Treatment of osteoarthritis of the knee joint at the stage of hydroarthrosis. (Especially from the viewpoint of its histological findings).
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Biomedical subjects
Publications and source records attributed to H Harada.
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A case of oral cancer that had derived from a 19-year skin graft on the left buccal mucosa is reported. The patient had had three previous operations due to squamous cell carcinoma, erosion, and squamous cell carcinoma of the left buccal mucosa, respectively. In the last two operations, skin was transplanted, and the present cancer is believed to have derived from the latter one. The tumor was resected, and a new skin was grafted. In situ hybridization of human papilloma virus (HPV) was carried out; the HPV 16 DNA could not be detected in the specimen. Eight months later, a cervical lymph node metastasis was detected; thus, a radical neck dissection was performed.
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The hepatitis C virus (HCV) genome was sought in the saliva of 76 chronic HCV carriers (mean age nearly 60 years) in a rural Japanese town, who had high serum titers of c-100 and anti-core second generation antibodies. In 27 samples (27 cases, 36%), the HCV-RNA genome was detected by the reverse transcriptase - polymerase chain reaction with either of two sets of primers covering two regions of the HCV genome: the 5'noncoding region and the region encompassing the putative envelope (E1). Transaminase values at the time of sampling were higher in the patients with than in those without detectable HCV RNA in saliva (p = 0.04 for alanine aminotransferase, p = 0.04 for aspartate aminotransferase; Wilcoxon test). The prevalence of the positivity was higher by 5'noncoding primers (14/59 vs. 15/68). Our data show that the severity and duration of hepatic dysfunction influence the detectability of the HCV genome in the saliva. This has been a controversial point among investigators.
Coenzyme Q, an important component of the electron transfer system in mitochondria, plays a central role in energy production aerobically. The effect of pretreatment with coenzyme Q10 (Co Q) on myocardial slow action potentials (APs) and accompanying contractions and on myocardial high energy phosphate content was studied in perfused hearts subjected to decreased perfusion pressure-hypoxia-substrate-free. Post-hatched chicks were treated i.p. with 10 mg/kg of Co Q daily for 5 days. To study the slow APs exclusively, the fast Na+ channels were voltage-inactivated by elevated K+ (25 mM) Tyrode solution. The Ca++-dependent slow APs were induced by elevating [Ca]o to 5.4 mM; hearts were paced at a rate of 40 per min. Hearts which had been pretreated with Co Q were protected against the deleterious effect of decreased perfusion pressure - hypoxia - substrate-free perfusion on mechanical performance accompanying the slow Ca++-Na+ APs. The slow APs in hearts pretreated with Co Q were also less affected than were non-treated hearts. However, the myocardial ATP and total adenine nucleotides were not affected by exogenous Co Q. It was suggested that exogenous Co Q could protect against the decline of cardiac contractions via improved availability of slow APs during decreased perfusion pressure - hypoxia - substrate-free, independently of the cellular high energy phosphate level.
The ability of taurine to protect the isolated heart against doxorubicin cardiotoxicity was examined. Chick hearts perfused for 20 min with medium containing 17 microM doxorubicin exhibited a decrease in contractility, an increase in resting tension and a dramatic depletion in tissue high energy phosphate content. Addition of 20 mM taurine to the perfusate attenuated the increase in resting tension and the decrease in myocardial adenosine triphosphate content induced by doxorubicin. The present study confirms our previous in vivo observations that taurine partially prevents doxorubicin-induced cardiotoxicity.
We measured regional gastric mucosal blood flow by laser Doppler flowmetry before and after control (n = 8) or cigarette smoking (n = 8) in healthy human beings. The control group showed no change in both antrum (from 1.15 +/- 0.32 to 1.20 +/- 0.39 V, NS) and corpus gastric mucosal blood flow (from 1.15 +/- 0.32 to 1.12 +/- 0.28 V, NS). In contrast, cigarette smoking caused a significant reduction in gastric mucosal blood flow in the antrum (from 1.08 +/- 0.31 to 0.71 +/- 0.22 V, p < 0.01) and in the corpus (from 0.99 +/- 0.26 to 0.66 +/- 0.24 V, p < 0.01). The magnitude of reduction in gastric mucosal blood flow was similar between the antrum and the corpus (-34% +/- 11% versus -33% +/- 15%, NS). We conclude that cigarette smoking induces a significant reduction in gastric mucosal blood flow and that no heterogeneous response occurs in regional gastric mucosa. In addition, the laser Doppler flowmeter appears to be a sensitive method to assess rapid change in gastric mucosal blood flow in human beings.
We studied oxygen saturation (SaO2) using a pulse oximeter in 120 patients undergoing non-sedated diagnostic upper gastrointestinal endoscopy. The baseline SaO2 was 98.3 +/- 1.0%. During the procedure, absence of oxygen desaturation (SaO2 > or = 95%) was found in 56%, mild oxygen desaturation (95% > SaO2 > or = 90%) in 35%, and severe oxygen desaturation (SaO2 < 90%) in 9%. Age (p = 0.56), gender (p = 0.47), smoking (p = 0.35), hemoglobin level (p = 0.52), body mass index (p = 0.27), or total endoscopy time (p = 0.72) was not related to the degree of oxygen desaturation. These results suggest that oxygen desaturation is frequently observed during non-sedated diagnostic upper gastrointestinal endoscopy although severe oxygen desaturation, which may induce rare but serious cardiopulmonary events, is not common. Furthermore, we cannot predict in which patients desaturation will occur. We therefore recommend continuous monitoring of arterial oxygenation in all patients during the procedure.
Oxygen saturation was studied with a pulse oximeter in 80 patients with cirrhosis (44 Pugh-Child's class A, 25 class B, and 11 class C) and 80 controls undergoing diagnostic esophagogastroduodenoscopy (EGD). No narcotic agent was used during the procedure. Baseline SaO2 was significantly lower in cirrhotics than in controls (97.7 +/- 1.0% versus 98.4 +/- 0.9%, p < 0.01). However, nadir SaO2 during EGD was similar for controls and cirrhotics (94.7 +/- 3.0% versus 94.9 +/- 3.3%, NS). Significant hypoxia was found in 29 (36%) control patients: mild hypoxia (95% > nadir SaO2 > or = 90%) in 22 patients and severe hypoxia (nadir SaO2 < 90%) in 7. Similarly, significant hypoxia was noted in 28 (35%) cirrhotic patients: mild hypoxia in 21 and severe hypoxia in 7. The mean duration of significant hypoxia during total EGD time was also similar for controls and cirrhotics (7.4 +/- 6.3% versus 9.2 +/- 10.7%, NS). When the degree of hypoxia during EGD was correlated with the severity of liver disease, analysis of variance (ANOVA) failed to show a significant relationship between Pugh-Child's class and nadir SaO2 or duration of significant hypoxia during total EGD time. These results suggest that oxygen desaturation during EGD occurs both in cirrhotic patients and in controls. We therefore conclude that a population of patients with cirrhosis does not have an increased risk of oxygen desaturation during non-sedated EGD.
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Complex cellular responses are often coordinated by a genetic regulatory network in which a given transcription factor controls the expression of a diverse set of target genes. Interferon regulatory factor (IRF)-1 and IRF-2 have originally been identified as a transcriptional activator and repressor, respectively, of the interferon-beta (IFN-beta) as well as of IFN-inducible genes. However, these factors have since been shown to modulate not only the cellular response to IFNs, but also cell growth, susceptibility to transformation by oncogenes, induction of apoptosis, and development of the T cell immune response. Furthermore, the evidence suggests that deletion and/or inactivation of the IRF-1 gene may be a critical step in the development of some human hematopoietic neoplasms. Subsequently, these factors have been shown to constitute a family of transcription factors, termed the IRF-family. Recent studies indicate that other IRF family members also involve the regulation of the IFN system and cell transformation. The IRF-family may be examples of transcription factors which can selectively modulate several sets of genes depending on the cell type and/or nature of the cellular stimuli, so as to evoke host defense mechanisms against infection and oncogenesis.
When stimulated with antigen, B cells are influenced by T cells to proliferate and differentiate into antibody-forming cells. Since it was reported that soluble factors could replace certain functions of helper T cells in the antibody response, several different kinds of lymphokines and monokines have been reported in B-cell growth and differentiation. Among these, human B-cell differentiation factor (BCDF or BSF-2) has been shown to induce the final maturation of B cells into immunoglobulin-secreting cells. BSF-2 was purified to homogeneity and its partial NH2-terminal amino-acid sequence was determined. These studies indicated that BSF-2 is functionally and structurally unlike other known proteins. Here, we report the molecular cloning, structural analysis and functional expression of the cDNA encoding human BSF-2. The primary sequence of BSF-2 deduced from the cDNA reveals that BSF-2 is a novel interleukin consisting of 184 amino acids.
Candidemia, a complication often affecting immunocompromised patients, is a common cause of acute lung injury. Yeast-phase Candida albicans has been shown to express a protein that is antigenically and structurally related to Mac-1. C. albicans is reported to stimulate intercellular adhesion molecule 1 (ICAM-1) expression on endothelial cells. In this study, the authors examined the role of ICAM-1 in acute lung injury induced by candidemia. The authors cultured rat pulmonary artery endothelial cells (RPAEC) and investigated the effect of anti-ICAM-1 antibodies on adhesion of C. albicans to RPAEC. In addition, the authors administered anti-ICAM-1 antibodies to rats to examine the effect of the antibodies on experimentally induced candidemia. Survival rates, lung wet-to-dry (W/D) weight ratios, bronchoalveolar lavage (BAL) fluid, histopathological findings, and colony-forming units (CFUs) of lung C. albicans were examined. The adherence of C. albicans to RPAEC was significantly decreased by anti-ICAM-1 antibodies. Anti-ICAM-1 antibodies significantly increased survival, decreased lung W/D weight ratios, decreased neutrophil counts in the BAL fluid, reduced microscopic lung injury, and decreased the quantity of lung C. albicans. These results indicate that ICAM-1 plays a role in adherence of C. albicans to pulmonary vascular endothelial cells, which likely leads to invasion of lung tissue by the organism.
An experimental and clinical tehcnique of measuring tissue pressures within closed compartments demonstrates a normal tissue pressure is approximately zero mmHg, and increased markedly in compartmental syndromes. There is inadequate perfusion and relative ischemia when the tissue pressure within a closed compartment rises to within 10-30 mm Hg of the patient's diastolic blood pressure. Fasciotomy is usually indicated, therefore, when the tissue pressure rises to 40-45 mm Hg in a patient with a diastolic blood pressure of 70 mm Hg and any of the signs or symptoms of a compartmental syndrome. There is no effective tissue perfusion within a closed compartment when the tissue pressure equals or exceeds the patient's diastolic blood pressure. A fasciotomy is definitely indicated in this circumstance, although distal pulses may be present. The measurement of tissue pressure aids in the early diagnosis and appropriate treatment of compartmental syndromes.