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Biomedical subjects

S Abe

Publications and source records attributed to S Abe.

At least 361 records · Page 20Linked to original sources

Perspectives on the role of the lateral pterygoid muscle and the sphenomandibular ligament in temporomandibular joint function.

The lateral pterygoid muscle plays an important role in the movement of the mandible and has been studied from several points of view, including structural and functional anatomy. What matters clinically is the relative position of the muscle fibers attached medially to the mandibular condyle. In the following study, we observed not only the attachment of the lateral pterygoid muscle fibers to the articular disk, but also the relative position of the mandibular condyle to a base line set up on the mandibular condyle. According to our observations, the lateral pterygoid muscle fibers attach to the articular disk at the inner point of the medial pole. Based on this finding, we can say that the muscle fibers can both draw the articular disk anteriorly and balance it by supporting it posteriorly. That is to say, the lateral pterygoid muscle has two actions: to elevate the articular disk anteriorly and to support the articular disk. Furthermore, the sphenomandibular ligament has continuity with the articular disk tissue medially. This relationship suggests that the ligament fibers attached to the articular disk draw the disk posteriorly in its course of mandibular closing, thus enabling the articular disk to move smoothly.

Adult↗

An anatomical study of a muscle bundle separated from the medial pterygoid muscle.

When mandibular dentures are fabricated, marginal sealing should be taken into consideration for the stability of the denture. We selected specimens of the medial pterygoid muscle showing insertion of an independent small muscle bundle at its insertion site, and evaluated the anatomical relationship between the morphology of the insertion site and the denture. The insertion of the pterygoid muscle was classified according to the insertion morphology of the independent small muscle bundle into three types using the retromolar pad as a reference: Type I, insertion of the independent muscle bundle posterior to the retromolar pad; Type II, insertion immediately below the retromolar pad; and Type III, insertion into the fascia of the mylohyoid muscle. Types II and III muscles seem to affect the denture because of their closeness to the mandibular denture. In the oral cavity, the independent small muscle bundle studied appeared as a streak-like structure. When such a structure is detected during examination for denture fabrication, the following consideration is necessary. Since the medial pterygoid muscle is a mouth-closing muscle, this independent small muscle bundle may contract during mouth closing, appearing more markedly in the oral cavity. Therefore, examination should be performed not only with the mouth closed but also with assumed centric occlusion.

Aged↗

Paratracheal air cysts communicating with the trachea: CT findings.

We reviewed the chest radiographic and thin-section computed tomography (CT) findings in three adult patients with air-filled paratracheal cysts communicating with the tracheal lumen. The air collections were located on the right side in each case. On plain radiographs, they appeared round or oval and were 1-2 cm in diameter. On CT scans, they appeared irregular with a small communication between the tracheal lumen and the cyst. Thin-section and three-dimensional reconstructed CT were useful in detecting the communication between the trachea and paratracheal cyst. In one case, the communication was recognized at surgical resection and in the other two cases, the orifice in the tracheal wall appeared as a tiny, well-circumscribed hole at fiberoptic bronchoscopy.

Adult↗

Genetic and clinical features of sensorineural hearing loss associated with the 1555 mitochondrial mutation.

Five Japanese families showing aminoglycoside-induced hearing loss were genetically as well as clinically investigated. A mitochondrial mutation at nucleotide 1555 was found in 28 out of 32 subjects. One hundred American control subjects did not show any evidence of the mutation at nucleotide 1555, suggesting that the 1555 A-->G (A1555G) mitochondrial mutation may be found more frequently among populations in the Asian continent. Many subjects who harbor this mitochondrial mutation exhibit a mild, high-frequency, progressive hearing loss even without aminoglycoside injection. The results presented here appear to support the hypothesis that the A1555G mutation may play a more general role in causing hearing loss.

Aminoglycosides↗

Primary mucinous carcinoma of the skin.

Primary mucinous carcinoma of the skin is a slow-growing tumor with a high recurrence rate. To improve the recognition of the clinical entity, two cases of this tumor were reported and were investigated histopathologically and histochemically. Both patients showed no evidence of metastatic mucinous adenocarcinoma int he breast or gastrointestinal tract. This tumor should be resected with wide margins. MRI is very helpful to plan the surgical margin.

Adenocarcinoma, Mucinous↗

Serum levels of cardiac troponin I and troponin T in estimating myocardial infarct size soon after reperfusion.

BACKGROUND: Cardiac troponin I (TnI) and troponin T (TnT) are highly specific myocardial markers. OBJECTIVE: To determine whether their serum levels can be used to estimate myocardial infarct size soon after reperfusion. METHODS: We measured the serum levels of TnI, TnT, and creatine kinase every 3 h, and the serum cardiac myosin light chain I (MLCI) every 24 h, in 42 patients with acute myocardial infarction in whom reperfusion therapy had successfully been performed. We calculated the severity of regional hypokinesis by analyzing the follow-up ventriculograms with the centerline method. RESULTS: The time from reperfusion to the peak level for TnI was 6.1 +/- 3.5 h, significantly shorter than those for creatine kinase (7.5 +/- 4.1 h) and MLCI (55 +/- 28 h). The time to peak level for TnT (6.8 +/- 4.0 h) differed significantly from that for MLCI but not from that for creatine kinase. There was a significant correlation between the peak levels of TnI and TnT (r = 0.86). The peak TnI and TnT levels were correlated well to the peak creatine kinase level (r = 0.67 and 0.69, respectively), total creatine kinase release (r = 0.66 and 0.66), and the peak MLCI level (r = 0.71 and 0.80). We observed excellent correlations between the peak levels of TnI and TnT, and regional hypokinesis (r = -0.84 and -0.85, respectively). These were comparable to the correlations between regional hypokinesis and the peak creatine kinase level (r = 0.75), total creatine kinase release (r = -0.72), and the peak MLCI level (r = -0.76). CONCLUSIONS: These results suggest that the peak serum levels of TnI and TnT in patients with successful reperfusion are accurate and early indices of infarct size.

Angioplasty, Balloon, Coronary↗

Augmented inhibition of growth of Candida albicans by neutrophils in the presence of lactoferrin.

The combined inhibitory effects of neutrophils and lactoferrins on the growth of Candida albicans were examined. Murine or human neutrophils partially inhibited growth of C. albicans when cultured with C. albicans in vitro. The growth inhibition was augmented by a combination of neutrophils and more than 30 microg/ml of bovine lactoferrin or 1 microg/ml of human lactoferrin, concentrations less than 1/10-1/200 their inhibiting concentrations when used alone. The inhibition of C. albicans was also enhanced by combination of neutrophils and bovine apolactoferrin or iron-bound holo-lactoferrin, but not by transferrin. Combination effects of neutrophils and lactoferrin were also observed in a condition where there was no contact between neutrophils and Candida cells. These results suggest that neutrophils inhibit the growth of C. albicans regardless of whether there is direct contact between them and Candida cells: neutrophil growth inhibition effects were augmented in the presence of a physiological concentration of lactoferrin, perhaps through some action of lactoferrin other than chelation of ferric ion.

Animals↗

[Poliovirus (Sabin strain) multiplication in human intestinal tract after oral polio vaccination].

Fecal specimens from a baby vaccine were collected every day from 1 to 51 days after primary vaccination and from 0 to 15 days after secondary vaccination. Polioviruses were isolated with GMK-2 cell line from 10% emulsion of the feces and titrated the virus contents in the emulsion of the feces. The isolated viruses were tested the reproductive capacity at 39.0 degrees C and 39.5 degrees C by the plaque method with primary cynomologous monkey kidney cells. Viruses were isolated from the feces during 28 days for type 1, 39 days for type 2 and 36 days for type 3 after primary vaccination, however, only type 1 viruses were isolated during 7 days after secondary vaccination. The multiplication of type 3 viruses in the intestine were increased after diminished the multiplication of type 1 and type 2. In plaque formation capacity at 39.0 degrees C and 39.5 degrees C, the isolates had shown to differ clearly among the types of poliovirus. After primary vaccination, type 1 isolates were not produced the plaques at 39.0 degrees C and 39.5 degrees C. Although type 2 isolates were not formed the plaques until the 14th day at 39.5 degrees C, the plaque formation capacity of the these isolates were increased gradually i.e.; on the 20th day (10(0.88) PFU/ml), the 26th day (10(2.00) PFU/ml) and the 39th day (10(2.63) PFU/ml) at 39.5 degrees C, and all of type 2 isolates tested were showed the plaque formation capacity (10(2.88 approximately 10(3.76) PFU/ml) at 39.0 degrees C. Type 3 isolates were formed plaques at 39.0 degrees C and 39.5 degrees C from the 7th day. After the secondary vaccination, type 1 isolates (7th day) was a little changed them. Neutralizing antibody titers were shown that type 1 was 320, type 2 was 110 and type 3 was 60 after 1 year of the second administration. These titers were closely similar the geometric mean titers of 2 year old babies in Japan.

Humans↗

Host range phenotype induced by mutations in the internal ribosomal entry site of poliovirus RNA.

Most poliovirus strains infect only primates. The host range (HR) of poliovirus is thought to be primarily determined by a cell surface molecule that functions as poliovirus receptor (PVR), since it has been shown that transgenic mice are made poliovirus sensitive by introducing the human PVR gene into the genome. The relative levels of neurovirulence of polioviruses tested in these transgenic mice were shown to correlate well with the levels tested in monkeys (H. Horie et al., J. Virol. 68:681-688, 1994). Mutants of the virulent Mahoney strain of poliovirus have been generated by disruption of nucleotides 128 to 134, at stem-loop II within the 5' noncoding region, and four of these mutants multiplicated well in human HeLa cells but poorly in mouse TgSVA cells that had been established from the kidney of the poliovirus-sensitive transgenic mouse. Neurovirulence tests using the two animal models revealed that these mutants were strongly attenuated only in tests with the mouse model and were therefore HR mutants. The virus infection cycle in TgSVA cells was restricted by an internal ribosomal entry site (IRES)-dependent initiation process of translation. Viral protein synthesis and the associated block of cellular protein synthesis were not observed in TgSVA cells infected with three of four HR mutants and was evident at only a low level in the remaining mutant. The mutant RNAs were functional in a cell-free protein synthesis system from HeLa cells but not in those from TgSVA and mouse neuroblastoma NS20Y cells. These results suggest that host factor(s) affecting IRES-dependent translation of poliovirus differ between human and mouse cells and that the mutant IRES constructs detect species differences in such host factor(s). The IRES could potentially be a host range determinant for poliovirus infection.

Animals↗

Visualisation of exercise-induced ischaemia of the right ventricle by thallium-201 single photon emission computed tomography.

OBJECTIVE: Exercise thallium-201 (201T1) single photon emission computed tomography (SPECT) has been used to detect potential ischaemia in the left ventricular myocardium but not in the right ventricle. The purpose of this study was to establish the clinical usefulness of a right ventricular polar map of 201T1 SPECT for visualisation of exercise-induced right ventricular ischaemia. METHODS: Myocardial 201T1 SPECT was obtained immediately after treadmill exercise in 97 patients with suspected coronary artery disease. A region of interest was placed over the right ventricle (RV) on post-stress transaxial images. Short axis images of this region were generated and reconstructed as a bull's eye polar map. Normal ranges of RV 201T1 uptake were determined in 12 patients with normal coronary arteries. Scintigraphic criteria for identifying RV perfusion abnormality were derived from 25 patients with right coronary artery (RCA) stenosis greater than 75%. These criteria were applied to 60 consecutive patients with suspected coronary artery disease. RESULTS: Perfusion defects in the RV were larger in patients with proximal RCA stenosis than in those with distal RCA stenosis (mean (SD) 28 (16)% v 6 (5)%, P < 0.001). The sensitivity and specificity of the RV polar map for the detection of proximal RCA stenosis were 67% (8/12) and 98% (47/48), respectively. RV perfusion defects became undetectable in 9 patients who had successful percutaneous transluminal coronary angioplasty to a proximal RCA lesion. CONCLUSIONS: A right ventricular polar map display was useful for visualising exercise-induced right ventricular ischaemia.

Adult↗

Inhibition of neutrophil elastase-induced interleukin-8 gene expression by urinary trypsin inhibitor in human bronchial epithelial cells.

BACKGROUND: Urinary trypsin inhibitor (UTI), a potential inhibitor for proteinases including neutrophil elastase (NE), trypsin, plasmin, cathepsin B and H has been used for the treatment of lung diseases with the absence of side effects in Japan. METHODS: In this study, we investigated the inhibitory effects of UTI on both purified NE and NE activities present in bronchoalveolar fluids from patients with chronic bronchitis. We also investigated the inhibitory capacity of UTI with regard to NE-induced interleukin-8 gene expression in human bronchial epithelial cells by Northern analyses. RESULTS: UTI inhibited NE activities in bronchoalveolar lavage fluid from patients with chronic bronchitis and of the purified enzyme. In addition, UTI inhibited NE-induced interleukin-8 gene expression and protein secretion in a human bronchial epithelial cell line. CONCLUSIONS: Our results suggest that UTI is applicable to patients with a variety inflammatory lung diseases in which NE plays a pivotal role.

Bronchi↗

Elevated levels of cytokeratin 19 in the bronchoalveolar lavage fluid of patients with chronic airway inflammatory diseases--a specific marker for bronchial epithelial injury.

Cytokeratin 19 (CK19) is a specific cytoskeletal structure of simple epithelia, including bronchial epithelial cells (BEC). Since CK19 is released from injured bronchial epithelium, we investigated the levels of CK19 fragments in the bronchoalveolar lavage fluid (BALF) of eight patients with chronic airway inflammatory diseases (CAID) using an enzyme-linked immunosorbent assay (ELISA). Included in our test group were four cases of chronic bronchitis, three cases of bronchiectasis, and one case of diffuse panbronchiolitis. There were also 15 control subjects (five asymptomatic smokers and 10 nonsmokers). BALF from the nonsmokers as well as from the asymptomatic smokers contained few CK19 fragments (0.2 +/- 0.2 and 1.9 +/- 0.8 pg/ml, respectively). In contrast, significantly high levels of CK19 were present in the BALF of patients with CAID (21.7 +/- 5.7 pg/ml; p < 0.01 versus nonsmoking controls). In addition, CK19 fragment concentrations in BALF correlated significantly with the number of neutrophils (r = 0.722, p < 0.01) but not with the numbers of macrophages or lymphocytes in BALF. BALF from patients with CAID contained high levels of neutrophil elastase (NE) activity, suggesting that NE might be an important stimulus for the release of CK19 from BEC. To prove this, we incubated BET-1A cells, a human immortalized bronchial epithelial cell line, both in the absence and the presence of inflammatory mediators (including NE, tumor necrosis factor-alpha [TNF-alpha], and hydrogen peroxide). We then measured the concentration of CK19 fragments in the culture supernatants with ELISA. BET-1A cells released CK19 fragments into their culture supernatants after treatment with NE but not after treatment with TNF or hydrogen peroxide. Further, we demonstrated that CK19 cleaved by NE could not be detected by ELISA. Our results suggest that CK19 measurement in BALF is useful for assessing the presence of bronchial epithelial injuries.

Adult↗

Hepatocyte growth factor in bronchoalveolar lavage fluids and cells in patients with inflammatory chest diseases of the lower respiratory tract: detection by RIA and in situ hybridization.

Pulmonary fibrosis is a chronic inflammatory disorder characterized by diffuse fibrous remodeling of alveolar spaces. Although much interest is focused on mechanisms of the inflammatory process in pulmonary fibrosis, little is known about the repair and regenerative process. Hepatocyte growth factor (HGF), originally discovered as a mitogen for hepatocyte regeneration, is now recognized as a multifunctional mesenchymal factor for epithelial regeneration, including the regeneration of alveolar type II epithelial cells. Involvement of HGF and its receptor (c-met) is evident in animal models of acute lung injury produced by hydrochloride inhalation. We studied the role of HGF in patients with idiopathic pulmonary fibrosis (IPF) (25 cases), lung fibrosis associated with rheumatoid arthritis (22 cases), and sarcoidosis (39 cases). Immunohistochemical evaluation demonstrated that hyperplastic alveolar type II epithelial cells, as well as alveolar macrophages, were strongly stained with anti-HGF antibody in tissues of patients with IPF. The concentration of HGF in bronchoalveolar lavage fluid (BALF) was significantly higher than in normal controls (0.23 +/- 0.09 pg/microg) in patients with IPF (0.77 +/- 0.88 pg of HGF/microg of albumin, P < 0.001), lung fibrosis associated with rheumatoid arthritis (0.50 +/- 0.64 pg/microg, P < 0.01), and sarcoidosis (0.41 +/- 0.61 pg/microg, P < 0.05). In situ hybridization revealed mRNA for HGF in alveolar macrophages (especially small monocytelike macrophages). These results indicate that the increase in HGF concentration in patients' peripheral air spaces is due to augmented HGF production by alveolar epithelial cells and alveolar macrophages. HGF, through a paracrine mechanism, may play an important role in the repair and healing of the inflammatory lung damage in pulmonary fibrosis.

Adult↗

Cis-acting region associated with lung cell-specific expression of the secretory leukoprotease inhibitor gene.

Secretory leukoprotease inhibitor (SLPI) is a serine protease inhibitor, produced locally in respiratory and genital glands, but not in the liver. In the present study the promoter region of this gene was analyzed to better understand the molecular mechanisms involved in transcriptional regulation. DNase-I hypersensitive sites were detected within 1 kbp upstream of exon I in chromatin structures of type II pneumocyte cell line A549 and utero-cervical cell line HeLa, both of which express SLPI mRNA transcripts. The function of the SLPI promoter encompassing these DNase-I hypersensitive sites has been studied by deletion analysis with the luciferase gene as a transient expression vector. In this analysis, we found three transcription control regions that function in A549 cells but not in nonlung cell lines, such as HeLa and hepatoma Hep G2. Among three cis-regulatory regions, a proximal 41-bp region (-132 to -92 bp relative to the transcription start site) is responsible for the most striking magnitude of transcriptional activity. This region corresponds to the transcriptional activating sequence detected in another lung cell line, HS-24, indicating that this 41-bp sequence is required for lung cell-specific expression. An electrophoretic mobility shift assay demonstrated that this 41-bp promoter region contains an 11-bp recognition sequence for two nuclear binding proteins, one of which is abundant in lung cell lines, and the other in nonlung cell lines. These results suggest that the ratio of these two nuclear binding proteins confers the cell type specificity on the expression pattern of the SLPI gene.

Adenocarcinoma↗

Three familial cases of hearing loss associated with enlargement of the vestibular aqueduct.

The present report describes three familial cases of recessive hearing loss associated with enlargement of the vestibular aqueduct (EVA). Six siblings from three families showed EVA. The common characteristic of these patients was the presence of congenital, high-frequency, fluctuating sensorineural hearing loss. These cases suggest that EVA may be a useful discriminator between different types of recessive hearing loss.

Adolescent↗

Serum and BAL Clara cell 10 kDa protein (CC10) levels and CC10-positive bronchiolar cells are decreased in smokers.

Cigarette smoking has diverse effects on the structure and function of the lung. Smoking appears to reduce the levels of Clara cell 10 kDa protein (CC10) in the alveolar lining fluid, but the influence of smoking serum on CC10 levels is still debated, and it has not been clear whether smoking reduces the number of CC10-producing lung cells. The aims of this study were to clarify the influence of smoking on CC10 levels in the alveolar lining fluid and bloodstream, and on the number of CC10-producing lung cells. CC10 concentrations were measured in sera and bronchoalveolar lavage (BAL) fluids, by means of enzyme-linked immunosorbent assay using monoclonal and polyclonal antibody, and the immunohistochemical expression of CC10 was examined in the lungs of nonsmokers and smokers using the monoclonal antibody, TY-5, against CC10/human urinary protein-1. CC10 concentrations in sera and in BAL fluids from healthy smokers were significantly lower than in healthy nonsmokers. Immunohistochemical expression of CC10 was found exclusively in nonciliated bronchiolar epithelial cells. As compared to that of nonsmokers, the mean percentage of CC10-positive bronchiolar epithelial cells was significantly decreased in lung tissue specimens obtained from smokers who had normal results in pulmonary function tests. It was concluded that smoking reduces the proportion of Clara cell 10 kDa protein-producing bronchiolar epithelial cells, resulting in decreased levels of Clara cell 10 kDa protein in the lower respiratory tract and in the bloodstream. The protein is a new blood biochemical and immunohistochemical marker, reflecting structural changes in peripheral airways induced by cigarette smoking.

Adult↗

Phase II study of irinotecan and etoposide in patients with metastatic non-small-cell lung cancer.

PURPOSE: To determine the effects of irinotecan (CPT-11) given in combination with etoposide (VP-16) in metastatic non-small-cell lung cancer (NSCLC), to evaluate response and survival rates, and to determine the qualitative and quantitative toxicities of the combination chemotherapy. PATIENTS AND METHODS: Sixty-one metastatic NSCLC patients received concurrent administration of CPT-11 and VP-16 for 3 days with recombinant human granulocyte colony-stimulating factor (rhG-CSF) support. RESULTS: Fifty-nine patients were assessable for response and all 61 patients were assessable for toxicity and survival. Fifty-six patients were treated with two or more courses of chemotherapy. Thirteen patients achieved a partial response (PR), 36 showed no change (NC), and 10 showed progressive disease (PD). The overall response rate was 21.3% (95% confidence interval, 12.9% to 33.1%). The median duration of PRs was 141 days (range, 62 to 299). Of the hematologic toxicities, 14 (23%) and 24 (39%) patients experienced grade 3 or 4 leukopenia and neutropenia, respectively. The toxicities were feasible. Treatment-related death occurred in one patient who suffered hypovolemic shock induced by hematemesis. The median survival time was 10.0 months and the 1-year survival rate was 36.1%. CONCLUSION: Combination chemotherapy with concurrent administration of CPT-11 and VP-16 with rhG-CSF support was only modestly effective against metastatic NSCLC, with feasible toxicities of moderate diarrhea and pulmonary toxicity. The results were equivalent to those expected with either cisplatin-based chemotherapy or with CPT-11 alone.

Adenocarcinoma↗