Pylori eradication rate between different durations of this quadruple therapy and Deforolimus purchase still remained further research. Key Word(s): 1. Helicobacter, pylori; 2. Drug therapy; 3. Levofloxacin; 4. Bismuth; Presenting Author: XI LIU Additional Authors: HONG CHENG, WEN GAO, XINHONG DONG, FULIAN HU Corresponding Author: HONG CHENG Affiliations: Peking Unversity First Hospital Objective: Increasing resistance to antibiotics is the main cause of failure in the Helicobacter pylori (H. pylori) eradication. The efficacy of the first-line therapy including proton pump inhibitors plus two antibiotics seems to have decreased. So many patients need to receive rescue therapy for the eradication of H. pylori after

first- or second-line therapies. We designed this study to collect patients who have

received furazolidone-based quadruple rescue therapy for two weeks and evaluate the efficacy, compliance and adverse effects of this regimen. Methods: A total of 210 patients with H. pylori positive [13C-urea breath test or rapid urease test positive] failing in previous treatment at least once were enrolled in this study. The average age of the patients was 51.6 years, ranging from 18 to 83 years. They have received a 14-day quadruple therapy with furazolidone, amoxicillin, bismuth citrate in combination MLN0128 price with proton pump inhibitors. To record the side effect profiles at the end of the treatment, H. pylori eradication was assessed with 13C-urea breath test 4 wk after therapy. Results: Two hundred and ten patients including seventy-two males completed this study. H. pylori eradication rate were 90.4% (190/210) according to per-protocol analyses. Mild and moderate adverse effects such as dizziness, nausea, and diarrhea were reported by 30 patients (14.3%). None of the 30 patients needed treatment

for their side effects. Conclusion: Regarding the eradication rate (PP > 90%), low price, and very low adverse effects, a 14-day quadruple therapy with furazolidone, amoxicillin, bismuth citrate and proton pump inhibitors can be an encouraging regimen for H. pylori infection treatment. Key Word(s): 1. H. pylori; 2. furazolidone; 3. efficacy; 4. safety; Presenting Author: YUEMIAO ZHANG Additional Authors: HONG CHENG, XUEZHI very ZHANG, WEN GAO, XINHONG DONG, FULIAN HU Corresponding Author: HONG CHENG, XUEZHI ZHANG Affiliations: Peking University First Hospital Objective: Antibiotic resistance is the main cause of failure of H. pylori infection treatment, especially when the strains resistant to clarithromycin, metronidazole and quinolone. Tetracycline and furazolidone resistance of H. pylori strains are both rare. The 4th Consensus Report of H. pylori infection in China has recommended tetracycline, furazolidone-containing quadruple regimen can be used for H. pylori eradication. However, the safety of this regimen has always been a concern.

4 The large degree of HCV genomic variation, the lack of protective immunity generated by HCV infection, and frequent opportunities for re-exposure through ongoing injection behaviors underpin the recognized occurrence of multiple HCV infections.5-10 Multiple infection is classified as either mixed infection (also sometimes referred to as coinfection), superinfection, and/or reinfection (see review by Blackard and Sherman11). Although multiple infection has been well studied for other viruses, relatively little is known about selleckchem multiple HCV infection. Primary HCV infection in chimpanzees

followed by re-exposure to viruses from either homologous or heterologous HCV strains has been reported to be associated with mild hepatitis and partial immune protection.12, 13 In humans, mixed HCV infection is generally transient, with evidence of replacement with the new strain or persistence of the primary strain.8,

14, 15 The reasons for the transient nature of mixed infection have yet to be elucidated but may relate to a more effective immune response against one virus (in contrast to the other),16 competition between the two viruses (with the fitter strain Wnt assay having an advantage),17 or a combination of these factors. There are limited data regarding the clinical associations of multiple infections. One cross-sectional study by Fujimura et al.10 of 96 HCV-infected patients with hemophilia reported higher alanine aminotransferase levels reflecting greater hepatocellular injury in nine patients (12%) who had mixed HCV genotypes. Another study by Kao et al.18 observed that mixed infection was more often associated with acute exacerbations during chronic hepatitis C infection than monotypic infection. The reported prevalence of multiple infection in HCV-infected

subjects ranges from 5% in a cohort of patients coinfected with HCV and human immunodeficiency virus19 to 39% in a cohort of IDUs.5 The high prevalence of multiple infection in IDUs and the association with high-risk behavior indicates that ongoing injection and needle sharing following primary infection can lead to subsequent acquisition of new HCV strains.5, 6, 20 Longitudinal studies to estimate the incidence of multiple infection include a small number of case series8-10, not 15 as well as prospective5-7, 21 and retrospective22, 23 analyses of stored samples. One of the retrospective studies within an IDU population reported a 1.8-fold higher incidence of reinfection (31/100 person-years; 95% confidence interval [CI] 17-62/100 person-years) compared with naïve infection (17/100 person-years; 95% CI 14-20/100 person years).22 In a recent IDU-based prospective study, the incidence rate of reinfection was 2.5-fold higher than primary infection and was associated with injection risk behavior.

Put into perspective, treatment-emergent grade 3 or 4 liver dysfunction was documented in 5% of placebo-treated and 7% of sorafenib-treated selleckchem patients in the pivotal SHARP (Sorafenib HCC Assessment Randomized Protocol)

trial.30 Regarding survival analysis, when the joint contribution of single-vector prognostic factors are considered in a multivariate model, the performance status, disease burden (intrahepatic and extrahepatic) and liver function (as measured by total bilirubin >1.5 mg/dL) provide further indications of predicted clinical outcome. Because these factors are considered by the BCLC staging system, it is no surprise that survival is progressively worse for each BCLC stage. In the background of BCLC staging, increased tumor burden (as reflected by multinodularity and bilobar involvement) or aggressiveness

(as determined by high alpha-fetoprotein, portal vein thrombosis , or poor performance status) and worsened liver function (as reflected by increased bilirubin or INR) provide additional prognostic information. The survival outcomes in specific cohorts compare favorably with other locoregional treatment options (chemoembolization and arterial embolization) that would typically be considered for unresectable patients in BCLC stages Y-27632 manufacturer A and B, as has also been shown recently.31 Data from our series show that survival after radioembolization appears particularly promising for the subset of patients with intermediate stage HCC who are considered poor candidates for chemoembolization (i.e., those with bilobar and/or multiple [>5] tumors; median, 15.4-16.6 months) as well as for those who had failed prior chemoembolization or arterial embolization (median, 15.4 months). Survival is also promising for the group of patients with advanced stage disease (BCLC C), particularly those with portal vein thrombosis , where radioembolization compares well to that observed after

sorafenib treatment and is well tolerated. A potential find more confounding effect on survival due to sorafenib therapy given after radioembolization was ruled out. The main limitation of this study is its retrospective nature, although many patients were in fact followed prospectively and more than 98% of the data were available for the multivariate model. Due to this retrospective nature, we could not assess intention-to-treat patients who were evaluated for radioembolization but were considered inappropriate due, for instance, to insufficient liver function or technical considerations such as uncorrectable vasculature that would have led to the misdirection of microspheres to the gastrointestinal tract and other nontarget organs or excessive shunting of radiation to the lung. In addition, strict recommendations from the manufacturer and consensus guidelines23 were not always followed (e.g., patients compromised by poor liver function or with ECOG performance status >2 were treated showing unsurprising poor outcomes).

Collectively, BTK phosphorylation these results indicate that mTOR activation could suppress LHBs expression through a negative feedback loop that repressed pre-S1 promoter activity. To determine the critical elements responsible for pre-S1 promoter repression by mTOR signal, we constructed three 5′-deletion mutants of pre-S1 promoter reporter plasmids (Fig. 5Aa,b,c). As shown in Fig. 5Ba,b,c, luciferase activities of all these deletion mutants consistently showed that only approximately 50% of the activities were detected in pre-S2 mutant-expressed cells, compared with those in control cells, indicating that nucleotide 2789-2845 of the pre-S1 promoter was the minimal

region for mediating mTOR signal-induced transcriptional repression. A computer search further revealed that this region contains three putative transcription factor binding sites at nucleotide AZD2014 2794-2801 (site 1), 2812-2816 (site 2), and 2820-2825 (site 3) of the pre-S1 promoter. We, therefore, generated pre-S1 promoter constructs with mutations at each one of these three sites (Fig. 5Ad,e,f) for further assays. As shown in Fig. 5Bd,f, activities of pre-S1 promoter-carrying mutations at site 1 or site 3 still showed mTOR activation-dependent repression, indicating that these

two sites were not responsive elements for the mTOR signal. Interestingly and unexpectedly, the mutation at site 2 resulted in a relatively low or insignificant luciferase activity of the pre-S1 promoter (Fig. 5Be), suggesting that site 2 was transcriptionally necessary for pre-S1 promoter activity. To further evaluate the role of site 2 in pre-S1 promoter repression by mTOR, we created

one additional mutant construct, in which site 2 remains intact, but site 1 and site 3 are mutated (Fig. 5Ag). We observed that this mutant construct could negatively respond to mTOR activation (Fig. 5Bg). Therefore, the 2812-2816 site appeared to be not only transcriptionally important for pre-S1 promoter activity, but also capable of mediating a suppressive effect under the status of mTOR activation. Because sequence analysis revealed that the 2812-2816 site of pre-S1 promoter is the putative binding site for transcription factor YY1, we performed EMSA and DAPA to confirm Anacetrapib the binding of YY1 to this site. In the EMSA experiment, two major shifted bands (a and b) were detected using WT probes containing the 2812-2816 site, one (a band) of which was not detected using the Mut probes, which destroyed the 2812-2816 site (Fig. 6A). Coincubation with competitors abrogated the formation of these two bands. The data suggest that the slower migrating band (a), but not the faster migrating band (b), represented the YY1-probe complex. To further confirm this speculation, we additionally added YY1 antibody to the reaction mixtures and observed specifically reduced intensity of the slower migrating band (a). This data further verified the interaction of YY1 with the 2812-2816 site.

2 Our study evaluated virtually all patients treated for hepatitis C in a Brazilian state, so differences with respect to the clinical trials cannot be explained by the treatment of minorities; besides, our state population is predominantly European in origin and does not fit within the groups suspected Pifithrin-�� datasheet of having worse responses. It also seems important to consider that even Caucasian patients

in Feuerstadt et al.’s cohort had worse results than those in the efficacy trials. Although the sustained virological response (SVR) rate ranged from 54% to 63% (42%-52% for genotype 1) in the trials,3-5 Feuerstadt et al.1 showed an SVR rate of 21% (14% for genotype 1 and 37% for genotype 2/3) in a sample of 255 patients with a mean age of 50 years (60% were male, 68% had genotype 1, and 29% had cirrhosis). We, on the other hand, found an SVR rate of 35.3% in a sample of 323 genotype 1–monoinfected individuals with a mean age of 51.1 years (55.7% were male, 57% had a pretreatment

viral load > 600,000 IU/mL, 73.9% had a METAVIR score of F3 or F4, and 30% had cirrhosis).2 The mean age and the proportion of patients with advanced fibrosis were much greater in both cohorts in comparison with the clinical trials.1-5 In Feuerstadt et al.’s study, 23% of the patients discontinued treatment because of side effects, whereas only 10.2% did so in our study. For both cohorts, intention-to-treat analysis was used.1, 2 A factor that could help to explain the differences between these two effectiveness studies is that for Feuerstadt et al.,1 26% of the patients were

lost to follow-up, Regorafenib chemical structure whereas we did not have such a problem,2 probably in part because the treatment is offered by the Brazilian Government, which provides more rigid control and ensures that the treatment is delivered until its completion once it has been started. It is important to remember that losses of more than 20% in cohort studies may diminish the confidence in their results. It is true that other authors have published cohorts with results closer to those shown in the trials. A recent review of the matter claims that the results of most cohorts collectively confirm those of the trials.6 We understand, however, that a careful evaluation must be performed see more before such a conclusion can be drawn; the aforementioned review is not systematic and includes results published in abstracts and in preliminary analysis and other results with important methodological flaws. A systematic review of this matter is of the utmost importance, although our impression is that the results of the clinical trials do not entirely correspond to those we find in real life, as already shown for interferon and ribavirin in the past.7 Ângelo Zambam de Mattos M.D.*, Paulo Roberto Lerias de Almeida Ph.D.* †, Cristiane Valle Tovo Ph.D.

“
“The global incidence of fatty liver disease (FLD) has eclipsed

nearly every other hepatic pathology, largely due to the obesity epidemic. Steatosis is the first requisite step in progression to steatohepatitis and cirrhosis, the more severe forms of FLD. Lifestyle changes remain the most effective treatment for FLD; however, waistlines continue to expand in parallel with a booming weight-loss industry, indicating that lifestyle changes are both difficult to achieve and ineffective for many patients. Thus, targets for therapeutic intervention are sought. A study in this issue of Hepatology[1] suggests a novel pathway that contributes to steatosis, opening new avenues for designing drugs to alleviate FLD. Many investigators studying hepatic injury have A769662 focused on the role of reactive oxygen species (ROS), such as hydrogen

peroxide (H2O2). High levels of ROS can result in severe cell dysfunction or death. Some studies suggest that ROS can cause FLD, while many others focus on the consequence of ROS once FLD has formed. Promising results from clinical trials using antioxidants in patients with nonalcoholic[2] and alcoholic[3] FLD (i.e., nonalcoholic fatty liver disease [NAFLD] and alcoholic liver disease [ALD], respectively) Mitomycin C support the theory that ROS can cause steatosis as well as the hepatic injury associated with FLD. The work by Nussbaum et al.[1] in this issue of Hepatology challenges this theory by demonstrating a paradoxic role for ROS in FLD: instead of contributing

to the pathogenesis of FLD, low (i.e., homeostatic) levels of ROS appear to prevent steatosis and addition of antioxidants promotes steatosis. Moreover, they uncover a previously unrecognized link between purine metabolism, ROS, and regulation of lipid droplet formation and utilization in hepatocytes. This study benefited from the use of zebrafish, a small vertebrate with high reproductive capacity and a fully sequenced genome that shows high conservation with humans.[4] The larval liver has a cellular composition comparable to mammals, and their hepatocytes all can synthesize, store, and metabolize lipids. Thus, zebrafish, like mammals, get FLD.[5] These attributes make zebrafish the only vertebrate amenable to forward genetic screening, which provides an unbiased approach to identify novel genes involved in FLD. Additionally, zebrafish larvae are transparent, providing an unparalleled view inside of the growing organism. The authors capitalize on this feature to develop a novel means to measure steatosis. Confocal imaging of the liver sections of larvae, where the contours of the hepatocytes are outlined with green fluorescent protein (GFP) and a fluorescent dye that labels the lipid droplets, allows quantification of cells containing lipid droplets as well as the number of droplets per cell, and also generates exquisite 3D images, rendering this pathology at subcellular resolution.

“
“The pathogenesis and diagnostic methods for idiopathic normal pressure

hydrocephalus (iNPH) have been active areas of research in recent years. This study was performed to determine whether there is a venous return abnormality in the intracranial circulation of patients with iNPH. The subjects were 20 patients with iNPH (Group N) and 24 normal controls (Group C). MR venography (MRV) was performed at the superior sagittal sinus 2 cm above the confluence of the sinuses, and the flow velocities were compared between Groups N and C. During normal breathing, the maximum velocities were significantly lower in Group N (18.8 cm/second) than in Group C (22.9 cm/second; (P < .01). During the Valsalva maneuver, compared to normal breathing, the velocity decreased in both groups, but both the maximum CH5424802 (Max V) and minimum (Min V) velocities were significantly ABT-263 cost lower in Group N than in Group C (P < .01). The flow velocity at the superior sagittal sinus was lower and the flow velocity during the Valsalva maneuver decreased more in patients with iNPH than in controls. The results may reflect the presence of abnormal intracranial venous flow in iNPH. J Neuroimaging 2011;21:365-369. "
“Requests for after-hours emergent spine MR imaging seem to be increasing. We sought to review the

trend in after hours spine MRI utilization at our institution and to determine how these results impacted therapeutic intervention. Following Institutional Review Board approval, reports from 179 after hours spinal MRI’s performed over the past 13 years were obtained and Lepirudin the relevant electronic medical records were reviewed. Emergent after hours spine MRI utilization increased from 7 per year to 23 over 13 years. Fifty-eight percent (104/179) had significant findings. Twenty-nine percent (52/179) of all patients imaged underwent surgery to treat pathologies identified on MR. Surgery was performed in only 2% (4/179) of these patients within 3 hours and 6% (10/179) within 6 hours of MRI completion. Five percent (8/179) had findings

that were treated with radiation therapy and in 78% of these it was performed within 6–12 hours. Of those in whom steroids or antibiotics were initiated, 41% and 50% were treated within 3 hours of MR scanning, respectively. Clinical use of emergent after hours spine MRI is steadily increasing at our institution. While MR imaging often discerned significant pathologies, performing these emergent studies rarely resulted in immediate surgical or radiotherapeutic intervention. “
“Distinguishing BNCT from chordoma with imaging is critical because of the profound differences in prognosis and management. Yet few reports define the variable imaging characteristics of BNCT. This study aims to evaluate the prevalence and characteristics of BNCT. A total of 916 patients with 64-section CT and 1.

It should be considered, however, that fibrosis, inflammation, and increased cell turnover are key processes implicated in the development

selleck chemical of liver cancer.28 Therefore, by reducing liver fibrosis and exerting antiinflammatory effects this therapy might in fact reduce the risk of liver carcinogenesis. Interestingly, multifocal bile duct proliferation, a process that precedes carcinogenesis in the TAA model, was markedly decreased in SVIGF-I-treated rats.29 Moreover, in rats with CCl4-induced cirrhosis, IGF-I therapy favors hepatocellular differentiation (up-regulation of HNF4α and down-regulation of WT-1), which may oppose tumorigenesis (Fig. 7). In fact, up-regulation of WT-1 has been shown to be associated with HCC development,18 suggesting that the effect of IGF-I in suppressing its expression may inhibit tumor formation. According to this idea it has been shown that a sharp decrease of IGF-I production by the cirrhotic liver increases the risk of hepatocellular carcinoma (HCC).30 Although there is activation of IGF-IR in HCC, the levels of IGF-I in tumor tissue are markedly diminished, whereas there is check details up-regulation of IGF-II, suggesting that the latter, and not the former, is the ligand involved in IGF-IR signaling in the tumor.31 As shown above, our data indicate that

in the cirrhotic liver IGF-IR is mainly expressed by nonparenchymal cells present in fibrous septa. The very poor expression of this receptor in hepatocytes would minimize any direct effect of the molecule on these cells. However, IGF-I gene therapy should not be administered to patients with cirrhosis who have already developed HCC because this therapy may

enhance tumor growth due to the abundance of IGF-IR in already transformed hepatocytes. In summary, we show that gene transfer of IGF-I to the cirrhotic liver sets in motion a curative process involving 17-DMAG (Alvespimycin) HCl increased expression of cytoprotective and antifibrogenic molecules and reduced expression of profibrogenic factors. IGF-I seems to be able to reprogram the liver from a “scar formation” response, which leads to cirrhosis, to a “tissue repair” circuit that favors cirrhosis regression. According to these findings IGF-I gene therapy might be of value for patients with advanced cirrhosis who do not have access to timely liver transplantation. We thank Pilar Peréz and Uxue Latasa for help with liver cells isolation, Maria Vera for SVIGF-I production, Ana Sandoval for the thioacetamide model, and Monica Enguita and Erkuden Casales. Additional Supporting Information may be found in the online version of this article. “
“Immunization with effective cancer vaccines can offer a much needed adjuvant therapy to fill the treatment gap after liver resection to prevent relapse of hepatocellular carcinoma (HCC). However, current HCC cancer vaccines are mostly based on native shared-self/tumor antigens that are only able to induce weak immune responses.

14–16 In the most recently-updated cancer staging manual by the American Joint Committee on Cancer and International Union against Cancer, the entire section of gastric cardiac cancer involving the distal esophagus has been removed from the chapter on the stomach into that of the esophagus.17 The manual requires using the esophageal cancer-staging criteria for pathological staging of cancers arising in the proximal stomach with esophageal involvement.17 This dramatic

change in paradigm has prompted us to critically review the histological selleck inhibitor evidence on CG in the proximal stomach published in the recent English literature. In 1961, Salenius published a histological study on gastric mucosal development at different gestational ages.18 The formation of gastric click here pits was found at week 8 in all portions of the stomach, except for the pylorus and cardia. Parietal cells were the first differentiated, glandular

cells, while pyloric glands and CG started to develop at week 13.18 These findings were confirmed by the data from a recent, similar study in 2003.19 Using the PAS–alcian blue stain, the investigators showed the presence of CG in all embryonic specimens.19 In their report, the CG formed a single layer of the epithelium lined with tall columnar cells, with a mucus-filled, apical cytoplasm containing both neutral and sialylated mucins, which differed from parietal cells conspicuously on hematoxylin–eosin (HE)-stained sections. Only neutral mucin was present in most superficial foveolar CG. From gestational age 15 weeks onwards, these mucus cells started to form

the CG that opened into pits. At week 23, the squamous mucosa with remnant ciliated columnar cells replaced the primitive esophageal mucosa, and was positioned proximally to the CG. In the last trimester, Terminal deoxynucleotidyl transferase the CG were further differentiated. At week 41, all CG secreted neutral mucin. The authors emphasized that both the CG and the CM were present in all sections of all cases19 (Table 1). This conclusion was similar to, but differs to some extent from, that of an earlier fetal study in 2001.20 In that report with routine, histological sampling, the CG and oxyntocardiac glands in the transition zone were found in 6% and 52% of cases, respectively.20 Both studies found that the number of CG increased with increasing gestational age.19,20 In 2003, Park et al.21 studied the same transition zone with either HE or PAS staining (Table 1). They found that this transition zone measured <0.4 mm, always contained oxyntic cells, but lacked CG in 20% of cases. This observation is different from that reported by De Hartogh et al.,19 who stated that the “CM was distal to, or straddled, the angle of His in all cases”.

A marked increase in the level of NOX1 mRNA was demonstrated in WT liver at day 3 and reached up to 6-fold at day 10 after BDL (Fig. 1A). In both genotypes the levels of NOX2 mRNA were similarly increased at day 10 after BDL. Meanwhile, the expression of NOX4 mRNA was unchanged (Supporting Fig. 1). To examine the effect of Nox1 deficiency on liver injury, serum ALT and AST levels were measured. Ten days after BDL, both parameters were significantly higher in WT than those in Nox1-deficient mice (Nox1KO) (Fig. 1B).

Furthermore, increased levels of collagen 1α (col-1α) mRNA and hydroxyproline, an amino acid specifically contained in collagen, were significantly suppressed in the liver of Nox1KO after BDL (Fig. 1C). These findings suggest that liver injury and fibrosis Gefitinib mw were attenuated in the absence of NOX1. In line with these findings, histological

analyses demonstrated marked collagen deposition in WT liver, whereas less deposition was observed in Nox1KO after BDL (Fig. 1D). As activated HSCs are the major source of collagen matrix, expression of α-SMA, a marker of activated HSCs, was examined at 10 days after BDL. A marked increase in mRNA and protein levels of α-SMA was observed in WT, whereas the levels were significantly suppressed in Nox1KO (Fig. 2A,B). Histological analyses also illustrated that α-SMA-positive HSCs were less PD98059 order apparent in Nox1KO (Fig. 2C). Several cytokines, such as PDGF, TGF-β1, tumor necrosis factor alpha (TNF-α), and macrophage chemoattractant protein-1 (MCP1) are Sodium butyrate known to take part in the development of liver fibrosis.1,

18-20 Following BDL, levels of PDGF, TGF-β1, TNFα, and MCP1 mRNAs in the liver were markedly increased, but no difference was observed between WT and Nox1KO (Supporting Fig. 2). We next investigated whether similar findings are observed in a different model of liver fibrosis. Repeated administration of the chemical hepatotoxin CCl4 elicited a significant increase in NOX1 mRNA in the liver. In contrast to the BDL model, however, the levels of col-1α and α-SMA protein were unaffected by Nox1 deficiency after 8 weeks of CCL4 treatment (Supporting Fig. 3). In the liver, expression of NOX1 was reported in hepatocytes and HSCs, but not in Kupffer cells.21 We therefore isolated hepatocytes and treated them with chenodeoxycholic acid, one of the key components involved in the pathogenesis of BDL-induced fibrosis. No change in the level of NOX1 mRNA was observed, whereas activation of caspase-3 induced by bile acid was significantly diminished in hepatocytes isolated from Nox1KO (Supporting Fig. 4A,B). We next isolated HSCs and the expression of NOX1 mRNA was assessed in primary culture. It is known that HSCs in culture are spontaneously activated.22 As shown in Fig. 3A, a time-dependent increase in NOX1 mRNA, which was undetectable until day 3, was demonstrated in cultured HSCs. Concomitantly, increased expression of α-SMA and col-1α mRNAs was demonstrated (Fig. 3B).