Doppler ultrasound examination of prosthetic function and ventricular blood flow after mitral valve replacement

Two-dimensional color Doppler echocardiography enables delineation of the spatial and temporal distribution of blood flow in the heart. In this study, the method was applied for investigation of flow dynamics in multiple planes in the region of prosthetic mitral valves for comparison with that of native mitral valves. In 15 healthy subjects there was normal flow toward the transducer, coded in red, in the left ventricle along the posterolateral wall (left ventricular inflow region) and blue-coded flow away from the transducer in the left ventricular outflow region during diastole. In 40 patients with St. Jude mitral valve prosthesis and 17 with bioprosthesis the flow pattern in the left ventricle was reversed. Mitral inflow was directed against the interventricular septum, accordingly, into the left ventricular outflow region while the outflow pattern was displaced posterolaterally into the left ventricular inflow region during diastole. The angle between the aortic valve ring and the mitral annulus was significantly smaller than in the healthy subjects. The angle between the central axis of the mitral prosthesis and the mitral inflow, which was 0 degrees in healthy subjects, was increased by the medial deviation in particular, in those with mechanical St. Jude prostheses. The maximal transprosthetic velocity, measured in 70 patients, and the maximal pressure gradient calculated according to the Bernoulli equation was substantially greater than the values in healthy subjects. In contrast to findings associated with normally-functioning prostheses, in four patients with prosthetic malfunction there was a diastolic peak velocity of more than 2 m/s as well as marked turbulence in the inflow region.     

Effect of H. pylori on COX-2 expression in gastric remnant after distal gastrectomy

BACKGROUND/AIMS: Helicobacter pylori infection is known to induce gastritis, oxidative stress, and cyclooxygenase (COX)-2 expression in the gastric mucosa. However, the effect of H. pylori infection on remnant gastritis has not been studied. We investigated whether the severity of remnant gastritis and COX-2 expression were affected by H. pylori infection after distal gastrectomy. METHODOLOGY: The study included 97 patients with gastric cancer who underwent curative distal gastrectomy with lymphadenectomy in our department between May 1999 and April 2001. All patients underwent endoscopic examination 2 weeks before and 12 weeks after surgery. The presence of H. pylori infection was determined by urease activity, hematoxylin-eosin staining, and immunochemical staining. Histologic remnant gastritis was graded based on the degree of neutrophil infiltration using the updated Sydney System. COX-2 expression was estimated immunohistochemically. RESULTS: Both the degree of neutrophil infiltration and the level of COX-2 expression were significantly higher in patients with than without H. pylori (p<0.05). There was a significant correlation between the degree of neutrophil infiltration and the degree of COX-2 expression (p<0.001). CONCLUSIONS: H. pylori eradication may become a treatment for preventing both remnant gastritis as well as remnant gastric carcinoma after distal gastrectomy.     

Telmisartan treatment decreases visceral fat accumulation and improves serum levels of adiponectin and vascular inflammation markers in Japanese hypertensive patients.

Hypertension contributes to the occurrence and progression of cardiovascular diseases. The angiotensin II type 1 receptor blocker telmisartan is reported to activate the peroxisome proliferator-activated receptor gamma and improve insulin sensitivity. We investigated the effects of telmisartan treatment on visceral fat, serum adiponectin and vascular inflammation markers in Japanese hypertensive patients. This was an open-label, non-controlled study. Twenty-eight essential hypertensive patients (22 men and 6 women; age 60.6+/-1.9 years; body mass index [BMI] 25.5+/-0.6 kg/m(2)) participated. Fat area was assessed with computerized tomography. All the subjects were started on telmisartan 40 mg/day, which was increased to 80 mg/day to achieve the blood pressure target of less than 130/80 mmHg. We assessed the visceral and subcutaneous fat areas, serum adiponectin levels, and vascular inflammation markers at baseline and 24 weeks of telmisartan treatment. There were significant reductions in visceral fat area (from 103.1+/-7.9 to 93.3+/-8.4 cm(2), p<0.01) and pulse wave velocity (from 1,706+/-52 to 1,587+/-51 cm/s, p<0.01) at 24 weeks. In contrast, significant increases in serum high-density lipoprotein cholesterol (from 5.06+/-0.15 to 5.32+/-0.13 mmol/L, p<0.05) and adiponectin levels (from 8.27+/-0.76 to 9.13+/-0.81 microg/mL, p<0.05) were observed. Also, there were reductions in the interleukin-6 level (from 2.26+/-0.27 to 1.60+/-0.14 pg/mL, p<0.01). We also conducted these investigations in male subjects alone and similar findings were obtained for all of these parameters. In conclusion, telmisartan treatment was associated with an improvement of vascular inflammation, reductions in visceral fat and increases in serum adiponectin.     

Hepatocyte growth factor gene transfer with naked plasmid DNA ameliorates dimethylnitrosamine-induced liver fibrosis in rats

Aim: Hepatocyte growth factor (HGF) has various biological properties, including antifibrogenic activity. In the present study, we tested the efficacy of HGF gene therapy using naked plasmid DNA in dimethylnitrosamine (DMN)-induced liver fibrosis in a rat model. Methods: Naked plasmid DNA encoding human HGF was injected once, together with a hypertonic solution, into the hepatic artery after DMN treatment on three consecutive days per week for 3 weeks. Naked plasmid DNA encoding beta-galactosidase was injected similarly in the DMN-treated control rats. DMN treatment was continued once weekly after gene transfer for additional 3 weeks. Results: The human HGF protein expression was detected in livers transfected with human HGF naked plasmid DNA, gradually decreasing by day 21. The expression of the endogenous rat HGF protein was also upregulated after human HGF gene transfer. Phosphorylation of c-Met, a HGF receptor, was detected only in livers transfected with human HGF plasmid DNA. Fibrosis was attenuated significantly in livers transfected with the human HGF plasmid. Attenuation wasaccompanied by decreased expression of alpha-smooth muscle actin. Increased portal vein pressure after treatment with DMN was suppressed significantly by HGF gene transfer. The upregulated hepatic protein expression of transforming growth factor-beta (TGF-beta) in response to DMN was markedly attenuated by HGF gene transfer accompanied by the increased protein expression for matrix metalloproteinases (MMP)-3 and -13. Conclusion: The hepatic arterial injection of human naked plasmid HGF DNA was effective in suppressing liver fibrosis induced in rats by DMN. The mechanisms by which HGF expression attenuated liver fibrosis may include the suppression of hepatic TGF-beta expression and the induction of MMP expression.     

MLL gene rearrangement in t(9;11) acute myelogenous leukemia with minimal myeloid differentiation (FAB subtype M0)

A 25-year-old man was diagnosed with acute myelogenous leukemia (AML), French-American-British (FAB) subtype M0, based on cytochemical and flow cytometric findings. Cytogenetic analysis revealed the chromosome translocations t(9;11)(p22;q23), and MLL gene rearrangement was identified by Southern blotting. In adult AML, MLL gene rearrangement was initially reported in FAB M4 and M5 cases, and recently in M1 and M2 cases, but was rare in M0 or M3 cases. Because the sensitivity of detecting MLL gene rearrangement by cytogenetic analysis is extremely low compared with Southern blotting analysis, the MLL gene may be involved in substantial numbers of adult AML cases, regardless of FAB subtype.     

Molecular investigation of pathogenic factors of suspected-diarrheogenic Escherichia coli isolates from patients feces

One hundred fifty-one O serotypable Escherichia coli strains which were assumed diarrheogenic E. coli among 2,240 strains of E. coli isolated from the in- and outpatients stools with or without gastrointestinal symptoms at Kyorin University Hospital from February 1994 to September 1996 were examined for the relationship between the possession of eight pathogenic factor-related genes and gastrointestinal symptoms of the patients using the polymerase chain reaction (PCR) for these strains. The rate of possession of pathogenic factor-related genes in the E. coli examined was 20.5% (31 strains) and gastrointestinal symptoms were found in all the patients with these strains except one. In the patients without gastrointestinal symptoms, E. coli isolates that possesses these genes was detected in only one case during 61 cases. The respective genes detected were eaeA and astA in each 14 strains, VT1 in 6, VT2 in 5, ST1b in 4, aggR in 3 and LT in 2, ST1a and invE gene was not detected. In particular, the O157 strains were found in 55.6% (5/9 strains) for these genes, and individual strains had VT1, VT2, eaeA and astA genes simultaneously. In contrast, none of these related genes was found in 9 strains of enteroinvasive serotype but enteropathogenic E. coli-related genes were found in 3 strains. The rate of possession of the genes related to enterotoxigenic E. coli, O159 which was most frequently isolated was low as 2.3% (1/43 strains, astA gene) and there were strains showing low correlation to the state of possession of the genes with the O serotype. Since the prevalence of the gastrointestinal symptoms is clearly high for the case which possesses the strain of which the pathogenic factor-related gene was detected, it was suggested that detection of pathogenic factor-related genes in E. coli isolates from feces using the PCR could be an effective means to decide whether the bacteria concerned was a causal bacteria or not in clinical practice.