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Chronic kidney disease (CKD) is known as a risk factor for cardiovascular disease. In recent years, several experimental and epidemiological studies have suggested that CKD is associated with endothelial dysfunction; thereby, a CKD state may initiate both large and small vessel damage. The association between renal dysfunction and asymptomatic lacunar infarction was reported in a hospital-based study, whereas the relationship between cerebral small vessel disease (SVD)-related lesions and CKD could not be clarified in a community-based study. We performed a cross-sectional study to determine the relationship between silent cerebral SVD-related lesions and CKD in a total of 625 community-based Japanese elderly. In this study, subjects with lower estimated glomerular filtration rate levels tended to have more lacunar infarcts and higher grades of white matter lesions (WMLs). In addition, the mean grades of WMLs or the mean numbers of lacunar infarction in the subjects with albuminuria were greater than those in subjects without albuminuria. In the logistic regression analysis, the association between the presence of CKD and lacunar infarction or moderate WMLs (Fazekas grades 2 and 3) was statistically significant (odds ratio [OR]: 1.86 and 1.50, respectively). Furthermore, as we performed additional analysis, excluding the subjects with stage 2 hypertension (those with casual blood pressure >or=160/100 mm Hg) or diabetes, CKD remained to be an independent risk for cerebral SVD-related lesions. This is the first study showing the relationship between silent SVD-related brain lesions and the presence of CKD, independently of conventional cardiovascular risk factors, in community-based elderly.

Pulmonary hypoplasia has been associated with absent or hypoplastic pulmonary artery in four cases in humans. Despite these reports, the effects of decreased pulmonary arterial flow on fetal lung growth have not been adequately studied. This study defines the effects of left pulmonary artery (LPA) ligation on fetal lung growth in sheep by comparing morphometrically determined pulmonary volumes from LPA-ligated, sham-operated, and un-operated control fetuses. LPA ligation (n = 5) or sham operation (n = 4) was performed at 105- to 114-d gestation. lungs were intratracheally fixed for light microscopy. At 112 d (n = 4) and at 140 d (n = 4), unoperated control fetuses were similarly delivered. Absolute pulmonary volumes were then measured using standard stereologic methods. Normal growth of the left lung from 112 to 140 d resulted in significant increases in wet and dry wt, displacement volume, and volumes of future airspace and capillary contents. LPA ligation caused significant decreases in left lung wet and dry wt, displacement volume, and in absolute volumes of fine nonparenchymal, future airspace, parenchymal tissue, and capillary contents compared to sham-operated and 140-d controls. Parenchymal tissue volume was also less than in 112-d controls. In addition, lung wt, displacement volume, and future airspace volume were significantly decreased in sham-operated fetuses compared to 140-d controls. The effects of LPA ligation on bronchial collateral circulation and factors known to affect lung growth (i.e. lung fluid volume) remain to be determined. Clearly, during the canalicular and alveolar stage of fetal lung development, pulmonary arterial flow is necessary for normal lung growth.

We report a patient with primary amenorrhea accompanied by adrenal adenoma. A 21-year-old woman was admitted to our hospital because of primary amenorrhea and hyperprogesteronemia without virilization. Venous sampling showed progesterone overproduction at the left adrenal gland. Computed tomography revealed a 7 cm mass in left adrenal gland. Serum pregnenorone, 17-hydroxypregnenorone, dehydroepiandrosterone, 17-hydroxyprogesterone, deoxycorticosterone, and 11-deoxycortisol were elevated. The diagnosis of steroid hormone producing tumor was made. Following tumor resection, serum progesterone normalized 4 days later, and menarche occurred 51 days after operation. The present case indicated that adrenal functioning tumor should not be overlooked in patients with primary amenorrhea.

Recent studies have indicated that platelet aggregation might be mediated by a decrease in CAMP from basal levels and prostaglandins (PGs) play a major role in mediating platelet aggregation. On the other hand, platelet function is altered in atherosclerosis and thrombosis. In these diseases, platelet adhesion is incleased, platelet's sensitivity to aggregating agents is increased and platelet secresion is enhanced. The administration of antiaggregating drugs is thought to modify and supress one or more of these functions and consequently prevents or delays the formation of thrombi, but in the treatment of these diseases, anticoagulants were not effective sometimes.One of these reasons is that probably mechanism of inhibition of platelet function by antiaggregating agents is varied. In consideration of this point, it is important to clarify the modes of action of antiaggregating drugs in the treatment of these diseases. Drugs such as Heparin, Trasylol, Dextran sulfate, Carbocromen, Prenylamine, Dipyridamole, CDP-choline and α-Tocopherol were incubated with human platelet suspension. The effects of those drugs on platelet aggregation were studied and those on the formation of PGs and cAMP.Material and MethodsHuman platelets were obtained from platelet rich plasma by centrifugation and were suspended in 134mM NaCl-15mM Tris-HCl buffer pH 7.4. After treatment with drugs, the platelet suspension was separated into two.One was used for platelet aggregation test by aggregometer. The other was further separated into supernatant and platelet fraction by centrifugation, which was used for assays of PGs and cAMP by RIA methods.ResultsHeparin, Dextran sulfate, and Carbocromen showed the dosedependent inhibitory effect on platelet aggregation induced by thrombin as well as aspirin or PGE1 did.On the other hand, Trasylol, Prenylamine, CDP-choline and Dipyridamole did not show inhibitory effect in vitro at concentrations lower than those of clinical use.Prenylamine and CDP-choline showed inhibitory effect in vitro at concentrations higher than those of clinical use, but α-Tocopherol did not show inhibitory effect in vitro.(Fig. 1) PGs formation showed stepwise decrease both in supernatant and platelet fraction by Heparin and Dextran sulfate.(Fig. 2) PGs formation showed stepwise decrease in platelet fraction by Aspirin and Trasylol, and no change in supernatant fraction.(Fig. 3.) In platelet fraction, PGs formation showed decrease by the high concentration of CDP-choline and stepwise decrease by Carbocromen. In supernatant fraction, Carbocromen showed slight increase of PGs formation at pg order.(Fig. 4.) The high concentration of Prenylamine depressed PGE, PGF2α formation in platelet fraction. On the other hand, it increased cAMP production.(Fig. 5) Group I did not supress the PG formation, and was further separated into subgroups A and B by the ability of cAMP formation. Group II inhibited the PG formation and was further separated into subgroups 1 and 2 by the ability of PG formation in platelet fraction.ConclusionThe mechanisms of inhibitory effect in platelets by antiaggregating drugs were varied.It is important to consider the modes of action of each antiaggregating drug in the clinical treatment of thromboembolism.

Mercury (Hg) vapor is released from dental "silver" tooth fillings into human mouth air after chewing, but its possible uptake routes and distribution among body tissues are unknown. This investigation demonstrates that when radioactive 203Hg is mixed with dental Hg/silver fillings (amalgam) and placed in teeth of adult sheep, the isotope will appear in various organs and tissues within 29 days. Evidence of Hg uptake, as determined by whole-body scanning and measurement of isotope in specific tissues, revealed three uptake sites: lung, gastrointestinal, and jaw tissue absorption. Once absorbed, high concentrations of dental amalgam Hg rapidly localize in kidneys and liver. Results are discussed in view of potential health consequences from long-term exposure to Hg from this dental material.

少なくとも約5年間にわたり持続している慢性心房性頻拍症の36才男子例について報告した.心電図上第I誘導のP波は陰性,心房拍動数は1分間120～150のことが多く比較的緩徐であり,かつ,多くの場合にWenckebach周期あるいは2: 1の房室ブロックを伴なった. PP間隔,および房室間伝導は自然にも変動する他に,情動,体動,体位変換などにより容易に変化し,その範囲は1分間約190の1: 1房室伝導にまで及び,他方, Aschner試験によりPP間隔は1秒以上にまで延長した. digitalis薬, procaineamide,迷走神経反射などにより,異所性調律の消失はきたさなかつた.本頻拍は発作性頻拍症とは種々の点で著しく異なるまれな頻拍症であり,この点につき文献的考察を行なつた.

Four cases with two-chambered right ventricle are presented; Cases 1 and 2 were associated with infundibular pulmonary stenosis, Case 3 with co-arctation of the aorta, and Case 4 with ventricular septal defect and essential hypertension. Case 4 was 52 years old, being the oldest case ever reported in the literature. Physical, roentgenologic, electrocardiographic, vectorcardiographic, cardiac catheterization and angiocardiographic findings are discussed. Although selective right ventriculography is gene-rally the most reliable and definitive procedure for diagnosis, the coexistence of the following clinical findings would be helpful for diagnosis of two-chambered right ventricle prior to the cardiac catheterization and angiocardiography, especially in cases with isolated or predominant two-chambered right ventricle; (1) a widely distributed, diamond-shaped systolic murmur with the maximum point at the left lower sternal border, (2) a diminished second heart sound at the pulmonary area, (3) a cardiomegaly of somewhat globular shape with absence of poststenotic dilatation, (4) a predominant R pattern in V1 through V6 with absence of significant late R in aVR, and (5) a QRS loop inscribed mostly anteriorly and leftwards in the vectorcardiogram.

Idiopathic normal pressure hydrocephalus (iNPH) is clinically important as a treatable gait disturbance and/or preventable dementia by shunt operation. iNPH usually occurs as a sporadic onset; however, genetic factor(s) is suggested to be involved in the pathogenesis of iNPH because of the presence of familial onset (two or more patients with NPH in a single family) of the disease, whose clinical and brain MRI features are indistinguishable from those of iNPH. Up to the present time, the genetic risk factor(s) for iNPH remains undetermined.