A surgical case of combined valvular disease complicated by absent right superior vena cava and persistent left superior vena cava.

A 74-year-old man with combined valvular disease with a recent cerebral infarction was admitted. While undergoing thorough examination for valvular disease, absent right superior vena cava (RSVC) and persistent left superior vena cava (PLSVC) were recognized. Chest X-ray film suggested a right arch protrusion, and CT and venogram confirmed the diagnosis. During surgery, replacement of the mitral and aortic valves and annuloplasty of the tricuspid valve were performed. A blood draining cannula was inserted in retrograde fashion from the coronary sinus into the PLSVC, without any difficulties in the tricuspid valve repair. Due to bradycardic atrial fibrillation, we believed that it would be difficult to insert an endocardial electrode postoperatively, hence myocardial electrode was placed in the right ventricular wall. Absent RSVC combined with PLSVC is very rare, and a patient who underwent combined valve surgery with this rare anatomical abnormality is herein presented.     

Anti-Candida albicans activity of essential oils including Lemongrass (Cymbopogon citratus) oil and its component, citral]

The effects of 12 essential oils, popularly used as antifungal treatments in aromatherapy, on growth of Candida albicans were investigated. Mycelial growth of C. albicans, which is known to give the fungus the capacity to invade mucosal tissues, was inhibited in the medium containing 100 micro g/ml of the oils: lemongrass (Cymbopogon citratus), thyme (Thymus vulgaris), patchouli (Pogostemon cablin) and cedarwood (Cedrus atlantica). Not only lemongrass oil but also citral, a major component of lemongrass oil (80%), in the range of 25 and 200 micro g/ml inhibited the mycelial growth but allowed yeast-form growth. More than 200 micro g/ml of citral clearly inhibited both mycelial and yeast-form growth of C. albicans. These results provide experimental evidence suggesting the potential value of lemongrass oil for the treatment of oral or vaginal candidiasis.     

Basic and clinical studies of cefotiam in neonates and premature infants

The effect of cefotiam (CTM) on neonates and premature infants was examined in basic and clinical studies. Minimum inhibitory concentrations of CTM against 190 clinically isolated strains kept by this department were investigated. This drug was found to have a strong antibacterial effect against Escherichia coli, Klebsiella spp., Proteus mirabilis and Streptococcus agalactiae, Staphylococcus aureus and Staphylococcus epidermidis, although some strains were resistant. The CTM was given to 0-3, 4-7, and greater than or equal to 8 day-old premature infants and neonates by intravenous injection at the dose of 20 mg/kg, and we studied changes in serum CTM levels over time. Mean serum CTM levels were 62.3 micrograms/ml at 15 minutes and 16.4 micrograms/ml at 6 hours after the injection, with the half-life of 3.6 hours, for the 0-3 day-old premature infants. They were 38.5 micrograms/ml at 15 minutes and 10.1 micrograms/ml at 6 hours, with the half-life of 2.9 hours, for the 0-3 day-old neonates. Those levels were 22.5 micrograms/ml at 15 minutes and 2.9 micrograms/ml at 6 hours, with the half-life of 1.9 hours, for the 4-7 day-old neonates, and 51.8 micrograms/ml at 15 minutes and 1.0 micrograms/ml at 6 hours, with the half-life of 1.1 hours, for the greater than or equal to 8 day-old neonates. The CTM was given to 0-3 and greater than or equal to 8 day-old premature infants and neonates by 1-hour intravenous drip infusion at the dose of 20 mg/kg, and changes in serum CTM levels after the infusion were followed. The 0-3 day-old premature infant (there was only one subject) had a peak serum CTM level of 21.0 micrograms/ml 1 hour after the start of the infusion (that is, at the time of its completion), with the level decreased to 8.6 micrograms/ml at 7 hours and the half-life was 5.4 hours. The mean peak serum CTM level in 0-3 day-old neonates were 36.7 micrograms/ml at 1 hour, which decreased to a mean of 7.0 micrograms/ml at 7 hours; the half-life was 2.3 hours.(ABSTRACT TRUNCATED AT 400 WORDS)     

Different postnatal ontogenic profiles of neurons containing beta (beta 1, beta 2 and beta 3) subunit mRNAs of GABAA receptor in the rat thalamus.

The postnatal ontogeny of neurons containing different GABAA receptor beta (beta 1, beta 2 and beta 3) subunit mRNAs were examined in the rat thalamus using in situ hybridization histochemistry. Neurons containing beta 1 or beta 2 subunit mRNA developed remarkably postnatally, while most neurons were already strongly labeled with beta 3 probe at birth. However, beta 3 subunit mRNA decreased rapidly after birth, few cells being labeled with this probe at day 35 and thereafter.     

Morphologic examination of CD3–CD4bright cells in rat liver

Recently, we found CD3-CD4(bright) cells with comparative specificity for normal rat liver. In the current study, we investigated the type and form of both CD3-CD4(bright) cells and CD3-CD4(dull) cells in the rat liver. The surface phenotype of hepatic mononuclear cells in Lewis rats was identified by using monoclonal antibodies including anti-CD4, anti-CD3, and antimacrophage in conjunction with two- or three-color immunofluorescence analysis. CD3-CD4(bright) cells and CD3-CD4(dull) cells were examined morphologically using May-Giemsa staining and scanning electron microscopy. The distribution of CD3-CD4(bright) cells and CD3-CD4(dull) cells 48 hours after intravenous administration of liposome-encapsulated dichloromethylene diphosphate was also investigated. In comparison to CD3-CD4(dull) cells, CD3-CD4(bright) cells were slightly larger macrophages with abundant cytoplasmic granules, being present with comparative specificity for normal rat liver and showing negligible effects by intravenous liposome-encapsulated dichloromethylene diphosphate administration. These data suggest that in normal young rat liver these CD3-CD4(dull) and CD3-CD4(bright) cells may be dendritic cells and Kupffer cells that shift from the liver to the spleen or vice versa. These cells may also be able to locally proliferate in liver or spleen due to changes in the developing liver.