SUMMARY: The authors report a rare case of fracture separations at both ends of the radius combined with an epiphyseal and diaphyseal fracture of the ipsilateral ulna. A seven-year-old girl fell one story and sustained a closed injury of her forearm. A closed reduction was unsuccessful, and an open reduction was performed with three of the four fractures being secured with Kirschner wires. These wires were removed one month later, and range-of-motion exercises were started. Thirty months after surgery, both forearms were equal in length, although the proximal radial epiphyseal line appeared partially closed. Joint motions, including forearm rotation, were normal. Radiologically, the ulnar diaphysis and the radial neck were posteriorly convex 20 degrees and 18 degrees, respectively.

Child↗

PubMedDate not supplied

An angiotensin-converting enzyme inhibitor protects against doxorubicin-induced impairment of calcium handling in neonatal rat cardiac myocytes.

1. The effects of doxorubicin (DOX) on intracellular calcium transients were examined in neonatal rat cultured cardiac myocytes, as were the cardioprotective effects of an angiotensin-converting enzyme (ACE) inhibitor on DOX-induced impairment of calcium handling. 2. Cultured cardiac myocytes isolated from neonatal Wistar-Kyoto rats were treated with DOX for 24 h. Field-stimulated calcium transients in single myocytes were measured in the presence or in the absence of isoproterenol using fura-2/AM. Calcium transients were also measured after the addition of DOX to myocytes pretreated with M-I (an active metabolite of delapril HCL, an ACE inhibitor. 3. Doxorubicin reduced the amplitude and maximum velocity of increase and decrease of calcium transients, prolonged the time-course of calcium transients and impaired the beta-adrenoceptor responsiveness of calcium transients in a dose-dependent manner. The DOX-induced impairment of calcium transients and beta-adrenoceptor responsiveness was improved by M-I. 4. Doxorubicin impaired both the mobilization and sequestration of intracellular calcium ions in contraction-relaxation cycles and the response of calcium transients to beta-adrenoceptor stimulation. The ACE inhibitor ameliorated DOX-induced impairment of calcium dynamics, suggesting ihat M-I, an active metabolite of delapril, protects against DOX-induced abnormal calcium handling leading to cardiac dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗

PubMedDate not supplied

Study on placental transmission of Pneumocystis carinii in mice using immunodeficient SCID mice as a new animal model.

Placental transmission of Pneumocystis carinii in mice was examined in 39 animals obtained by caesarean section from 17 pregnant SCID females experimentally infected with P. carinii. When examined with toluidine blue O, DAPI and immunofluorescent antibody stains, P. carinii was detected in the lungs of infected mothers but not in the lungs of caesarean section-derived neonates even after the neonates were treated with dexamethasone for 8 weeks. However, 13 neonates born to five infected females developed P. carinii pneumonia. These results indicate that P. carinii cannot be transmitted transplacentally in mice.

Animals↗

PubMedDate not supplied

Effect of sulfamethoxazole-trimethoprim and sulfadoxine-primethamine against fatal pneumocystosis in SCID mice.

The effect of sulfamethoxazole-trimethoprim (S-T) and sulfadoxine-primethamine (S-P) against Pneumocystis carinii (Pc) were examined in severe combined immunodeficiency (SCID) mice which are known to be susceptible to Pc. These animals develop fatal pneumocystosis without treatment with any immunosuppressant. The results suggested that S-T and S-P were effective against both trophic and cystic forms of Pc in SCID mice.

Animals↗

PubMedDate not supplied

Effects of environmental factors and disinfectants on the survival of Pneumocystis carinii outside the host.

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Animals↗

PubMedDate not supplied

[Contrast echocardiographic detection of pulmonary arteriovenous shunt in a hypoxemic patient with liver cirrhosis].

A 62-year-old man with liver cirrhosis and hypoxemia was admitted to evaluate the etiology of hypoxemia. The patient had noticed exertional dyspnea for three years. Physical examination, laboratory tests, ultrasonography and liver scintigraphy revealed liver cirrhosis. The arterial blood gas test showed hypoxemia (PO2 46.3 mmHg). Chest roentgenogram showed old pulmonary tuberculosis and the pulmonary function test demonstrated decreased FEV 1.0% and %DLco, which did not account for the marked hypoxemia. Contrast echocardiography was performed by injecting hand-agitated saline into the antecubital vein. Three seconds after the right ventricle was opacified, the contrast echoes appeared in the left atrium and then the left ventricle. Pulmonary arteriography revealed no pulmonary arteriovenous fistula. Hemodynamic data showed low pulmonary vascular resistance. Contrast echocardiography by injecting hand-agitated saline from the catheter tip was performed at both pulmonary arteries and the left atrium was opacified by each injection. The hypoxemia was mainly attributed to a intrapulmonary arteriovenous shunt. Although the etiology of hypoxemia in liver cirrhosis seems to be multifactorial, the intrapulmonary arteriovenous shunt is the most important factor. Contrast echocardiography was useful for detecting this shunt.

Arteriovenous Fistula↗