Background and Aim Cytokines and matrix metalloproteinases (MMPs) beta (IL-1b), IL-1 receptor antagonist (IL-1 RN), transforming growth factor beta 1 (TGF-b1), MMP-1, MMP-3, and MMP-9 and the prognosis of hepatitis C virus (HCV)-related hepatocellular carcinoma (HCC). Methods We enrolled 92 HCV-related HCC patients in the study, and gene polymorphisms of IL-1b -31 C/ T, IL-1 RN variable number of tandem repeats (VNTR), TGF-b1 +869 C/T, MMP-1 -1,607 1G/2G, MMP-3 -1,171 5A/6A, and MMP-9 -1,562 C/T were analyzed. Results In HCC clinical features, TGF-b1 C carriers and MMP-3 5A carriers had significantly larger HCC diameters than TGF-b1 T and MMP-3 6A homozygotes. In HCC prognosis, IL-1b T homozygotes and

The divergent synthesis of natural withasomnines and analogues was achieved from 4-hydroxypyrazoles, which was prepared via alkaline hydrolysis of the Baeyer-Villiger oxidation products from 4-formylpyrazoles. Key steps of this synthesis are regioselective Claisen rearrangement of 4-allyloxypyrazoles and the Suzuki-Miyaura coupling of 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazol-3-yl trifluoromethanesulfonate and commercially available arylboronic acids. The Suzuki-Miyaura coupling at the final step of this strategy enabled facile access to natural withasomnines and their analogues. The biological activities of the twelve synthesized compounds against cyclooxygenases-1 and -2 (COX-1 and COX-2) were evaluated.

Objective The inter-individual difference in response to liver injury appears to be important in the progression of liver fibrosis. Interleukin 10 (IL-10) is an anti-inflammatory cytokine, and several functional gene polymorphisms have been found. The aim of this study was to examine the possible association of IL-10 polymorphisms with the progression of liver fibrosis in hepatitis C virus (HCV)-related chronic liver disease patients. Methods We examined the IL-10 -1087 A/G and -824 T/C gene polymorphisms in 184 Japanese patients with HCV-related chronic liver disease: 94 chronic hepatitis (CH) and 90 with liver cirrhosis (LC). Results There were no significant differences in the genotype distributions or allele frequencies of IL-10 -824 T/C and -1087 A/G between the CH and LC groups. However, among the cirrhotic patients, the lower transcriptional allele, -824 T homozygotes had significantly lower serum albumin and platelet counts, and a higher Child-Pugh score than the -824 C carriers, and the lower transcriptional allele, -1087 A homozygotes had a higher ICG-R 15 compared with -1087 G carriers. Haplotype analysis of IL-10 -1087/-824 showed no significant difference between the CH and LC groups, but the combinations of AT and AC haplotypes (AT/ AT, AT/AC and AC/AC) had a significantly higher ICG-R 15 than the GC carriers. Conclusion IL-10 lower transcriptional -824 T allele, -1087 A allele, and -1087/-824 haplotypes AT and AC are risk factors for the progression of liver fibrosis in HCV-related chronic liver disease.

We examined the association of TIMP-1 and TIMP-2 gene polymorphisms with the progression of chronic liver disease related to the hepatitis C virus (HCV). We used PCR to analyze 188 patients with HCV-related liver disease (95 with chronic hepatitis and 93 with cirrhosis) for TIMP-1 372 T/C and TIMP-2 -418 G/C polymorphisms. Comparing chronic hepatitis and cirrhosis, there were no significant differences in TIMP-1 and TIMP-2 gene polymorphisms. Among chronic hepatitis patients, TIMP-2 -418 G homozygotes showed significantly faster fibrosis progression than C carriers. Among cirrhotic patients, males with the TIMP-1 372 T allele developed cirrhosis at a younger age, and patients who were homozygous for the higher-transcription TIMP-2 -418 G allele had significantly lower serum albumin concentrations. These results suggest that faster progression of liver fibrosis could be associated with TIMP-2 -418 G homozygotes.

There are few reports of acute kidney injury (AKI) associated with influenza viral infection. We treated a case of AKI that developed after an influenza B viral infection. A 35-year-old man visited a local physician for a fever and was diagnosed with influenza B. He was prescribed laninamivir, then returned to the physician 5 days later with dyspnea and was referred to Hospital A. Upon admission, respiratory arrest developed, for which he received tracheal intubation and mechanical ventilation. AKI was noted after admission and the patient was transferred to our hospital the next day. AKI and disseminated intravascular coagulation (DIC) were present at the time of transfer, thus a transfusion and continuous hemodiafiltration (CHDF) were performed, and administrations of thrombomodulin alpha and antithrombin III were initiated. Although the patient had DIC, AKI, and disturbance of consciousness, and was in a clinical state resembling influenza-associated encephalopathy, there was no clear abnormality shown in CT scans of the head. Urine output, renal function, and respiratory condition gradually improved, thus CHDF was stopped and extubation performed. The patient had no complications and was discharged on hospital day 22. Some reports have been presented regarding cases of AKI due to rhabdomyolysis associated with influenza viral infection, whereas our patient developed AKI as a complication of an influenza B viral infection without rhabdomyolysis or hemolytic uremic syndrome. Influenza B may cause AKI and DIC, and affected patients can be in a serious condition requiring immediate attention.