[Evaluation for medical management on catamenial pneumothorax].

Catamenial pneumothorax (CP) is one of the clinical manifestations of endometriosis, therefore the systemic hormonal therapy is indispensable and should be the 1st choice for CP treatment. However, it is refractory and repeats a recurrence, so that a combined or sequential adjuvant treatment becomes necessary. From 2003 to 2009, 5 patients with CP were treated at our institution. All patients had right-sided pneumothorax and the history of pelvic endometriosis. By thoracoscopic examination, diaphragmatic abnormalities, such as defect, pinhole, or brown spot, were identified in all patients. We performed hormonal therapy combined with chemical pleurodesis using OK-432, as an initial treatment. Two patients have been free of recurrence for 24 and 53 months, respectively. Three patients who refused or interrupted hormonal therapy caused a recurrence, but were successfully managed with the addition of pleurodesis and continuing hormonal therapy. At present, all patients are asymptomatic with 13 to 92 months recurrence-free period. From the long-term results, our therapeutic strategy consisted of hormonal therapy and chemical pleurodesis is considered appropriate.

Cloning of an auxin-responsive 1-aminocyclopropane-1-carboxylate synthase gene (CMe-ACS2) from melon and the expression of ACS genes in etiolated melon seedlings and melon fruits.

Two cDNA fragments (pCMe-ACS2 and 3) encoding auxin-responsive 1-aminocyclopropane-1-carboxylate synthase (ACS; EC.4.4.1.14) have been isolated from melon, and the expression patterns of the genes in etiolated melon seedlings and melon fruit have been determined by RT-PCR analysis. The deduced amino acid sequences of pCMe-ACS2 and 3 were homologous to those of AT-ACS6 and 4, which were auxin-responsive ACS genes of Arabidopsis. Both CMe-ACS2 and 3 were auxin-responsive ACS genes and their expressions in roots and hypocotyls were induced by treatment with indole acetic acid (IAA, 100 µM). The mRNA level of CMe-ACS2 in the fruit increased after pollination. Those of both CMe-ACS2 and 3 temporarily increased in the mesocarp tissues at the preclimacteric stage (from day 3 to day 5 after harvest) during ripening, while that of CMe-ACS3 was lower than that of CMe-ACS2. The increase in the mRNA level of CMe-ACS1 (wound- and ripening-induced gene, T. Miki, M. Yamamoto, N. Nakagawa, O. Ogura, H. Mori, H. Imaseki, T. Sato, Nucleotide sequence of a cDNA for 1-aminocyclopropane-1-carboxylate synthase from melon fruits, Plant Physiol. 107 (1995) 297-298.) in the mesocarp tissue was not observed until 5 days after harvest. A genomic DNA encoding CMe-ACS2 was isolated and its nucleotide sequence was determined. Nucleotide sequences resembling the auxin-responsive elements (AuxRE) D1 and D4 (the TGTCTC element) in the GH3 gene from soybean, and the auxin-responsive domain (AuxRD) B in PS-IAA4/5 from pea were found in the 5'-flanking region of the CMe-ACS2 gene.

Removal of endotoxin and cytokines by plasma exchange in patients with acute hepatic failure.

OBJECTIVES: To compare the circulating concentrations of endotoxin and cytokines in patients with fulminant hepatitis and patients with the severe form of acute hepatitis, and to assess the effects of plasma exchange on the circulating concentrations of these inflammatory mediators in patients with acute hepatic failure. DESIGN: Prospective, consecutive entry study of patients meeting fulminant hepatitis criteria and the severe form of acute hepatitis criteria. SETTING: University hospital, intensive care unit. PATIENTS: Five patients with fulminant hepatitis, eight patients with the severe form of acute hepatitis, two patients with acute-on-chronic hepatic failure, and one patient with postoperative hepatic failure. INTERVENTIONS: Plasma endotoxin, serum tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 were determined on admission in five patients with fulminant hepatitis and eight patients with the severe form of acute hepatitis. Circulating concentrations of the inflammatory mediators were measured before and after a single course of plasma exchange in eight patients with acute liver failure, including five patients with fulminant hepatitis, two patients with acute-on-chronic hepatic failure, and one patient with postoperative hepatic failure. MEASUREMENTS AND MAIN RESULTS: TNF-alpha and IL-6 in patients with fulminant hepatitis were significantly higher than in patients with the severe form of acute hepatitis, whereas endotoxin concentrations did not differ between patients with fulminant hepatitis or the severe form of acute hepatitis. IL-1beta was not detectable in patients with either fulminant hepatitis or the severe form of acute hepatitis. Plasma endotoxin concentrations decreased immediately after plasma exchange. Serum concentrations of TNF-alpha and IL-6 were significantly lower after plasma exchange than before plasma exchange. CONCLUSION: TNF-alpha and IL-6 may be important in the pathogenesis of the clinical symptoms that differentiate fulminant hepatitis from the severe form of acute hepatitis, and plasma exchange removes these inflammatory mediators from the circulation of patients with severe liver disease.

Treatment with a novel lipid A analogue, FS-112, and partial hepatectomy causes submassive liver necrosis and impaired liver regeneration in mice.

A novel experimental model of submassive liver necrosis with impaired regeneration has been established. A novel lipid A analogue, FS-112, was injected intravenously into male BALB/c mice, followed 2 days later by a 70% partial hepatectomy. Over the next 9 days, mice became severely jaundiced, with a peak total bilirubin (TBil) concentration of (mean +/- s.d.) 12.9 +/- 2.1 mg/dL 7 days postoperatively. In contrast, the TBil concentration in vehicle-treated mice remained less than 2 mg/dL. Significant elevations of L-alanine:2-oxoglutarate aminotransferase (ALT) were also observed 3-7 days after the operation in mice pretreated with FS-112, compared with mice pretreated with the vehicle. Submassive liver necrosis was observed with extensive mononuclear cell infiltration in mice treated with FS-112 and subjected to partial hepatectomy. Furthermore, both the BrdU and the proliferating cell nuclear antigen (PCNA) labelling index (LI) 1 day following partial hepatectomy in mice pretreated with FS-112 (8.6 +/- 4.3 and 7.9 +/- 4.2%, respectively) were significantly lower than levels in vehicle-treated mice (25.8 +/- 3.8 and 26.5 +/- 10.5%, respectively). The time course of changes in the BrdU LI in liver specimens from mice treated with both FS-112 and partial hepatectomy did not increase, even 3, 5, and 7 days postoperatively. Excellent liver regeneration with a PCNA LI 10-fold higher than the resting level was observed in mice treated with D-galactosamine hydrochloride. These results strongly suggest that this animal model of submassive liver necrosis may be suitable for clarifying the mechanisms of impaired liver cell regeneration often seen in fulminant hepatitis.

Direct evidence that hepatocyte growth factor is a hepatotrophic factor for liver regeneration and has a potent antihepatitis effect in vivo.

Hepatocyte growth factor, a potent mitogen for mature hepatocytes in vitro, seems to function as a hepatotrophic factor for liver regeneration. We examined the mitogenic effect of hepatocyte growth factor on mouse liver in vivo. The labeling index of hepatocytes was markedly increased when recombinant human hepatocyte growth factor was injected intravenously into mice subjected to 30% hepatectomy (control, 1.7% +/- 0.1%; 1 microgram hepatocyte growth factor, 6.4% +/- 1.3%; 5 micrograms hepatocyte growth factor, 18.3% +/- 0.2%) and into mice administered carbon tetrachloride (control, 12.7% +/- 1.0%; 1 microgram hepatocyte growth factor, 26.3% +/- 2.8%) or alpha-naphthylisothiocyanate (control, 0.4% +/- 0.1%; 1 microgram hepatocyte growth factor, 3.8% +/- 1.1%; 5 micrograms hepatocyte growth factor, 14.2% +/- 2.0%). In addition, weights of the remnant livers in mice given hepatocyte growth factor 60 hr after 30% hepatectomy were significantly greater than those of untreated control mice (control, 0.93 +/- 0.04 gm; 5 micrograms hepatocyte growth factor, 1.06 +/- 0.04 gm). Hepatocyte growth factor prevented any marked increase in the serum levels of liver enzymes and bilirubin when it was administered to mice also treated with alpha-naphthylisothiocyanate (control: ALT, 394 +/- 278 IU/L; lactate dehydrogenase, 2,644 +/- 1,109 IU/L; bilirubin, 9.6 +/- 2.6 mg/dl; and 5 micrograms hepatocyte growth factor: ALT, 135 +/- 7.9 IU/L; lactate dehydrogenase, 1,672 +/- 626 IU/L; bilirubin, 1.0 +/- 0.8 mg/dl). Our findings show that intravenously injected hepatocyte growth factor stimulates the growth of hepatocytes in mouse liver and protects the integrity of hepatocytes in vivo against hepatitis caused by hepatotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of changes in the size of ischemic region on ST-segment potential distribution in isolated canine hearts.

In order to investigate how a change in the size of a ischemic region is reflected in ST-segment mapping studies, we produced two different sizes of ischemic regions by occluding proximal or distal portions of the left circumflex artery for five minutes, using ten isolated canine heart preparations. We examined the relationship between the geometry of the ischemic region and ST-segment potential distribution on the epicardial surface and that in the "precordium", in which the heart was suspended. The extent of the ischemic region was reflected differently on epicardial and "precordial" sites, in that the magnitude of epicardial ST-segment elevation decreased (p less than 0.001) while the "precordial" one increased (p less than 0.01). In the epicardium the degree of ST-segment elevation was almost uniform over the ischemic region, whereas in the "precordium" it was maximal at sites overlying the center of the ischemic region and progressively decreased approaching the periphery. However, frequent occurrence of intraventricular conduction disturbance was observed near the center of the ischemic region. As a result, the magnitude of epicardial ST-segment elevation near the center became larger than in the periphery. These results suggest that the classical solid angle theory provides a useful approximation of the ST-segment deflection in very acute ischemic phase, until development of the intraventricular conduction delay.