Search

The syntheses, crystal structures, and magnetic properties of 2-D Hofmann-like motif {FeII(alkyl-pyridine)2[AuI(CN)2]2} (alkyl = 3,4-dimethyl (1), 4-ethyl (2), 4-isopropyl (3)), {FeII(alkyl-pyridine)2[AuI(CN)2]2}∙1/2(alkyl-pyridine) (alkyl = 3,5-dimethyl (4)), and {FeII(X-Isonicotinate)2[AuI(CN)2]2} (X = allyl (5), phenyl (6)) have been investigated. In spite of a wide range of substituent sizes, the structures of 1-3, 5, and 6 are almost crystallographically identical. The 2-D layer consists of an octahedral FeII ion coordinated with the nitrogen atoms in [AuI(CN)2] linear units at equatorial positions and monodentate py derivatives at axial positions. The adjacent two layers interact via intermetallic Au–Au interactions, forming a bilayer structure. The distance between stacking bilayers is associated with bulky substituent ligands. With increasing bulkiness, the interlayer distance expands without any transformation in the crystal structure. Compound 4 possesses guest space where uncoordinated 3,5-dimethyl-pyridine is present. Compounds 1-4 and 6 undergo spin transitions. Only 5 retains the high-spin state characteristic. These constant structures are similar to formerly reported Ag derivatives {FeII(alkyl-pyridine)2[AgI(CN)2]2}. The related Ag and Au families are compared and discussed. [ABSTRACT FROM AUTHOR]

We studied the synthesis and crystal structures of a new two-dimensional (2D) coordination polymer, {FeII(1-Ethyl-imidazole)2[NiII(CN)4]}n (1), and one-dimensional (1D) coordination polymers, {FeII(1-benzyl-imidazole)4[NiII(CN)4]}n (2) and {FeII(1-Allyl-imidazole)4[NiII(CN)4]}n (3). Compound 1 has a 2D sheet structure, which is a traditional Hofmann-like structure. In compound 1, an octahedral FeII ion is coordinated with the nitrogen atoms of the [NiII(CN)4] planar unit at equatorial positions and monodentate imidazole derivatives at axial positions. The layers construct a parallel stacking array. Compounds 2 and 3 have a 1D chain structure. In compounds 2 and 3, the FeIIN6 coordination environment is formed with four imidazole ligands and two [NiII(CN)4]2− metalloligands. In the [NiII(CN)4]2− unit, two CN substituents act as bidentate ligands that form infinite –Ni–C–N–Fe–N–C–Ni– chains. Herein, we discuss the systematic design of polymeric dimensionality. [ABSTRACT FROM AUTHOR]

Hepatocyte growth factor (HGF) has various effects especially on epithelial cells. However, the precise role of HGF on lipogenesis is still not fully understood. A high-fat diet was administered to HGF transgenic mice and wild-type control mice in vivo. Furthermore, recombinant human HGF (rhHGF) was administered to HepG2 cell line in vitro. We performed an analysis regarding the factors relating to lipid metabolism. An overexpression of HGF dramatically ameliorates a high-fat diet-induced fatty liver. HGF transgenic mice showed an apparently reduced lipid accumulation in the liver. The activation of microsomal triglyceride transfer protein (MTP) and apolipoprotein B (ApoB) accompanying higher triglyceride levels in the serum were found in HGF transgenic mice on a normal diet. Interestingly, this upregulation of the MTP activation became more apparent in the high-fat diet. In addition, the administration of rhHGF stimulated MTP and ApoB expression while reducing reduced the intracellular lipid content in HepG2 cell line. However, this induction of MTP and ApoB by HGF was clearly inhibited by PD98059 (MAPK inhibitor). In conclusion, the data presented in this study indicated that HGF ameliorates a high-tat diet-induced fatty liver via the activation of MTP and ApoB. hepatocyte growth factor: fatty liver; microsomal triglyceride transfer protein; apolipoprotein B doi:10.1152/ajpgi.00021.2007

Purpose: Helicobacter pylori (HP) infection is reported to increase 18F‐fluoro‐2‐deoxyglucose (FDG) accumulation in the stomach. The accumulation of FDG by positron‐emission tomography (FDG‐PET) in the stomach for the voluntary health examinees of cancer checkup was examined before and after the HP eradication. Subjects and Methods: From March 2013 to October 2015, eighty‐one subjects were performed FDG‐PET to detect cancer at the health checkup. All of them were also surveyed by esophagogastroduodenoscopy. Subjects were classified as the 33 cases of HP positive (group A), 38 cases of originally negative (group B), and the 10 negative cases by HP eradication therapy (group C). Group A was treated by combination of amoxicillin, clarithromycin, and proton pump inhibitor for a week, and all of them eradicated HP. A part of group A (n = 7) was serially performed FDG‐PET one to five years after the treatment and compared the maximum standard uptake value of FDG (SUV) around the fundic gland region. Results: SUV of group A (3.55 ± 0.69) was significantly higher than those of both group B (2.96 ± 0.72) and group C (2.89 ± 0.51) (p < 0.01, respectively). Groups B and C are almost comparable and showed no significant difference during the course. In group A, HP eradication significantly decreased the SUV to 3.1 ± 0.43 (P <.01). SUV after the eradication was significantly reduced (P <.01) in the mild to moderate atrophy (C1–C3) group according to Kimura and Takemoto classification of chronic gastritis of group A. Although SUV in the advanced atrophy group (O1–O3) tended to decline after the eradication, the change was not significant. Conclusion: HP‐infected stomach showed higher FDG uptake in the fundic gland region and HP eradication decreased the uptake in the mild to moderate atrophic gastritis but not in the severe atrophic gastritis. [ABSTRACT FROM AUTHOR]

Abstract Background Transforming growth factor α (TGFα) protects against gastric mucosal injury and facilitates wound healing. However, its overexpression is known to induce hypertrophic gastropathy resembling Menetrier's disease in transgenic (TG) mice on an FVB background, as one of the authors reported previously. We studied another TGFα-expressing mouse line on a CD1 background, whose gastric mucosa appears normal. Since this TG mouse had a strong resistance to ethanol-induced gastric injury, we considered the long-term effect of TGFα on several gastric protection mechanisms. Methods TGFα-expressing transgenic (TG) mouse lines bearing human TGFα cDNA under the control of the mouse metallothionein gene I promoter were generated on a CD1 mouse background, and analyzed their ethanol injury-resistant phenotypes produced by TGFα. Results In the TG mucosa, blood flow was well maintained after ethanol injury. Further, neural and inducible types of NO synthases were consistently and widely expressed in the TG mucosa, compared with the limited distribution of neural type NO synthase in the luminal pit region of the wild-type (WT) mucosa. COX-2 and its upstream transcription factor NfkB were constitutively elevated in the TG mucosa even before ethanol administration, whereas they were induced in the same region of the WT mucosa only after ethanol injury. Two anti-apoptotic proteins, HSP70 and Bcl-2, were upregulated in the TG mucosa even before ethanol administration, while they were not expressed in the WT mucosa before the injury. Furthermore, pro-caspase 3 activation was inhibited in the TG mucosa, while it was converted to the active form in the WT mucosa following ethanol administration. Conclusion We conclude that TGFα maintains the gastric mucosal defense against gastric injury by integrating other cytoprotective mechanisms.

Broncho-biliary fistula (BBF) is a rare but severe disorder defined as abnormal communication between the biliary system and bronchial tree. Cases of BBF have occasionally been reported, but no standard treatment has been established. We report two cases of BBF that developed after the treatment of hepatocellular carcinoma (HCC) and reviewed the relevant literature. Case 1, a man in his early eighties was diagnosed with BBF 4 months after undergoing surgical resection for HCC (diameter, 7 cm; location, segments 4 and 5). Percutaneous drainage and endoscopic nasobiliary drainage (ENBD) improved BBF without recurrence for more than a year. Case 2, a woman in her late sixties was diagnosed with BBF after percutaneous radiofrequency ablation for HCC. Although the BBF was treated with ENBD, bronchial occlusion, and percutaneous transhepatic portal vein embolization, these treatments were unsuccessful and the patient died. Although non-invasive treatments have been developed, refractory BBF still exists. The prediction of BBF and the development of more effective treatments are necessary to improve outcomes. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to evaluate the real‐world efficacy and safety of 12‐week sofosbuvir/velpatasvir (SOF/VEL) treatment for patients with decompensated liver cirrhosis caused by hepatitis C virus (HCV) infection. Methods: A total 72 of patients with Child–Pugh (CP) class B or C were enrolled. We evaluated the sustained virologic response at 12 weeks after the end of treatment (SVR12), adverse events (AEs), and changes in the liver function. Results: All participants had genotype 1 or 2 HCV infection. At baseline, the numbers of patients with CP class B and C were 59 and 13, respectively. The overall SVR12 rate was 95.8% (69/72); 94.9% (56/59) in CP class B and 100% (13/13) in CP class C. The serum albumin level, prothrombin time and ascites were significantly improved (P < 0.01); however, the serum bilirubin level and encephalopathy did not improve. Among patients who achieved SVR12, 75.0% showed an improvement in their CP score, while 5.9% showed a worsening. The presence of large portosystemic shunt (diameter ≥6 mm) and hyperbilirubinemia (≥2.0 mg/dL) were independent factors that interfered with the improvement in the CP score (P < 0.05). The most common AEs were encephalopathy (15.3%) and skin symptoms (7.9%). Two patients discontinued SOF/VEL due to AEs. Conclusions: Treatment with SOF/VEL for 12 weeks was relatively safe and effective for patients with decompensated cirrhosis. An SVR provided an improvement of the liver function in the majority of patients. However, large portosystemic shunt and hyperbilirubinemia were independent factors that interfered with the improvement in the CP score. [ABSTRACT FROM AUTHOR]

Background and Aim: We investigated the prognosis of late elderly patients (≥75 years old) after the achievement of a sustained viral response (SVR) by direct‐acting antivirals (DAAs). Methods: One hundred and four late elderly patients and 251 young patients (≤74 years old) who had achieved an SVR were included. We compared the cumulative hepatocellular carcinoma (HCC) incidence rates and survival rates after DAA administration. Furthermore, the factors associated with HCC incidence and the causes of death after DAA administration were also investigated. Results: The cumulative HCC incidence rates for 1 and 3 years were 2.9% and 11.7% in the late elderly patients and 2.4% and 5.4% in the young patients, respectively. The cumulative survival rates for 1 and 3 years were 100% and 95.6% in the late elderly patients and 100% and 96.4% in the young patients, respectively, with no significant differences in those rates noted (P = 0.133, P = 0.322, respectively). In the late elderly patients, only a history of HCC was a significant factor associated with HCC incidence after DAA administration. Five late elderly patients died after achieving an SVR, and malignant liver tumor was the cause of death in three of those patients. Conclusions: The prognosis did not differ markedly between late elderly patients and young patients. The factor most strongly influencing the prognosis of late elderly patients was likely liver disease, including HCC. DAAs should be introduced even in late elderly patients who can be expected to have a relative long‐term survival. [ABSTRACT FROM AUTHOR]