Intraperitoneal rupture of the ureter as a cause of generalized peritonitis: report of a case.

We report a rare case of generalized peritonitis caused by nontraumatic, intraperitoneal rupture of the ureter. An 80-year-old woman with a history of bilateral vesicoureteral reflux and long-term urethral indwelling catheter drainage presented with a very distended abdomen. Computed tomography showed massive ascites and intraperitoneal free gas.

[Effects of immunoglobulin on murine myocarditis caused by influenza A virus: experimental study].

Objectives: Influenza A viruses play the largest role in the worldwide epidemiology of infectious diseases. We examined the effects of intact type and F(ab')2 type of immunoglobulin preparations on murine influenza A virus myocarditis in mice.

Methods And Results: In vitro study showed that intact type and F(ab')2 type of immunoglobulin preparations had antiviral activities against many substrains of influenza A virus and other cardiotropic viruses, and that dose-dependent suppression of an influenza A virus (NWS type) was demonstrated by the treatment of both intact immunoglobulin and F(ab')2 fragments of immunoglobulin.

Effects of immunoglobulin upon murine myocarditis caused by influenza A virus: superiority of intact type to F(ab')2 type.

Influenza viruses play the largest role in the worldwide epidemiology of infectious diseases. Management of some inflammatory disease (eg, Kawasaki disease) with immunoglobulin has been demonstrated to be effective. We examined the effects of intact type and F(ab')2 type of immunoglobulin preparations upon murine influenza A virus myocarditis in mice.

An in vivo model of autoimmune post-coxsackievirus B3 myocarditis in severe combined immunodeficiency mouse.

Objective: Severe combined immunodeficiency (SCID) mice possess neither T nor B lymphocytes and are thus suitable recipients for adoptively transferred lymphocytes. Because autoimmune mechanisms may be involved in the pathogenesis of coxsackievirus B3 (CB3) myocarditis, we attempted to assess the in vitro cellular damage caused by antigen-sensitized lymphocytes and to determine whether splenic lymphocytes from BALB/c mice with chronic CB3 myocarditis could cause myocarditis into SCID mice.

Methods And Results: Cytotoxic cellular damage against non-myocytes and myocytes was demonstrated using 51Cr-release assay by lymphocytes cultured from myocarditis specimens or splenocytes from mice with chronic CB3 myocarditis.

Amyocarditic coxsackievirus B3 causes myocarditis in immunocompromised mice.

In the present study, we investigated the role of the immune status of the host in the pathogenesis and development of coxsackievirus B3 myocarditis. We compared the disease expression in myocarditic coxsackievirus B3 (CB3M)-infected BALB/c wild-type mice and severe combined immunodeficient (SCID) mice and in amyocarditic coxsackievirus B3 (CB3O)-infected BALB/c wild-type mice untreated or treated with immunosuppressive agents and SCID mice. There were no differences in viral growth in vitro between CB3M and CB3O.

Oral L-arginine prevents murine coxsackievirus B3 myocarditis.

We have previously demonstrated that administration of nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), aggravated murine coxsackievirus B3 myocarditis. In the present study, we evaluated the effects of L-arginine, a precursor of NO, upon acute and chronic myocarditis. Dietary L-arginine and L-arginine plus L-NAME (L-arginine+L-NAME group) were administered to coxsackievirus B3 (CB3)-infected C(3)H/He mice for 2 weeks (experiment I), and to CB3-infected mice from the second week until the fourth week after virus inoculation (experiment II).

Oral administration of L-arginine prevents congestive heart failure in murine viral myocarditis.

It was previously demonstrated that administration of the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME) aggravated viral myocarditis in mice. In the current study, the effects of l-arginine, a precursor of nitric oxide, on congestive heart failure (CHF) in myocarditis were evaluated. Dietary l-arginine and l-arginine plus l-NAME (l-arginine + l-NAME group) were administered to encephalomyocarditis virus-infected BALB/c mice over 4 weeks (experiment I) and to encephalomyocarditis virus-infected DBA/2 mice from the 4th through 12th weeks after the virus inoculation (experiment II).

Clinical utility of ursodeoxycholic acid in preventing flutamide-induced hepatopathy in patients with prostate cancer: a preliminary study.

Background: The present study was designed to ascertain retrospectively the validity of ursodeoxycholic acid (UDCA) in the treatment of prostate cancer in terms of prophylactic effects on the occurrence of flutamide-induced hepatopathy in a large number of patients surveyed in a multi-center cooperative study.

Methods: One hundred and eighty-one patients (74.1 +/- 4.