Microbial extracranial aneurysm of the internal carotid artery: complication of cervical lymphadenitis.
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Biomedical subjects
Publications and source records attributed to T Endo.
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Tumor necrosis factor-alpha (TNF-alpha) is known to modulate the expression of thyroid-specific genes, such as thyroglobulin (TG), contributing to the pathogenesis of autoimmune thyroid disease. In the present study, we show that TNF-alpha suppresses DNA-binding activity of thyroid transcription factors, Pax-8 and thyroid transcription factor-1 (TTF-1), which is, in part, involved in TNF-alpha-induced decrease in TG gene expression. Transfected into rat thyroid FRTL-5 cells, the activity of reporter plasmid containing the rat TG promoter ligated to a luciferase gene was significantly suppressed in the presence of TNF-alpha. In gel mobility shift analyses, protein-DNA complexes formed by TTF-1 and Pax-8 were reduced when the nuclear extracts prepared from TNF-alpha-treated FRTL-5 cells were used. The suppressive effect of TNF-alpha on TTF-1-DNA complex formation is, in part, caused by suppression of TTF-1 gene transcription by TNF-alpha. Expressions of TTF-1 messenger RNA and protein, which were assessed by Northern blot and Western blot analyses, respectively, were decreased by TNF-alpha treatment of FRTL-5 cells. In contrast, TNF-alpha did not affect the expression of Pax-8 messenger RNA. Treatment of FRTL-5 cells with TNF-alpha caused a decrease in Pax-8 protein in nuclear extracts and accumulation of the protein in the cytoplasm, as assessed by Western blot analyses. Mutation of the TTF-1/Pax-8-binding site lost the TNF-alpha-induced decrease in TG promoter activity in a transfection experiment. These results indicate that TNF-alpha suppresses the activity of TTF-1 and Pax-8 by different mechanisms, which, in part, seem to be involved in TNF-alpha-induced decrease in TG gene expression.
Tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) are cytokines that can individually or additively suppress thyroid cell function and the expression of thyroid-specific genes, such as thyroglobulin (TG) and thyroperoxidase (TPO). Thyroid transcription factor-2 (TTF-2) is a DNA-binding protein that modulates the expression of TG and TPO genes. In the present study, we examine the effects of TNF-alpha and IFN-gamma on TTF-2 gene expression, as well as the DNA-binding activity of TTF-2. FRTL-5 cells were maintained in 5H medium containing 0.2% calf serum for 7 days, then incubated with TNF-alpha, IFN-gamma, or TNF-alpha plus IFN-gamma. Total RNA was isolated and Northern blotted. TNF-alpha (50 ng/ml) only slightly suppressed (61+/-2% compared with control), whereas IFN-gamma (100 U/ml) modestly decreased TTF-2 messenger RNA (mRNA) levels (34+/-4%). TNF-alpha and IFN-gamma simultaneously caused a marked decrease in TTF-2 mRNA levels (13+/-2%). The suppressive effects of TNF-alpha and IFN-gamma on TTF-2 mRNA levels were concentration dependent and maximal at 50 ng/ml TNF-alpha with 100 U/ml IFN-gamma. The suppressive effect was also time dependent, reaching a maximum 12 h after exposure. Moreover, the suppressive effects of TNF-alpha and IFN-gamma upon rat TG and TTF-2 mRNA levels were similar. To test whether TNF-alpha and IFN-gamma alter TTF-2-binding to DNA, we performed electrophoretic mobility shift assays using a TTF-2-binding element in the rat TG gene as a probe. Formation of the TTF-2/DNA complex was decreased by TNF-alpha and/or IFN-gamma. Our results demonstrate that TNF-alpha and IFN-gamma additively reduce the gene expression and DNA-binding of TTF-2. These data suggest that TTF-2 is involved in the TNF-alpha and IFN-gamma-induced suppression of thyroid-specific gene expression.
Isatin (indole-2,3-dione), an endogenous inhibitor of monoamine oxidase (MAO), has several physiological properties for stress and anxiety. We previously identified isatin in the brain of stroke-prone spontaneously hypertensive rats (SHRSP) using gas-chromatography mass spectrometry. This study elucidated the effects of isatin on the ACh and DA levels of brain tissues in rats. Furthermore, we evaluated the effect of isatin on DA levels in a rat model of Parkinson's disease induced by Japanese encephalitis virus. Striatal ACh and DA levels significantly increased at 2 hours after isatin (50-200 mg/kg, i.p.) administration. Perfused through a microdialysis probe, isatin (10(-6)-10(-4) M) also produced a significant and concentration-dependent increase in the ACh and DA concentrations in the perfusate from the rat striatum. Furthermore, urinary isatin concentrations in patients with Parkinson's disease tend to increase according to the severity of disease. Isatin (100 mg/kg, i.p.) significantly increased striatal DA levels in a rat model of Parkinson's disease. These results suggest that urinary isatin may become a diagnostic marker for the clinical severity of Parkinson's disease and that endogenous isatin, a new biological modulator, may play a role in the regulation of the brain levels of ACh by increasing the level of DA under stress.
The effects of a mixture of organisms on cecal fermentation and cholesterol metabolism in sham-operated and cecectomized rats were investigated. Male F344 rats, allocated into four groups: cecectomized rats fed a mixture of organisms (CEMO), cecectomized rats fed rice bran (CERB), sham-operated rats fed a mixture of organisms (SHMO), and sham-operated rats fed rice bran (SHRB) for 4 weeks. The diets had 0.5% cholesterol and 0.125% sodium cholate added. There were no significant differences in the body weight gain and food intake among the groups. The cecal pH in the SHMO group was significantly lower than that in the other groups. The total cholesterol and (VLDL + IDL + LDL)-cholesterol concentrations in serum were significantly lower in the SHMO group than that in the SHRB group, and the triacylglycerol concentration in the sham-operated rats tended to decrease compared to the cecectomized rats. The fecal cholesterol excretion in the CERB group was higher than that in the other groups, and that in the SHMO group was significantly higher than in the SHRB group. The acetic acid, propionic acid, n-butyric acid, and total short-chain fatty acid concentrations in the cecum contents were significantly higher in the SHMO group than those in the other groups. Streptococcus, Bifidobacterium, and Lactobacillus in the SHMO group tended to be higher than the other groups and Bacteroidaceae in the CEMO and CERB groups were significantly higher than that in the SHMO group. The results demonstrate that the mixture of organisms was fermented with the cecal contents and that the metabolites such as short-chain fatty acid lowered the serum total cholesterol and liver cholesterol concentrations in the rats fed a cholesterol-containing diet.
The effects of a probiotic (a mixture of Bacillus, Lactobacillus, Streptococcus, Clostridium, Saccharomyces and Candida) on the lipid metabolism, and caecal flora and metabolites of cocks were studied. The cholesterol level of the liver and serum was significantly decreased in the cocks fed on the cholesterol-enriched diet containing the probiotic. The distribution and frequency of occurrence of flora, and the chemical characteristics of the metabolites in the caecal content of the cocks were also affected by the inclusion of the probiotic in the basal and cholesterol-enriched diets. The Enterobacteriaceae species were significantly decreased in number, while the Bacillus, Streptococcus, Bifidobacterium and Lactobacillus species were significantly increased. The presence of yeast was observed, and the ammonia level was significantly reduced. The pH value, however, was not affected. The concentration of short-chain fatty acids in the caecal content of the cocks fed on the cholesterol-enriched diet supplemented with the probiotic was increased. It is, therefore, suggested that the incorporation of a probiotic in the diet would improve the balance of the intestinal flora and metabolites. Furthermore, it would also suppress the serum and liver cholesterol levels of cocks fed on the cholesterol-enriched diet.
By the selective breeding of obese male mice of the ddY strain and using indices of the heavy body weight and appearance of urinary glucose, we established two inbred strains in 1992: one with obesity and urinary glucose (Tsumura, Suzuki, Obese Diabetes: TSOD) and the other without them (Tsumura, Suzuki, Non Obesity: TSNO). The male TSOD mice constantly showed signs of obesity and urinary glucose with increases in food and water intake, body weight and some fat weight. The body mass index (BMI) clearly showed moderate obesity. Increases in the levels of diabetic blood parameters (glucose, insulin and lipids) were also found in males, in which the levels of blood glucose and insulin were high to the ages past the growth peak. In the histological studies, pancreatic islets of the TSOD males were found hypertrophic without any signs of insulitis or fibrous formation. Among these diabetic characteristics, some of which were similar to the reported models of non-insulin-dependent diabetes mellitus (NIDDM), the stable appearances of the hyperglycemia, the hyperinsulinemia and the hypertrophy of pancreatic islets to the ages past the growth peak were the prominent features. In these respect the TSOD mouse may be a useful model for researching the mechanisms of human diabetes and its complications.
Gonadotropin-releasing hormone (GnRH) and its agonist analog (GnRHa) are well known to have luteolytic effects. We previously reported that prolactin (PRL) stimulated matrix metalloproteinase (MMP)-2 activity to degrade collagen type IV as a mechanism of structural luteolysis. The effects of GnRHa treatment on developed corpora lutea are unknown. In this study we assessed the effect of GnRH on MMP expression and induction of structural involution of developed corpora lutea of superovulated rats using GnRHa. Pregnant mare serum gonadotropin-human chorionic gonadotropin (hCG)-synchronized ovulation and luteinization were induced in immature female rats, followed by daily treatment with GnRHa from 5 days after hCG treatment. GnRHa-induced involution of corpora lutea was evident 3 days after the treatment, as shown by their markedly smaller size (60% of the control weight). Nine days after hCG injection, serum progesterone and 20alpha-dihydroprogesterone concentrations were as low as those associated with structural luteolysis. These findings revealed that GnRHa has the ability to induce structural luteolysis in superovulated rats in the same way that PRL does. To gain information on mechanisms of luteal involution induced by GnRHa, we performed gelatin zymography. This showed a significant increase in the active form of MMP-2 in the luteal extract of GnRHa-treated rats (more than twofold that of the control). Activation of pro-MMP-2 by membrane type-MMP (MT-MMP) is reported to be a rate-limiting step for catalytic function. Another function of MT-MMP is to degrade collagen types I and III. The plasma membrane fraction of corpora lutea of GnRHa-treated rats activated pro-MMP-2 of fetal calf serum, resulting in a marked shift of the 68-kDa band to the 62-kDa band in the zymogram. A Northern hybridization study also revealed simultaneous significant increases in expression of MMP-2 mRNA and MT1-MMP mRNA in corpora lutea of GnRHa-treated rats (more than threefold the control level). In summary, hormonal and histological features of corpora lutea of GnRHa-treated superovulated rats correspond to those of structural luteolysis. GnRHa stimulated the expression of MMP-2 and MT1-MMP in developed corpora lutea associated with involution. These findings support the conclusion that MMP-2, activated by MT1-MMP, and MT1-MMP itself, remodel the extracellular matrix during structural luteolysis induced by GnRHa.
The purpose of the present study is to examine changes of the circadian period in humans during temporal isolation, where the circadian rhythm is free-running. Twelve young males each spent 22 d alone in a temporal isolation room. Rectal temperature was continuously recorded and plasma melatonin was measured on day 3 (D3) and from days 10 to 13 (D10-D13). The light intensity in the room was less than 100 lx during the waking period. The free-run period of temperature rhythm from D3 to D10 (24.75 h) was not significantly different from those of the plasma melatonin rhythm (24.63 h) and sleep-wake cycle (24.69 h). The free-run period of temperature rhythm was 24.58 h in S-1 (D2-D6), which was gradually and significantly lengthened to 24.84 h in S-2 (D6-D10), 25.16 h in S-3 (D12-D16), and 25.18 h in S-4 (D18-D22). The free-run period of rectal temperature rhythm was steadily lengthened throughout the isolation period, which was probably due to the after-effect of previous entrainment to 24-h time cues.
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Dry cough and exertional dyspnea developed in a 78-year-old man after aorto-coronary bypass surgery for angina pectoris. Chest X-ray films showed small nodular shadows in the upper and middle fields of both lungs. The patient's condition was exacerbated despite treatment with antibiotics. Chest high-resolution computed tomography disclosed small nodular and reticulo-linear shadows predominantly in the interlobular septa and bronchovascular bundles. Transbronchial lung biopsy specimens revealed micro-granulomas with necrosis, suggesting miliary tuberculosis. Antituberculosis drugs were started and the patient's symptoms and radiographic findings gradually resolved. Cases of cellular immunosuppression have beer reported in patients following open-heart surgery that utilized antifical heart and lung apparatus. Such procedures, together with hemodialysis, deserve consideration as potential risk factors for miliary tuberculosis.
Differences in the N-linked oligosaccharides on isoforms of the neural cell adhesion molecule (N-CAM) on astrocytes were found using a lectin, namely, Datura stramonium agglutinin (DSA). Integral proteins of astrocytes prepared from newborn rat cerebella were solubilized with Nonident P-40 and then separated into two fractions, an unbound fraction and a bound fraction, by a DSA-agarose column. Both fractions thus obtained were subjected to immunoblotting using an anti-N-CAM monoclonal antibody. In the DSA-bound fraction, N-CAM 180 was found as well as N-CAM 120 and N-CAM 140. On the other hand, N-CAM 180 was not detected in the unbound fraction, whereas N-CAM 120 and N-CAM 140 were. Furthermore, N-CAM 180 did not carry the HNK-1 epitope, whereas the other two isoforms did. Although the presence of N-CAM 180 on astrocytes was controversial until recently, the results shown here indicate that N-CAM 180 exists on rat astrocytes and exclusively carries a glycan structure reacting with DSA. This is the first demonstration of the production of N-CAM glycoforms carrying different oligosaccharides by a homogeneous astrocyte preparation. These results suggest that the glycosylation of each N-CAM isoform might be regulated independently. Whether each N-CAM with different glycans participates in different functions remains to be established.
Recent advantages of medical treatment for severe and fulminating ulcerative colitis are described. When considering therapeutic alternative for patients with severe and fulminating UC, it is the most paramount importance to assess accurately severity of disease. Next, the following is helpful guides to treat, (1)general management of patients illness, including correction of electrolytes imbalance, and sufficient fluid and alimentation therapy to avoid life-threatening complications, (2)timely surgical intervention, if disease is intractable. Two new promising approaches to severe and fulminating UC are introduced herein. One is fast-acting cyclosporine continuous intravenous administration, the other is leucocytapheresis employing new membrane filter, Cellsoba, manufactured by Asahi Medical Co. However, it remains controversial when and how physicians should abandon to surgical intervention.
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In order to elucidate the role of emetic action, the effects of talipexole and bromocriptine, two antiparkinsonian dopamine receptor agonists, on serotonin (5-HT) release from enterochromaffin (EC) cells were studied by measuring 5-HT concentrations in the perfusate of the isolated rat ileum. Bromocriptine (10(-8)-10(-6) M), which exerts agonistic effects on D1 and D2 receptors, increased 5-HT release in a concentration-dependent manner. No significant increase in 5-HT release was seen after addition of talipexole, which selectively stimulates D2 receptors and blocks 5-HT3 receptors, even at 10(-6) M. The increase in 5-HT release caused by bromocriptine at 10(-6) M was inhibited by administration of 10(-6) M of D1 receptor antagonist SCH 23390, D2 receptor antagonist spiperone, 5-HT3 receptor antagonist granisetron or tetrodotoxin (TTX). These results showed the involvement of both dopaminergic and serotonergic mechanisms in the 5-HT release from EC cells following the administration of dopamine receptor agonists. Bromocriptine might induce 5-HT release by stimulating D1, D2 and 5-HT3 receptors and depolarizing neurons in the ileum. On the other hand, talipexole might weaken 5-HT release from EC cells elicited by D2 receptor stimulation with its 5-HT3 receptor blocking property. It is suggested that the emetic effect of dopamine receptor agonists involves the peripheral gastrointestinal tract as their site of action.
We used a self expandable metalic stent (SEMS) on 24 patients (average age 68.6 years, 20 males, 4 females) with malignant upper gastrointestinal stenosis from August, 1997 to March, 1999. The primary diseases of the 24 patients were gastric cancer (13 cases: 54%), esophageal cancer (10 cases: 42%) and paraesophageal lymph node metastasis of breast cancer (one case: 4%). In this study, we present a "Home Index" as an indicator to evaluate a patient's quality of life, and investigated the efficacy and problem of SEMS.
The object of this study was to evaluate the involvement of 5-HT3 receptors in the regulation of 5-HT release from the small intestine using ferrets, an animal model of emesis. 2-Methyl-5-HT, a 5-HT3 receptor agonist, produced a concentration-dependent increase of 5-HT from the ferret ileum. This increase in 5-HT release was significantly inhibited by granisetron (10(-7) and 10(-6) M) or azasetron (10(-7) and 10(-6) M) in a concentration-dependent manner. Ondansetron (10(-7) M) and ramosetron (10(-6) M) also significantly inhibited the 2-methyl-5-HT-induced increase in 5-HT release. When the concentration of ondansetron was increased from 10(-7) M to 10(-6) M, inhibition of 5-HT release was reduced. Ramosetron, for which 5-HT3 receptor binding of the rat brain is remarkably stronger than for any other 5-HT3 receptor antagonists, inhibited the 5-HT release at only the highest concentration of 10(-6) M. Based on these observations that the mode of action on the 2-methyl-5-HT induced 5-HT release is different among 5-HT3 receptor antagonists, it is suggested that there is a possibility that the neuronal 5-HT3 receptors and the 5-HT3 receptors on the EC cells may represent two distinct subtypes.