprotein has no prognostic role in compensated cirrhosis patients with a single, small HCC diagnosed during surveillance and treated with curative intent. These findings emphasize the futility of serum alpha-fetoprotein determination in a clinical setting where surveillance for HCC may provide its maximal benefit in terms of amenability to curative treatment and patients survival. New, more accurate markers are therefore needed to improve our current ability

to predict the outcome of patients diagnosed with early HCC. Other members of the ITA.LI.CA group: Dipartimento di Medicina Clinica, Alma Mater Studiorum, 上海皓元 Università di Bologna, Italy: Mauro Bernardi, Maurizio Biselli, Romina Cassini, Paolo Caraceni, Marco Domenicali, Virginia Erroi, Marta Frigerio, Annagiulia Gramenzi, Barbara Lenzi. Dipartimento di Medicina Interna, dell’Invecchiamento e Malattie Nefrologiche, Azienda Ospedaliero-Universitaria di Bologna, Italy: Donatella Magalotti. Divisione di Medicina, Azienda Ospedaliera Bolognini, Seriate, Italy: Claudia Balsamo, Maria Di Marco, Elena Vavassori. Divisione di Medicina, Ospedale Treviglio-Caravaggio, Treviglio, Italy: Lodovico Gilardoni, Mario Mattiello.

46, 47 This study undoubtedly has some limitations. In the current version of the ITA.LI.CA database, data regarding tumor recurrence after treatment are not

available, and therefore in this study the influence of alpha-fetoprotein levels on some important composite AP24534 price endpoints such as recurrence plus death could not be assessed. Furthermore, as expected in our country, hepatitis virus infection was the cause of cirrhosis in most cases, and therefore it remains to be established whether these results can be generalized to HCC patients with other etiologies.48, 49 Lastly, although the ITA.LI.CA database includes more than 3,000 HCC patients, the selection find more criteria for this study were very strict, and therefore the study population was limited to 205 patients. A post-hoc analysis shows that this sample size had a statistical power of 22% to detect a difference between the observed 5-year survival rates of patients with alpha-fetoprotein below (61%) and above (55%) 20 ng/mL. With such survival rates, a sample size

of 2,118 patients with compensated cirrhosis and single, small HCC treated with curative intent, derived from a population of more than 30,000 patients with HCC, would have been needed to achieve a power of 80%. All in all, we feel that even these figures, if framed in the context of clinical practice, confirm the bland prognostic potential of alpha-fetoprotein in the subset of patients we selected. In conclusion, we found that serum alpha-fetoprotein has no prognostic role in compensated cirrhosis patients with a single, small HCC diagnosed during surveillance and treated with curative intent. These findings emphasize the futility of serum alpha-fetoprotein determination in a clinical setting where surveillance for HCC may provide its maximal benefit in terms of amenability to curative treatment and patients survival. New, more accurate markers are therefore needed to improve our current ability

to predict the outcome of patients diagnosed with early HCC. Other members of the ITA.LI.CA group: Dipartimento di Medicina Clinica, Alma Mater Studiorum, medchemexpress Università di Bologna, Italy: Mauro Bernardi, Maurizio Biselli, Romina Cassini, Paolo Caraceni, Marco Domenicali, Virginia Erroi, Marta Frigerio, Annagiulia Gramenzi, Barbara Lenzi. Dipartimento di Medicina Interna, dell’Invecchiamento e Malattie Nefrologiche, Azienda Ospedaliero-Universitaria di Bologna, Italy: Donatella Magalotti. Divisione di Medicina, Azienda Ospedaliera Bolognini, Seriate, Italy: Claudia Balsamo, Maria Di Marco, Elena Vavassori. Divisione di Medicina, Ospedale Treviglio-Caravaggio, Treviglio, Italy: Lodovico Gilardoni, Mario Mattiello.