Dramatic recovery of counter-regulatory hormone response to hypoglycaemia after intensive insulin therapy in poorly controlled Type I diabetes mellitus.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Iida.
Explore the source record for details and available documents.
PURPOSE: To describe the double-contrast radiographic features of lupus-associated enteropathy. MATERIALS AND METHODS: Six patients with systemic lupus erythematosus involving the small bowel were assessed by double-contrast radiography of the duodenum and small intestine, with reference to clinical manifestations and jejunoscopic findings. RESULTS: Lupus-associated enteropathy could be categorized into two types: acute onset enteritis in four patients and protein-losing enteropathy with hyperlipidaemia in two patients. The former group presented with irregular thickening and spiculation in the folds of the multiple segments of the duodenum to the terminal ileum, and they were frequently accompanied by thumbprinting, suggestive of ischaemic change. The latter group was characterized by mildly thickened folds with multiple submucosal nodules in the upper portion of the jejunum. In one patient from this group, jejunal biopsy demonstrated lymphangiectasia. Both groups were successfully treated by high-dose prednisolone. Follow-up radiography in the former group showed a complete improvement within 2-7 weeks, whereas radiographic abnormalities in the latter remained even after 2 months. CONCLUSIONS: Lupus-associated enteropathy cases may be divisible into two types; an acute ischaemic enteritis type and a protein-losing enteropathy type, each presenting distinct radiographic features.
OBJECTIVE: To compare the gastrointestinal features of isosporiasis and strongyloidiasis. METHODS: Two patients with isosporiasis and three patients with strongyloidiasis were assessed by double-contrast radiography of the duodenum and small intestine, with reference to histology of the duodenal biopsy specimens. RESULTS: Both conditions affected the duodenum and the proximal jejunum, and showed similar radiographic changes as the diseases progressed. Thus, three patients with diarrhoea lasting 1 year or less showed only minimal or irregularly thickened mucosal folds, which seemed to result from mucosal inflammation. Two patients with long-standing disease periods (17 years and 30 years) presented a markedly granular mucosal appearance with effacement of the folds on radiography. These chronological differences in the radiographic features seemed to reflect the degree of villous atrophy. CONCLUSION: Isosporiasis has similar radiographic features of strongyloidiasis.
BACKGROUND & AIMS: Calcitonin gene-related peptide (CGRP) protects the gastric mucosa against injurious stimuli in various experimental models. The underlying mechanism could be the increase in gastric mucosal blood flow (GMBF). A number of endogenous vasodilators exert their effects through the activation of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels on vascular smooth muscle. The present experiments were performed to elucidate whether CGRP increases GMBF through the activation of KATP channels and whether the channels are involved in the protection by CGRP of gastric mucosa. METHODS: GMBF was determined by the hydrogen-clearance technique in male Wistar rats. Mucosal lesions were produced by intragastric superfusion with 0.15N HCland 15% ethanol for 40 minutes. Effects of an agonist (Y-26763, intra-arterially) and an inhibitor (glibenclamide, intravenously) of KATP channels were tested. RESULTS: Y-26763 increased GMBF, which was abolished by glibenclamide, and a CGRP-induced increase in GMBF was attenuated by glibenclamide. Macroscopic and microscopic lesions were exacerbated by human CGRP-(8-37) (a CGRP-1 receptor antagonist; intra-arterially) and glibenclamide but were ameliorated by exogenous CGRP (intra-arterially). CONCLUSIONS: CGRP protects the gastric mucosa against ulcerogenic stimuli, at least in part, through the activation of KATP channels in rats.
Explore the source record for details and available documents.
BACKGROUND: Unlike gastric lymphoma, the endoscopic features of low-grade, mucosa-associated lymphoid tissue (MALT) lymphoma of the colorectum have not been defined. METHODS: We analyzed colonoscopy, endoscopic ultrasonography, and histologic findings in six patients with MALT lymphoma restricted to the colorectum. Histologic confirmation of the proliferation of centrocyte-like cells with lymphoepithelial lesions formed the criteria for the selection of patients. RESULTS: Based on endoscopic findings, the patients were divided into cases of solitary (4 patients) or multifocal (2 patients) involvement. Endoscopic findings in cases of solitary involvement were uniform in that the lesions were either smooth or nodular protrusions, demonstrated by a hypoechoic mass under endoscopic ultrasonography. Multifocal involvement was endoscopically recognized as protrusions, dilated vasculature, or small ulcers. CONCLUSIONS: Protruding lesions are the main pattern of involvement in MALT lymphoma of the colorectum, although variable and multifocal involvement is also possible in this type of lymphoma.
Explore the source record for details and available documents.
The aim of the present study was to determine whether a tap on the forehead evokes a vestibulospinal reflex in sternocleidomastoid muscles in normal human subjects and patients with central or vestibular lesions. While first positive-negative short-latency EMG potentials with a mean positive potential peak of about 12 ms and a mean negative potential peak of about 17 ms were found in the bilateral sternocleidomastoid muscles in normal subjects, they disappeared or were attenuated in patients with central or peripheral vestibular lesions.
Ovarian steroid hormones exert major influences on eating behaviour and body weight regulation of female rats. Ovariectomy (OVX) results in an increase in food intake and a concomitant increase in body weight, while estradiol (E2) replacement reverses these effects. In this study, we examined the influence of OVX on obese (ob) gene expression in rat adipose tissues and serum leptin concentration. Female Wistar rats, 10 weeks old, were divided into three groups: sham-operated control rats receiving corn oil (group 1, n = 4), ovariectomized rats receiving corn oil (group 2, n = 5), and ovariectomized rats receiving 17beta-E2 (10 microg/kg/day) replacement (group 3, n = 4). After 4 weeks, the rats and food consumption were weighed and serum E2 and leptin levels were measured by radioimmunoassays. Furthermore, the expression levels of ob mRNA obtained from the bilateral perimetric fat pads were estimated by Northern blot analysis. The mean weight and food consumption in group 2 were significantly (p < 0.01) heavier than those in group 1. But there were no significant differences between group 1 and group 3. The expression levels of ob mRNA in group 2 were lower than those in group 1, however, the levels of group 3 were restored to the level of group 1. On the other hand, no significant differences among the 3 groups as to serum levels of leptin were observed. The data herein clearly indicate that ovarian steroid hormones may be one of the factors involved in the regulation of ob gene.
BACKGROUND: Activation of adenosine triphosphate-sensitive K+ channels causes cerebral vasodilation. To assess their contribution to volatile anesthetic-induced cerebral vasodilation, the effects of glibenclamide, an adenosine triphosphate-sensitive K+ channel blocker, on the cerebral vasodilation induced by isoflurane and sevoflurane were studied. METHODS: Pentobarbital-anesthetized dogs (n = 24) assigned to one of two groups were prepared for measurement of pial vessel diameter using a cranial window preparation. Each dog received three minimum alveolar concentrations (MAC; 0.5, 1, and 1.5 MAC) of either isoflurane or sevoflurane, and the pial arteriolar diameters were measured in the presence or absence of glibenclamide (10(-5) M) infused continuously into the window. Mean arterial pressure was maintained with phenylephrine. Furthermore, to assess the direct effect of isoflurane and sevoflurane on cerebral vessels, artificial cerebrospinal fluid was administered topically by being bubbled with isoflurane or sevoflurane. The blocking effect of glibenclamide on the vasoactive effects of these anesthetics also were evaluated. RESULTS: Isoflurane and sevoflurane both significantly dilated large (> or = 100 microm) and small (< 100 microm) pial arterioles in a concentration-dependent manner (6% and 10%, 3% and 8% for 0.5 MAC; 10% and 19%, 7% and 14% for 1 MAC; 17% and 28%, 13% and 25% for 1.5 MAC). Glibenclamide attenuated the arteriolar dilation induced by these anesthetics (not significant in isoflurane). Topical application of isoflurane or sevoflurane dilated large and small arterioles both in a concentration-dependent manner. Such vasodilation was inhibited completely by glibenclamide. CONCLUSION: The vasodilation of cerebral pial vessels induced by isoflurane and sevoflurane appears to be mediated, at least in part, via activation of adenosine triphosphate-sensitive K+ channels.
A 35-yr-old, immunocompetent male was admitted complaining of severe odynophagia. He was diagnosed as having herpes simplex esophagitis and was started on intravenous acyclovir 5 mg/kg every 8 h on the day of admission. His response was dramatic. Within 24 h he was virtually asymptomatic. Acyclovir therapy in immunocompetent adults with esophagitis has been described in only a handful of cases in the literature, although the therapy is well established in immunocompromised patients. We review the English literature and discuss the efficacy of the therapy. Acyclovir therapy may be beneficial in immunocompetent patients with particularly severe odynophagia.
AIMS: To investigate the clinicopathological findings in cases with intraepithelial haemorrhage of the oesophagus (IHO). METHODS: Necropsy records and the histopathology findings in the oesophagus were reviewed for the period 1990 to 1995. Six cases (0.7%) of IHO were found among 919 necropsy cases. Clinical records of these patients and gross and microscopic slides were reviewed in detail. RESULTS: The ages of the IHO cases ranged from 42 to 82 years (average 68 years), with a male to female ratio of 1:2. All cases had underlying haematological disorders with thrombocytopenia, but disseminated intravascular coagulation was not evident in any case. Macroscopically, solitary (two cases) or multiple (four cases) haemorrhagic lesions ranging from 6 to 79 mm in size were identified within the distal oesophagus. Microscopically, there was no inflammatory infiltration, destruction of red blood cells, or submucosal scar formation. CONCLUSIONS: IHO seems to occur shortly before death as a terminal event in haematological disorders. Based on these observations, the term "terminal IHO" can be suggested for this type of oesophageal lesion.
This study was designed to investigate whether anti-IgE-induced or ionophore A23187-induced histamine release from human basophils is regulated by exogenous nitric oxide (NO), and to assess some similarities between the effect of NO on basophils and that on rat peritoneal mast cells (RPMC). The NO donor, sodium nitroprusside (SNP), inhibited A23187-induced histamine release from crude human basophils and crude RPMC in a dose-dependent fashion. This downregulation was still observed when SNP was washed out just before the cell stimulation, indicating that the effect of SNP was irreversible. The downregulation disappeared in both purified cell populations after the removal of contaminating cells. However, when purified cells were preincubated with SNP in the presence of 5 mM N-acetylcysteine (NAC), increasing the bioavailability of NO, the downregulation was recovered. The presence of NAC significantly augmented the downregulation of SNP on A23187-induced histamine release from both crude cell populations. In contrast, SNP had no effect on anti-IgE-induced histamine release from either crude or purified basophil preparation in the absence of NAC, and SNP plus NAC inhibited anti-IgE-induced histamine release from both cell preparations. The same results were obtained with crude and purified RPMC preparations under the same conditions. These results show that SNP similarly downregulated exocytosis of basophils and RPMC, and acquired the potent effect in the presence of NAC, indicating that exogenous NO plays a part in the regulation of basophil and mast cell activation.
BACKGROUND AND PURPOSE: Although randomized clinical trials have demonstrated the benefit of antihypertensive treatment in preventing stroke, the effectiveness of community-based programs is largely unknown. We investigated long-term community-based prevention activities. METHODS: In rural northeastern Japan, people aged > or = 30 years numbered 3219 in the full intervention community and 1468 in the minimal intervention community in 1965. Systematic blood pressure screening and health education began in 1963. Stroke was registered through 1987. RESULTS: More than 80% of people aged 40 to 69 years were screened in both communities in the 1960s. One community charged for screening services after 1968, whereas the other community intensified intervention; subsequently, screening rates and the follow-up of hypertensive individuals declined in the minimal intervention community, especially in men. In men, stroke incidence declined more (P < 0.001) in the full intervention (42% in the period 1970 to 1975, 53% in the period 1976 to 1981, and 75% in the period 1982 to 1987) than in the minimal intervention community (5% increase, 20% decrease, and 29% decrease, respectively); in women, the stroke incidence declined about 45% to 65% in both communities. Changes in stroke prevalence paralleled those in stroke incidence. Trends in systolic blood pressure levels tend to explain the differential stroke rates in men. CONCLUSIONS: Delivery of hypertension control services through intensive, free, community-wide screening and health education was effective in prevention of stroke for men in a community.
BACKGROUND AND PURPOSE: The effects of acute smoking on cerebral circulation are controversial. This study was designed (1) to clarify any differences between the effects of cigarette smoking and nicotine infusion and between the effects of single- and multiple-cigarette smoking on cerebral vessels and (2) to probe the mechanism(s) underlying the vascular responses. METHODS: In pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats, pial vessel diameters were measured with the use of a cranial window preparation. We studied the effects of (1) 60 puffs per minute of mainstream cigarette smoke from cigarettes having 2 nicotine levels (0.1 and 1 mg per cigarette), (2) administration of nicotine (0.05 mg per body IV), and (3) repeated smoking (four 1 mg nicotine-containing cigarettes at 30-minute intervals) (n=6 each). RESULTS: Inhalation of smoke from a 0.1 or 1 mg nicotine-containing cigarette for 1 minute caused pial arterioles to constrict at 30 seconds (7.2% and 7.3%, respectively) and then to dilate (peak at 5 to 10 minutes; 4.6% and 17.9%, respectively). Nicotine infusion caused pial vasodilation (35.7%) without an initial vasoconstriction. Repeated smoking suppressed the pial vasodilation but not the initial vasoconstriction. The vasodilation induced by a single cigarette was greatly inhibited by pretreatment with mecamylamine or glibenclamide and attenuated by propranolol or Nomega-nitro-L-arginine methyl ester; the initial vasoconstriction was inhibited by seratrodast, a thromboxane A2 receptor antagonist (n=6 in each case). CONCLUSIONS: Single-cigarette smoking had a significant biphasic effect on cerebral arteriolar tone. The vasodilation was attenuated by repeated smoking. The vasodilation is most likely an effect of nicotine, at least in part mediated via sympathetic activation, NO production, and K+ channel activation. The vasoconstriction is partially due to thromboxane A2 induced by cigarette smoke.
This 8-year-old boy presented with a rare case of epidural hematoma of the clivus and atlantoaxial dislocation caused by a hyperflexion injury sustained in a traffic accident. Magnetic resonance (MR) imaging demonstrated an epidural hematoma in the posterior fossa that compressed the pons and medulla. On admission, the patient was confused and had bilateral abducens palsy. He was treated conservatively, and 6 months after admission, the epidural hematoma on the clivus had disappeared on MR imaging and the bilateral abducens palsy was cured. Only two such cases have been reported in the literature. In this report, the authors discuss the mechanism of hematoma formation in this region of the brain.
It has been shown that the neural channels from the otolith organs and the vertical semicircular canals connect to the cyclo-rotatory oculomotor system. However, only a few studies have been conducted to examine the relationship between the cyclo-rotatory optokinetic (COK) and the vestibular inputs. Accordingly, we have analyzed the cyclo-rotatory oculomotor output evoked by a COK stimulus, in 30 subjects; 21 normal adults, 4 elderly persons, and 5 persons with unilateral vestibular dysfunction. In addition, the spinal motor output was simultaneously recorded and comparatively analyzed. The increase in COK nystagmus (COKN) was less than that in horizontal and vertical OKN. There was a significant decline in the maximum slow phase eye velocity in the elderly subjects as well as in the subjects with unilateral vestibular dysfunction, compared to that in the normal adult subjects. Regarding the spinal motor output, in the subjects with unilateral vestibular dysfunction, a pronouned increase in the sway distance from the center of gravity was found with COK stimulus forward the lesioned side. However, with the COK stimulus, there was no significant correlation between the output functions of the cyclorotatory oculomotor system and those of the spinal motor system.
It is not known whether the optokinetic afternystagmus (OKAN) can be evoked by cyclo-rotatory optokinetic stimulation (C-OKst) or not. Accordingly, this study was designed to investigate the problem by using a rotating white dome with random dots. Optokinetic nystagmus (OKN) and OKAN in standing upright, supine, and prone positions were recorded and analyzed with an infrared-ray CCD camera and computed picture analyzer. During stimulation, rotatory OKN showed clearly, but there was no slow-rise component. The OKAN was continuously recorded and analyzed. The component of this OKAN was found only in the head-horizontal direction (yaw axis) in all different head positions. It appeared fairly constantly in the prone posture. The velocity storage mechanism (VSM) had to be charged by the C-OKst, but the OKAN (1st phase) appeared only in the yaw axis, not in the roll axis.