No abstract

SLIT was effective and safe in the treatment of cedar pollinosis.

Sphingomyelinosis (spm), an autosomal recessive mutation in mice originally occurred in the C57BL/KsJ inbred strain. Spm/spm mice of this genetic background show striking hepatosplenomegaly with a marked accumulation of sphingomyelin and cholesterol due to a deficiency of sphingomyelinase. However, in spm/spm mice of C57BL/6J and DBA/2J backgrounds, hepatosplenomegaly was not pronounced in spite of marked elevation of hepatic lipid concentrations. The lifespan of C57BL/6J-spm/spm and DBA/2J-spm/spm mice was shorter than that of C57BL/KsJ-spm/spm mice. This appeared to be associated with the comparatively rapid rise in hepatic lipid concentrations, which in turn might be related to the absence of hepatomegaly. Histological study revealed the formation of massive foam cell clusters in the livers and spleens of C57BL/KsJ-spm/spm mice, whereas in the case of C57BL/6J-spm/spm and DBA/2J-spm/spm mice, diffusely scattered foam cells were found. These findings suggest that the functions of reticuloendothelial system (RES) play a crucial role in the development of hepatosplenomegaly in response to lipid accumulation.

SUMMARYMany cardiac surgeries are performed with blood cardioplegia. However, some studies suggest that activated neutrophils form blood cardioplegia can cause reperfusion injury. In this study we assessed myocardial protection using a leukocyte-depleted cardioplegic solution.Patients undergoing elective coronary artery bypass grafting (CABG) with continuous blood cardioplegia were divided into two groups: the LD group, which received leukocyte-depleted blood cardioplegia (n = 11); and the control group, which received nonfiltered blood cardioplegia (n = 11). IL-6, IL-8, CK-MB, and troponin T were measured in the coronary sinus blood immediately after the release of the aortic cross-clamp. Cytokine concentrations were also measured upon the patient's return to the ICU. The total dopamine and dobutamine doses, hemodynamic measurements after surgery, and the leukocyte filtration rate were also measured.During antegrade cardioplegia infusion, leukocytes were almost completely removed (filtration rate: 85.8 ± 4.0%). However, during terminal warm cardioplegia, leukocyte removal decreased (filtration rate: 39.9 ± 7.8%). Immediately after the release of the aortic cross-clamp, plasma CK-MB and troponin T concentrations were significantly lower in the LD group (17.7 ± 1.9 U / l and 0.017 ± 0.002 ng / ml, respectively) than in the control group (30.3 ± 3.6 U / l and 0.072 ± 0.029 ng / ml, respectively). The IL-6 and IL-8 concentrations were similar in the LD group and the control group. After the return to the ICU, the CK-MB and troponin T concentrations were similar in the two groups. No significant differences were found in the total doses of dopamine or dobutamine after surgery in the two groups (99 ± 77 vs 101 ± 128 µg / kg / min). No significant differences were found in the hemodynamic parameters after surgery in the two groups.In patients undergoing CABG with continuous blood cardioplegia, leukocytedepleted blood cardioplegic solution may attenuate reperfusion injury. (Jpn Heart J 2000; 41: 425-433)

The expression of atrial natriuretic polypeptide (ANP) in the ventricles of human hearts with myocardial infarction (MI) was studied immunohistochemically. Immunoreactive myocytes were identified in the ventricular tissues of all of 16 hearts with old MI (both with and without heart failure) and in all five hearts with subacute MI, but not in any of the eight hearts without MI nor in the five with acute MI. In the nonfailing hearts with MI, ANP positive myocytes surrounded the areas of infarction, and were also seen in the subendocardium of the infarcted segment. In the failing hearts with MI, ANP expression was noted in the whole ventricular subendocardial region, in addition to the border of infarcts. The sites of ANP expression corresponded well to those of marked stress attributable to tissue shrinkage or fibrosis due to MI, haemodynamic overload, or both. It thus appears that ANP expression is augmented in human hearts with MI regardless of the presence or absence of heart failure, and it is suggested that regional mechanical stress on the ventricular myocardium, as well as haemodynamic overload, may be very closely associated with ventricular ANP expression.