In addition, episodes of serious bleeding may result in long periods of inactivity. Finally, co-morbidities such as HIV and hepatitis C and their treatment may lead to bone mass loss. Thus, haemophilia has a number of predisposing factors associated with decreased BMD and such patients are at higher risk than the general population to develop osteoporosis [28,29]. One of the first clinical studies in haemophilia involved 19 men with severe haemophilia A (HIV negative, but 18/19 were positive Selleck PLX4032 for hepatitis C antibodies) [30]. Compared with age/sex matched controls BMD was significantly lower in the lumbar spine

(P = 0.018) and the femoral neck (P < 0.0005) in patients with haemophilia. Serum levels of total alkaline phosphatases and gamma-glutamyl

transferase were markedly elevated. This led the authors to suggest that the osteopenia observed in this haemophiliac cohort may be due to liver dysfunction, although they acknowledged that other factors such as relative immobility may TSA HDAC also be relevant [30]. More recently, Gerstner and colleagues [28] studied 30 patients with moderate to severe haemophilia to ascertain risk factors associated with decreased BMD. In this trial 70% of haemophiliac patients had decreased BMD, 43% had osteopenia and 27% osteoporosis. Factors associated with increased bone loss were: 1  Decreased joint mobility (P = 0.046). Table 3 presents findings from some representative studies on adults and children with haemophilia in which BMD data were reported [31–35]. They all show that BMD is lower in haemophiliac patients compared with controls. Pathophysiological changes associated with osteoporosis are almost irreversible as they involve loss of bone microarchitecture, and therefore preventative strategies in patients with haemophilia are the preferred option. There is good evidence that long-term factor prophylaxis from early childhood to prevent bleeding helps preserve 上海皓元 normal BMD [29]. In those countries where primary prophylaxis is not economically viable prompt treatment

with clotting factor to stop the bleeding is advocated, followed by stabilization of the joint. After the bleeding is resolved early mobilization is recommended. Physicians should then encourage participation in suitable regular physical activities [35,36]. Figure 2 outlines various treatment options for haemophiliac men with low BMD. In those with osteopenia various non-prescription medications and lifestyle changes such as calcium, vitamin D and increased exercise may help. However, in patients with osteoporosis drug therapy is required and a number of drug classes are available including the bisphosphonates, estrogens, calcitonins and monoclonal antibodies. 1  Osteoporosis can cause significant morbidity and mortality in the general population.

These values were averaged for each photograph and the relative fluorescence of all photographs was averaged for each replicate. Mean fluorescence for wounded and sham-wounded samples incubated without DCFH-DA were subtracted from the values for samples incubated with DCFH-DA to correct for background fluorescence. When 10% of replicates were re-measured, they were on average

<5% different from the original measured value. Cellular accumulation of strong oxidants after grazing was determined for P. decipiens, the only species of macroalgae AP24534 included in this study that is palatable to the amphipod G. antarctica, by measuring the oxidation of DCFH in vivo. Circular, paired P. decipiens samples (n = 5, 8–10 mm diameter) were excised with a cork borer 24–48 h prior to experimentation and held in flowing seawater until use. Both samples from each individual were placed in a plastic bottle containing five G. antarctica in filtered seawater. Bottles were floated in an aquarium containing flow-through ambient seawater (~1.5°C) for 2 h to allow grazing. Samples were removed from grazers and one sample was incubated

with DCFH-DA, while its paired sample was incubated in the same manner, but without DCFH-DA, as described previously. Samples were viewed microscopically and imaged according to the previous section with the exception that three photographs were taken of each sample, each photograph containing Talazoparib concentration a haphazardly chosen section of grazed

edge with a substantial portion of inner, ungrazed thallus. Since G. antarctica feed on edges (authors’ personal observations), photographs were analyzed for brightness using ImageJ as above, but the five randomly determined sections analyzed for grazed tissue were chosen from directly along the grazed thallus edge and the five randomly determined sections analyzed for control tissue were chosen from directly along the side of the photograph nearest the inner, ungrazed thallus. Strong oxidants in the seawater medium were quantified medchemexpress by measuring the oxidation of DCFH in the presence of esterase and peroxidase using a fluorometer (following Weinberger et al. 1999) before and 1 min after wounding. Paired samples of A. mirabilis, H. grandifolius, T. antarcticus (n = 10), and D. anceps and P. decipiens (n = 9) were placed in 15 mL SFSW under constant rotation on ice. Samples were wounded by multiple punches using a sterile plastic 5 mL pipette tip over the entire thallus surface. Paired, control tissue was treated in the same way as wounded samples with the exception of wounding. To sample, 1,000 μL of the seawater medium was combined with either 500 U catalase (Sigma C9322) in DI or the same volume of DI water.

73 copies/mL (4.04-9.11 copies/mL), 3.58 IU/mL (1.17-5.10 IU/mL), and 1.71 Paul Ehrlich (PE) IU/mL (−0.64 to 2.63 PE IU/mL), respectively. For the prediction of VR (HBV DNA

< 60 copies/mL at 24 months) in HBeAg(+) LY294002 purchase patients, baseline alanine aminotransferase (P = 0.013), HBV DNA (P = 0.040), and qHBsAg levels (P = 0.033) were significant. For the prediction of VR, the area under the curve for the baseline log qHBsAg level was 0.823 (P < 0.001); a cutoff level of 3.98 IU/mL (9550 IU/mL on a nonlogarithmic scale) yielded the highest predictive value with a sensitivity of 86.8% and a specificity of 78.9%. As for SR (HBeAg loss at 24 months), the reduction of qHBeAg was significantly greater in the SR(+) group versus the SR(−) group. The sensitivity and specificity were 75.0% and 89.8%, respectively, with a decline of 1.00 PE IU/mL at 6 months. With ETV therapy, the correlation between HBV DNA and qHBsAg peaked at 6 months in HBeAg(+) patients. Conclusion: Both qHBsAg and qHBeAg decreased significantly with ETV therapy. The baseline qHBsAg levels and the on-treatment decline of qHBeAg in HBeAg(+) patients were proven to be highly useful in predicting VR and SR, respectively. The determination of qHBsAg and qHBeAg can help us to select the appropriate strategy for the management of patients with CHB. However, the dynamic interplay between qHBsAg,

qHBeAg, and HBV DNA during antiviral therapy remains to be elucidated. (Hepatology 2011;) Chronic infection with hepatitis B virus (HBV) is a worldwide health problem, with more than 400 million people thought to www.selleckchem.com/products/rxdx-106-cep-40783.html be infected. Moreover, these patients are at increased risk for disease progression to cirrhosis and hepatocellular carcinoma.1 Large cohort studies have shown that elevated levels of HBV DNA are closely associated with the development of cirrhosis and hepatocellular carcinoma, and reducing HBV DNA to undetectable levels is one of the primary goals in patients receiving antiviral therapy.2,

3 The current gold standard in monitoring viral loads is real-time 上海皓元 polymerase chain reaction (PCR), which offers high sensitivity and accuracy.4 Data from these assays reflect the disease status and are employed by most clinical studies.2, 3 The shortcomings of PCR, however, are its relatively high cost and unavailability in some areas. Moreover, viral activity can still be monitored in patients with undetectable HBV DNA through the measurement of hepatitis B surface antigen (HBsAg) and/or hepatitis B e antigen (HBeAg) titers. HBsAg has long served as a qualitative serological marker for the diagnosis of HBV. Recent advances in the development of HBsAg assays with a quantitative, analytical approach have led to the exploration of its potential role in monitoring disease and therapy outcome. Since 2004, when Deguchi et al.

However, because the net result of global miRNA deficiency in hepatocytes was impaired

S phase Y-27632 price entry, loss of miR-378 appears to be insufficient to compensate loss of miR-21 during liver regeneration. Specific inhibition of miR-21 and miR-378 in vivo could be used to delineate their individual contributions to regulation of liver regeneration.30 Because a single miRNA typically targets many genes, the effects of miR-21 and miR-378 during liver regeneration are most likely not restricted to inhibition of Btg2 and Odc1. For example, in addition to Tgfbi and Smad7, the TargetScan algorithm predicts Tgfbr2, Acvr1c (activin A receptor 1C), and Acvr2a (activin A receptor 2A) as direct and conserved miR-21 targets

involved in TGFβ and activin signaling. miR-21 might target these genes to limit the inhibitory effect of TGFβ and activin signaling on G1 to S phase transition of hepatocytes after 2/3 PH.25 The levels of the proliferation-promoting gene Ccnd1 were increased in hepatocytes with global miRNA deficiency before 2/3 PH. Our selleck miRNA profiling revealed that miR-16, an miRNA known to inhibit Ccnd1 in the prostate, is expressed in the liver.31 Thus, loss of miR-16 may explain de-repression of Ccnd1 in Dgcr8del/fl, Alb-Cre+/− mice. In analogy, it is possible that loss of other miRNAs normally expressed in hepatocytes but not induced by 2/3 PH may contribute to impaired liver regeneration in Dgcr8del/fl, Alb-Cre+/− mice. This could explain the spontaneous oval cell activation in a subset of Dgcr8del/fl, Alb-Cre+/− mice. In addition, mouse miRNAs continue to be identified and we cannot rule out that miRNAs not represented on our arrays play a role in liver regeneration. However, in contrast to findings after DGCR8 inactivation in the skin,32 miR-21 was depleted in whole liver samples of mice 上海皓元医药股份有限公司 with hepatocyte-specific DGCR8 deficiency. This shows that miR-21 is mainly

expressed in hepatocytes in the liver and supports our conclusion that miR-21 directly regulates cell cycle progression in hepatocytes. Specific induction of miR-21 in G1 phase after 2/3 PH and impaired G1 to S phase transition in both hepatocytes with global miRNA deficiency and in those with FoxM1 deficiency further suggest that miR-21 plays a leading role in miRNA regulation of liver regeneration. Our analyses focused on miRNA target genes that are conserved between mouse and human. Although little has been reported about miR-378′s regulation or function, the expression of miR-21 is known to be increased in primary human liver cancer.33, 34 Moreover, miR-21 has been shown to promote proliferation of human liver cancer cell lines by inhibition of the phosphatase and tensin homolog (PTEN) tumor suppressor.33 Therefore, it is likely that miR-21 inhibits Btg2, and potentially other regulators of hepatocyte proliferation, also in human liver regeneration. The authors thank Dr.

Our data show that this is not the case, implying the lack of any major iron regulatory role of putative muscle-derived sHjv under physiological conditions. We do not expect that the small genetic background differences of the mice would substantially affect iron parameters, as between distinct pure inbred strains.43, 44 Nevertheless, direct measurement of sHjv levels in the serum of mice with tissue-specific disruption of Hjv and wildtype controls, as well as assessment of its capacity to inhibit

BMP signaling, are required to further validate the origin and the function of circulating sHjv. In conclusion, our overall data demonstrate that hepatic Hjv is necessary and sufficient to prevent iron overload and control hepcidin expression, whereas muscle Hjv is dispensable. Similar conclusions were drawn in a report that was recently published while this http://www.selleckchem.com/products/bgj398-nvp-bgj398.html article was under review.45 We thank Dr. Mike Rudnicki (University of Ottawa) for the MCK-Cre mice and Dr. Nancy EPZ-6438 concentration Andrews (Duke University) for the Hjv−/− mice. We also thank Dr. Naciba Benlimame for assistance with histology. K.P. holds a Chercheur National career award from the Fonds de la Recherche en Santé du Quebéc (FRSQ). K.G. is supported by doctoral awards from the J. Latsis and A. Onassis Public Benefit Foundations. Additional Supporting Information may be found in the online version of this article.

MCE公司 “
“Aim:  The aim of this prospective study was to determine cow’s milk protein allergy (CMPA) cases in a tertiary care hospital in India and to study its clinical presentations and outcome following treatment. Methods:  Consecutive children with chronic diarrhea from June 2004 to December 2007 were evaluated with hemogram, anti-endomysial antibody, upper gastrointestinal endoscopy, sigmoidoscopy and intestinal biopsies. Initial diagnosis of CMPA was based on characteristic intestinal biopsy (> 6 eosinophils/HPF) and diagnosis was confirmed by positive milk challenge. Results:  Forty CMPA cases (25 boys, with a mean age of 17.2 ± 7.8 months and symptom duration

of 8.3 ± 6.2 months) presented with diarrhea (bloody in 16, watery in 16, combined in three, recurrent hematemesis in two, rectal bleeding in one and one case each with pain in the abdomen with vomiting and anemia with occult bleeding). Sigmoidoscopy revealed aphthous ulcers in 82% of cases and rectal biopsy was positive in 97% of cases. All children improved on a milk-free diet. Milk challenge was positive in 100% of cases when it was done early (within 6 months). On follow up of 15 ± 9 months, milk was successfully restarted in 25 cases after a median milk-free period of 15 months, 10 were still on a milk-free diet and five were lost to follow up while on a milk-free diet. Conclusions:  CMPA is not uncommon in a developing country such as India.

Genetic relationships between individuals can, in turn, affect BTK inhibitor their social behaviour and the emergent

social organization of the population. Using combination of behavioural and genetic data from the wild boar Sus scrofa population in Białowieża Primeval Forest (eastern Poland), we evaluated the socio-genetic structure of wild boar groups, the spatial genetic structure of the population and dispersal patterns. We found that wild boar post-weaning movements were largely spatially limited to the vicinity of maternal range, with female boars showing a tendency to settle in the direct neighbourhood of the kin and male boars dispersing further away from the natal area. Consequently, such dispersal patterns were reflected in the kin-based social organization and the spatial genetic structure of the population, which was manifested at a spatial scale corresponding to the size of a few home ranges (<5 km). A negative relationship between geographic distance and genetic relatedness, which was particularly strong in female boars, indicated a presence

of local kin clusters dominated by female boars and the importance of female philopatry in shaping the structure of wild boar population. This was confirmed by the genetic profile and composition of social groups. This study showed the role dispersal decisions can play in the emergence Akt inhibitor of the kin-based and matrilineal social system of wild boars. “
“Morphological adaptations of amphisbaenians for a fossorial life constrain their ecological demands in a greater way than for epigeal reptiles. Studies on the diet of amphisbaenians suggest that most species are generalists, although others seem more selective. However, there is no information on the diet preferences of almost any species because most studies

did not evaluate the availability 上海皓元医药股份有限公司 of prey in the environment. We analysed the spring diet selection of a population of the amphisbaenian Trogonophis wiegmanni from the Chafarinas Islands, in North Africa. We specifically examined diet estimated from faecal material collected from live amphisbaenians and compared diet with the availability of invertebrates in the soil. Results indicate that the diet of T. wiegmanni amphisbaenians consists of some of the types of invertebrates that are more commonly found under rocks used by amphisbaenians, such as insect larvae, snails, isopods, beetles and ants. This diet could be initially considered generalist, and probably opportunistic. However, the comparison of proportions of prey types in the diet and those available in the habitat revealed that T. wiegmanni does not eat prey at random, but selects some particular prey types (insect larvae and pupae and, surprisingly, snails), while others (ants and isopods) are consumed less than expected by their abundance. We did not found differences between sexes or age classes in diet composition.

However, the incidence and prevalence of IBD has increased rapidly over the last two to four decades. These changes may correlate to the life changes in Asia close to the Western country. We will see the characteristic of our IBD patients from colonoscopy findings. Methods: Descriptive study to describe Inflammatory Bowel Disease (IBD) patients characterized who underwent colonoscopy at Cipto Mangunkusumo

Hospital (RSCM) from 2009 until 2013. We had 2,234 patients who underwent colonoscopy from January 2009 until December 2013. Results: From colonoscopy OSI-906 nmr patients, there were normal colonoscopy 14.2%, hemorrhoid 66.3%, tumor 20.5%, polyp 13.2%, IBD 9.8%, infective colitis 6.2% and ileitis 5.7%.The incidence of IBD 9.8% (219 cases of IBD from 2,234). The ulcerative colitis

(UC) was 192 cases (87.7%) which male gender 44.8%, female 55.2%, and average age 47.8 ± 15.75 years. Crohn’s Disease (CD) was 27 cases (12.3%) which male gender 40.7%, female 59.3%, and average age 40.96 ± 16.24 years. There are significant difference for average age between UC and CD (47.81 ± 15.75 vs 40.96 ± 16.25, selleck chemical p = 0.04). Most of the clinical symptoms are chronic diarrhea 78.6%, then abdominal pain 55%, hematochezia 46.8%, abdominal mass 5% and constipation 5%. Chronic diarrhea was the most of clinical symptoms for UC and CD. Conclusion: The incidence of IBD is still only below 10% from colonoscopy patients.

Most of them are UC. Female was a most gender MCE公司 for both UC and CD. There are significant differences for average age between UC and CD. Key Word(s): 1. Colonoscopy; 2. inflammatory bowel disease Presenting Author: TADAKAZU HISAMATSU Additional Authors: JUN MIYOSHI, KATSUYOSHI MATSUOKA, MAKOTO NAGANUMA, KIYOTO MORI, HIROKI KIYOHARA, KOSAKU NANKI, TOMOHARU YAJIMA, YASUSHI IWAO, HARUHIKO OGATA, TOSHIFUMI HIBI, TAKANORI KANAI Corresponding Author: TADAKAZU HISAMATSU Affiliations: Tokyo Dental College Ichikawa General Hospital, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Keio University School of Medicine, Kitasato University Kitasato Institute Hospital, Keio University School of Medicine Objective: We evaluated the clinical efficacy of adalimumab (ADA) for Crohn’s disease (CD) and analyzed predictive factors for induction and maintenance of clinical remission. Methods: We retrospectively reviewed the medical records of 45 patients treated with ADA for CD at Keio University Hospital between October 2010 and October 2013. Clinical remission was defined as a Harvey-Bradshaw index of ≤4. Results: Twenty-eight of 45 patients (62.2%) achieved clinical remission at week-4.

13 Furthermore, TGF-β derived from HSCs acted on tumor cells and governed tumorigenesis in a paracrine fashion, leading to tumor-progressive and autocrine TGF-β signaling in tumor cells.18 Recently, stromal cell-derived factor 1 (SDF-1) was found to be released by MK-8669 datasheet activated HSCs within the liver metastases, and CXCR4 (chemokine [C-X-C motif] receptor 4), the ligand of SDF-1, was found to be expressed in colorectal cancer cells.22In

vitro, this SDF-1/CXCR4 paracrine signaling promoted tumor cell invasion and protected tumor cells from apoptosis.22 In unpublished data, we have also demonstrated that myofibroblast-derived PDGF-BB is a potent survival factor for cholangiocarcinoma cells. Taken together, these data support the concept that activated RGFP966 ic50 HSCs promote tumor cell growth by supplying them with growth factors and cytokines. A high degree of ECM remodeling favors tumor invasion and progression in the liver.23 Both MMP and TIMP2 play a key role in degrading basement membranes, thereby allowing cancer cells to cross tissue boundaries and develop into metastases. By performing

in situ hybridization and zymography, Musso et al. found that both MMP2 and TIMP2 messenger RNA were expressed in activated HSCs at the invasive front of liver metastases, and a higher level of MMP2 messenger RNA and enzymatic activity was detected in liver metastases than in nontumoral liver samples.24, 25 In addition, activated 上海皓元医药股份有限公司 HSCs at the invasive front of human liver metastases were found to express a secreted form of ADAM9 (a disintegrin and metallopeptidase 9).16 This molecule was shown to be able to cleave laminin and bind to tumor cells, thus promoting invasion of tumor cells.16 These data indicate that HSCs may facilitate tumor invasion by producing proteolytic enzymes involved in the degradation of ECM. Activated HSCs are a major cell type for ECM production during the pathogenesis of liver fibrosis,4, 5 and this process may

also contribute to the prometastatic growth effects of HSCs. In the liver tumor microenvironment, TGF-β1 released by tumor cells induces HSCs to produce increased amounts of ECM constituents such as fibronectin and collagen I. These ECM components constitute a microenvironment in which tumor cells adhere and grow. In addition to providing a physical support to tumor cells, these ECM components also regulate the adhesion, migration, and survival of tumor cells by binding to and activating integrins on the surface of tumor cells.26, 27 For example, ECM-mediated activation of phosphoinositide 3-kinase and its downstream targets in tumor cells protects tumor cells from genotoxin-induced cell cycle arrest and subsequent apoptosis, contributing to tumor chemoresistance.28 In addition, the poorly vascularized architecture associated with desmoplasia contributes to tumor chemoresistance by imposing a barrier to drug delivery.

[28, 29] A previous study showed that

the 3-year cumulative occurrence rate of liver cancer was 12.5% in cirrhotic patients and 3.8% in chronic hepatitis patients, suggesting that hepatitis B and C virus infection and high AFP values are risk factors.[30] Ascha and colleagues reported that HCC developed in 12.8% of cirrhotic patients with non-alcoholic steatohepatitis (NASH) and 20.3% of cirrhotic patients with hepatitis C virus (HCV) infection (P = 0.03) during a median follow-up period of 3.2 years; the cumulative incidence of HCC was 2.6% per year for NASH-cirrhosis and 4.0% in HCV-cirrhosis (P = 0.09).[31] As for the morphological aspects, a coarse parenchymal echo pattern in the liver is a risk factor for the development of HCC in patients with Nutlin-3a solubility dmso HCV-related cirrhosis.[32] The incidence of HCC differed depending JNK inhibitor library on the echo pattern of liver parenchyma; that is, HCC developed in 9 of 11 (82%) cases with a coarse-nodular pattern, 3 of 7 (43%) with a coarse pattern, and only 1 of 20 (5%) with a fine pattern. The study found that the incidence of a coarse-nodular pattern of liver parenchyma was significantly higher in the high DNA synthesizing group than in the low DNA synthesizing group; thus, increased DNA synthesis by hepatocytes may account for the increased risk of developing HCC. Additionally, hepatic lesions showing hypo-density in both the arterial and equilibrium

phases of contrast-enhanced CT were associated with an annual HCC incidence rate 上海皓元 of 15.8%.[33] This incidence rate was higher than in our study,

a discrepancy that may have been due to the marked differences with respect to lesion characteristics between the studies. The appearance of hepatic lesions in the so-called postvascular phase is based on microbubble accumulation using Sonazoid or Levovist.[10-15] Sonograms of this phase allow us to predict histological findings and to characterize focal hepatic lesions.[2, 6, 7] However, postvascular-phase findings are not specific because PIELs encompass a wide spectrum of hepatic lesions. In particular, PIELs may include well-differentiated HCC in cirrhotic patients, and may present an alternation from non-hypervascular lesion to hypervascular lesion. In our study, three PIELs had an arterial-phase hypervascular appearance, which is strongly suggestive of a malignant lesion. However, these lesions did not change the imaging findings during follow-up, indicating that arterial vascularity may not always be predictive for the development of HCC from a PIEL. The mean diameter of HCC lesions that occurred in our study was 15.1 mm, being sufficient to be cured by local treatment alone.[34] The time interval between HCC detection and the last imaging was 4.0 months, which is considered to be an acceptable duration. In fact, the American Association for the Study of Liver Diseases recommends a 6-month interval for HCC screening in cirrhotic patients.

6%) of the 10 769 commune health stations which provide health services in Viet Nam found that liver cancer is the most common cause of cancer RAD001 death in Viet Nam,6 accounting for 27.1% of cancer deaths (31.04% in men and 19.91% in women).

It is thought that over 90% of these liver cancer deaths reflected the high prevalence of HBV infection in Viet Nam.23 Alcohol and HCV infection are other likely contributors to this high rate of liver cancer. In one study of patients diagnosed with HCC, the majority (85%) had evidence of CHB; almost one in seven patients had evidence of HCV.24 For prevention of liver cancer in Viet Nam, the first long-term focus should be HBV vaccination, thus effecting primary prevention of all liver cancers that are related to this virus. In addition, it will be important to use the best available treatments to profoundly suppress HBV and HCV in the chronically infected to lessen HCC risk. It will also be important to address alcoholic liver disease well before it reaches the stage that can

lead to cancer. There are many challenges that exist in Viet Nam related to providing the type of total integrated approach to liver disease that could substantially decrease both morbidity and mortality. Although 70–75% of Viet Nam’s 84 million people dwell in rural and mountainous regions where medical care is substantially limited, almost all of the 10 769 communes have a health center which provides both primary health care and preventive health-care activities,25 a potentially valuable resource for addressing liver disease. Providing the health centers with simple accurate guides on proper screening and vaccination procedures Olaparib nmr for HBV, screening medchemexpress for HCV, and treatment for those with CHB and CHC could guide them to proper care of liver disease patients. Because these commune health centers already have information flowing to and from the Ministry of Health, a national mandate to improve liver disease services could efficiently reach the local commune level. It will also

be important to enlist private health-care providers as in some areas there are more private providers than public ones.26 The non-profit health organizations that provide health care in Viet Nam are also valuable resources. All provinces and most communes (95.7%) have a Red Cross Society branch that provides free health checks for the poor and other vulnerable groups, including children, the elderly, and women,25 so enlisting their help in the campaign against liver disease might be invaluable. Re-use of contaminated needles, syringes, and inadequately sterilized medical equipment is another major challenge that must be addressed. Recent Vietnamese studies have identified as major risk factors for HBV infection a history of hospitalization and of acupuncture4 as well as a history of surgery.9 HCV prevalence is particularly high in patients on maintenance hemodialysis (54%) and those with hemophilia (29%).