[Percutaneous radiofrequency ablation therapy with left single lung ventilation for liver carcinoma in the hepatic dome].

OBJECTIVE: To evaluate the advantages of percutaneous radiofrequency ablation (PRFA) therapy with contralateral single lung ventilation (SLV) for liver carcinoma in the hepatic dome (LCHD). METHODS: The clinical data of 10 patients (the SLV group) with LCHD consecutively treated from January to December 2006 were retrospectively analyzed. And another 10 cases (the control group) with LCHD treated from January 2004 to December 2005 were selected with a strict inclusion criterion for compared test according to rules of same diagnosis, similar tumor bulk and site, same sex, similar age and liver function. The patients' ages and tumor diameters of the 2 groups were compared with t-test and the rates of complications and incomplete tumor ablation were compared with chi2-test. RESULTS: There was no statistical difference in ages and tumor diameters between the 2 groups (P > 0.05). The average number of radiofrequency ablation needle punctures in the SLV group was significantly less than the control group (3.4 +/- 0.4 vs. 6.1 +/- 0.8, P < 0.01). There was no bronchial intubation related complications like hypoxemia, atelectasis, lung infection and no puncture related complications like pneumothorax, hemothorax, hemoperitoneum and bile leakage in the SLV group. Two cases in the control group had complications including pneumothorax (n = 1) and pleural effusion (n = 1). There was no mortality in the 2 groups. Though the rate of incomplete tumor necrosis in the SLV group was not statistically lower than that in the control group (10% vs. 40%), the occurrence rate of the undesirable event (complication and incomplete tumor necrosis) of the SLV group was significantly lower than that of the control group (10% vs. 60%, P < 0.05). The durations and costs of operating procedure were not significantly different between the 2 groups. CONCLUSION: Left SLV makes PRFA for LCHD more efficient, effective and safe.

Elevated levels of mitochonrial respiratory complexes activities and ATP production in 17-ß-estradiol-induced prolactin-secretory tumor cells in male rats are inhibited by melatonin in vivo and in vitro.

BACKGROUND: Our earlier studies indicate that melatonin inhibits the proliferation of prolactinoma and induces apoptosis of pituitary prolactin-secreting tumor in rats. Melatonin has also been shown to induce apoptosis and to reduce the production of ATP in breast tumor cells. This study analyzed the levels of the four mitochondrial respiratory complexes and the production of ATP and also the effects of melatonin treatment of prolactinoma. METHODS: In the in vivo study, mitochondria were harvested from control pituitaries or prolactinoma collected from the pituitaries of melatonin- and 17-ß-estradiol (E2)-treated male rats. In the in vitro study, prolactinoma cells mitochondria were harvested. Activities of the four mitochondrial respiratory complexes were assayed using fluorometer. ATP production of prolactinoma cells was estimated using bioluminescent methods. RESULTS: Elevated levels of four mitochondrial respiratory complexes activities and ATP production were recorded in prolactinoma cells. Moreover, in both in vivo and in vitro studies, melatonin inhibited the activities of mitochondrial respiratory complexes and the production of ATP in prolactinoma cells. CONCLUSIONS: There is a link between mitochondrial function increase and tumorigenesis. Melatonin induces apoptosis of pituitary prolactin-secreting tumor of rats via the induction of mitochondrial dysfunction and inhibition of energy metabolism.

[Relationship between dissolved organic carbon and DBP in the Pearl River water].

Dissolved organic carbon (DOC) in the Pearl River system in Guangdong Province was fractioned by using XAD resins into humic substances and other fractions. The concentration and distribution of DOC, SUVA254, trihalomethanes formation potential (THMFP) and relationships between DOC and THMFP were analyzed. The 2-year study demonstrated that the DOC concentration of Pearl River ranged from 0.7 to 33.0 mg x L (-1). On the other hand, the trihalomethanes formation potential (THMFP) in Pearl River was 30.39-1 091.52 microg x L(-1), which showd a linear relationship with the DOC concentration. Spatially, the DOC concentration and THMFP increased downstream along each tributary; however, the humic substances mitigated to the opposite. During the chlorination, humic substances were the main precursors of disinfection by-products (generating 64.6% of THM) in Pearl River and the specific trihalomethanes formation potential (STHMFP) of humic substances was over 2 times higher as the other fractions. In addition, SUVA254 was proved to provide a reference indicator in testing the precursors of disinfection by-products.

[The protective effect of the limb ischemia preconditioning on the hepatic injury related to NO/ET-1 system in rats].

OBJECTIVE: To study the relationship between the disturbance of nitric oxide/endothelin-I (NO/ET-1) and the hepatic injury following limb ischemia/reperfusion (I/R) in rats as well as the regulation of NO/ET-1 system by limb ischemia preconditioning (IPC). METHODS: Using limb ischemia/reperfusion injury model rats, animals were randomly divided into three groups (n = 6): control group, I/R group and IPC group. The contents of alanine aminotransferase (ALT), aspartate aminotransferase (AST) in the plasma as well as nitric oxide (NO), endothelin-1 (ET-1), nitric oxide/endothelin-1 (NO/ET-1) in the plasma and the liver were measured. The levels of total nitric oxide synthase (tNOS), inducible nitric oxide synthase (iNOS), constitutive nitric oxide synthase (cNOS) in the liver were determined. The expression of iNOS and endothelial NOS (eNOS) were detected by the immunohistochemical method. The morphologic changes stained with hematoxylineosin were observed under microscope. RESULTS: It was found that the levels of NO, ET-1 in the plasma and the liver tissue all increased after reperfusion, while the values of ALT, AST, NO/ET-1 decreased. Liver pathology revealed that after limb I/R there were edema, villous microvascular congestion, infiltration of polymorphonuclear neutrophil (PMN), cell degeneration in part cells of the liver. The hepatic damage was deteriorated. While the expression of iNOS elevated, cNOS (mainly eNOS) reduced and total NOS increased. The protection of the limb IPC attenuated the disturbance of NO/ET-1. CONCLUSION: The hepatic injury following limb I/R is related to the disturbance of NO/ ET-1. The protection of the limb IPC might be conducted by its regulation of NO/ET-1 system. The elevation of endothelial NOS and the reduction of non-endothelial NOS generated the NO in this situation.