Cathepsin E expressed in pancreatic cancer.
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Adenocarcinoma↗
Biomedical subjects
Y Nishikawa
Publications and source records attributed to Y Nishikawa.
Clinical and magnetic resonance image correlation in idiopathic cerebellar ataxia.
Sixty-one patients who fulfilled the clinical criteria for idiopathic cerebellar ataxia and who had symptoms at least for 3 years were examined clinically and by magnetic resonance imaging (MRI). Based on the clinical signs, they were divided into patients with pure cerebellar signs (Group 1), patients with additional mild rigidity and/or hyperreflexia (Group 2) and patients with additional severe rigidity and hypokinesia (Group 3). Patients in Group 1 had milder disability and better prognosis than patients in Group 2 or Group 3 (ataxic score: 14.9 vs. 28.6 and 36.0; annual progression ratio: 0.26 vs. 0.65 and 0.70, respectively). We measured the area of the cerebellar vermis, ventral pons and dorsal brainstem on midsagittal T1-weighted MR images for all patients and age- and sex-matched controls. The cerebellar vermis as well as the ventral pons of patients were significantly smaller than corresponding structures in controls (p < 0.001). The ventral pons of patients in Group 2 and Group 3 was significantly smaller than that of patients in Group 1 (p < 0.0001, respectively), and the dorsal brainstem of patients in Group 2 and Group 3 was also significantly smaller than that of patients in Group 1 (p < 0.001, respectively). The ventral pons of patients in Group 3 was significantly smaller than that of patients in Group 2 (p < 0.05) as well. There was a significant correlation between the area of the ventral pons and the annual progression ratio (p < 0.001). With MRI, slight but definite hyperintensities were demonstrated in the pontine base and the medulla of 22 patients on proton density images. In the longitudinal study, patients in Group 2 and Group 3 had atrophy of the ventral pons already at an early stage. The ventral pons of patients in Group 3 was smaller at the initial MR examination than that of patients in Group 2. These observations suggest that patients with smaller ventral pons may have rapid progression and poor prognosis. Thus, even a relatively simple quantitation of the area of the ventral pons may be useful to predict the prognosis of patients, in addition to neurologic assessment at intervals.
Adult↗
Simultaneous combination of endoscopic sclerotherapy and endoscopic ligation for esophageal varices.
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Combined Modality Therapy↗
Catabolite repression of the adhesion of Vero cytotoxin-producing Escherichia coli of serogroups O157 and O111.
The virulence traits that mediate Vero cytotoxin-producing E. coli (VTEC) adherence are unclear. Many VTEC strains possess the eaeA gene which is involved in the attaching and effacing effects of enteropathogenic E. coli (EPEC). Most eae-positive VTEC adhered to HEp-2 cells in a localized manner; however some strains did not adhere. Thus we investigated the adhesion of poorly adherent strains, especially those of serogroups O111 and O157. To establish a model, the adherence to HEp-2, INT407 and Caco-2 cells of 12 O157 VTEC and six O111 VTEC isolated from cases of human infection were studied after growth of the bacteria under different conditions. For adhesion tests mannose is usually added during prior broth culture of the bacteria, and during the period of attachment, so that any adhesion due to mannose-sensitive type 1 pili is inhibited. Bacteria cultured in peptone water in the absence of mannose adhered to all three lines; there were localized clusters of bacteria on 1%-82% cells, whether mannose was present during the attachment period or not. Bacteria grown in the presence of D-mannose, or any other sugar that was metabolized, showed little adherence (range 0-9%). alpha-Methyl-glucoside also caused marked inhibition of adhesion. It was concluded that inhibition of adhesion was due to catabolite repression.
Animals↗
Endotoxin-induced left ventricular depression is blocked by nitrogen mustard or dimethylthiourea in rabbits.
We examined endotoxin-induced myocardial depression in 31 anesthetized rabbits using left ventricular end-systolic and end-diastolic pressure-volume relationships (sonomicrometers). In the control group, endotoxin (100 micrograms/kg iv) induced systolic depression (> 10% increase in end-systolic volume at matched end-systolic pressure) in 9 of 16 and diastolic dilation (> 10% increase in end-diastolic volume at matched end-diastolic pressure) in 8 of 16 rabbits within 7 h, unrelated to hypotension, acidosis, or hypoxia. Seven rabbits were pretreated with nitrogen mustard (1-2 mg/kg iv 4 and 2 days before) to decrease circulating neutrophils and monocytes by 98%. Endotoxin did not induce systolic depression in any rabbit (P = 0.01 compared with control), and diastolic dilation developed in one rabbit (P = 0.12). In eight rabbits pretreated with dimethylthiourea (DMTU; 500 mg/kg iv 30 min before), an intracellular free radical scavenger, systolic depression developed in one (P = 0.05) and diastolic dilation in five (P = 0.44). We conclude that cells inhibited by nitrogen mustard (e.g., neutrophils, monocytes, or macrophages) mediate endotoxin-induced left ventricular systolic depression. DMTU inhibited endotoxin-induced systolic but not diastolic dysfunction.
Animals↗
Differential inhibitory mechanisms in VPL versus intralaminar nociceptive neurons of the cat: I. Effects of periaqueductal gray stimulation.
Nociceptive thalamic units receiving afferent input from the greater splanchnic nerve (SPL) were recorded from the nucleus ventralis posterolatealis (VPL) and intralaminar nuclei in urethane-chloralose anesthetized cats. The effects of stimulating the periaqueductal gray (PAG), or the nucleus raphe dorsalis (NRD) on responses of nociceptive thalamic units were investigated. Forty-eight nociceptive specific (NS) and 20 wide dynamic range (WDR) units with SPL input were found in the shell region of the caudal VPL. Following electrical stimulation of either the ventral PAG or the NRD, responses to SPL input were inhibited in all NS and WDR units tested. Responses of these units to electrical stimulation of spinothalamic tract fibers in the ventrolateral funiculus (VLF) were also inhibited following the PAG/NRD stimulation. These results suggest that PAG/NRD stimulation-produced inhibition of both NS and WDR units may be partially mediated by an ascending antinociceptive mechanism. Intralaminar nociceptive units with SPL input were found in the nuclei centralis lateralis (CL), paracentralis (Pc), and parafascicularis (Pf). The effects of conditioning electrical stimulation of either the ventral PAG or the NRD on responses of intralaminar nociceptive units were studied. Of 113 intralaminar nociceptive units studied, 68 units were unaffected, 23 units were excited and 22 units were inhibited following the conditioning stimulation. In the units in which responses to SPL stimulation were inhibited, responses elicited by electrical stimulation of the mesencephalic reticular formation (MRF) were also inhibited. These data suggest that although there is an ascending inhibitory pathway from PAG/NRD to intralaminar nuclei, this system is far less potent compared with the ascending inhibitory system acting upon the VPL.
Afferent Pathways↗
Differential inhibitory mechanisms in VPL versus intralaminar nociceptive neurons of the cat: II. Effects of systemic morphine and CCK.
In urethane-chloralose anesthetized cats, the effects of intravenous morphine on responses of thalamic nociceptive units were studied. In both nociceptive specific (NS) and wide dynamic range (WDR) units recorded from the nucleus ventralis posterolateralis (VPL), intravenous morphine suppressed unit responses to the greater splanchnic nerve (SPL) stimulation, but had little effect on responses to stimulation of spinothalamic tract fibers in the ventrolateral funiculus. In nociceptive units recorded from nuclei centralis lateralis (CL) and parafascicularis (Pf) of the intralaminar nuclei, intravenous morphine suppressed responses to stimulation of the mesencephalic reticular formation as well as to SPL stimulation. Intravenous cholecystokinin (CCK) antagonized the suppressive action of morphine on responses of VPL units, but did not antagonize the suppressive action of morphine on responses of intralaminar units. The results suggest that intravenous morphine inhibits synaptic transmission of nociceptive impulses in the intralaminar nuclei as well as in the spinal cord, but not in the VPL, and that CCK antagonizes the antinociceptive action of morphine in the spinal cord, but not in the intralaminar nuclei.
Animals↗
[Continuous subcutaneous injection therapy with interferon-alpha for renal cell carcinoma patients with bone metastasis].
Thirteen patients with renal cell carcinoma who had proven bony metastases were treated with multimodal treatment including surgery, radiotherapy and immunotherapy in the form of subcutaneous continuous injection of by natural type interferon-alpha (INF). The mode of administration of IFN was as follows: IFN, 2,5000 x 10(4) unit dissolved in 60 ml saline, was continuously injected (0.5 ml/hr) via a subcutaneous route as one course of the treatment and was given two courses in two weeks preoperatively. Postoperatively, IFN was given every week and the number of courses totally amounted to 15. In some cases IFN was given thereafter either every week or every other week. In four patients whose serum concentration of IFN was measured during and after administration of continuous IFN, the concentration of IFN rose after injection and showed 40.5 IU/ml in average 24 hours later. The concentration was kept measurable in six to eight days long and the maximum concentration was 167 IU/ml. In IFN-treated patients nine survived including two CRs, two NCs, five PDs and four deaths. The five year survival rate was 53%. Continuous subcutaneous injection of IFN in combination with surgery and/or radiotherapy is effective in the treatment of bony metastasis from renal cell carcinoma.
Aged↗
[A battery model of the eyeball to calculate standing potential of the eye].
Variation of the resting potential caused by eye movements was analyzed by applying a battery model to the eyeball. A formula that gives the potential between the inner canthus and the outer canthus of the eye was derived on the basis of the electric theory in electromagnetics, on the assumption that the eyeball was floating in a homogeneous conductor. The variations of the resting potentials were represented using the distance from the center of the eyeball to the potential detecting position and the deflection angle of the position with respect to the optical axis of the eyeball. To verify the validity of the formula, the variation of the resting potential caused by the various amplitudes of bilaterally symmetrical eye movements were measured. The calculated results were found to be in good agreement with the experimental ones.
Electrooculography↗
[Adenosine deaminase isoenzymes in patients with Graves' disease].
CD26, the T cell activation antigen, is identical to the ADA binding protein and is considered to interact with ADA to activate the T cells on the surface. Therefore, we examined the activity of serum ADA isoenzymes in patients with Graves' disease in whom CD26 presented T cells were increased. The activities of total ADA and ADA2 were significantly higher in Graves' disease than normals. We also observed that the levels of soluble interleukin-2 receptor (sIL-2R) and neopterin, markers of T cell activation, were significantly higher in Graves' disease. The correlation coefficients among ADA2, neopterin, and sIL-2R were significantly high (p < 0.001). Among these parameters, only sIL-2R was correlated with the thyroid hormones. ADA2 activity was considered to reflect the activated state of T cells and to be, independent of the thyroid hormone levels.
Adenosine Deaminase↗
Abnormal evoked potentials of Kearns-Sayre syndrome.
We examined eight patients with Kearns-Sayre syndrome (KSS) to investigate a dysfunction in the central nervous system (CNS) using PTN-SEP, MN-SEP and BAEP. We found a significant increase in the P37 latency of PTN-SEPs and the central conduction time of MN-SEPs, and interpeak latencies of BAEPs. Delayed SEPs or BAEPs were caused by a dysfunction of the somatosensory or lateral lemniscus pathways which could be related to mitochondrial abnormalities in the CNS. Long-term therapy with CoQ showed an improvement of the latencies of SEPs after about half a year from the start of CoQ therapy in our patients. The improvement of the latencies of SEPs were preserved during CoQ therapy. It could be demonstrated that CoQ therapy had the beneficial effects on abnormal functions of the CNS in patients with KSS.
Adult↗
Involvement of the central nervous system in myotonic dystrophy.
To investigate the etiological factors responsible for intellectual impairment and mood changes in patients with myotonic dystrophy (DM), we evaluated 14 patients with DM by means of neuropsychological evaluation and magnetic resonance images (MRI). There were significant differences between patients and controls in regard to the Barthel index, Zung's depression scale, attention, verbal fluency and digit span. All patients had ventricular enlargement and white matter abnormalities on MRI. However, the severity was variable and there was no difference in neuropsychological testing between patients with mild ventricular dilatation and those with severe dilatation. On the other hand, significant differences were present between patients with mild white matter lesions and those with severe white matter abnormalities in regard to verbal fluency and attention. Neuropathologic examination of an autopsied brain showed an increase in the interfascicular space of the white matter which produced pallor on myelin staining. The present findings suggested that the white matter abnormalities were the cause of cognitive impairment among patients with DM.
Activities of Daily Living↗
Effect of dynamic exercise on left atrial function in conscious dogs.
1. Dynamic changes in left atrial (LA) function during treadmill exercise were studied in ten conscious dogs instrumented to measure left ventricular (LV) pressure and diameter, LA pressure and diameter, and pulmonary venous blood flow (PVF, transit time flowmeter). 2. Systolic PVF volume (reservoir volume; a measure of LA reservoir function) increased from 38 +/- 4% of total PVF volume at baseline to 52 +/- 8% of total PVF volume during exercise, and diastolic PVF volume (conduit volume; a measure of LA conduit function) decreased from 62 +/- 5% at baseline to 48 +/- 8% during exercise (P < 0.005). 3. The increases in reservoir volume and the decrease in conduit volume were due not only to a greater decrease in diastolic interval than systolic interval but were also caused by a significantly greater increase (P < 0.05) in the mean systolic filling rate (93%) than in the mean diastolic filling rate (51%). 4. During exercise the pattern of LV filling derived from changes in LV diameter showed that a greater percentage of LV filling occurred during the second half of diastole at the time of atrial contraction (P < 0.05), suggesting that LA booster function was enhanced. 5. Changes in LA dimension revealed that during exercise more blood volume was reserved in the LA during systole and that this change was associated with an increase in the LA dimension at the beginning of LA contraction (r = 0.61, P < 0.05). 6. We conclude that LA reservoir and booster functions were augmented during exercise, whereas conduit function was not. Increased reservoir function may play an important role in accelerating LV filling by helping to maintain an enhanced atrioventricular pressure gradient during diastole and also by increasing LA booster function through an increase in LA preload.
Animals↗
Autocrine factor enhancing the secretion of M(r) 95,000 gelatinase (matrix metalloproteinase 9) in serum-free medium conditioned with murine metastatic colon carcinoma cells.
We previously reported that murine tumor cells with a high spontaneous metastatic potential to the lung secrete higher amounts of M(r) 95,000 gelatinase (matrix metalloproteinase 9, MMP9) than do poorly metastatic cells. The present study, conducted to clarify the mechanisms underlying the increase in MMP9, revealed an autocrine factor that enhances the secretion of M(r) 95,000 gelatinase (MMP9). The secretion of MMP9 by highly metastatic colon carcinoma LuM1 cells, detected by zymography, was augmented 10-fold when cultured in medium supplemented with serum-free medium conditioned with LuM1 cells. Because the secretion of M(r) 60,000 gelatinase (MMP2), as well as total protein, by the same cells was not affected under these conditions, the augmentation appears specific for MMP9. The steady-state level of MMP9 mRNA was elevated in LuM1 cells cultured in the presence of the supernatant. The amount of the factor in the culture medium increased with time in culture, indicating that it was produced by the LuM1 cells. It was found to be heat stable but sensitive to trypsin digestion. Conditioned medium from poorly metastatic NM11 cells did not stimulate the secretion of gelatinases by NM11 cells, suggesting that autocrine stimulation of MMP9 secretion is a characteristic of metastatic cells. This factor could account for the augmented secretion of MMP9 by murine tumor cells with spontaneous metastatic potential to the lung.
Animals↗
Redistribution of glutamate and GABA in the cerebral neocortex and hippocampus of the Mongolian gerbil after transient ischemia. An immunocytochemical study.
The redistribution of glutamate and GABA in postischemic brains was examined immunocytochemically using the gerbil model of unilateral 1 h cerebral ischemia. In the cerebral neocortex, the majority of neurons underwent recovery processes after 5 h of recirculation, while neurons in the hippocampus were irreversibly damaged. Glutamate-like immunoreactivity (LI) was highly increased in the degenerating hippocampal CA3 pyramidal cells after recirculation, while in the neocortex and the hippocampal CA1 sector, the pyramidal cells showed only slightly increased glutamate-LI. GABA-LI-positive punctae in the neuropil, corresponding to neuronal processes of GABAergic neurons, were accentuated after recirculation both in the cerebral neocortex and the hippocampus. Although the astrocytes on the nonischemic side showed neither glutamate-LI nor GABA-LI, the swollen astrocytes and their foot processes, which were observed after recirculation, often showed strong glutamate-LI and GABA-LI. These data suggest (1) the accumulation of glutamate or glutamate-like substances, especially in the CA3 pyramidal cells, (2) the excitation of the GABAergic neurons and their subsequent uptake of GABA, and (3) the sequestration of the extracellular neurotransmitters by astrocytes in the postischemic period.
Animals↗
A case of apocrine adenocarcinoma associated with hamartomatous apocrine gland hyperplasia of both axillae.
We report an apocrine adenocarcinoma of the left axilla associated with hamartomatous apocrine gland hyperplasia of both axillae. The patient, a 69-year-old man, presented with no symptoms or complaints other than an oval mass felt in the left axilla. The mass was resected and histopathological examination revealed a papillary apocrine adenocarcinoma located within hyperplastic apocrine glands. Because gallium scintigraphy performed after the operation still showed bilateral abnormal uptakes, skin and subcutaneous tissues of the bilateral axillary areas were resected. Histological examination demonstrated marked multilobular hyperplasia of the apocrine glands. These hyperplastic glands did not show distinct atypia, and there was no evidence of tumor remnants in the left axilla. The patient has shown no signs of local recurrence or metastasis at 20 months' follow-up. To our knowledge, this is the first case of malignant transformation of hamartomatous apocrine gland hyperplasia (apocrine gland organic hamartoma or apocrine nevus).
Adenocarcinoma↗
Adhesion to and invasion of human colon carcinoma Caco-2 cells by Aeromonas strains.
The enteropathogenicity of Aeromonas strains that showed mannose-resistant adhesion to INT407 cells was evaluated by infecting Caco-2 cells and observing them by light and electronmicroscopy. Five of six strains adhered in large numbers to Caco-2 cells in the presence of mannose and caused cytopathic effects. Two strains of Aeromonas spp. seemed to invade Caco-2 cells, as membrane-bound bacteria were seen within the cytoplasm of these cells; however, staining by acridine orange-crystal violet appeared to show intracellular fluorescent bacteria in three strains. Fimbriae did not appear to play an important role in adhesion because fimbrial structures were not seen by transmission electronmicroscopy. Adhesion of four strains was inhibited by the addition of L-fucose. The strains were negative in the fluorescence actin staining test, which in enteropathogenic Escherichia coli strains correlates with the ability to attach and efface intestinal microvilli. The DNA of the Aeromonas strains did not hybridise with the E. coli eae and ipaB probes, associated with attaching and effacing ability and invasion, respectively. These results give support to the enteropathogenicity of adhesive strains of Aeromonas spp., although the mechanisms of adhesion, and possibly invasion, remain to be elucidated.
Acridine Orange↗
Ca2+ influx initiates death of hepatocytes injured by activation of complement.
To clarify the role of cytosolic Ca2+ in hepatocellular death, we exposed cultured hepatocytes to human serum and a monoclonal antibody directed against rat liver plasma membranes to produce complement-mediated cell injury. The change in cytosolic Ca2+ concentration was measured by fura2 and fluo3 fluorescence. With the addition of monoclonal antibody, an increase in cytosolic Ca2+ was observed, followed by cell death. Both the increase in intracellular Ca2+ and cell death were prevented by intracellular Ca2+ chelation or removal of extracellular Ca2+. We conclude that an increase in cytosolic Ca2+ plays a major role in hepatocellular injury induced by exposure of the cell membrane to monoclonal antibody.
Animals↗