A comparative clinicopathological study was retroscpectively performed in 61 children and 51 adults with IgA nephropathy. Hematuria and/or proteinuria as a chance finding was the most common initial clinical sign, being observed in 82.0% of the children and in 52.9% of the adults. At renal biopsy, hypertension and severe proteinuria were found in 9.8 and 33.3% of the adults and in 0 and 14.8% of the children (both p < 0.05), respectively. Elevations of blood urea nitrogen and serum creatinine were found at this time of biopsy in 21.6 and 9.8% of the adults, but in none of the children (p < 0.001 and p < 0.05, respectively). Histologically, focal glomerulosclerosis and tubular atrophy were found in 52.9% of the adults and in 32.8% of the children (p < 0.05). However, some features of the disease seen in both groups were similar, including the incidences of IgA nephropathy, sex ratio, the mode of onset, incidences of gross hematuria, and high IgA levels in the sera. Furthermore, the relationships between the severity of proteinuria and renal lesions were similar: mesangial proliferation, glomerulosclerosis, and tubular atrophy increased with the degree of the severity of proteinuria. These results suggest that IgA nephropathy is essentially identical in children and adults, although adult patients tend to be further advanced in their disease course at the time of diagnosis, and that focal glomerulosclerosis with tubular atrophy is correlated with deterioration of renal function.

Lipopolysaccharide (LPS) is a pathogen-associated large molecule responsible for sepsis-related endotoxic shock, and the heart is one of the most common organs adversely affected. LPS is reported to increase serum TNFalpha levels and reduce Per1 and Per2 gene expression. Therefore, in this experiment, we determined the time-dependent effects of LPS on heart rate (HR) and circadian gene expression in the mouse heart and liver. HR of the LPS group was significantly elevated 2 and 8 h after injection compared to the control group. A significant percent increase in HR was observed at ZT6, 12, and 18. LPS increased Tnfalpha mRNA expression in the heart and liver at ZT6, 18, and 24. A time-dependent effect of LPS on reduction of Per1 and Per2 gene expression was also observed in the heart and liver. In order to examine the effect of LPS on cell damage, we examined apoptosis-related gene expression after LPS injection. Bax mRNA expression level of the LPS group was higher than that of the control group 8 and 26 h after injection. On the other hand, Bcl2 mRNA expression level of the LPS group was lower than that of the control group 2 and 26 h after injection. Dexamethasone strongly attenuated the LPS-induced increase of serum TNFalpha without significant change in Per1 and Per2 gene expression in the heart. In conclusion, the present results demonstrated that LPS exerts a time-dependent inhibitory effect on Per1 and Per2 gene expression in the heart and liver. The chronopharmacological lethal effect of LPS may be related to the time-dependent increase of serum TNFalpha level and simultaneously high level of Per2 gene expression in the heart and liver between ZT12-18. Taken together, chronopharmacological effect of LPS may be related to not only sickness behavior syndrome and mortality, but also circadian rhythm systems.

Abstract-The effect of naloxone given at various times after morphine administration on the development of tolerance to and dependence on a single dose of morphine was studied.Naloxone antagonized the analgesic effect of morphine and the development of tolerance to and dependence on morphine, dose dependently.

Positron emission tomography was performed using an oxygen-15 gas inhalation technique to measure regional cerebral blood flow, metabolic rate for oxygen, oxygen extraction fraction, and cerebral blood volume in 13 patients with subarachnoid hemorrhage during the period of delayed vasospasm after surgery as well as in 10 volunteers as controls. Compared with the controls, the patients showed decreased hemoglobin concentration and decreased total arterial oxygen content due to postoperative hemodilution. Global reductions in the metabolic rate for oxygen and in the tissue oxygen supply were noted even in the apparently normal cortex of the patients in spite of adequate blood flow and adequate oxygen extraction fraction. In addition, regional reductions in blood flow and in perfusion reserve were seen in the cortical territory corresponding to cerebral vasospasm. Our results indicate that two processes are involved in the pathophysiology of cerebral vasospasm: 1) generalized impairment of oxygen metabolism with a reduced tissue oxygen supply, even in the apparently normal cortex, and 2) additional impairment of regional perfusion in the territory of vasospasm. (Stroke 1989;20:1504-1510 C erebral vasospasm is one of the most important causes of cerebral dysfunction after aneurysmal rupture. It is generally believed that neurologic symptoms become overt as arteries narrow and blood flow falls below the ischemic threshold.1 However, cerebral function during vasospasm might be affected by factors other than low perfusion, such as possible toxicity from subarachnoid clots 2 -4 or changes in the patient's general condition due to postoperative management. 56Cerebral vasospasm also differs from other causes of cerebral ischemia in its pathogenesis, in the duration and distribution of vascular narrowing, and in the reversibility of low perfusion. Thus, the hemodynamic and metabolic sequences during vasospasm may not necessarily be similar to those Received February 1, 1989; accepted June 23, 1989. during acute ischemia, which have been described in humans in previous positron emission tomography (PET) studies. 7 -8 The aim of our study was to investigate the pathophysiologic mechanism of cerebral dysfunction during the period of delayed vasospasm after subarachnoid hemorrhage (SAH), in addition to clarifying the problems of current postoperative management of SAH patients under usual clinical settings. Subjects and MethodsWe selected 13 SAH patients, nine women and four men, mean age 50 (range 25-70) years between June 1986 and June 1988. We also selected 10 persons without SAH, seven men and three women with a similar age range, to serve as controls.The patients had SAH due to an initial aneurysmal rupture in the anterior circulation; no history of other intracranial, cardiopulmonary, or metabolic disease; no intracerebral hematoma either on admission or during their entire clinical course; and underwent successful neck-clipping of aneurysms without any complications related to either surgery or anesthesia. The dia...

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