Although the classical NF-κB activation pathway is important in m

Although the classical NF-κB activation pathway is important in many cellular Doxorubicin chemical structure processes, the noncanonical NF-κB pathway is also important for normal and pathological processes. NF-κB is restricted to the cytoplasm by inhibitory proteins that are degraded when they are specifically phosphorylated; this permits NF-κB to enter the nucleus and activate target genes. Different combinations of NF-κB subunits induce transcription with different timing sequences and recognize different sequences of NF-κB binding sites. The noncanonical pathway is based on processing of the NF-κB2 gene product p100.11, 12 The p52 subunit is generated

from p100 processing by I kappa B kinase alpha, one of the kinase complexes.11, 12 Once produced, p52 can enter the nucleus and induce genes that regulate many processes.12 In other systems, including androgen-sensitive LNCaP cells in vitro and lymphoma cells, NF-κB/p52 encourages cellular growth by protecting cells from apoptosis and stimulating cyclin D1 expression.16, 17 Coculturing of bone marrow stromal cells with lymphoma cells resulted in active p52 generation, which then translocated to the nucleus

and was associated with increased XIAP and cIAP expression; this was similar to what was seen in our system.17 Investigators have shown a significant relationship between NF-KB, XIAP, and the JNK find more cascade.18-20 Bubici and colleagues18 showed that NF-KB–mediated apoptosis suppression involves inhibition of the JNK cascade, which is related to up-regulation of a variety of mediators, including XIAP, which block aspects of the JNK cascade. Similarly, Kaur and colleagues20 showed that XIAP inhibits JNK activation by transforming growth factor β1 and counteracts transforming growth factor β1–induced apoptosis. This is consistent with our findings, in which CXCR2

knockout mice increased XIAP levels, decreased JNK levels, and Resveratrol decreased apoptosis and mortality. Other investigators have used leflunomide with APAP toxicity and have shown a protective effect due to the inhibition of APAP-induced JNK activation. This decreased Bcl-2 and Bcl-XL activation and decreased apoptosis.19 This is also consistent with our studies. In contrast, other investigators have shown that APAP-induced activation of JNK promotes necrosis by a direct effect on mitochondria.21, 22 “
“Liver transplantation is an effective, life-prolonging procedure for selected patients with end-stage liver disease due to a wide variety of etiologies, including autoimmune, cholestatic and metabolic liver diseases, viral hepatitis and certain malignancies.

Posted in Antibody | Leave a comment

22, 31 In our study, neither the AMA at diagnosis nor that at que

22, 31 In our study, neither the AMA at diagnosis nor that at questionnaire was associated with fatigue (P > 0.05), hence not supporting this hypothesis. Using a backwards selection

procedure to perform multivariate analysis, with significance defined as P < 0.05, we identified calcium and vitamin D use, elevated BMI, stage of disease at diagnosis, presence of varices, clinically reported fatigue at questionnaire, and pruritus as the significant predictors of fatigue when evaluated formally in the PBC-40 questionnaire (Table 5). This broad modeling of our data reinforces the concept that fatigue in PBC is multifactoral. Within each variable it remains highly likely that there are related factors that we are unable to capture or define accurately that contribute to fatigue severity. The Toronto criteria for treatment response is derived from this clinic practice and predicts no histological progression Ixazomib at 10 3Methyladenine years if patients have ALP values less than 1.67 × upper limit of normal after 2 years of UDCA.30 Comparative criteria were also applied as per Pares (normalization of ALP or >40% reduction of ALP after 1 year of UDCA)28 and Corpechot

(ALP <3 × upper limit of normal and aspartate aminotransferase less than 2 × upper limit of normal and bilirubin less than 1 mg/dL after 1 year of UDCA).29 Student t tests were used to compare PBC-40 responses between treatment responders and nonresponders. Complete biochemistries for at least one treatment response were available in 261 patients. As demonstrated in Table 6, there were significantly lower symptom scores in all domains other than Fatigue and Cognition, if patients responded as per the Toronto definition. Thymidine kinase Applying the alternative definitions of treatment response also demonstrated significantly lower total PBC-40 scores in responders than

in nonresponders (range, 8.7-14.9 points lower; P < 0.05). Itch scores were significantly lower, absolute difference 1.1-1.9, according to the Toronto (P = 0.02) and Corpechot (P = 0.001) criteria, but not Pares (P = 0.71). Responders by any criteria scored lower values in the Social and Emotional domains; range 3.5-4.1 points lower; P < 0.05. Fatigue is a common but complex symptom that is poorly understood and lacks effective treatment. Up to 85% of patients with PBC will complain of fatigue, and it is often a symptom that negatively impacts on the quality of life of patients, as well as having been suggested to be associated with early mortality.32 In this study, we set out to explore and describe the frequency and severity of fatigue in patients with PBC, through the use of a multidomain disease-specific QOL tool, the PBC-40, and to specifically define the role of comorbidities in fatigue. We confirm the importance of this symptom for patients with PBC but clearly show the relevance of comorbidities in determining fatigue severity.

Posted in Antibody | Leave a comment

Mounting evidence implicates that Mesenchymal Stem Cells (MSCs) h

Mounting evidence implicates that Mesenchymal Stem Cells (MSCs) have properties of low immunogenicity, immunomodulation and anti-inflammatory in vitro and in vivo, especially regulate T-cell responses. Therefore, we transplanted MSCs into an experimental model of IBD to investigate their potential therapeutic effects in vivo. Methods: A rectal enema of trinitrobenzene sulfonic acid (TNBS) (100 mg/kg body weight) was applied

to female BALB/c mice. Bone marrow mesenchymal stem cells (BMSCs) were derived from male green fluorescent protein (GFP) transgenic mice and were transplanted intravenously into animal models after onset of disease. Clinical activity scores, histological changes were evaluated. GFP and Sex determining Region Lumacaftor datasheet Y gene (SRY) expression were used for cell tracking. Ki67 positive cells and Lgr5-expressing cells were detected to observe proliferative activity.

Inflammatory response was determined by measuring levels of different inflammatory mediators in colon and serum. The inflammatory cytokines include tumor necrosis factor-α(TNF-α),interferon-γ(IFN-γ),interleukin-2(IL-2),IL-6,IL-17,IL-4,IL-10,transforming growth factor(TGF-β).Master regulators of Th1 cell (T-box INK 128 price expressed in T cells,T-bet),Th17 cell(retinoid related orphan receptor gammat,RORγt),Th2 cell (GATA family of transcription factors 3,GATA3) and regulatory T cell O-methylated flavonoid (forkhead box P3,Foxp3) were also detected. Results: Systemic infusion of GFP-BMSCs ameliorated the clinical and histopathologic severity of colitis, including body weight loss, diarrhea, inflammation and increasing survival (P < 0.05). Cell tracking

study showed that MSCs homed to the injured colon. MSCs promoted proliferation of intestinal epithelial cells and differentiation of intestinal stem cell (P < 0.01). This therapeutic effect was mainly mediated by down-regulating both Th1-Th17 driven autoimmune and inflammatory responses (IL-2, TNF-α, IFN-γ, T-bet; IL-6, IL-17, RORγt), while by up-regulating Th2 activities (IL-4, IL-10, GATA-3) (P < 0.05). MSCs also induced activated CD4 + CD25 + Foxp3+ regulatory T cells (TGF-β, IL-10, Foxp3) with suppressive capacity on Th1-Th17 effecter responses and promoted Th2 differentiation in vivo (P < 0.05). Conclusion: MSCs emerge as key regulators of immune and inflammatory responses and as an attractive candidate for a cell-based therapy for IBD. Key Word(s): 1. MSCs; 2. IBD; 3. transplantation; 4. immunomodulation; Presenting Author: XUESONG YANG Additional Authors: LIPING ZHANG, WEI FU, AIYING WANG Corresponding Author: XUESONG YANG Affiliations: No Objective: To study the clinical characters and endoscopic manifestation of ulcerative colitis associated colorectal cancer (UC-CRC).

Posted in Antibody | Leave a comment

The few individuals grouped together in the third cluster move ve

The few individuals grouped together in the third cluster move very little, at low frequency and stay hidden more, resulting in round trips of longer duration. The three behavioural clusters were identified using

clustering methods that take into account all behavioural variables under the assumption that each behavioural strategy shows a normal distribution in a population. The retrieved clusters were then cross-validated using an independent clustering method, which showed that the grouping was robust (Fig. 2). Interestingly, the grouping of individuals in either two or three clusters was equally robust with the reassignment of individuals showing the same two individuals being misclassified. The three individuals comprising the third cluster, although being classified as belonging to the second cluster if only two groups are predefined, show a distinct and unique behaviour compared with the entire sample characterized by extremely low levels of exploration. In JAK inhibitor review summary, three groups differing in the amount of exploration and the time to the onset of exploration were detected. van Oers et al. (2004) showed the importance of the latency of the first movement when investigating

avian exploration syndromes as this reflects the willingness of individuals to take risks. Our analysis demonstrated differences among the three clusters in the latency to the first movement. Indeed, animals in cluster one start moving earlier than individuals in group

two, with the maximal latency observed for individuals in cluster two. Generally, frogs moved close to the walls of the tank and did not explore the centre much. This behaviour involving exploration close to a physical structure such as a wall reduces visibility to predators and provides some shelter while exploring. Similar behaviours where animals disperse and explore using landscape elements have been demonstrated for other taxa (Baguette et al., 2013). Among our behavioural clusters, animals in cluster three showed significantly less movement away from the walls of the those cage compared with the animals in the other two clusters. Behavioural syndromes (bold vs. shy) are typically recovered in studies analysing exploration behaviour (Dingemanse & de Goede, 2004; Wilson & Godin, 2009). Bold individuals are defined, in this context, as those that show curiosity and a willingness to explore; they move a lot at high frequency and take risks by moving away from walls or other structures that provide shelter. On the opposite end, shy individuals stay hidden long, explore little and use landscape elements during exploration to avoid open space. When analysing the behavioural clusters discovered in our data, it becomes evident that animals in cluster one can be characterized as bold, those in cluster three as shy and those in cluster two as intermediate. Indeed, our data show a large group of male X.

Posted in Antibody | Leave a comment

1) Recognizing that failure

1). Recognizing that failure Romidepsin molecular weight to provide the extra liver with a normal portal venous supply could handicap the allograft in the same way as the native livers were damaged in my nontransplant portal diversion models, I began the development of versatile transplant procedures to study the special qualities of splanchnic venous blood in dogs. One of the models was a method of total recipient hepatectomy, the unique feature of which was preservation of the retrohepatic inferior vena

cava2 as in the first stage of today’s piggy-back human liver transplantation. For liver allograft implantation, it was technically easier to simply remove this portion of the recipient vena cava click here and replace it with the comparable segment of the donor liver’s vena cava into which all of the hepatic veins empty.3 Operative survival with the complete canine replacement operation (Fig. 2) was not accomplished until a few days after I moved to Northwestern in June 1958 for a final 12 months of cardiovascular surgical

training that was expected to culminate in an academic practice in thoracic surgery. Instead, two steps were taken during the summer of 1958 that ensured pursuit of the liver research for at least 5 years beyond completion of the thoracic residency. The first step was the submission of a four-page NIH grant focused on metabolic studies in which liver replacement was one of the experimental models. The second step was my nomination by Northwestern for a John and Mary Markle Scholarship. Here, the emphasis was radically different. Markle Scholar candidates were expected to identify an open-ended career objective. Ignoring check details advice to develop a “more realistic” project in the emerging field of open heart surgery, I proposed the life goal of clinical liver transplantation. In the autumn of 1958, I learned

that the NIH grant would be fully funded for 5 years, and shortly thereafter that I had been selected as a Markle Scholar. The first phase of the canine liver project was nearly completed by the time I finished the thoracic residency and the dual revenue streams began on July 1, 1959. In addition, a second operation had been perfected in which the liver was transplanted as part of an allograft that contained all of the other intra-abdominal viscera (Fig. 3).6, 7 The magnitude of the Markle proposal should have been intimidating, but it did not seem so at the time. The slate of liver transplantation was nearly blank in 1958, but what had to be done was transparent: make the operation biologically sound, make it practical, and find a way to prevent allograft rejection. I was not the only person to think that way. Although I did not learn of it until a year later, Francis D.

Posted in Antibody | Leave a comment

The treatment with this formulation was proved effective overall

The treatment with this formulation was proved effective overall in the three treatment modalities considered, and the majority of patients including patients with type 3 VWD achieved haemostatic responses rated as ‘good’ to ‘excellent’, with no significant differences between disease subtypes. These results confirmed those of a preplanned ad interim analysis of the study

[12]. The new formulation was therefore at least as effective as the previous one, also associated with clinical responses rated excellent/good in the majority of patients [9, 13-17]. Our efficacy findings were also in line with those of recently published studies with other commercially available VWF/FVIII MK-8669 manufacturer concentrates [18-20]. During the 24-month follow-up period, there was an increase in the number of patients receiving Haemate® P VR for long-term prophylaxis (n = 31) compared with those

on prophylaxis at baseline (n = 16). The role of prophylaxis with VWF/FVIII concentrates in VWD is still a matter of debate. So far, few studies Buparlisib clinical trial have evaluated the use of secondary prophylaxis in VWD. [21-27]. In the study by Berntorp et al. [23] in 35 patients with VWD, mostly with type 3 VWD, prophylaxis was associated with a substantial decrease in the annual number of bleeding events [23, 24]. Also, patients who started prophylaxis at a young age had no joint bleeds and no clinical signs of arthropathy. Similar results were obtained in a recently published cohort study in 32 patients with a median prophylaxis duration of 3 years leading to the resolution of recurrent bleeding in 31 of the 32 patients [21]. Our results show that prophylactic treatment with Haemate® P VR, both for short-term and long-term bleeding prevention, was effective across all disease subtypes. To our knowledge, the treatment of VWD has not been evaluated in pharmacoeconomic analysis

so far. This type of analysis is strongly needed and is likely to contribute also to establishing the role of long-term prophylaxis in the treatment of VWD. We thus collected data describing the impact this website of VWD on a set of pharmacoeconomic variables. During the 24-month follow-up almost half of the patients lost days of school or work and about one-third was hospitalized because of the disease, whereas another third underwent invasive procedures made necessary by the condition. As no previous studies have addressed this aspect it is difficult to make any comparison. However, these figures are in keeping with the presence of significant bleeding histories and morbidity, as shown by the high average BS observed at enrolment. Haemate® P VR was well-tolerated and the switch to this new formulation was not associated with any serious or unexpected adverse event, including thromboembolic events or inhibitor development, in agreement with previous findings [12].

Posted in Antibody | Leave a comment

For example, a frequent amplification target is COL4A1 on 13q34,

For example, a frequent amplification target is COL4A1 on 13q34, and a frequent deletion this website target is SERPINA5 on 14q32.13. Moreover, the differential expressions of eight DEGs in several of these new CNAs were also validated by q-PCR

(Supporting Fig. 2B). Additionally, SERPINA5 was also observed to inhibit the migration ability of HCC cells in this study (Supporting Fig. 7). To the best of our knowledge, this is the first study to use high-resolution copy number analysis of a relatively large numbers of paired specimens to create a comprehensive catalog of CNAs in HCC genomes. Several findings have emerged from our studies, mainly based on the opportunity provided by integrated analysis of genomic and transcriptional profiles. One finding is that several regulatory modules were identified as functioning in a concerted manner, including involved in cell adhesion,

cell cycle, regulation of the actin cytoskeleton, and WNT signaling pathways, which have all been implicated in HCC.33, 34 Another finding is the identification of three novel cancer genes related to HCC, including one tumor suppressor candidate TRIM35 and two possible oncogenes buy Luminespib HEY1 and SNRPE. TRIM35 is a member of the Ring finger, B box, coiled-coil (RBCC), or Tripartite motif (TRIM) family.35 It was originally isolated as a gene up-regulated during an erythroid-to-myeloid lineage switch, and independently as a proapoptotic gene activated during macrophage maturation.31, 35 It is notable that enforced expression of TRIM35 in HeLa cells could inhibit cell proliferation and tumorigenicity.31 However, the functions of this gene in HCC are largely unknown. In this study we found that TRIM35 was located in a frequently deleted region of 8p21.2-21.1. Consistently, the mRNA and protein levels of TRIM35 were also significantly down-regulated in HCC

specimens. However, it is worth noting that additional regulatory mechanisms other than its genomic loss for TRIM35 down-regulation in HCC exist. Therefore, we examined the methylation status of CpG selleck inhibitor islands within TRIM35 promoter using quantitative real-time methylation-specific PCR on 31 out of 58 paired HCC and nontumor tissues. We found that the frequency of hypermethylation was approximately 45.2% (14/31) in HCC tissues compared with the nontumor tissues, which might account for the down-regulation of TRIM35 mRNA and protein level in HCC tissues in addition to that caused by genomic loss of 14q32.13 loci (17.2%). Furthermore, we found that TRIM35 could significantly suppress the in vitro cell proliferation and in vivo tumorigenicity of HCC cells. Most important, the expression level of TRIM35 was negatively correlated with the tumor grade, tumor size, and serum AFP level of HCC patients.

Posted in Antibody | Leave a comment

For example, a frequent amplification target is COL4A1 on 13q34,

For example, a frequent amplification target is COL4A1 on 13q34, and a frequent deletion p38 MAPK inhibitors clinical trials target is SERPINA5 on 14q32.13. Moreover, the differential expressions of eight DEGs in several of these new CNAs were also validated by q-PCR

(Supporting Fig. 2B). Additionally, SERPINA5 was also observed to inhibit the migration ability of HCC cells in this study (Supporting Fig. 7). To the best of our knowledge, this is the first study to use high-resolution copy number analysis of a relatively large numbers of paired specimens to create a comprehensive catalog of CNAs in HCC genomes. Several findings have emerged from our studies, mainly based on the opportunity provided by integrated analysis of genomic and transcriptional profiles. One finding is that several regulatory modules were identified as functioning in a concerted manner, including involved in cell adhesion,

cell cycle, regulation of the actin cytoskeleton, and WNT signaling pathways, which have all been implicated in HCC.33, 34 Another finding is the identification of three novel cancer genes related to HCC, including one tumor suppressor candidate TRIM35 and two possible oncogenes Wnt inhibitor HEY1 and SNRPE. TRIM35 is a member of the Ring finger, B box, coiled-coil (RBCC), or Tripartite motif (TRIM) family.35 It was originally isolated as a gene up-regulated during an erythroid-to-myeloid lineage switch, and independently as a proapoptotic gene activated during macrophage maturation.31, 35 It is notable that enforced expression of TRIM35 in HeLa cells could inhibit cell proliferation and tumorigenicity.31 However, the functions of this gene in HCC are largely unknown. In this study we found that TRIM35 was located in a frequently deleted region of 8p21.2-21.1. Consistently, the mRNA and protein levels of TRIM35 were also significantly down-regulated in HCC

specimens. However, it is worth noting that additional regulatory mechanisms other than its genomic loss for TRIM35 down-regulation in HCC exist. Therefore, we examined the methylation status of CpG click here islands within TRIM35 promoter using quantitative real-time methylation-specific PCR on 31 out of 58 paired HCC and nontumor tissues. We found that the frequency of hypermethylation was approximately 45.2% (14/31) in HCC tissues compared with the nontumor tissues, which might account for the down-regulation of TRIM35 mRNA and protein level in HCC tissues in addition to that caused by genomic loss of 14q32.13 loci (17.2%). Furthermore, we found that TRIM35 could significantly suppress the in vitro cell proliferation and in vivo tumorigenicity of HCC cells. Most important, the expression level of TRIM35 was negatively correlated with the tumor grade, tumor size, and serum AFP level of HCC patients.

Posted in Antibody | Leave a comment

For example, a frequent amplification target is COL4A1 on 13q34,

For example, a frequent amplification target is COL4A1 on 13q34, and a frequent deletion LBH589 solubility dmso target is SERPINA5 on 14q32.13. Moreover, the differential expressions of eight DEGs in several of these new CNAs were also validated by q-PCR

(Supporting Fig. 2B). Additionally, SERPINA5 was also observed to inhibit the migration ability of HCC cells in this study (Supporting Fig. 7). To the best of our knowledge, this is the first study to use high-resolution copy number analysis of a relatively large numbers of paired specimens to create a comprehensive catalog of CNAs in HCC genomes. Several findings have emerged from our studies, mainly based on the opportunity provided by integrated analysis of genomic and transcriptional profiles. One finding is that several regulatory modules were identified as functioning in a concerted manner, including involved in cell adhesion,

cell cycle, regulation of the actin cytoskeleton, and WNT signaling pathways, which have all been implicated in HCC.33, 34 Another finding is the identification of three novel cancer genes related to HCC, including one tumor suppressor candidate TRIM35 and two possible oncogenes Sirolimus in vivo HEY1 and SNRPE. TRIM35 is a member of the Ring finger, B box, coiled-coil (RBCC), or Tripartite motif (TRIM) family.35 It was originally isolated as a gene up-regulated during an erythroid-to-myeloid lineage switch, and independently as a proapoptotic gene activated during macrophage maturation.31, 35 It is notable that enforced expression of TRIM35 in HeLa cells could inhibit cell proliferation and tumorigenicity.31 However, the functions of this gene in HCC are largely unknown. In this study we found that TRIM35 was located in a frequently deleted region of 8p21.2-21.1. Consistently, the mRNA and protein levels of TRIM35 were also significantly down-regulated in HCC

specimens. However, it is worth noting that additional regulatory mechanisms other than its genomic loss for TRIM35 down-regulation in HCC exist. Therefore, we examined the methylation status of CpG click here islands within TRIM35 promoter using quantitative real-time methylation-specific PCR on 31 out of 58 paired HCC and nontumor tissues. We found that the frequency of hypermethylation was approximately 45.2% (14/31) in HCC tissues compared with the nontumor tissues, which might account for the down-regulation of TRIM35 mRNA and protein level in HCC tissues in addition to that caused by genomic loss of 14q32.13 loci (17.2%). Furthermore, we found that TRIM35 could significantly suppress the in vitro cell proliferation and in vivo tumorigenicity of HCC cells. Most important, the expression level of TRIM35 was negatively correlated with the tumor grade, tumor size, and serum AFP level of HCC patients.

Posted in Antibody | Leave a comment

However, a limitation of this study was that our patients had INR

However, a limitation of this study was that our patients had INR values on the lower end of spectrum in both cohorts and inter-laboratory variability of INR has been shown to be greater with higher mean INRs (Am J Transplant 2007, 7:1624-280) Disclosures: Neeral L. Shah – Grant/Research Support: Boehringer Ingelheim RGFP966 concentration Stephen H. Caldwell – Advisory Committees

or Review Panels: Vital Therapy; Consulting: Wellstat diagnostics; Grant/Research Support: Genfit, Gilead Sciences Patrick G. Northup – Grant/Research Support: Hemosonics, Bristol Meyer Squibb Curtis K. Argo – Consulting: Wellstat Diagnostics; Independent Contractor: Genentech/Roche The following people have nothing to disclose: Dennis Kumral, Nicolas M. Intagliata “
“Genetic variation near the IL28B gene and substitution of amino acid (aa) 70 and 91 in the core

region of hepatitis C virus (HCV) genotype 1b can predict the response to pegylated interferon (PEG-IFN)/ribavirin combination therapy, but its impact on triple therapy of telaprevir/PEG-IFN/ribavirin is not clear. The aims of this study were to investigate the predictive factors of sustained virological response to a 12-week or 24-week regimen of triple therapy in 72 of 81 Japanese adults infected with HCV genotype 1. Overall, sustained virological response and end-of-treatment response were achieved by 61% and 89%, respectively. Especially, the sustained virological response was achieved by 45% and 67% in the 12- and 24-week regimens, respectively. Multivariate analysis identified rs8099917 near the IL28B gene (genotype TT) and substitution at aa 70 (Arg70)

as significant determinants of sustained virological response. Prediction of response MK-1775 purchase to therapy based on a combination of these factors had high sensitivity, specificity, and positive and negative predictive values. The efficacy of triple therapy selleck was high in the patients with genotype TT, who accomplished sustained virological response (84%), irrespective of substitution of core aa 70. In the patients having genotype non-TT, those of Arg70 gained high sustained virological response (50%), and sustained virological response (12%) was the worst in patients who possessed both genotype non-TT and Gln70(His70). Conclusion: This study identified genetic variation near the IL28B gene and aa substitution of the core region as predictors of sustained virological response to a triple therapy of telaprevir/PEG-IFN/ribavirin in Japanese patients infected with HCV genotype 1b. (HEPATOLOGY 2010) Hepatitis C virus (HCV) usually causes chronic infection that can result in chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma (HCC).1, 2 At present, treatments based on interferon (IFN), in combination with ribavirin, are the mainstay for combating HCV infection. In Japan, HCV genotype 1b (HCV-1b) in high viral loads (>100 KIU/mL) accounts for more than 70% of HCV infections, making it difficult to treat patients with chronic hepatitis C.

Posted in Antibody | Leave a comment