The aim of the present study was to examine pain threshold and pain recovery in patients with burning mouth syndrome (BMS) and matched no-pain controls. Twenty female patients diagnosed with BMS without organic gross changes were enrolled in the study. Twenty control subjects were chosen from age-matched healthy female volunteers. We compared the thermal pain threshold using heat beam dolorimeter on the finger and tongue between patients and controls. Warm (at 50°C for 5 s), cold (at 0°C for 30 s) and mechanical (stimulation by electric tooth brush for 15 s) stimulation was applied to the tongue for both groups. Participants were asked to rate the subjective pain using a visual analogue scale (VAS). Although there was no significant differences between patients and controls in terms of the threshold on the finger, the threshold on the tongue was significantly higher in patients than in controls. We suggest there were peripheral dysfunction at the tongue, and/or central dysfunction in patients with BMS. Among the three types of stimulation, the patients perceived significantly the highest pain from the mechanical stimulation for the first 5 min after the stimulation. Furthermore, when patients with BMS perceived some pain, they continued to complain of the pain longer and more intricately than the controls. This indicates that the pain of the patients is strongly affected not only at a sensory component but also at an affective/motivational component than the controls. However, we should be cautious of simply advancing psychogenic theory in this etiology.

We investigated whether depressed plasma antithrombin and protein C activity, considered as a specific finding of disseminated intravascular coagulation (DIC), is due to consumption coagulopathy in septic patients with DIC. An analysis of hemostatic parameters was performed in 139 septic patients (68 with DIC and 71 without DIC). Plasma activity of antithrombin and protein C tended to be significantly decreased in septic patients with DIC but not in those without DIC (p < 0.001). However, when the septic patients were classified into three groups according to the albumin (or choline esterase) level, no significant differences in antithrombin activity or protein C activity were observed between the patients with and without DIC in any of the subgroups. Notably, neither the plasma activity of antithrombin nor protein C was decreased even in septic patients with DIC who had normal plasma levels of albumin (or choline esterase). No significant correlation was observed between plasma levels of thrombin-antithrombin complex (TAT) and antithrombin activity, or between plasma levels of TAT and protein C activity either in septic patients with DIC or without DIC. It is reasonable to conclude that the markedly reduced plasma activity of antithrombin and protein C is not due to consumption coagulopathy in septic patients with DIC.

Statistical studies on anorexia nervosa in Japan were carried out by our research group. Questionnaires were sent to physicians at 1,030 representative institutions throughout Japan and data were collected from 315 institutions. The total number of patients with anorexia nervosa in 1981 was 940 outpatients and 372 inpatients. The number of patients in 1981 was twice as high as in 1976. Detailed data on 1,011 patients were investigated. As most of the patients had certain endocrinological abnormalities which improved after weight gain, indications are that at least a part of the endocrinological abnormalities might be secondary changes due to weight loss.

Tissue factor (TF) and lipopolysaccharide (LPS) are frequently used to induce disseminated intravascular coagulation (DIC) in experimental animal models. Although the pathophysiology of DIC may differ depending on which agent is used for induction, previous studies on models of DIC have not distinguished which DIC-inducing agent was used. In the present paper, we evaluate the characteristics of TF-induced and LPS-induced DIC using two types of DIC models, with special reference to selected hemostatic parameters and pathological findings within the kidney. Male Wistar rats were administered TF (3.75 U/kg; sustained infusion for 4 h) or LPS (30 mg/kg; sustained infusion for 4 h) via the tail vein, and blood sampling was performed at 0, 1, 3, 4, 5, 7, 9, 11, and 28 h. Judging from changes in the levels of thrombin-antithrombin complex, fibrinogen levels, and platelet counts, it is reasonable to conclude that the severity of both types of experimental DIC is similar with regard to hemostatic activation and consumption coagulopathy. A marked elevation in the level of D-dimer was noted without any organ dysfunction or much fibrin deposition in the kidney upon administration of TF. However, a markedly prolonged period of elevation in plasminogen activator inhibitor activity, a prolonged depression in antithrombin III activity, severe organ failure, and a markedly prolonged period of fibrin deposition in the kidney was observed following LPS administration. A modest number of the rats from the TF-induced DIC model died during the experimental period, whereas a large number of rats died during LPS-induced DIC, especially after 9 h. Since the time course of the pathophysiology differed remarkably among the TF-induced and LPS-induced DIC models in rats, we recommend that TF-induced and LPS-induced DIC be approached as distinct models in order to determine the implications of their experimental and clinical use.

Previous cross-sectional studies have demonstrated that blood pressure measurements at home (HBP) in the morning display stronger predictive power for micro- and macrovascular complications in type 1 and 2 diabetic patients than casual/clinic blood pressure (CBP) measurements. This longitudinal study investigated which of these measurements offers stronger predictive power for outcomes over 6 years. At baseline, 400 Japanese patients with type 2 diabetes were classified as hypertensive or normotensive based on HBP and CBP measurements. Mean (+/-SD) survey duration of all patients was 42.1 +/- 20.0 months (range, 3-72 months). Primary and secondary endpoints were death and new, worsened, or improved micro- and macrovascular events, respectively. Differences in outcomes for each endpoint between hypertensive and normotensive patients in each group were analyzed using survival curves from Kaplan-Meier analysis and log-rank testing. Associated risk factors related to outcomes were assessed using Cox proportional hazards modeling. On the basis of HBP, cumulative events of death and new or worsened microvascular diseases were significantly higher in hypertensive patients than in normotensive patients. On the basis of CBP, no significant differences were identified. New or worsened macrovascular events were significantly higher in hypertensive patients than in normotensive patients on the basis of both HBP and CBP. One associated risk factor was morning hypertension. A longitudinal study of type 2 diabetic patients demonstrated that elevated HBP in the morning is predictive of micro- and macrovascular complications.