[A case of nutcracker esophagus complicated with angina pectoris].
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Angina Pectoris↗
Biomedical subjects
A Kawakami
Publications and source records attributed to A Kawakami.
[Clinical characteristics of near-fatal asthma attack induced by NSAIDs].
Despite advance in the treatment of asthma, asthma-related deaths have not declined. One of the reasons in those cases may be that there is a surprising lack of information on death from asthma since most of asthma deaths take place outside the hospital. Learning about near-fatal asthma attack (NFA) patients is useful to understand the mechanisms of asthma deaths because NFA patients and fatal asthma possess common clinical characteristics. It is well-known that there are two types of severe asthma exacerbation, that is, "sudden onset" and "slow onset attaches", in terms of clinical, functional and blood gas parameters. On the other hand, NSAIDs is one of the factors leading to exacerbation of asthma or asthma-related death. We examined the characteristics of NSAIDs-induced asthma and the pattern of respiratory arrest in the NSAIDs-induced NFA group compared to non-NSAIDs group at a Kyoto National Hospital from 1986 to 1997. A Total of 30 patients (34 cases) with NSAIDs-induced asthma among 265 admissions with asthma attack were reviewed involving 15 women and 15 men, mean age 46 +/- 14 years old. Six patients (8 cases) of NSAIDs group and 13 patients of non-NSAIDs group had intubation for their NFA. NSAIDs group showed more severe respiratory insufficiency with higher arterial CO2 level compared to non-NSAIDs group (91.5 +/- 16.3 vs 76.3 +/- 17.0 Torr) and significant lower pH level (7.02 +/- 0.14 vs 7.18 +/- 0.07, p < 0.05). But, NSAIDs group showed significantly more short weaning time than that of non-NSAIDs group (p < 0.01). We suggest that many sporadic cases of rapid onset severe asthma attacks may result from the ingestion of NSAIDs.
Adult↗
Hemisphere specialization of Go experts in visuospatial processing.
To investigate hemisphere function of experts, Go experts and novices were given two Salthouse-type visuospatial tasks. In Experiment 1, stimuli of 4 digits in 6 cells were projected to the left (LVF) or right visual field (RVF). There was no prominent group difference in identification of digits and locations. In Experiment 2, stimuli of 4 digits in 16 cells were projected to the LVF or RVF. Go experts showed more accurate performance than novices. Both groups showed the same laterality, an RVF advantage, in the number identification. However, in the location identification, Go experts showed no visual field difference, whereas novices showed an RVF advantage. Based on these findings, the relationship between task demand and hemisphere function of experts is discussed.
Adult↗
Increased Fas-mediated cytotoxicity of CD4-positive T cells in patients with human T-lymphotropic virus type I-associated myelopathy.
Using a 51Cr release assay, we investigated Fas-mediated cytotoxicity of peripheral blood CD4+ T cells of patients with human T-lymphotropic virus type-I (HTLV-I)-associated myelopathy (HAM) against T98G, a glioblastoma cell line which expresses Fas. Cytotoxic activity of CD4+ T cells against T98G was significantly higher in HAM patients than in controls. Moreover, when CD4+ T cells of HAM patients were preincubated with a monoclonal antibody to human Fas ligand (FasL), cytotoxic activity against T98G was significantly suppressed. These results suggest that damage to nervous tissues by the Fas/FasL system is involved in the pathogenesis of HAM.
Aged↗
Insulin-like growth factor I stimulates proliferation and Fas-mediated apoptosis of human osteoblasts.
In vitro studies have shown that insulin-like growth factor I (IGF-I) is a potent growth factor for osteoblasts, although both bone formation and resorption are upregulated by IGF-I in vivo. To understand the difference in the action of IGF-I observed in vitro and in vivo experiments, we examined the effect of IGF-I on the proliferation and Fas-mediated apoptosis of human osteoblasts in vitro. Human osteoblastic cell line MG63 and human primary osteoblast-like cells obtained from biopsy specimens were used as human osteoblasts. Cells were cultured with or without various concentrations of IGF-I followed by determination of the proliferative response and Fas-mediated apoptosis. IGF-I dose dependently stimulated the proliferation of cultured human osteoblasts. Both Fas expression and the degree of anti-Fas IgM-induced apoptosis of human osteoblasts was also augmented by IGF-I. Furthermore, the cytotoxicity of Fas ligand (FasL) cDNA transformants against human osteoblasts was increased when IGF-I-stimulated osteoblasts were used as target cells, indicating that stimulation of IGF-I increased functional Fas expression on human osteoblasts as well as their proliferation. The addition of DEVD-CHO, a specific inhibitor of CPP32, to the culture resulted in a significant inhibition of Fas-mediated apoptosis of both unstimulated and IGF-I-stimulated osteoblasts, although it did not affect the proliferative response or Fas expression. Our data suggest that activation of CPP32 is necessary for Fas-mediated apoptosis of human osteoblasts, and treatment of IGF-I increased this signaling pathway. In contrast, regulation of proliferation and Fas expression of the cells were probably not affected by CPP32 activation. Our results suggest that IGF-I acts on cultured human osteoblasts by increasing their proliferation and induction of Fas-mediated apoptosis by neighbouring FasL+ cells such as osteoclasts, thus probably functioning as a local coupling factor in the bone in vivo, stimulating both bone formation and resorption.
Apoptosis↗
Effects of transjugular intrahepatic portosystemic shunt (TIPS) on esophageal motor function and gastroesophageal reflux.
The effects of transjugular intrahepatic portosystemic shunt (TIPS) placement on esophageal motor function and gastroesophageal reflux were investigated in patients with esophageal varices. In six men with esophageal varices, esophageal manometry and upper gastrointestinal endoscopy were performed before and 15-20 days after TIPS placement. Intraesophageal pH monitoring was performed in the four patients with severe esophageal varices (defined as the largest sized varices) following TIPS placement. Findings were compared with those in six healthy men (controls) who underwent esophageal manometry and intraesophageal pH monitoring. The esophageal varices resolved or were reduced after TIPS placement. Resting lower esophageal sphincter (LES) pressures were similar in the study group before and after TIPS placement and in the control subjects. The incidence and progression of esophageal contractions were similar in the study group before and after TIPS placement and in the control subjects. At 3 cm above the LES, the amplitude of esophageal contraction after TIPS placement was significantly higher than that before TIPS placement. At 3 and 8 cm above the LES, the amplitude of esophageal contraction in the control subjects was significantly higher than that in the study group before and after TIPS placement. Esophageal acid exposure time after TIPS placement was similar to that in the controls. TIPS placement is a useful treatment that improves esophageal motor function without the occurrence of pathologic gastroesophageal reflux.
Esophageal and Gastric Varices↗
Expression and function of Fas and Fas ligand on peripheral blood lymphocytes in normal subjects.
We investigated the expression and function of Fas and Fas ligand (FasL) on peripheral blood lymphocytes (PBLs). The cells were stimulated with various cytokines or 12-0-tetradecanoyl phorbol 13-acetate (PMA) plus ionomycin. About 30% of unstimulated PBLs expressed Fas, and the expression was augmented by interleukin-1beta (IL-1beta), IL-2, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), or PMA plus ionomycin. Although only minimal FasL expression was detected on unstimulated PBLs, FasL expression was markedly induced by IL-2 or PMA plus ionomycin, suggesting that Fas and FasL were both expressed on IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs. Although IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs were positive for both Fas and FasL, no significant increase in apoptosis was demonstrated in these activated PBLs. In addition, treatment of PBLs with IL-2 or PMA plus ionomycin did not change anti-Fas-induced apoptosis, although these activated PBLs expressed Fas strongly when compared with unstimulated PBLs. Only IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs killed Fas+ target cells efficiently via the interaction of Fas on target cells with FasL of PBLs. Bcl-2 was constitutively expressed on unstimulated PBLs, but its expression was significantly augmented by IL-2 or PMA plus ionomycin. The expression of Bax was clearly induced only on IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs and that of other Bcl-2 family proteins such as Bcl-x and Bad could not be detected on human PBLs, including IL-2-stimulated or PMA-plus-ionomycin-stimulated PBLs. Our results suggest that PBLs activated by IL-2 or PMA plus ionomycin express both Fas and FasL and that they kill Fas+ target cells by using FasL on the surface. The resistance of these activated PBLs to Fas-mediated apoptosis may be due to the augmented Bcl-2 expression or the presence of Bcl-2:Bax heterodimers on these cells.
Adult↗
Association of endogenous insulin secretion and mode of therapy with body fat and serum leptin levels in diabetic subjects.
Insulin is one of the hormonal regulators of leptin synthesis and participates in adipose tissue maintenance. The present study was undertaken to clarify the association of endogenous insulin secretion and mode of therapy with body fat and serum leptin levels in diabetic subjects. We measured the fasting serum C-peptide level, as an estimate of endogenous insulin secretion, and the serum leptin level in 176 Japanese diabetic subjects (79 men and 97 women; age, 55.9+/-14.3 years; body mass index [BMI], 23.8+/-4.1 kg/m2 [mean+/-SD]). Thirty-one subjects were treated with diet therapy alone, 66 with sulfonylurea (SU), and 79 with insulin (including 29 with type I diabetes mellitus). Body fat was analyzed by the impedance method. Serum leptin levels significantly correlated with the BMI and body fat and were higher in women, mainly because of their greater body fat. Serum C-peptide concentrations positively correlated with body fat and serum leptin in subjects treated with diet and SU. In insulin-treated type II diabetic subjects, both serum C-peptide and the daily insulin dose were weakly associated with body fat and serum leptin. In those subjects, despite a lower percent body fat and body fat mass, serum leptin concentrations (10.3+/-8.4 ng/mL) were comparable to the levels in subjects treated with diet (8.8+/-8.5 ng/mL). When compared within the same BMI and body fat groups (BMI 20 to 25 and > 25 kg/m2) including the control subjects matched for age and sex, serum leptin levels were higher in insulin-treated type II diabetic subjects versus the control subjects and diabetic patients treated with diet or SU. Stepwise regression analysis for all of the diabetic subjects showed that both the serum C-peptide level and exogenous insulin administration, as well as the BMI, gender, and age, were determinants of the serum leptin level. In conclusion, endogenous insulin secretion is closely associated with body fat and serum leptin in diabetic subjects treated with diet therapy and SU. In Japanese insulin-treated type II diabetic subjects, both endogenous and exogenous insulin are associated with body fat and serum leptin, which is maintained at levels comparable to or somewhat higher than the levels in control subjects and diabetic patients treated without insulin.
Adipose Tissue↗
Apoptosis in labial salivary glands from Sjögren's syndrome (SS) patients: comparison with human T lymphotropic virus-I (HTLV-I)-seronegative and -seropositive SS patients.
Apoptosis is a type of cell death that occurs during morphogenesis and development of the immune system. One of the mechanisms is mediated through the Fas and Fas ligand (FasL) pathway. To determine the possible involvement of Fas and its ligand in salivary gland destruction, we analysed the appearance of nuclei with DNA fragmentation by using nick end labelling (TUNEL) and the expression of Fas and FasL by immunohistochemistry in labial salivary glands. Furthermore, we compared the features of apoptosis in labial salivary glands between HTLV-I- and HTLV-I+ SS. When the frozen sections of 10 primary SS patients in the absence of anti-HTLV-I antibody were examined, several apoptotic cells were found in the acinar and ductal epithelial cells as well as infiltrated mononuclear cells. Both Fas and FasL were detected in the infiltrated mononuclear cells. Acinar epithelial cells, which are surrounded by FasL+ mononuclear cells, were also double-positive with Fas and FasL, although the expression of FasL was localized at their apical border, suggesting that apoptosis of mononuclear cells was achieved by activation-induced mechanisms through Fas/FasL pathways, and that of acinar epithelial cells was mediated by FasL derived from either acinar epithelial cells themselves or infiltrated mononuclear cells. Interestingly, Fas expression in ductal epithelial cells was localized around the lumen side of the ducts, indicating that FasL secreted from acinar epithelial cells may induce Fas-mediated apoptosis of ductal epithelial cells. We also studied the labial salivary glands from nine SS patients with anti-HTLV-I antibodies. There was no significant difference in the occurrence of apoptotic cells or in the expression of Fas and FasL between HTLV-I+ and HTLV-I- SS patients. It was of note that neither the expression of Fas and FasL nor the presence of apoptotic cells were determined in labial salivary glands from subjects without SS. These findings indicate that Fas-mediated apoptosis in salivary glands could be involved in the pathological manifestations of SS, irrespective of HTLV-I seropositivity.
Adult↗
CD4+ T-cell-mediated cytotoxicity against staphylococcal enterotoxin B-pulsed synovial cells.
Apoptosis of synovial cells in rheumatoid arthritis (RA) synovium determined in vivo is suggested to counteract the overgrowth of synovium. Immunohistological examination has revealed the infiltration of activated CD4+ T cells, which express Fas ligand (FasL), in RA synovium. The presence of a putative antigen (Ag) of autoimmune disorders in a target organ may induce the activation of specific T cells in the inflammatory region such as RA synovium. We examined the possible role of CD4+ T cells activated by synovial cells in a staphylococcal enterotoxin B (SEB)-dependent manner, inducing synovial cell apoptosis. Synovial cells were cultured with or without interferon-gamma (IFN-gamma) and further incubated with CD4+ T cells in the presence of SEB. After the cocultivation, both the cytotoxicity and FasL expression of CD4+ T cells were investigated. Constitutive Fas expression was detected on both unstimulated and IFN-gamma-stimulated synovial cells. CD4+ T cells did not kill SEB-pulsed unstimulated synovial cells efficiently. In contrast, when CD4+ T cells were incubated with IFN-gamma-stimulated synovial cells with SEB whose human leucocyte antigen (HLA)-DR and -DQ expression was markedly induced, significant cytotoxicity by these cells against synovial cells was detected. The addition of anti-HLA-DR and -DQ monoclonal antibodies (mAbs) or human Fas chimeric protein (hFas-Fc) reduced this cytotoxicity. FasL expression of CD4+ T cells cocultured with IFN-gamma-stimulated synovial cells with SEB was significantly induced. Furthermore, the addition of mAbs against CD54, CD58 and CD106 inhibited both the cytotoxicity and FasL expression of CD4+ T cells induced by IFN-gamma-stimulated synovial cells in the presence of SEB, indicating the importance of costimulatory molecules on synovial cells in activating CD4+ T cells. Our results suggest that CD4+ T cells are activated by synovial cells by an SEB-dependent manner and express FasL, inducing Fas-mediated apoptosis of the latter cells. These phenomena may regulate the overgrowth of synovial cells in RA synovium.
Antibodies, Monoclonal↗
Correlation between tectum formation and expression of two PAX family genes, PAX7 and PAX6, in avian brains.
Heterotopic transplantation of brain vesicles between chick and quail were performed, and the correlation between tectum formation and the expression of two PAX family genes, PAX7 and PAX6, analyzed. Reciprocal transplantation between the prosencephalon and mesencephalon showed that formation of the tectum always coincided with induction/maintenance of PAX7 and suppression of PAX6, indicating that switch-on or -off of these two PAX family genes in region specific manners are responsible for the differentiation of brain vesicles into the tectum. On the other hand, transplantation of the mesencephalic floor plate into the dorsal mesencephalon suppressed PAX7 expression in the dorsal mesencephalon and changed its fate from the tectum to the tegmentum, indicating that factors in the mesencephalic floor plate suppress PAX7 and limit tectum territory to the dorsal part of the mesencephalon.
Animals↗
Inhibitory effect of glucocorticoid for osteoblast apoptosis induced by activated peripheral blood mononuclear cells.
Recent studies suggest a protective effect of glucocorticoid against progression of bone erosion and periarticular osteoporosis in patients with rheumatoid arthritis (RA), although this steroid hormone itself is believed to increase bone loss. To understand the antagonistic effect of glucocorticoid for osteopenic process in RA patients, we examined the effect of dexamethasone on Fas-mediated apoptosis of cultured human osteoblasts induced by either anti-Fas IgM or activated peripheral blood mononuclear cells (PBMC). Human osteoblastic cell line MG63 and primary osteoblast-like cells obtained from biopsy specimens were used in this study. PBMC isolated from healthy donors were cultured with or without recombinant interleukin-2 (rIL-2) followed by 12-O-tetradecanoyl-phorbol 13-acetate (PMA) with ionomycin in the presence or absence of dexamethasone. Fas was functionally expressed on MG63 and primary osteoblast-like cells, and treatment of these cells with dexamethasone affected neither Fas expression nor anti-Fas IgM-induced apoptosis. Activated PBMC expressing membrane-type Fas ligand (mFasL) efficiently killed both MG63 and primary osteoblasts-like cells, and the addition of human Fas chimeric protein (hFas-Fc) significantly diminished the cytotoxicity, indicating that interactions between mFasL of activated PBMC and Fas on human osteoblasts induce apoptosis of the latter. Although dexamethasone did not affect apoptosis of MG63 and primary osteoblast-like cells induced by anti-Fas IgM, treatment of activated PBMC with dexamethasone markedly inhibited both mFasL expression and cytotoxicity of these cells against human osteoblasts, suggesting that dexamethasone preferentially acts not on osteoblasts but PBMC. Cultured supernatants from activated PBMC induced apoptosis of human osteoblasts and the addition of hFas-Fc also inhibited the cytotoxicity of the supernatants. In addition, soluble form FasL (sFasL) was detected in the supernatants of activated PBMC. Furthermore, both the cytotoxicity and sFasL concentration of cultured supernatants of activated PBMC incubated with dexamethasone was significantly lower than that in the absence of dexamethasone. Our data suggest that glucocorticoid suppresses the apoptotic process of osteoblasts by inhibiting the expression of both mFasL and sFasL derived from activated PBMC, mediating a protective effect against periarticular bone loss and bone erosion in inflammatory arthritis such as RA.
Apoptosis↗
Coordinated expression of Hoxa-11 and Hoxa-13 during limb muscle patterning.
The limb muscle precursor cells migrate from the somites and congregate into the dorsal and ventral muscle masses in the limb bud. Complex muscle patterns are formed by successive splitting of the muscle masses and subsequent growth and differentiation in a region-specific manner. Hox genes, known as key regulator genes of cartilage pattern formation in the limb bud, were found to be expressed in the limb muscle precursor cells. We found that HOXA-11 protein was expressed in the premyoblasts in the limb bud, but not in the somitic cells or migrating premyogenic cells in the trunk at stage 18. By stage 24, HOXA-11 expression began to decrease from the posterior halves of the muscle masses. HOXA-13 was expressed strongly in the myoblasts of the posterior part in the dorsal/ventral muscle masses and weakly in a few myoblasts of the anterior part of the dorsal muscle mass. Transplantation of the lateral plate of the presumptive wing bud to the flank induced migration of premyoblasts from somites to the graft. Under these conditions, HOXA-11 expression was induced in the migrating premyoblasts in the ectopic limb buds. Application of retinoic acid at the anterior margin of the limb bud causes duplication of the autopodal cartilage and transformation of the radius to the ulna, and at the same time induces duplication of the muscle pattern along the anteroposterior axis. Under these conditions, HOXA-13 was also induced in the anterior region of the ventral muscles in the zeugopod. These results suggest that Hoxa-11 and Hoxa-13 expression in the migrating premyoblasts is under the control of the limb mesenchyme and the polarizing signal(s). In addition, these results indicate that these Hox genes are involved in muscle patterning in the limb buds.
Animals↗
Contribution of a missense mutation (Trp64Arg) in beta3-adrenergic receptor gene to multiple risk factors in Japanese men with hyperuricemia.
Epidemiological data reveal that hyperuricemia is a risk factor of atherosclerosis. The risk is possibly caused by a link between hyperuricemia and insulin resistance-related metabolic syndrome. Recently it has been proposed that a missense mutation (Trp64Arg) in the beta3-adrenergic receptor (beta3-AR) gene may contribute to the accumulation of multiple risk factors related to insulin resistance. The present study was undertaken to further clarify an association between the Trp64Arg mutation and the metabolic syndrome in 47 Japanese men with hyperuricemia, who are substantially at high risk of atherosclerosis. One patient (2%) had the homozygous mutation, 12 (26%) were heterozygous for the mutation, and 31 (72%) had no mutation found by the PCR-RFLP analysis. The Trp64Arg mutation was not related to past maximal body mass index (BMI), BMI and waist/hip ratio. The subjects with the heterozygous mutation showed a slightly higher incidence of impaired glucose tolerance and diabetes mellitus in the 75 g oral glucose challenge (67%), as compared with those without the mutation (39%). Serum insulin response at 60 min and the sum of serum insulin in the glucose challenge were greater in the former subjects than those in the latter subjects (P=0.041 and 0.076, respectively). An increase in serum lipoprotein(a) was also observed in the subjects with the heterozygous mutation, but the Trp64Arg mutation was not associated with other dyslipidemia, blood pressure or ischemic changes on the electrocardiogram. These results indicate that the heterozygous mutation of Trp64Arg in the beta3-AR gene partly contributes to the accumulation of multiple risk factors in male subjects with hyperuricemia. A larger prospective study is necessary to elucidate a possible role of the Trp64Arg mutation in atherosclerotic diseases in future.
Adult↗
Central diabetes insipidus associated with a missense mutation in the arginine vasopressin gene that replaces Ala at the carboxyterminus of the signal peptide with Thr.
We report an 18-year-old male with a history of polyuria, polydipsia, and thirst since childhood. In a hypertonic saline infusion test, the patient's plasma vasopressin rose only to 0.28 pg/ml. In a water deprivation test, his urinary osmolality rose only to 189 mosmol/kg and then rose to 538 mosmol/kg by vasopressin administration. A T1-weighted magnetic resonance imaging (MRI) scan revealed a loss of the posterior pituitary bright spot. Sequencing of the vasopressin gene showed a heterozygous point mutation that replaced Ala at the carboxyterminus of the signal peptide with Thr. His father also had similar history, and we therefore diagnosed his illness as familial central diabetes insipidus.
Adolescent↗
Semantic priming of Kanji words in the cerebral hemispheres.
Two experiments were conducted to investigate how the spreading activation arose in hemispheres using single and 2-letter Kanji words. Results suggested that single- and 2-letter Kanji words were processed differentially and the semantic activation mechanisms seemed to be different from that of English words.
Brain↗
[Effect of inhalation of ipratropium bromide on nonspecific esophageal motility disturbance--case report].
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Administration, Inhalation↗
[A case of hypertensive lower esophageal (LES) sphincter that psychological factors may contribute to the onset].
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Esophageal Motility Disorders↗