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Biomedical subjects

S Endo

Publications and source records attributed to S Endo.

At least 343 records · Page 19Linked to original sources
PubMed1995

Detection of Helicobacter pylori infection in early stage gastric cancer. A comparison between intestinal- and diffuse-type gastric adenocarcinomas.

BACKGROUND: Helicobacter pylori (H pylori) infection has been suggested to be a risk factor for gastric carcinogenesis. However, those previous studies have been concerned with advanced cancer cases. To the authors' knowledge, no detailed investigation on the prevalence of H pylori in early stage gastric cancer tissue has been performed. The relationship between early stage gastric cancer and the prevalence of H pylori was studied by a immunohistochemical staining analysis. METHODS: Sixty-eight patients who were endoscopically and surgically diagnosed as having early stage gastric cancer were enrolled in this study. All tissue specimens were obtained from patients by endoscopic biopsy, and were classified histopathologically as the intestinal-type of early stage gastric cancer in 34 patients (male-to-female ratio, 28:6; age, 64 +/- 11 years) and the diffuse-type of early stage gastric cancer (male-to-female ratio, 23:11; age, 57 +/- 14 years) in the other 34 patients. The amount of H pylori in tissue samples was graded from 0 (no characteristic bacteria) to 3 (numerous bacteria) using the fluorescent microscopic and an immunohistochemical technique. RESULTS: Twenty-nine of the 34 cases of the intestinal-type of gastric cancer had H pylori infection, as compared with 11 of the 34 cases of diffuse-type early stage gastric cancer. A significantly higher incidence (85%; P < 0.001) of H pylori infection and, thus, higher grading scores of the number of H pylori were found in the intestinal-type early stage gastric cancer. CONCLUSIONS: These findings suggest that the infection of H pylori may have a crucial relationship to the early stages of carcinogenesis of intestinal-type gastric cancer.

Adenocarcinoma↗
PubMed1995

Stability of alpha-helices in a molten globule state of cytochrome c by hydrogen-deuterium exchange and two-dimensional NMR spectroscopy.

To distinguish between intrinsically stable helices and those stabilized by the protein three-dimensional structure, we report the hydrogen-deuterium exchange (H2H) rates of 29 amide protons of ferricytochrome c in a molten globule state (at 35 degrees C, pH 2.0 with 0.5 M KCl), monitored by 2D-NMR. The results of the H2H-exchange experiments have been analyzed to calculate the protection factors. The helices were not uniformly stable and amide protons of residues belonging to the N and C-terminal helices had high protection factors. The protection factors of amide protons involved in the 50's helix were low, and could not be determined quantitatively. In the 60's helix we found two amide protons with protection factors comparable to those of the N and C-terminal helices. These results, compared with previously reported intrinsic helicities of peptide fragments, indicate that the relative helicities of isolated fragments are not directly reflected in the stability of the helices in the molten globule state, even though this state has no rigid tertiary structure. This suggests that loose interactions between helices are present in the molten globule state of cytochrome c, and that they are essential for keeping the helicity of the helical segments. The loose tertiary interactions discussed here differ from the usual tertiary interaction found in the native state in that the specific interdigitization between side-chains is absent.

Amino Acid Sequence↗
PubMed1995

Control of crystal forms of apoferritin by site-directed mutagenesis.

Surface charges of protein molecules are not only important to biological functions but also crucial to the molecular assembly responsible for crystallization. Appropriate alteration in the surface charge distribution of a protein molecule induces new molecular alignment in the proper direction in the crystal and, hence, controls the crystal form. Apoferritin molecules are known to crystallize in two- and three-dimensional forms in the presence of cadmium ions, which bridge neighboring protein molecules. Here we report a controlled transformation of the apoferritin 2-D crystal by site-directed mutagenesis. In mutant apoferritin, two amino acid residues binding a cadmium-ion through their negative charge, were replaced by one type of nonionic amino acid residues. The amino acid residues, Asp-84 and Gln-86 in the sequence of recombinant (i.e., wild-type) horse L-apoferritin, were replaced by Ser. The wild-type apoferritin yielded a hexagonal lattice 2-D crystal in the presence of cadmium ions. In contrast, the mutant apoferritin yielded two types of oblique crystals independent of the presence of cadmium ions. Image reconstruction of electron micrographs of the mutant crystals made clear that the mutant apoferritin molecules oriented themselves with the 2-fold symmetry axis perpendicular to the crystal plane in both crystals, while the wild-type apoferritin molecules oriented themselves with the 3-fold symmetry axis perpendicular to the crystal plane. The changes of crystal forms and molecular orientation in the 2-D crystals were well explained by a change of the electrostatic interactions induced by the mutagenesis.

Animals↗
PubMed1995

Portal and peripheral endotoxins in patients with esophageal varices undergoing surgery.

Under the hypothesis that portal endotoxemia, which has been considered evidence of endogenous endotoxemia, is actually a false-positive reaction of the Limulus test, the conventional method of determination, Toxicolor (TOX) and a new endotoxin-specific method, Endospecy (ES) were investigated, whereby portal endotoxemia was reexamined. Peripheral and portal blood samples were collected from 12 patients at various intervals during surgery for esophageal varices, and then evaluated by TOX and ES, the normal values of which are under 60.0 pg/ml and under 9.8 pg/ml, respectively. The mean peripheral and portal endotoxin (Et) levels by TOX were 23.1 pg/ml and 38.9 pg/ml, 1.5 h after the start of surgery, which continued to increase thereafter, the corresponding levels being 48.1 pg/ml and 58.7 pg/ml 8 h after the start of surgery, respectively. The portal Et levels were significantly higher by ES, indicating portal endotoxemia, the mean peripheral and portal Et levels being 6.9 pg/ml, and 6.5 pg/ml, 1.5 h after the start of surgery, these levels showing changes within a similar range. The levels determined by the conventional TOX method increased with time, to a portal Et level of 5.0 pg/ml 8 h after the start of surgery, whereas those determined by ES changed within the same range suggesting that the onset of portal endotoxemia primarily involves the G-factors and that endogenous endotoxemia does not occur.

Blood Specimen Collection↗
PubMed1995

The use of computed tomography in the prediction of delayed cerebral infarction following acute aneurysm surgery for subarachnoid haemorrhage.

In order to predict the occurrence of cerebral infarction after aneurysmal surgery in patients with subarachnoid haemorrhage, we measured the amount of subarachnoid blood on initial and on postoperative computed tomograms. We used a reliable grading method to estimate the amount of blood on computed tomograms in 24 patients with infarction due to vasospasm and 45 patients without cerebral infarction, all of whom underwent aneurysmal surgery within 48 hours after the ictus. The total amount of subarachnoid blood on admission and on the day after operation was more in the cerebral infarction group than in the non-infarction group. The clearance rate of subarachnoid blood by surgery was lower in patients with cerebral infarction than in patients without infarction and the predominant site of subarachnoid blood corresponded with the site of the infarct. Of 24 patients with cerebral infarction, 22 (92%) belonged to the group whose initial total blood score was more than 10 on admission and whose clearance rate by surgery was less than 50%. Therefore, we propose this range to be an indication for the occurrence of cerebral infarction in postoperative patients due to cerebral vasospasm. The presence of intracerebral haematoma and the amount of ventricular blood and their clearance by surgery were also estimated for the prediction of delayed cerebral infarction after aneurysmal surgery. However, they had no relation to the occurrence of cerebral infarction due to vasospasm.

Adult↗
PubMed1995

Plasma platelet-derived growth factor-B chain is elevated in patients with extensively large brain tumour.

The plasma concentration of the platelet-derived growth factor (PDGF)-B chain and the plasma platelet factor 4 (PF4) levels were measured in 17 healthy controls and 55 brain tumour patients. In the 17 normal controls, the plasma PDGF-B and PF4 levels were 523 +/- 157 pg/ml (mean +/- SD) and 84 +/- 37 ng/ml, respectively. In the brain tumour patients, these values were 881 +/- 854 pg/ml and 93 +/- 64 ng/ml, respectively. The plasma PDGF-B concentration was elevated above the upper limit of normal individuals in 12 (22%) of the 55 patients. However, since the corresponding PF4 levels suggested the platelet activation, the increased plasma PDGF-B may have originated from platelets. To address this, platelet releasing experiments were performed on citrated blood samples from 5 normal individuals. The plasma PDGF-B and PF4 levels from the 17 normal controls and those observed in the platelet releasing experiments correlated with a regression line of Y = 240 + 4.86X (Y:PDGF, X:PF4). There were only 6 (11%) patients whose plasma PDGF-B level was elevated above the 95% confidence limit estimated from the corresponding PF4 value. In these patients, the tumour volumes were extensively large, and those elevated PDGF-B values decreased after treatment and became elevated again in three patients with recurrent glioblastoma. Although the plasma tumour-derived PDGF-B was detected only in an extensively large brain tumour, it might be a useful plasma marker evaluating the effects of therapy and prognosis in such patients.

Adolescent↗
PubMed1995

Anti-phospholipid antibodies and cerebral vasospasm following subarachnoid haemorrhage.

Delayed ischaemic deficits due to cerebral vasospasm contribute to the high morbidity and mortality rates associated with subarachnoid haemorrhage. We evaluated the usefulness of measuring anti-phospholipid antibodies (aPLs) for prediction of the occurrence of symptomatic vasospasm and the outcome after subarachnoid haemorrhage. 32 consecutive patients with subarachnoid haemorrhage due to ruptured cerebral aneurysms were studied. They were admitted and operated on within 72 hours after the onset of subarachnoid haemorrhage. aPLs such as lupus anticoagulants, anti-cardiolipin IgG and anti-cardiolipin IgM were measured repeatedly after admission. Furthermore, platelet count, platelet aggregability and plasma platelet factor 4 were also measured. Eleven among the 32 patients (34.4%) showed positive in the examination for aPLs. Although aPLs could not predict symptomatic vasospasm, once symptomatic vasospasm occurred, patients with aPLs frequently demonstrated cerebral infarction and therefore their outcome was worse. aPLs were associated with a severe initial clinical grade and SAH grade on CT scan. Therefore it may explain the association of aPLs with worse outcome. aPLs were detected between 1 and 7 days. Four of 6 patients (67%) with aPLs became negative between 7 and 13 days after subarachnoid haemorrhage. The mechanism of transient aPLs is unclear but it is more likely to occur in the severer grade patients. The reduction in platelet count, the increased platelet aggregability, and the increased plasma platelet factor 4 concentration were also observed in aPLs-positive patients with symptomatic vasospasm.

Adult↗
PubMed1995

Platelet-activating factor (PAF) and the formation of chronic subdural haematoma. Measurement of plasma PAF levels and anti-PAF immunoglobulin titers.

In order to estimate the contribution of platelet-activating factor (PAF) to the formation of chronic subdural haematomas (CSH), we measured plasma PAF and anti-PAF antibody levels in head-injured patients with and without CSH and normal volunteers. Plasma PAF and anti-PAF IgG levels were higher in patients with CSH than in patients without CSH or in normal volunteers. Furthermore, plasma PAF and anti-PAF IgG levels increased in a time-dependent manner over the first 35 days following head injury. These data suggest that PAF may be involved in the generation of CSH.

Adult↗
PubMed1995

Delirium in critical care unit patients admitted through an emergency room.

Two hundred thirty-eight patients admitted consecutively to a critical care unit through an emergency room were assessed prospectively for the presence of delirium. Thirty-eight patients (16%) developed delirium. Delirium occurred with equal frequency in all disease categories. The presence of abnormal head imaging which required medical intervention did not predict the development of delirium. The median delay between admission and the development of delirious was 4 days, however, one-fourth of the patients were delirious on the day of admission. The patients with abnormal head imaging who required medical intervention had a higher frequency of onset of delirium on the first day compared with patients without. The delirium lasted a median of 5 days and resolved within a week in over 70% of patients. These results confirm that delirium is frequently present in patients who require acute critical care after emergency room evaluation. In this population, serious medical disease is a better predictor of the development of delirium than the presence of abnormal brain imaging which required medical intervention. Although delirious patients have longer lengths of stay, the presence of delirium does not predict higher mortality, as has been reported in other populations. This could be because delirious patients admitted to the critical care unit through the emergency room have fewer premorbid medical problems predisposing them to poor outcome.

Adult↗
PubMed1995

Plasma concentrations of type II phospholipase A2, cytokines and eicosanoids in patients with burns.

The plasma concentrations of type II phospholipase A2 (type II PLA2) and eicosanoids, such as leukotriene B4 (LTB4), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TXB2), were determined by radioimmunoassay in 23 patients with burns covering at least 20 per cent of their body surface. Cytokines such as tumour necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and interleukin 8 (IL-8) were determined by enzyme-immunosorbent assay. There was no increase in type II PLA2 concentration in the early stage of burns, but an increase in type II PLA2 concentration was triggered by infection (P < 0.0001). The level of type II PLA2 was significantly higher in the non-surviving group than in the surviving group (P = 0.0006), suggesting that it reflects the severity of the disease. There was a significant correlation between the maximum level of type II PLA2 and TNF-alpha (r = 0.6346, P = 0.0011). There was a significant correlation between the maximum level of type II PLA2 and the accompanying plasma concentrations of LTB4, 6-keto-PGF1 alpha, and TXB2 throughout the observation period (r = 0.4814, P = 0.0200; r = 0.5943, P = 0.0028; r = 0.4368, P = 0.0372 respectively). Plasma levels of LTB4, and TXB2 were significantly higher in the burn patients who died than in those who survived (P = 0.0493; P = 0.0493 respectively).

Adult↗
PubMed1995

Generators of somatosensory evoked potentials investigated by dipole tracing in the monkey.

Generators of somatosensory evoked potentials, elicited by electrical stimulation of the median nerve in anaesthetized monkeys (Macaca fuscata), were investigated by submitting a three-dimensional reconstructed brain model to dipole tracing, which can equate surface potential distributions to an approximate corresponding equivalent dipole. The following components of the somatosensory evoked potentials were simultaneously recorded from 21-27 epidural electrodes: P7 (the letter indicates positive or negative polarity; the number indicates the approximate latency of the peak in ms) was recorded widely from various locations on both the left and right hemispheres, P10 was recorded near the anterior side of the central sulcus contralateral to the stimulation side, N10 was recorded near the posterior side of the contralateral central sulcus, P12 was recorded on both sides of the contralateral central sulcus, and P18 was recorded posterior to the contralateral central sulcus. Current source generators (dipoles) of each component of somatosensory evoked potentials were localized by dipole tracing: a dipole for P7 was located in the thalamus contralateral to the stimulation side; a dipole for P10 and N10 in the posterior wall of the contralateral central sulcus (area 3b); a dipole for P12 in the contralateral post central gyrus (areas 1 and 2); and a dipole for P18 in the anterior wall of the contralateral intraparietal sulcus (area 5). The locations and latencies of dipoles that generated cortical components of somatosensory evoked potentials, estimated by dipole tracing, were confirmed by direct cortical surface recording from a 16-25 electrode array placed directly on the cortical surface; and multiple unit recording from the anterior and posterior parietal cortices. After excision of area 5, P18 and N18 were abolished, whereas P10, N10, and P12 were not affected. The results suggest that dipoles for somatosensory evoked potentials progressed from the thalamus to area 5 via the primary somatosensory area. This progress is consistent with the hierarchical sequence of somatosensory information processing.

Anesthesia↗
PubMed1995

Physiological results of monkey brain ischemia, and protection by a calcium blocker.

Physiological and histological investigation was undertaken to examine dynamic and metabolic changes due to transient ischemic insult of the monkey brain with and without postischemic treatment by the calcium entry blocker, NC-1100 (1 mg/kg, IV). Monkeys were subjected to temporary occlusion of the eight major arteries: bilateral common carotid, internal and external carotid, and vertebral arteries. Blood flow was restored after 5-, 10-, 13-, and 15-min ischemia in different monkeys. The amplitudes of extradural, cortical, and hippocampal electroencephalograms decreased severely within 1-6 min after beginning occlusion. Complete recovery of these electroencephalograms required more than 1 h. During ischemia, significant change was obvious in arterial glucose, and systolic, diastolic, and mean blood pressure, all of which increased. There were no significant physiological differences between the untreated and NC-1100-treated groups, except decreased diastolic blood pressure and slightly lower postischemic heart rate in the treated group. These small differences might be accounted for by the effect of the calcium blocker. Ten to 15 minutes ischemia caused cell changes, including cell death, which were confined almost exclusively to the CA1 subfield of untreated hippocampi examined the fifth day after occlusion. However, no ischemia-induced cell change was observed in the CA1 subfield of hippocampi subjected to 10 to 15 min ischemia in the NC-1100-treated group. It was concluded that a calcium entry blocker can protect neurons from mild ischemia-induced injury and might ameliorate morphological damage and functional impairment of the brain due to ischemia in patients who suffer transient anoxic or hypoxic injury. The present physiological data should contribute to their clinical treatment.

Analysis of Variance↗
PubMed1995

Ischemic neuronal damage specific to monkey hippocampus: histological investigation.

We previously reported lesions confined specifically to the hippocampus when produced by occluding eight vessels (the bilateral vertebral, common, internal, and external carotid arteries), which supply blood to the brain. However, histopathological changes in the primate brain, caused by ischemic injury, have not previously been thoroughly investigated. In the present study, macaque monkeys were subjected to 5-18-min ischemia by occluding the eight vessels. After the brains were perfused and fixed 5 days after the occlusion, all regions were histologically investigated for ischemic cell changes. Ischemia for 5 min produced no ischemic cell change. Ischemia for 10-15 min produced cell death limited to the deeper portion of the pyramidal cell layer of the CA1 subfield in the hippocampus. In most monkeys, no cell death was observed in any brain region outside of the hippocampus after ischemia for up to 15 min. Ischemia for 18 min produced more widespread cell death in the CA1 subfield of the hippocampus, and cell death was no longer confined to the hippocampus, but was observed in layers III, V, and VI of the neocortices, the striatum, and some other regions. Brains that were perfused and fixed 1 year after 15-min ischemic insult revealed no ischemic cell morphological change in any region, but the number of pyramidal cells in the CA1 subfield was decreased to about half. The results indicate that the CA1 subfield of the monkey hippocampus is the precise region of the brain most susceptible to ischemic insult in the primate forebrain, and after a critical time (15-min ischemia in this procedure) ischemic cell changes occur suddenly and extensively. Ischemia due to occlusion of eight arteries for 10-15 min could produce a model of human amnesia caused by transient ischemic insult.

Amnesia↗
PubMed1995

Clinical assessment of squamous cell carcinoma of the nasal cavity proper.

The subjects were 14 patients with squamous cell carcinoma or undifferentiated carcinoma of the nasal cavity treated at Nihon University Hospital between October 1984 and November 1991, who were followed for at least 3 years. The site of the tumor origin within the nasal cavity was the lateral wall in 8 patients, the nasal septum in three patients, and unknown in three patients. Histologically, there were 13 squamous cell carcinomas in (3 well differentiated, 7 moderately differentiated, and 3 poorly differentiated) and 1 undifferentiated carcinoma. Treatment was by a combination of radiotherapy, chemotherapy, and surgery in 8 cases, a combination of radiotherapy and surgery in 5 cases, and surgery alone in 1 case. The 3-year and 5-year Kaplan-Meier survival rates were 86 and 69%, respectively. A total of 6 patients suffered a recurrence, with local recurrence occurring in 4 patients and pulmonary metastasis in 2 patients. Tumor control was achieved in 3 of the 4 cases of local recurrence by reoperation, and by surgery in 1 of the 2 cases of pulmonary metastasis. The duration of the recurrence-free interval in the patients who developed local recurrences, 18 to 46 months after the completion of the initial course of therapy, was of considerable interest.

Carcinoma, Squamous Cell↗
PubMed1995

Protein phosphatase-1 regulates outward K+ currents in sensory neurons of Aplysia californica.

The peptide neurotransmitter Phe-Met-Arg-PheNH2 (FMRFamide) increases outward K+ currents and promotes dephosphorylation of many phosphoproteins in Aplysia sensory neurons. We examined FMRFamide-induced current responses in sensory neurons injected with thiophosphorylated protein phosphate inhibitor-1 and inhibitor-2 (I-1 and I-2), two structurally different vertebrate protein phosphatase-1 (PP1) inhibitors to define a role for PP1 in the physiological actions of FMRFamide. Thiophosphorylated I-1 and I-2 both reduced the amplitude of outward currents elicited by FMRFamide by 50-60% and were as effective as microcystin-LR, which inhibited both PP1 and protein phosphatase-2A in Aplysia neuronal extracts. These data suggested that of the two major neuronal protein serine/threonine phosphatases, FMRFamide utilized primarily PP1 to open serotonin-sensitive K+ (S-K+) channels. Earlier studies showed that a membrane-associated phosphatase regulated S-K+ channels in cell-free patches from sensory neurons. Utilizing its unique substrate specificity and inhibitor sensitivity, we have characterized PP1 as the principal protein phosphatase associated with neuronal plasma membranes. Two protein phosphatase activities (apparent M(r) values of 170,000 and 38,000) extracted from crude membrane preparations from the Aplysia nervous system were shown to be isoforms of PP1. These biochemical and physiological studies suggest that PP1 is preferentially associated with neuronal membranes and that its activity may be required for the induction of outward K+ currents in the Aplysia sensory neurons by FMRFamide.

Animals↗