Reversed circadian blood pressure rhythm is associated with occurrences of both fatal and nonfatal vascular events in NIDDM subjects.

To assess the significance of reversed circadian blood pressure (BP) rhythms as a predictive factor of vascular events in NIDDM, vital status after an average 4-year follow-up was determined in 325 NIDDM subjects in whom the circadian BP profile had been monitored between 1988 and 1996. Circadian BP rhythm was analyzed by the COSINOR (a compound word for cosine and vector) method, as previously described. After exclusion of 37 dropped-out subjects, 288 were recruited to the further analysis, of which 201 had a normal circadian BP rhythm (group N) and the remaining 87 had a reversed one (group R). There was no difference in sex, HbA1c, the prevalence of smokers, serum lipids, or serum electrolytes between groups N and R at baseline, whereas age, the prevalence of hypertension, serum creatinine, and diabetic complications were more pronounced in group R than in group N. During the follow-up period (which averaged 52 months in group N and 36 months in group R), fatal and nonfatal vascular (cerebrovascular, cardiovascular, peripheral vascular arteries, and retinal artery) events occurred in 20 subjects in group N and 56 in group R. Unadjusted survival times and event-free times were estimated by the Kaplan-Meier product-limit method, and there was a significant difference in both unadjusted survival and event-free survival rates between groups N and R (P < 0.001 each; log-rank test). The Cox proportional-hazards model adjusted for age, sex, circadian BP pattern, duration of diabetes, therapy for diabetes, various diabetic complications, and hypertension demonstrated that circadian BP pattern and age exhibited significant, high adjusted relative risks for fatal events, and that diabetic nephropathy, postural hypotension, and hypertension as well as circadian BP pattern exhibited significant, high adjusted relative risks with respect to the occurrence of various nonfatal vascular events. These results suggest that reversed circadian BP rhythm is associated with occurrences of both fatal and nonfatal vascular events in NIDDM subjects.

Presynaptic inhibition of tooth pulp afferents in the trigeminal nucleus during REM sleep.

In order to find whether presynaptic inhibition of tooth pulp afferents is enhanced in any phase of sleep or wakefulness, the orthodromic mass response of the trigeminal nucleus to electrical stimulation of the ipsilateral tooth pulp and the antidromic mass response of the tooth pulp to stimulation of the trigeminal nucleus were recorded in the cat. Both responses were stable in amplitude during different phases of sleep and wakefulness. However, attenuation of the orthodromic response and augmentation of the antidromic one were sometimes observed during the burst of rapid eye movements during paradoxical sleep, suggesting that presynaptic inhibition is massively enhanced only on those occasions.

Attenuation during paradoxical sleep of signals from tooth pulp to thalamus.

Quantitative evaluation of the response of thalamic neurons to tooth pulp stimulation was made in chronically prepared cats. The latency, duration and intensity of the responses were measured from the post-stimulus time histograms to estimate, from various aspects, the alteration in the responsiveness during different phases of sleep and wakefulness. During slow wave sleep, tooth pulp-evoked impulses tended to be transmitted to the thalamus in a similar or slightly higher intensity compared to wakefulness. In contrast, during paradoxical sleep the signals were often attenuated in many aspects. The results seem to be in favor of the idea that the impairment of signal to noise ratio in a variety of neuronal networks is one of the characteristics of paradoxical sleep.

Rapidly progressive glomerulonephritis concomitant with diabetic nephropathy.

We describe a rare case of a rapidly progressive glomerulonephritis (RPGN) superimposed on diabetic nephropathy. A 68-year-old woman with non-insulin-dependent diabetes mellitus (NIDDM) complicated with diabetic triopathy demonstrated a rapid deterioration of renal function. Her urinary sediment contained many red blood cell (RBC) cells and casts, suggesting an additional renal disease accompanying diabetic nephropathy. Renal biopsy revealed crescent formation in many glomeruli characteristic of the pauci-immune type of RPGN. Steroid pulse therapy transiently halted the deterioration in renal function, but the patient died of pneumonia complicated with methicillin-resistant staphylococcus aureus (MRSA) infection. The unusual findings in diabetic nephropathy indicated the coexistence of primary glomerulonephritis and diabetic glomerulosclerosis in this case.

Congenital pericardial defect associated with cardiac incarceration: case report.

1. A 4-year-old boy with the congenital partial defect of the left pericardium who presented with myocardial infarction, died of incarceration of the left ventricle. 2. This is the fourth reported case of death from this anomaly in the world. 3. Because this anomaly occasionally causes sudden death, it is important to diagnose the condition while the patient is alive.

[Inhibition, by electro-acupuncture, of the scalp evoked potential induced by painful stimulation of the tooth in man]. / Inhibition, par électro-acupuncture, du potentiel cortical évoqué au niveau du scalp par la stimulation douloureuse de la dent chez l'homme.

Scalp potentials evoked by electrical stimulation of the tooth pulp can be diminished in amplitude by electroacupuncture. This diminution goes generally in inverse with the increase in subjective pain threshold.

[Effect of electro-acupuncture on the response of the trigeminal nucleus evoked by electric stimulation of dental pulp in the cat]. / Effet de l'électro-acupuncture sur la réponse du noyau trigéminal évoquée par la stimulation électrique de la pulpe dentaire chez le chat.

The potential in the spinal trigeminal nucleus evoked by electrical tooth pulp stimulation is depressed by electro-acupuncture given to the acupuncture point in the course of the nerve innervating the stimulated tooth.

Potentiating effects of calcium chelators on basal and stimulated aldosterone production by bovine adrenal glomerulosa cells in vitro.

We previously reported the potentiation of basal aldosterone production by the addition of the calcium chelator ethyleneglycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) to an extracellular solution of bovine adrenal glomerulosa cells in vitro. To assess whether the addition of the calcium chelators ethylenediamine-N,N,N',N'-tetraacetic acid (EDTA) and EGTA can potentiate basal and stimulated aldosterone production, we compared the effect of EDTA with that of EGTA on basal and the agonist (potassium; 8 mM, angiotensin II; 10 nM, ACTH; 10 nM)-stimulated aldosterone production by the cells in vitro. These two chelators lowered the extracellular ionized calcium ([Ca2+]o) concentration in a similar manner. The levels of basal and the agonist-stimulated aldosterone production in the presence of EDTA (1 mM) and EGTA (1 mM) were significantly (P < 0.01 or less) increased when compared with those in the absence of EDTA and EGTA, respectively. These results show that the addition of EDTA and EGTA to an extracellular solution potentiates basal and the agonist-stimulated aldosterone production in vitro. Although an increase in basal aldosterone production in the presence of EDTA (1 mM) and EGTA (1 mM) was completely inhibited by the voltage-dependent calcium channel antagonist nifedipine (1 microM) or the calmodulin antagonist pimozide (1 microM), the potentiation of the agonist-stimulated aldosterone production does not seem to be induced by CA2+/calmodulin-dependent nor cAMP-dependent systems. These findings suggest that calcium chelators such as EDTA and EGTA may possess activating effect on basal and stimulated aldosterone production in bovine adrenal glomerulosa cells.

Mitochondrial DNA point mutation at nucleotide pair 3316 in a Japanese family with heterogeneous phenotypes of diabetes.

A mitochondrial DNA (mtDNA) point mutation at nucleotide pair (np) 3316 has been reported in relation to diabetes. We recently encountered a non-obese family with this type of mutation. The proband in the affected family, a 49-year-old woman who had been previously diagnosed as having an insulin-requiring non-insulin-dependent diabetes mellitus (NIDDM), was referred to our hospital for treatment of diabetic gangrene in her left foot. Her insulin secretory capacity was markedly reduced, but the insulin sensitivity evaluated by the euglycemic hyperinsulinemic clamp technique was normal. In addition, her serum lactate level was markedly increased after a 5 min ambulation, although her serum pyruvate and ketones remained within the normal range. Twenty-year-old twin sons had been treated with insulin since the age of 7, when both were diagnosed with insulin-dependent diabetes mellitus (IDDM). The proband's mother, a 68-year-old, was nondiabetic at this time. MtDNA analysis revealed a point mutation at np 3316 in all family members, which was homoplasmic for the mutation on a photograph of agarose gel electrophoresis containing ethidium bromide under ultraviolet light. This mutation seemed to be maternally transmitted in the family, and the onset of diabetes was occurring earlier and the insulin secretory capacity was declining from generation to generation, so that these findings suggest that the point mutation at np 3316 is associated with various phenotypes of diabetes.