Studies of episodic memory problems in individuals with TBI, however, have found these problems to be persistent 4 and years after the trauma (Piolino et al., 2007). In summary, our study shows that patients with TBI exhibit impaired episodic memory as well as impaired episodic future thinking. The TBI patients presented even more pronounced difficulties in episodic event representations, when having to recall or imagine events further back or forth in time, indicating that mental

time travel into the distant past or future is a cognitively more demanding process. In our study, it seems likely that impaired executive functioning at least partly underlies the deficits in the ability to remember specific past events and imagine specific future events. Our finding that TBI patients show deficits regarding episodic future thinking may have several clinical implications. For example, selleck chemical difficulties with elaborating and maintaining a specific and detailed representations of future rewarding experiences could decrease anticipatory pleasure, thus leading to motivational deficits in pursuing

personal goals. Also, an impaired ability to simulate alternative plans of actions could severely disrupt adequate problem-solving, thus resulting in more inflexible and stimulus bound actions. Thus, one possible consequence of the observed impairment of episodic memory and episodic future thinking in TBI Selleckchem Sorafenib patients may be diminished temporally extended self-awareness. The ability to become aware of past and possible future states of oneself is thought to ensure continuity and a sense of self through time. Disorders of episodic memory and episodic future thinking might at least in part explain the impaired awareness of deficits, which is a frequent consequence of TBI (McGlynn & Schacter, 1989) and which represents one of the biggest challenges in the rehabilitation process (Prigatano, 1999, 2005). We thank the patients for giving their time; the Regional Hospital Hammel Neurocenter and in particular Eva Lind for clinical assistance and helpful suggestions. We also thank Lise Fischer-Mogensen

and Nadia Nielsen for their help. This work was supported by the Danish National Research Foundation as well as the Danish Council for Independent Research for the Humanities. “
“Conversion disorder (CD) is Buspirone HCl a condition where neurological symptoms, such as weakness or sensory disturbance, are unexplained by neurological disease and are presumed to be of psychological origin. Contemporary theories of the disorder generally propose dysfunctional frontal control of the motor or sensory systems. Classical (Freudian) psychodynamic theory holds that the memory of stressful life events is repressed. Little is known about the frontal (executive) function of these patients, or indeed their general neuropsychological profile, and psychodynamic theories have been largely untested.

1

In this issue Daporinad price of the Journal, Yamada et al. explore the impact of ultrasound-diagnosed fatty liver on the incidence of IFG or T2D in Japanese people undergoing a health checkup.11 A total of 12 375 individuals (6799 men and 5576 women) without hyperglycemia or T2D at baseline were re-assessed after 5 years. IFG and T2D were newly diagnosed in 7.6% and 1% of men, and 3.8% and 0.5% of women, respectively, within the study period. In both sexes, the prevalence of newly diagnosed IFG and T2D was significantly higher in the participants with fatty liver than among those without fatty liver, and after adjustment for the other risk factors, fatty liver remained an independent risk factor for IFG and/or T2D. The impact of fatty liver on incidence of IFG and T2D was stronger among participants with a lower BMI. Therefore, the presence of fatty liver may be a better predictor for development of T2D than obesity

itself, and it can be considered to be an early predictor of T2D. In general, this is a well written and concise manuscript with a clear message, and answers a question that is important and significant in public health. Furthermore, it has the strength of studying click here a large number of individuals. Some limitations of this study include the lack of liver enzymes and OGTT at baseline, the use of a single result of fasting plasma glucose (FPG) for diagnosis of diabetes at follow up, and lack of rigorous exclusion of other etiologies of fatty liver, making it difficult to draw conclusions regarding second the metabolic risk among subjects with NAFLD. It should be noted that regional guidelines recommend an OGTT be performed at diagnosis of NAFLD when FPG is more than 5.6 mmol/L12, and several studies now report a much higher prevalence of glucose intolerance and established T2D at diagnosis of NAFLD when OGTT is routinely performed.14–16 Both T2D

and hepatogenous diabetes (complicating cirrhosis) are associated with increased liver-related morbidity and mortality in cirrhotic patients regardless of etiology.1 Unlike the hepatogenous diabetes attributed to cirrhosis, T2D in NAFLD is more frequently associated with risk factors such as age, BMI and family history of T2D.1,4–11 It constitutes a risk factor for NASH, for fibrotic progression to cirrhosis and ultimately hepatocellular carcinoma. The finding of diabetes is thus associated with an increased risk of all-cause death and liver-related mortality in patients with NAFLD, and diabetic and cardiovascular risk may compete with liver-related complications in dictating the final outcome.1,3 The biological mechanisms by which NAFLD contributes to a higher risk of developing T2D are not fully understood. However, the fatty liver could contribute in the same way as visceral adipose tissue to insulin resistance, systemic inflammation and oxidative stress, while decreased serum adiponectin concentrations might also be part of the mechanism.

[6] Because of these unique mechanisms and the requirement for specialist knowledge of the complex anatomy and physiology of the orofacial AZD6738 supplier region, diagnosis may be difficult. Many patients have consulted multiple clinicians for their condition yet remain undiagnosed or with an incorrect diagnosis.[7, 8] Our aim is to provide the headache physician with a guide to orofacial pain presentations and diagnoses informed by our clinical experience in the fields of medicine as well as dentistry, and to review the literature relevant to these conditions. We provide an overview of the common presentations of orofacial pain including dental causes of pain, non-dental causes of intraoral pain, and extraoral facial pain syndromes,

as the signs and symptoms of many of these conditions can overlap significantly, causing diagnostic difficulty. We also present a discussion of history, diagnosis, and management considerations relating to the biopsychosocial model of diagnostic formulation and management. This approach is particularly relevant and important in the field of orofacial pain given the significant level of psychological distress and social dysfunction that is associated with these disorders.[9, 10] As with other types of chronic pain, there is often

a mismatch between the patient’s expectation of a cure for their pain, and the reality that for many types of chronic pain, a cure is seldom possible. Medicine alone does not have the tools to manage a condition that has a neurophysiological cause but is also experienced emotionally, socially, financially, and spiritually.[11] Recognition of psychological comorbidities Palbociclib is essential for appropriate diagnosis and successful pain management. This is a narrative, clinically orientated review of orofacial pain conditions encountered in a specialist orofacial pain clinic, with references to relevant literature. Quotations from patients are included to illustrate relevant points Acyl CoA dehydrogenase as these also form part of the evidence base.[12] The types of orofacial pain have been divided into sections as

shown in Figure 1 —. Information regarding dental causes of orofacial pain is included as this area is often unfamiliar to medical practitioners. Evidence-based management options, as far as possible, for the specific diagnoses are summarized and presented in a tabulated form (Table). In the second half of the paper, we discuss holistic management approaches to orofacial pain. There are few causes for dental pain; however, because of significant neural convergence in the jaws and face, it may be referred, poorly localized, or misdiagnosed. The 4 major causes of dental pain are pulpitis, cracked tooth syndrome, dental abscess, and dentine sensitivity.[13] These are often acute conditions, but because they are common, they may coexist with other chronic pains.[14] Both the dental pulp and periodontal ligament contain nociceptors.

[6] Because of these unique mechanisms and the requirement for specialist knowledge of the complex anatomy and physiology of the orofacial check details region, diagnosis may be difficult. Many patients have consulted multiple clinicians for their condition yet remain undiagnosed or with an incorrect diagnosis.[7, 8] Our aim is to provide the headache physician with a guide to orofacial pain presentations and diagnoses informed by our clinical experience in the fields of medicine as well as dentistry, and to review the literature relevant to these conditions. We provide an overview of the common presentations of orofacial pain including dental causes of pain, non-dental causes of intraoral pain, and extraoral facial pain syndromes,

as the signs and symptoms of many of these conditions can overlap significantly, causing diagnostic difficulty. We also present a discussion of history, diagnosis, and management considerations relating to the biopsychosocial model of diagnostic formulation and management. This approach is particularly relevant and important in the field of orofacial pain given the significant level of psychological distress and social dysfunction that is associated with these disorders.[9, 10] As with other types of chronic pain, there is often

a mismatch between the patient’s expectation of a cure for their pain, and the reality that for many types of chronic pain, a cure is seldom possible. Medicine alone does not have the tools to manage a condition that has a neurophysiological cause but is also experienced emotionally, socially, financially, and spiritually.[11] Recognition of psychological comorbidities ACP-196 solubility dmso is essential for appropriate diagnosis and successful pain management. This is a narrative, clinically orientated review of orofacial pain conditions encountered in a specialist orofacial pain clinic, with references to relevant literature. Quotations from patients are included to illustrate relevant points selleck chemicals as these also form part of the evidence base.[12] The types of orofacial pain have been divided into sections as

shown in Figure 1 —. Information regarding dental causes of orofacial pain is included as this area is often unfamiliar to medical practitioners. Evidence-based management options, as far as possible, for the specific diagnoses are summarized and presented in a tabulated form (Table). In the second half of the paper, we discuss holistic management approaches to orofacial pain. There are few causes for dental pain; however, because of significant neural convergence in the jaws and face, it may be referred, poorly localized, or misdiagnosed. The 4 major causes of dental pain are pulpitis, cracked tooth syndrome, dental abscess, and dentine sensitivity.[13] These are often acute conditions, but because they are common, they may coexist with other chronic pains.[14] Both the dental pulp and periodontal ligament contain nociceptors.

In vitro experiments have demonstrated not only that entecavir has stronger antiviral activity than lamivudine or adefovir against HBV wild strains, but it is also effective against lamivudine-resistant strains.[179] Entecavir has had health insurance approval in Japan since 2006, for administration of 0.5 mg per day in treatment-naïve cases. In Europe studies of entecavir therapy in patients naïve to NAs, in both HBeAg positive cases and negative patients, HBV DNA negative conversion rates and ALT normalization rates were higher for entecavir than for lamivudine.[14, 25, 180] The greatest characteristic

of entecavir is that it has a lower incidence of viral resistance than lamivudine. For this reason entecavir is currently the treatment of first choice when using NAs. Resistance to entecavir is exhibited by CHIR99021 amino acid mutation of either rtT184, rtS202 or rtM250, in addition to the lamivudine resistant amino acid mutations at rtM204V and rtL180M.[181] In the abovementioned study, increased Selleck AZD2014 HBV DNA levels were seen in 22 out of 679 patients until the 96th week of therapy. Only 1 case of entecavir-resistant HBV was confirmed at 1 year, and 1 more case at 96 weeks, in one of which lamivudine-resistant HBV had already been detected at the commencement of entecavir therapy.[180]

Long term results have been reported for entecavir administration for 5 years.[16, 182] The HBV DNA negative conversion rate was 55–81% at 1 year, 83% at 2 years, 89% at 3 years, 91% at 4 years and

94% at 5 years, and the ALT normalization rate was 65% at 1 year, 78% at 2 years, 77% at 3 years, 86% at 4 years and 80% at 5 years, while the incidence of resistant HBV was 0.2% at 1 year, 0.5% at 2 years, and 1.2% at 3–5 years. However, in these studies, entecavir 0.5 mg daily was not continuously administered Nutlin-3 in all cases. On the other hand, in a report from Hong Kong of continuous entecavir therapy for 3 years, the HBV DNA negative conversion rate was 81% at 1 year, 90% at 2 years and 92% at 3 years; the ALT normalization rate was 84% at 1 year, 88% at 2 years and 90% at 3 years; and the HBeAg seroconversion rate was 22% at 1 year, 41% at 2 years and 44% at 3 years.[19] From of these cases, 1 case of resistant HBV was confirmed at 3 years. In results from Japan concerning NAs naïve cases,[15, 18, 183] the HBV DNA negative conversion rate was 77–88% at year 1, 83–93% at year 2, 95% at year 3, and 96% at year 4. The ALT normalization rate was 83–87% at year 1, 88–89% at year 2, 92% at year 3, and 93% at year 4. The HBeAg seroconversion rate was 12–20% at year 1, 18–20% at year 2, 29% at year 3, and 38% at year 4. Histological evaluation also confirmed improvement in the Knodell necroinflammatory score and fibrosis score at 1 year and 3 years.[18] The incidence of entecavir-resistant HBV was 3.3% at 3 years.

Fewer than half of the haplotypes (25) occurred in more than one individual (Table S1, Fig. 3). The most common haplotype (h1) was within the restricted lineage and occurred in 31 individuals. Thirteen haplotypes belong in the restricted lineage (95 individuals) and 34 haplotypes in the widespread lineage (81 individuals including one from New Caledonia). Trees generated by BEAST provided posterior support probabilities of 1 for the widespread lineage and 0.9988 for the restricted one (data not shown). Figure 1

shows the numbers of representatives of each lineage from each sampled Doxorubicin mw locality in Australia and Table S1 gives details on distribution of each haplotype. The only sequences from Australian waters that did not belong to the widespread or restricted lineages were from two dugongs from Ashmore Reef (Fig. 1, 3), which lies on the edge of the Australian continental shelf almost Smoothened inhibitor 400 km off Western Australia and ~120 km from Timor from which it is separated

by a deepwater trench. A third dugong from Ashmore Reef carried a sequence representative of the widespread lineage. The Australian lineages were represented outside Australia by a single sequence (h44, widespread lineage) from New Caledonia, about 1,500 km east of the closest part of Queensland. All remaining sequences from outside Australia form a loose cluster in Figure 3, but given the diversity they exhibit and the very limited sampling, this cluster may not represent a single lineage (hence we did not present neutrality indices and some other analyses for this lineage alone). Overall, dugongs exhibit high haplotypic diversity (0.946) and rather low nucleotide diversity (0.026) (Table 2). The restricted lineage, despite including Nintedanib (BIBF 1120) a larger number of samples, displays much lower haplotypic diversity and nucleotide diversity than the widespread lineage (Table 2). When the data were explored for evidence of population growth, strikingly different results

were obtained for each lineage. Runs in Beast rejected the hypothesis of constant population size for the widespread lineage but not for the restricted one. The neutrality indices (Fu’s FS and R2; Table 2) did not support population growth for the restricted lineage. However, the highly significant value for Fu’s FS statistic indicates that the widespread lineage has experienced growth. Values for the R2 statistic did not reject the null hypothesis of constant population size in either lineage and was our only evidence against growth in the widespread lineage. The Bayesian skyline plot (Fig. 4a) suggests recent expansion for the widespread lineage after a period of near-stasis. Both median and mean values for effective population size (NE(FEMALE)) through time are shown in Figure 4a, b because they differ from one another more than we had expected and it is not clear which should be preferred.

Of the 48 patients with positive pH/impedance findings, 38 was normal on WLI (Figure 1A) except 10 with EE and 37 showed positive AFI manifestations indicating the presence of GERD(Figure 1B). The sensitivity and accuracy of AFI (77% and 67%, respectively) in detecting GERD were higher than those of

WLI (20% and 52%, respectively), although the specificity of AFI (53%) was lower than that of WLI (97%). Inter-observer reliability analysis of AFI findings indicated substantial agreement (Kappa = 0.630, p = 0.000). Multivariate analysis showed that positive AFI findings significantly correlated with pH/impedance results (odds ratio [OR] = 0.242, 95% confidence interval [CI] 0.087–0.673, p = 0.007). Conclusion: AFI can detect esophageal PD0325901 solubility dmso mucosal ACP-196 mw changes related

to acid reflux, invisible on conventional WLI, in patients with NERD, suggesting that AFI endoscopy may be effective in the endoscopic diagnosis of GERD. Key Word(s): 1. Autofluorescence; 2. Endoscopy; 3. GERD; 4. Acid Reflux; Presenting Author: XI HUANG Additional Authors: JIUHONG MA Corresponding Author: XI HUANG Affiliations: The First Affiliated Hospital of Nanchang University Objective: Endoscopy is widely performed in China, but the reprocessing of the endoscope’s still poses many problems, because many units do not strictly adhere with to the endoscope reprocessing standard. To identify the practices used for reprocessing of gastrointestinal endoscopes in China, a survey a was carried out including basic information about the hospital, rinsing, disinfection, storage as well as personnel protection,

etc. Methods: A survey tool with 53 questions was designed for the survey, and 181 endoscope centers were investigated for endoscope reprocessing Oxymatrine by questionnaire. Results: The results indicate that the main method for the reprocessing of endoscope’s in the hospital endoscopy center’s was mainly manual processing (51.4%) with 45.8% of the endoscope centers using a combination of both manual reprocessing and Automated endoscope reprocessing. Only 2.8% of the investigated endoscope centers completely used Automated endoscope reprocessing. A lot of infection risks will emerge inevitably with such a high proportion of manual reprocessing procedures, which will be shown in the following survey results. 68.5% of the investigated hospitals chose glutaraldehyde, 10% chose the ortho-phthalaldehyde, 11.6% chose acidified water, 10% chose Chlorine dioxide and PAA. Conclusion: Although there are many endoscopy procedures carried out in China, there are still lots of issue’s during endoscope reprocessing which have not attracted extensive attention this study hope’s to address some of these issues. Key Word(s): 1. Reprocessing; 2. GI endoscopy; 3. Cleaning; 4.

In these patients, palliative treatment is possible, employing systemic therapy. Genetic profiling has suggested that HCC progression is attributed PF-6463922 to a number of altered signaling pathways as well as epigenetic mechanisms. Thus, as in other tumor entities,

targeted agents are investigated as novel therapeutic options. Along this line, angiogenesis inhibition is a prime therapeutic target in solid tumors, especially in highly vascularized HCC. Since the successful completion of the SHARP study in 2007,2 the antiproliferative and angiostatic multi–tyrosin kinase inhibitor (TKI), sorafenib, has been approved as the first systemic agent for treatment of patients with unresectable or metastatic HCC and preserved liver function. Sorafenib primarily inhibits BRAF/vascular endothelial growth factor receptor (VEGFR)/platelet-derived growth factor receptor tyrosin kinases mediating

cell proliferation and angiogenesis; it also blocks many additional kinases, given its lack of selectivity.3 The mechanism underlying the antitumor effect of sorafenib is complex, and even RAF-independent signaling has recently been described as a significant pathway of sorafenib-induced cell death.4 At present, sorafenib represents the only drug with statistically significant, but clinically modest, benefit in terms of improvement in overall survival (OS), time to Rapamycin order progression (TTP), and disease control rate. Efficacy of sorafenib in HCC was demonstrated in two

large randomized, controlled trials (RCT): SHARP and the Asia-Pacific study,2, 5 sorafenib significantly reduces the risk of death and prolongs median OS by approximately 3 months. Survival benefit is based on an extended TTP. Sorafenib does not induce tumor-size reduction, and radiologic response has to be confirmed by a decrease in viable tumor mass. Therefore, to identify novel drugs with activity in HCC in future and PAK5 ongoing trials, modified Response Evaluation Criteria In Solid Tumors criteria have been proposed.6 FGF3/4, fibroblast growth factors 3 and 4; FGFR, FGF receptor; HCC, hepatocellular carcinoma; OS, overall survival; RCT, randomized, controlled trial; TKI, multi–tyrosin kinase inhibitor; TTP, time to progression; VEGFR, vascular endothelial growth factor receptor. Sorafenib is associated with relevant toxicities, especially in patients with compromised liver function (stage Child-Pugh B). Patients with cirrhosis suffer from fatigue, and in such patients, sorafenib may cause a rapid deterioration in quality of life. Therefore, predictive (bio)markers to guide therapy with sorafenib are urgently needed. Many clinical parameters and serum markers as well as genomic signatures have been suggested; for example, development of hypertension and diarrhea, known side effects of sorafenib, under therapy seem to be associated with a favorable outcome.

[48] Less data are available for the utility of serum CEA in CCA diagnosis. The Pittsburgh group reported that serum CEA level of > 5.2 ng/mL had a sensitivity of 68% and specificity of 82%.[44] One study showed that in patients with CCA, the biliary CEA level was about five times that of patients with benign strictures.[50] A combined index of serum CA 19-9 and CEA (CA 19-9 + [CEA × 40]) has been reported to correctly identified

10 of 15 patients with CCA, including 6 of 11 with radiographically occult disease; and without false positive.[46] This corresponded to an accuracy of 86% for CCA detection. A subsequent study however suggested that this score was no better than CA 19-9 alone in predicting the presence of CCA.[51] Rapamycin ic50 6. Cholangiography with tissue acquisition has been the traditional technique to diagnose HCCA. Cholangioscopy may be performed to increase the diagnostic yield. Level of agreement: a—80%, b—20%, c—0%, d—0%, e—0% Quality of evidence: II-2 Classification of recommendation: B Endoscopic tissue acquisition during ERCP can be performed either via papilla under fluoroscopic guidance or via mother–baby cholangioscopy. In general, the diagnostic

sensitivity of transpapillary biopsy under fluoroscopic guidance for CCA ranges from 40% to 60%.[40, 52-55] Transpapillary biopsy enables the collection of a relatively this website large amount of tissue because of the use of standard biopsy forceps. In contrast, mother–baby or spyglass or percutaneous cholangioscopy-assisted targeted

biopsy cannot always collect a sufficient amount of tissue because of the use of forceps with small jaws. In fact, the diagnostic sensitivity of cholangioscopy-targeted biopsy alone was previously reported to be suboptimal (49%).[56] However, the advantage of cholangioscopy is that it may additionally provide a cholangioscopic impression to better clarify some indeterminate cholagiographies. The pool data demonstrated that mother–baby cholangioscopy plus targeted biopsy can improve the sensitivity to detect biliary malignancy to 89–100% with the specificity of 87–96%.[57-59] 7. Cholangioscopy with image enhancement systems and triclocarban possible targeted biopsy or probe-based confocal laser endomicroscopy (pCLE) may improve the accuracy of HCCA diagnosis. Level of agreement: a—73%, b—21%, c—6%, d—0%, e—0% Quality of evidence: III Classification of recommendation: C Although peroral cholangioscopy such as conventional mother–baby scope and spyglass system can be useful for detecting CCA, the images’ quality is still suboptimal because of the limitation in resolution of the fiber-optic choledochoscope. With the advent in video endoscope and the image enhancement technology such as narrow band imaging, the vascular pattern of neoplasm in the bile duct can be better characterized by a new video choledochoscope.

As shown in Fig. 1B, IFN-γ and IL-4 were produced dominantly by hepatic iNKT (CD3+CD1d tetramer+) cells. Similarly, to analyze the antigen-presenting capacity of DCs, we evaluated surface marker expression 24 hours after α-GalCer injection compared to controls. Significantly increased expression levels of MHC class I (H-2Kb),

MHC class II (I-Ab), CD1d, CD80, CD86, and CD40 on DCs (CD11c+NK1.1− cells) in liver and spleen of mice administered with α-GalCer was noted compared to that of mice administered with PBS (Fig. 1C), suggesting that α-GalCer intravenously stimulated selleck kinase inhibitor the full maturation of DCs in liver and spleen. Four weeks postimmunization, serum autoantibodies IgM and IgG to PDC-E2 were significantly increased in α-GC/CFA/2-OA mice as compared to that of PBS/CFA/2-OA, α-GC, and α-GC/CFA control mice (Fig. 2A). Importantly, there was a significant increase in liver inflammation, portal inflammation, and bile duct damage in the α-GC/CFA/2-OA group compared to PBS/CFA/2-OA mice (Fig. 2B,C; Table 1). Further, ductular proliferation was observed in four out of five α-GC/CFA/2-OA mice but not in any (0/5) of the PBS/CFA/2-OA mice (Table 1). Furthermore, mild fibrous septa extension PD0325901 concentration (score = 2) was observed in three out of five α-GC/CFA/2-OA mice (Fig. 2C; Table 1). In addition,

there was significantly increased MHC class I, II, and costimulatory molecules CD86 and CD40 expression on the DCs of α-GC/CFA/2-OA mice compared to PBS/CFA/2-OA mice (Fig. 2D). There was a significant increase the in liver total mononuclear cells in α-GC/CFA/2-OA mice compared

to that of PBS/CFA/2-OA, α-GC, and α-GC/CFA control mice (Fig. 3A). In addition, significantly increased numbers of conventional T (CD3+ NK1.1−) cells and B cells were noted in α-GC/CFA/2-OA mice (Fig. 3B). Importantly, significantly increased absolute numbers of CD8+ T cells were noted in α-GC/CFA/2-OA mice compared to that of PBS/CFA/2-OA mice (Fig. 3C). Serum autoantibodies IgM and IgG to PDC-E2 were significantly increased in α-GC/CFA/2-OA mice as compared to PBS/CFA/2-OA, α-GC, and α-GC/CFA control mice (Fig. 4A). Examination of H&E-stained liver section revealed portal inflammation, bile duct damage, granulomas, proliferating bile ductules, and fibrous septa extension in the α-GC/CFA/2-OA group (Fig. 4B). In the α-GC/CFA/2-OA group, minimal to moderate (score = 1-3) liver inflammation, portal inflammation, and bile duct damage were observed (Fig. 4C; Table 1). Granulomas were found in 12/13 α-GC/CFA/2-OA mice (Fig. 4C; Table 1). In addition, fibrous septa extension was observed in all (13/13) α-GC/CFA/2-OA mice examined (Table 1). It is also important to note, as shown in Fig. 4D and Table 1, that 10/13 α-GC/CFA/2-OA mice demonstrated liver fibrosis as highlighted by silver staining and Azan staining.