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Volume 209 (2006)
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- Issue 3 Pages 169-
- Issue 2 Pages 75-
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Volume 209, Issue 2
June
Displaying 1-11 of 11 articles from this issue
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Invited Review
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Kohei Yamauchi2006 Volume 209 Issue 2 Pages 75-87
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSBronchial asthma has been characterized by chronic and allergic airway inflammation, which induces cytological and histological changes in the airway structure over time. These changes have been called airway remodeling, which includes goblet cell hyperplasia, subepithelial fibrosis, and hyperplasia and hypertrophy of airway smooth muscle cells. Airway epithelium in asthma is often occupied with goblet cells, which contain secretory granules. Airway wall thickness increases because of subepithelial fibrosis, and hyperplasia and hypertrophy of airway smooth muscle cells and submucosal glands. Airway remodeling, therefore, can often cause irreversible airflow limitation, an increase of airway hyperresponsiveness and severity of asthma. Recent studies have demonstrated the molecular and cellular mechanisms of goblet cell hyperplasia, subepithelial fibrosis, and hyperplasia and hypertrophy of airway smooth muscle cells. Several lines of evidence suggest that airway remodeling has been induced by cytokines and mediators produced in chronic allergic airway inflammation. Thus, early intervention with inhaled corticosteroid may prevent progress of airway remodeling by suppressing allergic airway inflammation.View full abstractDownload PDF (3738K)
Regular Contributions
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Junko Momiyama, Toshimitsu Hashimoto, Atsushi Matsubara, Kazunori Futa ...2006 Volume 209 Issue 2 Pages 89-97
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSInner ear hair cells play a major role in the auditory pathway that converts sound stimulation into electrical signals, and then into a neural code. However this function is often lost by aminoglycoside ototoxicity. The injury of inner ear hair cells from aminoglycoside treatment is considered apoptosis, and caspase is an important participant in the apoptosis pathway in many organs. It has been reported that calpain, a calcium-dependent protease, is essential for mediation and promotion of cell death. The purpose of the present study was to investigate effects of caspase and calpain inhibitors on the inner ear hair cells after aminoglycoside treatment, and to explore the cell death pathway. Cochlea explant cultures were prepared from mice of postnatal 6 days, cultured with neomycin and/or protease inhibitors, and then stained with phalloidin-fluorescein isothiocyanate (phalloidin-FITC), which was used as a marker to identify surviving hair cells. We demonstrated that neomycin (0.1-1 mM) reduced the number of outer hair cells in a dose-dependent manner. Furthermore, we showed that leupeptin, a calpain inhibitor, significantly protects against the neomycin-induced loss of outer hair cells, whereas a caspase inhibitor was effective only against a lower concentration of neomycin (0.2 mM). Using the TdT-mediated dUTP-biotin nick and labeling method, we also found that a calpain inhibitor, but not a caspase inhibitor, prevents apoptotic DNA fragmentation after treatment with 1 mM neomycin. These results suggest that calpain, rather than caspase, may be responsible for apoptosis induced by aminoglycoside. Thus, leupeptin may prevent hearing loss from aminoglycoside ototoxity.View full abstractDownload PDF (1436K) -
Ping Chen, Yaozong Yuan, Shiwen Wang, Leheng Zhan, Jiayu Xu2006 Volume 209 Issue 2 Pages 99-107
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSIt has been reported that matrix metalloproteinase 9 (MMP-9) disrupts basement membrane and increases vascular permeability. MMP-9 therefore might participate in the pathogenesis of severe acute pancreatitis (SAP). Captopril, an angiotensin-converting enzyme inhibitor, could reduce MMP-9 expression. However, the effect of captopril on the outcome of SAP is not ascertained. The aim of this study was to determine whether captopril attenuates the severity of SAP by reducing MMP-9 expression. Thirty Sprague-Dawley rats were randomly divided into 3 groups (n = 10 for each). Rats were given intraperitoneal injection of saline (SAP group) or captopril (4 mg/kg) (treated group), and then given retrograde infusion of 5% sodium taurocholate (1.5 ml/kg) into the pancreatic duct under laparotomy to induce SAP. One group of rats, injected with saline, underwent only sham operation (Control). Experimental samples were collected at 24 hrs after the induction of SAP or sham operation. Various markers of severity of SAP, such as serum levels of amylase and trypsinogen activation peptide and the vascular permeability, were increased in rats with SAP, but were significantly decreased in captopril-treated rats (p < 0.01). Likewise, the serum MMP-9 levels and expression levels of pancreatic tissue MMP-9 were significantly higher in rats with SAP than those in captopril-treated rats and control rats (p < 0.01 for both parameters), but showed no difference between captopril-treated and control rats. These results suggest that captopril may attenuate vascular permeability by reducing MMP-9 expression in SAP, thereby ameliorating severity of the disease. The use of captopril might become a new therapeutic agent for SAP.View full abstractDownload PDF (2463K) -
Masahiko Inoue, Yoshihiro Wakayama, Hiroko Kojima, Seiji Shibuya, Taka ...2006 Volume 209 Issue 2 Pages 109-116
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSMyoferlin is a novel protein of unknown function with high homology to dysferlin, the gene mutations of which cause limb girdle muscular dystrophy type 2B and Miyoshi myopathy. The myoferlin gene seems to be a candidate for the modifier, and because of the high homology to dysferlin myoferlin may work as a compensator for the absence of dysferlin in dysferlinopathy. This hypothesis is based on the observation that utrophin, which has 80% homology with dystrophin, is overexpressing in the dystrophin deficient myofibers. To test this hypothesis, we investigated the myoferlin expression by immunoblot and immunohistochemical analysis in muscles of five patients with dysferlinopathy. For this aim, we generated a myoferlin specific antibody that does not cross react with dysferlin, and performed the immunoblot, immunohistochemical and immunoelectron microscopic studies. Immunohistochemical analysis showed that the antibodies against myoferlin and dysferlin clearly stained the normal human myofiber surface membranes. The electron microscopy of single immunogold labeled samples for myoferlin showed the presence of the molecular signal along the normal muscle cell membrane. Immunoblot analysis showed that the intensity of 230-kDa myoferlin band of dysferlinopathy muscle extracts was similar to that of normal muscle extracts. The immunostaining of dysferlinopathy muscles with anti-myoferlin antibody revealed a weak immunoreactivity along the muscle cell surface. Thus, the compensatory overexpression of myoferlin was not detected in muscles with dysferlinopathy.View full abstractDownload PDF (3119K) -
Yoichi Shimada, Kazutoshi Hatakeyama, Takashi Minato, Toshiki Matsunag ...2006 Volume 209 Issue 2 Pages 117-123
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSWe have previously restored ambulation in paraplegics by performing hybrid functional electrical stimulation (FES) with medial linkage knee-ankle-foot orthosis (MLKAFO). The most common MLKAFO (hinge-type MLKAFO) has the hypothetical axis that is lower than the physiological hip joint position, resulting in slow velocity and short step length. A new MLKAFO (sliding-type MLKAFO), which uses sliding medial linkages, has been developed to correct the axial discrepancy of the hinge-type MLKAFO that causes limited hip joint excursion. There have been reports of instability associated with sliding medial linkages, but the mechanism of this instability is unclear. The purpose of the present study was to evaluate the effects of FES with MLKAFOs on ambulation in paraplegics. Two complete paraplegic patients (levels T8 and T12, respectively) participated in this study. Kinematics data during ambulation were obtained using a motion analysis system. We measured gait velocity and hip progression during the standing phase. The sliding-type MLKAFO produced faster gait velocity than did the hinge-type MLKAFO, but it caused pelvis instability without FES. Pelvis instability was controlled by hybrid FES using the sliding-type MLKAFO. With hybrid FES, the sliding-type MLKAFO provides better gait performance than the hinge-type MLKAFO, but the hinge-type MLKAFO provides greater pelvis stability during walking. Moreover, FES provides sufficient propulsion to allow the complete paraplegics to walk.View full abstractDownload PDF (948K) -
Tetsuya Adachi, Hiromasa Ogawa, Shinichi Okabe, Tomomi Kitamuro, Yoshi ...2006 Volume 209 Issue 2 Pages 125-134
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSHypoxia causes a life-threatening situation, and the ventilatory response to hypoxia plays an important role in preventing death. We have hypothesized that persons with a blunted hypoxic ventilatory response may have a weak defense response to hypoxic episodes and be susceptible to fatal respiratory disturbances. However, precise correlations between the hypoxic ventilatory response and respiratory disturbances are not well understood. In the present study we examined the hypoxic and hypercapnic ventilatory responses in nine inbred mouse strains (A/J, AKR/N, BALB/c, C3H/He, C57BL/6, DBA/2, NZW, SWR/J, and 129Sv). Breathing frequency, tidal volume and minute ventilation of unanesthetized and unrestrained mice were assessed by whole body plethysmography. Age-matched mice were exposed for 3 min to 10% O2 in N2 gas or 10% CO2 in hyperoxic gas to determine the acute ventilatory response to chemical stimuli. Basal respiratory variables and hypoxic ventilatory responses differed among the strains, but the hypercapnic ventilatory response did not differ. The hypoxic ventilatory response was the highest in AKR/N mice and the lowest in SWR/J mice. These findings suggest that genetic factors may have influenced the hypoxic ventilatory response but not the hypercapnic ventilatory response. To examine the effects of severe hypoxic stress on the respiratory cycle, we exposed the strain with the highest or lowest hypoxic ventilatory response to 6% O2 in N2 until the onset of apnea. The “appearance time of apnea”, which is defined as the time from the hypoxic loading to the onset of apnea, was shorter in the SWR/J strain than in the AKR/N strain. We suggest that a lower hypoxic ventilatory response may be a risk factor for apnea under hypoxia.View full abstractDownload PDF (627K) -
Ismet Melek, Ferit Akgul, Taskin Duman, Fatih Yalcin, Edip Gali2006 Volume 209 Issue 2 Pages 135-140
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSSickle cell disease (SCD) is a common form of hemoglobinopathy and is highly prevalent worldwide. Silent cerebral infarction, which represents infarction without clinical signs, is a risk factor for clinical stroke in patients with SCD. It is well known that silent infarction predisposes patients with SCD to overt stroke. The aim of the present study is to investigate the effect of silent infarction on neurological soft signs (NSS), which demonstrate subtle impairments in sensory integration, motor coordination and the sequencing of complex motor acts and to evaluate whether NSS can be used in clinical practice to evaluate the patients at risk of stroke in SCD patients with silent infarction. Fifty-nine SCD patients without any documented history of cerebrovascular accident and 28 healthy controls were included in this study. All the patients with SCD were evaluated with cerebral magnetic resonance imaging. We found that the NSS scores were significantly higher in patients with silent cerebral infarction than those in patients without silent infarction and control subjects (p < 0.05). Importantly, there was no significant difference in the NSS scores between the patients without silent infarction and control subjects. These results indicate that high NSS scores represnt an important finding for diagnosis of silent infarction in SCD patients. As silent infarction increases the risk for stroke in patients with SCD, NSS can be used to provide additional information in diagnosis of the patients with possible stroke risk during the course of SCD.View full abstractDownload PDF (590K) -
Lei Yu, Guojun Wu, Liguo Wang, He Wang, Geng Zhang2006 Volume 209 Issue 2 Pages 141-148
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSThe prostate tumor-inducing gene 1 (PTI-1) was originally identified by differential ribonucleic acid (RNA) display in human prostate carcinoma. PTI-1 is expressed in human prostate carcinoma but not in benign prostate hypertrophy or normal prostate tissue. PTI-1 may be a member of oncogenes that could affect protein translation and contribute to carcinoma development in human prostate. To investigate the role of PTI-1 in human prostate carcinoma, we constructed three different short interfering RNA (siRNA) vectors (pSilencer3.1-neo-Yu Lei [YL]1-2, -YL3-4 and -YL5-6), each of which was transfected into DU145 and PC3 human prostate cancer cell lines. Among these siRNAs, only pSilencer3.1-neo-YL1-2 could almost completely block the expression of PTI-1 in these two cell lines. The growth of the cell lines was then evaluated after transfection. The proliferation rate was retarded in DU145 and PC3 cells transfected with pSilencer3.1-neo-YL1-2, compared with the cells transfected with a control vector; namely, about 88.6% of DU145 and 80.2% of PC3 cancer cells were blocked at the G1 phase when transfected with pSilencer3.1-neo-YL1-2, compared to 62.0% in DU145 cells and 51.7% in PC3 cells, transfected with the control vector. Moreover, 68.3% of DU145 cells and 72.3% of PC3 cells were induced into apoptosis, while in control transfection, the population was 26.6% in DU145 cells and 28.4% in PC3 cells. These results indicate that blocking PTI-1 expression can inhibit the growth of certain prostate cancer cell lines. We suggest that PTI-1 may serve as a target for the gene-based therapy of human prostate carcinoma.View full abstractDownload PDF (635K) -
Yasushi Suwazono, Etsuko Kobayashi, Mirei Uetani, Katsuyuki Miura, Yuk ...2006 Volume 209 Issue 2 Pages 149-157
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSThe C825T variant of the G-protein β3 subunit (GNB3) gene has attracted renewed attention as a candidate gene for obesity, hypertension and hyperuricemia. The main role of G-protein is to translate signals from the cell surface into a cellular response. The 825T allele is associated with a splice variant of GNB3 protein and enhanced G-protein activation. We examined the relationship between this variant and the risk of hyperuricemia in Japanese workers. The study subjects were 1,452 men and 1,169 women selected from 3,834 men and 2,591 women in 1997. On the basis of common clinical criteria, hyperuricemia I was defined as serum uric acid ≥ 7.0 mg/dl in men and 6.0 mg/dl in women or taking antihyperuricemic medication. The hyperuricemia I group consisted of 186 men and 20 women and its control of 1,266 men and 1,149 women. Hyperuricemia II was defined as serum uric acid > 5.7 mg/dl (median) in men and 3.9 mg/dl (median) in women or taking antihyperuricemic medication. The hyperuricemic II group consisted of 684 men and 570 women and its control of 768 men and 599 women. To replicate previous significant results in young Caucasian men, we selected these criteria because the authors of the study in young Caucasian men adopted the median in their subjects as a cut-off. The statistical power was estimated as 99% based on the significant results in Caucasians. Genotype and allele distributions in men and women with hyperuricemia I and II were not significantly different from those in the corresponding control groups. Logistic regression analysis on hyperuricemia I and II, and multiple regression on serum uric acid level demonstrated no significant effect of the C825T genotype. Despite the sufficient statistical power, this study could not demonstrate the significant influence of C825T on hyperuricemia or serum uric acid. The targeting of this polymorphism is unlikely to be beneficial in the prevention of hyperuricemia in the general Japanese population.View full abstractDownload PDF (393K)
Case Reports
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Sumiko Yoshida, Yohtaro Numachi, Setsu Fukushima, Kazunori Matsumoto, ...2006 Volume 209 Issue 2 Pages 159-162
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSIt has been hypothesized that not only genetic but also environmental factors contribute to the onset of schizophrenia. We therefore conducted psychophysiological studies on a pair of identical twins discordant for schizophrenia, to differentiate non-genetic from genetic indexes possibly associated with this disease. The affected and unaffected twins were 28 year-old females. The affected twin was diagnosed as having schizophrenia based on the Diagnosis and Statistical Manual of Mental Disorders, third edition revised (DMS-III-R), whereas the unaffected twin had no psychiatric disorders. The brain potentials evoked by visual stimulation (visual event-related potential [visual ERP]) were recorded. The components of the visual ERP, which are believed to reflect pattern cognition, semantic processing and the failure to use preceding word information, were compared with normal subjects. Both twins showed abnormal semantic processing and similar failure to use preceding word information. Abnormality of semantic processing was marked in the affected twin. These results indicate that failure to use preceding word information might reflect only genetic factors, whereas abnormal semantic processing might reflect both genetic and non-genetic factors because the affected twin was considered to show accelerated deterioration after the disease onset. However, only the affected twin showed abnormal pattern cognition, which might be attributable to non-genetic factors such as an acquired vulnerability to schizophrenia. We suggest that the impairment of pattern cognition evaluated by visual ERP may be a critical index for the onset of schizophrenia.View full abstractDownload PDF (240K) -
Keisuke Wakusawa, Kazuhiro Haginoya, Taro Kitamura, Noriko Togashi, Ma ...2006 Volume 209 Issue 2 Pages 163-167
Published: 2006
Released on J-STAGE: May 17, 2006
JOURNAL FREE ACCESSHypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC) is a rare leukoencephalopathy presenting in the infantile period and characterized by diffuse cerebral hypomyelination, and atrophy of the basal ganglia and cerebellum. As patients with H-ABC lack remarkable laboratory findings, the diagnosis is based on brain magnetic resonance imaging findings alone. Only eight cases have been reported in the literature, and thus the natural course and treatment of this disease are not fully understood. We report a 35-month-old boy with H-ABC who had hemidystonia, hypomyelination, and cerebellar ataxia. We diagnosed H-ABC after considering a thorough differential diagnosis, excluding other diseases involving hemidystonia, hypomyelination, and cerebellar ataxia. Furthermore, technetium-99m ethyl cysteinate dimmer-single-photon emission computerized tomography (Tc-ECD-SPECT) and positron emission tomography with fluorodeoxyglucose 18F (FDG-PET) revealed decreased blood flow and glucose metabolism in the bilateral lenticular nucleus, thalamus, and cerebellum. A peroral levodopa preparation containing carbidopa (levodopa-carbidopa) was effective at ameliorating and stopping the progression of the patient's dystonia (final effective doses: levodopa, 200 mg/day and carbidopa, 20 mg/day). This is the first case report of a Japanese patient with H-ABC and treatment for this disease. Levodopa-carbidopa may be an effective treatment for H-ABC.View full abstractDownload PDF (1545K)
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