To study the relationship between the disturbance of nitric oxide/endothelin-1 (NO/ET-1) and the hepatic ischemia/reperfusion (I/R) injury as well as the regulation of the NO/ET-1 system by the hepatic ischemic preconditioning (IPC), the changes of the NO/ET-1 system and their relationship with the hepatic I/R injury were compared between the I/R group and the IPC+I/R group in a rat hepatic I/R model. 2 h after reperfusion, the liver tissues were examined for expressed inducible nitric oxide synthase (iNOS) mRNA by RT-PCR. In the acute phase of hepatic reperfusion, the ratio of NO/ET-1 was reduced, which was due to the significant reduction of NO₂⁻/NO₃⁻ (the metabolic product of NO) and significant elevation of ET-1 in the blood plasma. The content of ALT, AST, LDH and TNF-α in blood plasma, and level of MDA in liver tissue were increased but ATP in liver tissue was reduced, and the hepatic damage was deteriorated. The protection of the hepatic IPC was associated with the elevated ratio of NO/ET-1 caused by the elevation of NO₂⁻/NO₃⁻, and reduction of ET-1 as well. No iNOS mRNA was detected in the liver tissues. It was concluded that hepatic I/R injury was related to the disturbance of NO/ET-1. The protection of the hepatic IPC in the acute phase might be mediated by its regulation of NO/ET-1 system. The cNOS rather than the iNOS generated the NO in this scenario.

To understand the expression and effect of mismatch repair genes, hMSH2 and hMLH1, and to investigate anti-leukemic cell proliferation mechanism of curcumin, the levels of both genes were detected by multiple comparative RT-PCR. The protein of hMSH2 was determined by flow cytometry (FCM) and the gene mutation of hMSH2 and hMLH1 were detected by PCR-SSCP and microsatellite instability assay. After UV irradiation, the gene expression of hMSH2 and hMLH1 was not increased and showed no response. This phenomenon was not ascribed to gene mutation, because PCP-SSCP and microsatellite instability assay revealed no abnormal gel-shift band in both genes. After irradiation and addition of curcumin, the expression of hMSH2 mRNA increased and the cellular apoptotic rate also increased at the same time. The difference was statistically significant as compared with groups without addition of curcumin and control groups (P<0.05). Our results suggested that when MMR system was inhibited by the same agents, curcumin can remove this suppression and switch to cellular apoptosis.

To identify the knowledge of rare lymphoproliferative disorder, the clinical and biological features of three kinds of lymphoproliferative disorders with cytoplasmic projections were compared. The clinical manifestations, ultrastructure and immunophenotype were analyzed. The results showed that hairy cell leukemia (HCL), splenic lymphoma with villous lymphocyte (SLVL) and hairy cell leukemia-variant (HCL-V) had some common characters including splenomegaly, peripheral blood and bone marrow infiltration by villous lymphocyte and B lymphocyte immunophenotype; but these three disorders had specific features respectively. It was concluded that overall analysis of clinical and laboratory features might be contributive to the differential diagnosis of these three disorders.

We investigated the expression of heme oxygenase-1 (HO-1) gene and production of endogenous carbon monoxide (CO) in the rat lung tissue at different time points of chronic hypoxic pulmonary hypertension and the effect of hemin on the expression of HO-1 gene and pulmonary hypertension. A rat model of hypoxic pulmonary hypertension was recreated by exposure to intermittent normobaric hypoxic environment (10% O₂). Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to determine the level of HO-1 mRNA in the rat lung tissue and double wave length spectrophotometry was used to evaluate the quantity of COHb in arterial blood. Cardiac catheterization was employed to measure the right ventricular systolic pressure (RVSP) and HE staining was performed in dissected lung tissue to observe the pathological changes of the intra-acinar pulmonary arteries (IAPA). It was found that (1) There was a low level of HO-1 mRNA in normal rat lung tissue, but the level of HO-1 mRNA increased by 2–4 times in the lung tissue of hypoxic rats (P<0.01). The quantity of COHb was 2–3 times those of control group (P<0.01 orP<0.05). These were accompanied by the increased of RVSP and the thickened IAPA; (2) Hemin could keep the HO-1 mRNA and COHb in the hypoxic rat lung tissue at a high level, and partially suppressed the increase of rat RVSP, thereby ameliorating the pathological changes of IAPA. In conclusion, the upregulation of the expression of HO-1 gene and production of CO in the rat lung of hypoxic pulmonary hypertension plays a role of inhibition in the development of hypoxic pulmonary hypertension. Hemin has a therapeutic effect on hypoxic pulmonary hypertension.