[A case of antimitochondrial antibody (AMA) negative primary biliary cirrhosis (PBC) associated with Sjögren's syndrome and arthropathy].
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Biomedical subjects
Publications and source records attributed to S Endo.
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The whole mouth method gustatory test is a simple gustatory test. It can be applied easily, and can be used to assess overall taste which a subject is supposed to be feeling. In the present study, a new series of taste solutions for the use in the whole mouth gustatory test was prepared. In order to determine the normal range of gustation and relationships between each taste solution, gustatory threshold tests were conducted on 123 healthy volunteers (17-22 years old). The series of taste solutions represented 4 tastes, i.e., sweet, salty, sour, and bitter, and was prepared using sucrose, salt, tartaric acid and quinine, respectively. Recognition thresholds measured for each taste solution yielded normal ranges i.e., 0.0165 mol/l for the sweet solution, 0.0316 mol/l for the salty solution, 0.000734 mol/l for the sour solution, and 0.0000203 mol/l for the bitter solution which were almost the same as those published. The average thresholds obtained for all solutions were at almost always at the middle concentration level, i.e., level 6. Thus, this method can serve as a standard method of performing the whole mouth taste test. Principal component analysis of the thresholds obtained revealed that the primary component mainly demonstrated taste detection function, and that it could more or less be represented by the simple sum of each detection threshold. The analysis also showed that approximately 90% of taste threshold variation is explained by the 4 principal components. These findings provide further evidence that these four tastes comprise the basic elements of taste.
Plasma levels of type II phospholipase A2 (type II PLA2), cytokines and endotoxin were determined in patients with sepsis to investigate their interrelations and their role in the patient's prognosis. Type II PLA2 was measured by radioimmunoassay, tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and IL-8 were each measured by enzyme-linked immunosorbent assay (ELISA). Endotoxin was determined by a method based on an endotoxin-specific synthetic substrate. Plasma levels of type II PLA2 were significantly higher in the patients who died of sepsis than in those who survived the illness. There was a significant correlation between type II PLA2 and TNF-alpha and IL-6. Type II PLA2, TNF-alpha, IL-6, and IL-8 may be useful as indices of disease severity. The results suggest that TNF-alpha and IL-6 stimulate the production of type II PLA2 in the plasma of patients with sepsis.
We evaluated the roles of plasma endothelin-1 and plasma thrombomodulin in the development of disseminated intravascular coagulation (DIC) in patients with sepsis. Plasma endothelin-1 was measured by radioimmunoassay (RIA). Plasma thrombomodulin and tumor necrosis factor-alpha (TNF-alpha) were measured by enzyme-linked immunosorbent assay (ELISA), and serum protein C (protein C) was measured by the synthetic substrate method. Endotoxin was measured by the Endospecy test, a synthetic substrate method. A new perchloric acid method was used for the pretreatment of plasma. Blood levels of endothelin-1 and thrombomodulin were significantly higher in patients with DIC than in those without DIC (p < 0.0001). Endothelin-1 and thrombomodulin levels were positively correlated (r = 0.8645, p = 0.0001), as were endothelin-1 and TNF-alpha levels (r = 0.5441, p = 0.0002). Thrombomodulin and protein C levels were negatively correlated (r = -0.5627, p = 0.0001). Endotoxin was elevated above the normal level 14.3% (6/42) for these patients. TNF-alpha is involved in the production of endothelin-1 and thrombomodulin, which play a role in the pathogenesis of DIC and whose blood levels reflect its severity.
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Long-term potentiation (LTP) is a synaptic mechanism thought to be involved in learning and memory. Long-term depression (LTD), an activity-dependent decrease in synaptic efficacy, may be an equally important mechanism which permits neural networks to store information more effectively. One form of LTD that has been observed in the hippocampus requires activation of postsynaptic NMDA (N-methyl-D-aspartate) receptors, a change in postsynaptic calcium concentration, and activation of postsynaptic serine/threonine protein phosphatase 1 (PP1) or 2A (PP2A). The mechanism by which PP1 or PP2A is regulated by synaptic activity is unclear because these protein phosphatases are not directly influenced by calcium concentration. LTD induction may require activation of a more complex protein phosphatase cascade consisting of the Ca2+/calmodulin-dependent protein phosphatase, calcineurin, its phosphoprotein substrate, inhibitor-1, and PP1. We tested this hypothesis using calcineurin inhibitors as well as different forms of inhibitor-1 loaded into postsynaptic cells. Our results suggest a signalling pathway in which calcineurin dephosphorylates and inactivates inhibitor-1. This in turn increases PP1 activity and contributes to the generation of LTD.
A 21-year-old man developed signs of brainstem damage after being injured while playing rugby. Cervical x-ray films showed os odontoideum, and angiography revealed persistent occlusion of the right vertebral artery at the level of the second cervical spine. These findings indicated that atlantoaxial dislocation caused by os odontoideum may have induced vertebral artery occlusion, leading to brainstem infarction.
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Acetazolamide was given in the early stage of ischemic cerebral edema produced by unilateral permanent carotid occlusion in gerbils. The animals were studied 1, 4, and 6 hours after ischemia. The tissues were examined for water and electrolyte concentrations and ischemic areas were visualized by 2,3,5-triphenyltetrazolium chloride (TTC) and H-E staining. Acetazolamide injected just after occlusion showed a positive effect in reducing edematous changes. Later administration of the drug had neither positive nor harmful effect on the ischemic brains. Thus, acetazolamide seems to be useful for cerebrovascular response studies in the early stage of a brain lesion.
A case of neonatal intracerebral hemorrhage (ICH) secondary to rupture of an arteriovenous malformation (AVM) is reported. The baby began to vomit frequently 9 h after birth. Computed tomographic scan revealed the presence of an ICH. Intravenous digital subtraction angiography (IVDSA) demonstrated an AVM, which was successfully excised on the 2nd day after birth. It is stressed that IVDSA is safe and noninvasive in comparison with conventional angiography and is useful for diagnosis of cerebral vascular disease in neonates.
Among 231 patients with cervical injuries treated over 12 years, 15 had cervical spinal cord injury associated with ossification of the posterior longitudinal ligament. All of them were male and most had injuries due to a relatively weak external force. Four of them underwent surgery. There was little difference in improvement of paralysis between the conservatively and the surgically treated group.
We have previously established a human malignant glioma cell line, TM-1. TM-1 cells could proliferate in the serum-free medium. In the present study, immunochemical analysis demonstrated that platelet-derived growth factor (PDGF), transforming growth factor (TGF)-alpha, and TGF-beta are present in the serum-free medium conditioned by growing TM-1 cells. While the cells appeared to possess a single type of binding sites for epidermal growth factor (EGF) with properties comparable to those determined for other tumor cells, the conditioned medium did not contain EGF.PDGF, TGF-alpha, and EGF added exogenously to serum-free media stimulated thymidine incorporation into DNA of TM-1 cells. In addition, antibodies specific for PDGF and TGF-alpha suppressed this activity. These results indicate autocrine and stimulatory roles of PDGF and TGF-alpha for the proliferation of TM-1 cells. As observed for other tumor cells, TGF-beta by itself weakly suppressed thymidine incorporation by TM-1 cells. However, TGF-beta employed in combination with TGF-alpha or EGF appeared to stimulate thymidine incorporation, suggesting that a cooperative action of TGF-beta with different growth factors may be involved in the stimulatory growth regulation at least for TM-1 cells.
Congenital generalized lipodystrophy (CGL) is a rare disease, the main symptoms of which are a reduction of systemic subcutaneous fat, characteristic facial features, hypertrichosis, and insulin-resistant diabetes. We report herein the unusual case of a 25-year-old man with CGL in whom gas gangrene developed, an association which has never before been encountered.
The purpose of this study was to measure plasma platelet-activating factor (PAF) concentration, PAF-acetylhydrolase activities, anti-phospholipid antibody (aPLs) titers, and platelet function in patients with subarachnoid haemorrhage (SAH) and to assess the association of these variables with the development of cerebral vasospasm. Thirty-two patients with SAH due to ruptured cerebral aneurysm were studied. Plasma PAF concentration, PAF-acetylhydrolase activity, platelet count and aggregability, and plasma factor 4 (PF4) concentrations were measured regularly until approximately 2 weeks after SAH. aPLs, including lupus anticoagulant and anti-cardiolipin IgG and IgM were measured within 3 days after SAH. Plasma PAF concentration in patients with SAH showed the highest value on the occasion during 5 to 9 days after SAH. The concentrations were higher in patients with infarction due to vasospasm than in patients without cerebral infarction on any occasions after SAH. Plasma PAF-acetylhydrolase activities did not change in patients, regardless of the presence of cerebral infarction after SAH. Increased platelet consumption and aggregability and higher concentrations of PF 4 were detected in patients with cerebral infarction and not in patients without cerebral infarction. The patients with cerebral infarction due to cerebral vasospasm had aPLs more frequently than the control volunteers. Our findings indicate that increased plasma PAF and aPLs may contribute to the pathogenesis of cerebral vasospasm after SAH.
Platelet activating factor (PAF) content and PAF-acetylhydrolase (PAFAH) activity were measured in the plasma and haematoma of 34 chronic subdural haematoma (CSH) patients. The plasma PAF level in patients with CSH was higher than that in healthy controls. Although there was no correlation between the plasma PAF levels and the interval between the onset of symptoms and the day of sampling, namely, the interval after bleeding, the haematoma PAF level gradually decreased according to the interval after the onset of symptoms. There was no difference between plasma PAFAH activity in patients with CSH and that in healthy controls, and haematoma enzyme activity gradually increased correlated with the interval between the onset of symptoms and surgery. In addition, the localization of PAF in haematoma capsules was histochemically determined. PAF was solely localized to the peri-sinusoidal vessels in the outer membrane of haematoma capsules. Based on these biochemical and histochemical studies, we speculated that PAF may play a role in the development of chronic subdural haematomas.