Search PubMed⌕ Search

Biomedical subjects

H Yamakawa

Publications and source records attributed to H Yamakawa.

At least 19 recordsLinked to original sources
PubMed2006

Inheritance pattern of familial moyamoya disease: autosomal dominant mode and genomic imprinting.

BACKGROUND: Although the aetiology of moyamoya disease (MMD) has not been fully clarified, genetic analysis of familial MMD (F-MMD) has considerable potential to disclose it. OBJECTIVE: To determine the inheritance pattern and clinical characteristics of F-MMD to enable precise genetic analyses of the disease. METHODS: 15 highly aggregated Japanese families (52 patients; 38 women and 14 men) with three or more affected members were examined. The difference in categories of age at onset (child onset, adult onset and asymptomatic) between paternal and maternal transmission was compared by chi2 statistics. RESULTS: In all families there had been three or more generations without consanguinity, and all types of transmission, including father-to-son, were observed. Among a total of 135 offspring of affected people, 59 (43.7%) were patients with MMD or obligatory carriers. Affected mothers were more likely to produce late-onset (adult-onset or asymptomatic) female offspring (p = 0.007). CONCLUSIONS: The mode of inheritance of F-MMD is autosomal dominant with incomplete penetrance. Thus, in future genetic studies on F-MMD, parametric linkage analyses using large families with an autosomal dominant mode of inheritance are recommended. Genomic imprinting may be associated with the disease.

Adolescent↗
PubMed2005

Multi-aspect gene relation analysis.

Recent progress in high-throughput screening technologies has led to the production of massive amounts data that we can use to understand biological systems. To interpret this data, biologists often need to analyze the characteristics of a set of genes by using Gene Ontology (GO) annotation. We are proposing a novel method for assisting such an analysis. Given a set of genes, the method automatically extracts several analyzing aspects in terms of a subset of genes that are attached to some related GO terms. It then creates a gene-attribute bipartite graph that highlights the aspect selected by the user according to his/her interests. We describe this method in detail and report on an experiment where the proposed method is applied to the analysis of rat kidney expression data.

Animals↗
PubMed2002

Failure of stent-assisted endovascular treatment for ruptured dissecting aneurysms of the basilar artery.

We report two instructive cases of ruptured dissecting aneurysm of the basilar artery. Although stent-assisted endovascular treatment was successful, recurrent bleeding occurred 4 h after the procedure in one patient, and the other's basilar artery occluded 6 days after the procedure. These cases suggest that the high porosity of currently available stents may be insufficient to induce intraluminal thrombosis and merely stenting may fail to prevent bleeding, while postoperative anticoagulation alone may be inadequate to prevent occlusion of the stented vessel.

Adult↗
PubMed2001

p53 regulates ceramide formation by neutral sphingomyelinase through reactive oxygen species in human glioma cells.

The present study was designed to elucidate the relationship between p53 and ceramide, both of which are involved in apoptotic signaling. Treatment of human glioma cells with etoposide caused apoptosis only in cells expressing functional p53. p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2',7'-dichlorofluorescin (DCFH) into 2',7'-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase. Superoxide dismutase (SOD), a selective antioxidant for O2-*, had no effects on p53 expression but inhibited ceramide generation and apoptotic cell death caused by etoposide. However, catalase, a specific antioxidant for H2O2, only weakly inhibited and sodium formate, a hydroxyl radical (* OH) scavenger, unaffected etoposide-induced apoptosis. Like etoposide-induced cell death, treatment of glioma cells with the O2-*-releasing agent, pyrogallol, induced typical apoptosis and ceramide generation even in the presence of catalase. In contrast, human glioma cells lacking functional p53, either due to mutation or the expression of E6 protein of human papillomavirus, were highly resistant to etoposide and exhibited no significant change in the ceramide level. Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*. Taken together, these results suggest that p53 may modulate ceramide generation by activation of neutral sphingomyelinase through the formation of O2-*, but not its downstream compounds H2O2 or * OH.

Apoptosis↗
PubMed2001

Prognostic implication of Ki-67 immunostaining in treating subclinical pleural cancer found at thoracotomy in lung cancer patients.

BACKGROUND: Therapeutic principles for managing subclinical pleural cancer found unexpectedly during intraoperative examination are unclear. We analyzed prognostic factors including the tumor proliferative marker Ki-67 in these circumstances. METHODS: The cases of 65 surgically treated patients with lung cancer and subclinical T4 pleural cancer, microscopic in 25 and macroscopic in 40, were reviewed. RESULTS: The overall 5-year survival rate of patients undergoing lobectomy was 14.3%. For patients with T4 NO disease, the 5-year survival rate was 46.7%. In patients with a low Ki-67 labeling index, the 5-year survival rate was 28.6%. The Ki-67 labeling index was a significant (p < 0.05) indicator of survival. Multivariate analysis demonstrated Ki-67 labeling index, lymph node involvement, and tumor differentiation to be the most influential prognostic factors for postoperative survival (p < 0.01). CONCLUSIONS: In the treatment of lung cancer patients with subclinical pleural cancer found at thoracotomy, tumor resection is not necessarily contraindicated. Resection appears to be beneficial in patients with no nodal involvement or a low tumor Ki-67 labeling index. This index is a good therapeutic indicator for lung cancer patients.

Aged↗
PubMed2001

Healing of full-thickness tears of avian supracoracoid tendons: in situ hybridization of alpha1(I) and alpha1(III) procollagen mRNA.

Although clinically significant, much remains unknown about the healing of the torn rotator cuff tendon, because of unavailability of appropriate animal model. The human supraspinatus tendon faces the subacromial bursa superiorly, and the joint capsule inferiorly, while the digital flexor tendon is surrounded by the synovium. We hypothesized that the supraspinatus tendon heals by the process which is different from that observed with digital flexor tendons, in which epitenon cells migrate into the torn portion circumferentially. The avian supracoracoid tendon was adopted for this experiment because of its similarity to the human supraspinatus tendon. We developed a full-thickness tendon laceration followed by primary suture. The objective of this study was to detect localization of the responsible cells for repair of the tendon. We examined the process using histology and in situ hybridization. Starting at week 1 the peritendon cells of the bursal side proliferated and migrated into the laceration site. At week 6, the tendon stumps were continuous with new connective tissue. High-level expression of procollagen mRNA in the proliferating peritendon cells on the bursal side demonstrates to contribute to the reparative process, which progressed to the joint side. This mode of repair is different from that of the digital flexor tendon.

Animals↗
PubMed2001

Correlation of sodium-related factors with insulin sensitivity in young, lean, male offspring of hypertensive and normotensive subjects.

Pioneer studies have proposed that multiple metabolic abnormalities, such as insulin resistance, increased Na(+)-H(+) exchanger activity and abnormal intracellular calcium homeostasis, are frequently associated with a subset of essential hypertensive patients with low plasma renin activity (PRA). However, it is unclear whether insulin resistance is related to the low renin status in the very early phase of genetical hypertension. Besides, there is controversy on the subject of the in vivo effect of acute hyperinsulinaemia on sodium-related factors. We investigated the relationship between sodium-related parameters and insulin sensitivity, and the effects of euglycaemic hyperinsulinaemia on cyclic guanosine monophosphate (cGMP) and atrial natriuretic peptide (ANP) levels in 17 young, lean, normotensive male subjects, who displayed extreme predispositions for the development of hypertension. PRA was significantly lower in the positive than in the negative family history group (P < 0.05). Insulin sensitivity (M-value) was correlated with PRA before euglycaemic hyperinsulinaemic clamping (r = 0.577, P < 0.05), and was also inversely correlated with fractional excretion of sodium (FE(Na)) before clamping (r = -0.51, P < 0.05). Euglycaemic hyperinsulinaemia significantly decreased PRA (P < 0.0001) and increased cGMP (P < 0.05) and ANP levels (P < 0.01). In conclusion, insulin sensitivity may be partially determined by PRA levels and FE(Na) before clamping in young, lean, normotensive male subjects. Acute euglycaemic hyperinsulinaemia decreases PRA, and increases cGMP and ANP levels from the fasting condition.

Adult↗
PubMed2001

Transcriptionally and post-transcriptionally regulated response of 13 calmodulin genes to tobacco mosaic virus-induced cell death and wounding in tobacco plant.

We isolated 13 tobacco calmodulin (CaM) genes, NtCaM1-13, and analyzed their expression profile in response to pathogen infection and wounding using specific DNA probes for individual CaM genes and specific antibodies for CaM proteins in groups I (NtCaM1/2), II (NtCaM3/4/5/6/7/8/11/12 and 9/10) and III (NtCaM13), respectively. Synchronous cell death in tobacco mosaic virus (TMV)-infected N-gene-containing tobacco leaves accompanied a predominant accumulation of NtCaM1, 2 and 13 transcripts and NtCaM13-type protein, which is a possible ortholog of soybean defense-involved CaM (SCaM-4), preceding induction of PR-1 and PR-3 defense genes. Accumulation of NtCaM1, 2, 3 and 4 transcripts was induced within 30 min after wounding and NtCaM1-type protein accumulated transiently after wounding. NtCaM13-type protein, which was found at a low level in healthy leaves, decreased instantly after wounding. The treatment with a proteasome inhibitor, lactacystin, enhanced wound-induced accumulation of NtCaM1-type protein and inhibited wound-induced decrease of NtCaM13-type protein, suggesting that proteasome activity is involved in the degradation of these CaMs. Thus, our results indicate that levels of individual CaM proteins are differentially regulated both transcriptionally and post-transcriptionally in tobacco plants that are exposed to stresses such as pathogen-induced hypersensitive cell death and wounding.

Acetates↗
PubMed2001

Narcolepsy and other non-SAS hypersomnia in sleep breathing disorders clinic.

Four of the 708 snorers (0.56%), referred to our sleep breathing disorders clinic for the past 2 years were diagnosed as having narcolepsy-cataplexy. Detecting HLA DRB1*1501/DQB1*0602 positive was informative for differentiating genuine narcolepsy from non-sleep apnea syndrome (non-SAS) hypersomnia in our clinic. A non-SAS obese boy, diagnosed as having essential hypersomnia syndrome, was found to be HLA DRB1*1502/DQB1*0601 positive. His hypocretin concentration was 206 pg/mL in the cerebrospinal fluid.

Adolescent↗
PubMed2001

Effects of physiological cardiac pacing on sleep-disordered breathing in patients with chronic bradydysrhythmias.

In six patients with chronic bradydysrhythmias, polysomnographies were performed before cardiac pacemaker implantation and over the week following implantation. A patient with third-degree atrioventricular block (AVB) and two patients with sinus node dysfunction (SND) were associated with sleep-disordered breathing (SDB). Their cardiac pacemaker therapies, with the increase in the average heart rate, led to a reduction of apnea-hypopnea index and/or an improvement of Cheyne-Stokes breathing. It seems that chronic bradydysrhythmia is one of the causative factors leading to SDB.

Aged↗
PubMed2001

Interleukin-1-induced subacromial synovitis and shoulder pain in rotator cuff diseases.

OBJECTIVE: To determine the relationship between the expression of interleukin-1beta (IL-1beta) and IL-1 receptor antagonists (IL-1ra) in the subacromial bursa and shoulder pain in rotator cuff diseases. METHODS: Synovial specimens were analysed using various methods including reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry and in situ RT-PCR. Thirty-nine patients with rotator cuff diseases were candidates. The degree of their shoulder pain was evaluated using a visual analogue scale. RESULTS: The mRNA expression levels of the cytokines were significantly correlated with the degree of pain [IL-1beta: r=0.782; secreted IL-1ra (sIL-1ra): r=0.756; intracellular IL-1ra (icIL-1ra): r=0.806, P<0.001, respectively]. The combined results of immunohistochemistry and in situ RT-PCR analysis indicated that both synovial lining and sublining cells produce IL-1beta, while synovial lining cells predominantly produce icIL-1ra and sublining cells secrete sIL-1ra. CONCLUSIONS: The differential regulation of the two forms of IL-1ra mRNAs may play an important role in shoulder pain in rotator cuff diseases, regulating IL-1-induced subacromial synovitis.

Adult↗
PubMed2001

Spinal injuries in snowboarders: risk of jumping as an integral part of snowboarding.

BACKGROUND: The purpose of this study was to clarify the occurrence rate and characteristics of spinal injuries caused by snowboarding that were sustained at the Okumino skiing area in Gifu Prefecture, Japan, from 1988 to 2000. METHODS: This study was a retrospective review of 13,490 cases of snowboard- or ski-related injury treated at Sumi Memorial Hospital over this period. RESULTS: A total of 7,188 patients sustained snowboard-related injuries, and 238 of these had spinal injuries caused by snowboarding (3.3%), whereas 6,302 patients sustained ski-related injuries, and 86 of these had spinal injuries caused by skiing (1.4%). Although there were no significant differences in the difficulty of slope, location of vertebral fracture, or spinal cord injury between snowboarders and skiers, the incidence of transverse process fractures was significantly higher in snowboard-related than in skiing-related injury (p < 0.05). In addition, there was a significantly higher incidence of spinal injury among beginner snowboarders than among beginner skiers (p = 0.04). Furthermore, intermediate or expert snowboarders were more likely to be injured because of jumping than beginners (p < 0.001), whereas about 70% of spinal injuries caused by skiing resulted from a simple fall. CONCLUSION: Spinal injuries sustained while snowboarding are increasing considerably in incidence and are characterized as complex injuries. We must educate young snowboarders of the risk of this sport, to prevent these serious injuries.

Adolescent↗
PubMed2001

Crucial role of calpain in hypoxic PC12 cell death: calpain, but not caspases, mediates degradation of cytoskeletal proteins and protein kinase C-alpha and -delta.

Ca2+ influx is one of the main causative events in hypoxic PC12 cell death, because an extracellular Ca2+ chelator, ethylene glycol bis (2-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) inhibited and Ca2+ ionophore A23187 mimicked the hypoxic cell death. The hypoxic cell death was markedly prevented by a broad spectrum caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-FMK) as well as a calpain inhibitor, calpeptin, as assessed by nuclear staining with Hoechst 33258 and lactate dehydrogenase release. The processing of procaspase-3 was inhibited by z-VAD-FMK, but not by calpeptin. In contrast, z-VAD-FMK failed to block the proteolytic cleavage of fodrin-alpha, a preferential substrate for calpain. On the other hand, degradation of actin and fodrin-alpha was prevented by calpeptin but not by z-VAD-FMK. In addition, not only protein kinase C (PKC)-alpha but also PKC-delta were cleaved to generate approximately 46 kDa fragments. The PKC fragmentation was inhibited by calpeptin but not by z-VAD-FMK. These findings suggest that the extracellular Ca2+ influx induced by hypoxic stress activates calpain, resulting in the degradation of cytoskeletal proteins and generation of PKC fragments almost independently of caspase activation. Therefore, calpain may play an important role in hypoxic PC12 cell death.

Animals↗
PubMed2001

Cerebral ischemic complications following intracranial bleeding in patients with moyamoya disease--three case reports.

Three patients with bleeding-type moyamoya disease suffered ischemic complications following their first episode of intracranial bleeding. The patients presented with intraventricular hemorrhage and suffered cerebral infarction on the 14th, 16th, and 11th days after the ictus, respectively. The clinical records revealed no obvious hypotension before progression to infarction and suggested that dehydration accelerated by the administration of hyperosmotic drugs was a contributing factor to the infarction. Two patients underwent superficial temporal artery-middle cerebral artery anastomoses in the chronic stages and have never experienced further ischemic complications. The other patient died despite receiving intensive care. Hemodynamic reserve may be severely impaired in patients with bleeding-type moyamoya disease. Adequate control of hydration is important to prevent cerebral infarction after intracranial bleeding in patients with moyamoya disease.

Adolescent↗
PubMed2000

Type II brain 4.1 (4.1B/KIAA0987), a member of the protein 4.1 family, is localized to neuronal paranodes.

Histochemical analyses of type II brain 4.1/4.1B/KIAA0987, a member of the protein 4.1 family, were carried out in rat brain. In situ hybridization (ISH) showed that type II brain 4.1 mRNA is expressed in a variety of neuronal cells. In particular, type II brain 4.1 mRNA was actively transcribed in the cells of the mesencephalon and the brainstem, which have large myelinated nerve fibers. Expression of type II brain 4.1 mRNA was not observed at least in glial cells distributed in nerve fiber tracts. In immunohistochemical studies using anti-type II brain 4.1-specific antibody, the major immunosignals appeared as brilliant pairs of dots along nerve fibers. Such immunosignals were detected throughout the brain, but were highly concentrated in nerve fiber tracts. These data suggested that type II brain 4.1 is predominantly localized to neuronal paranodes. Detailed analysis concentrating on the nodal region indicated that type II brain 4.1 is present at the paranodal membrane but not in the axoplasm. Weaker type II brain 4.1-specific immunosignals were observed along the internodal membrane of myelinated axons and in the cytoplasm of some neuronal cells. Finally, comparative immunohistochemical studies using antibodies against the other three protein 4.1 family members, type I brain 4.1/4.1N/KIAA0338, erythroid type 4.1 (4.1R) and 4.1G, demonstrated that each of these proteins is distributed in a unique pattern in the cerebellum. Our results are the first to show that type II brain 4.1 is the only member of the protein 4.1 family localized to neuronal paranodes.

Animals↗
PubMed2000

Increased phospholipase D2 activity during hypoxia-induced death of PC12 cells: its possible anti-apoptotic role.

During hypoxic incubation (1% O2) of PC12 cells, the PLD activity was transiently increased within 12h, followed by a gradual decrease. In the in vitro assay, the increased PLD activity was independent of GTPgammaS required for PLD1 or of oleic acid for PLD(OA), suggesting the activation of PLD2. The level of PLD2 protein showed no change up to 12h but a gradual decrease after 24 h. Pretreatment of cells with S. chromofuscus PLD resulted in inhibition of hypoxia-induced apoptotic cell death. In contrast, 1-butanol, but not 2-butanol, potentiated cell death. Moreover, the number of apoptotic cells significantly reduced in PC12 cells over-expressing PLD2. These results raise the possibility that PLD2 activation may play an anti-apoptotic role in hypoxia-induced cell death.

1-Butanol↗