Biomedical subjects

T Homma

Publications and source records attributed to T Homma.

At least 73 records · Page 4Linked to original sources

PubMed1996

[Effects of pulmonary rehabilitation on vital capacity in patients with chronic pulmonary emphysema].

To evaluate the effects of pulmonary rehabilitation on pulmonary function, 15 patients with chronic pulmonary emphysema underwent pulmonary rehabilitation for six weeks as inpatients. Pulmonary rehabilitation consisted of relaxation techniques, breathing retraining, thoracic massage, physical exercise, and walking. In 8 of the 15 patients vital capacity increased by more than 200 ml (over 10%), and in 7 of the 15 patients the load of maximal exercise increased by more than 5 watts (over 10%). Increases in vital capacity were not associated with increases in maximal exercise load. The percent change in vital capacity associated with pulmonary rehabilitation correlated significantly with the percent change in tidal volume and the percent change in expiratory minute ventilation at the maximal load. The percent change in tidal volume at the maximal load correlated significantly with the percent change in maximum oxygen uptake. We attribute the increase in vital capacity to an improvement in thoracic cage movement. These findings suggest that pulmonary rehabilitation can increase vital capacity in some patients with chronic pulmonary emphysema, and that such an increase is not directly connected to increases in exercise capacity.

Aged↗

PubMed1996

[Psychological and physiological changes accompanying pulmonary rehabilitation in patients with chronic pulmonary emphysema].

In 14 patients with chronic pulmonary emphysema, the relations between changes in psychological status associated with pulmonary rehabilitation and exercise tolerance were studied with the Cornell Medical Index and the Yatabe-Guiford Personality Inventory. Although the scores on the latter did not change, the cardio-respiratory score on the Cornell Medical Index improved significantly (p < 0.05). The only index of exercise tolerance that improved significantly was the distance walked in 10 minutes (p < 0.05). The changes in the scores of "Lack of Objectivity" and "Rhathymia" correlated negatively with the change in the distance walked in 10 minutes (R = -0.80, p < 0.01; R = -0.81, p < 0.01). The change in psychological status that accompanied pulmonary rehabilitation has been related to the improvement in the distance walked in 10 minutes.

Aged↗

PubMed1996

Apoptosis of germinal centers in postnatal development of rabbit tonsil.

The purpose of this study was to clarify the relationship between the morphological maturation of the germinal center of newborn rabbit tonsil and the appearance of apoptosis in it. Germinal centers were observed using immunostaining. Apoptosis is shown to be scarce in immature type of germinal center, but abundant in mature type. The findings suggest apoptosis to have an important function in the germinal center of the tonsil.

Animals↗

PubMed1996

Cell dynamics in the germinal center of the human tonsil.

Apoptosis of the human tonsillar germinal center was studied by means of immunocytochemical methods. It is generally accepted that the germinal center of the lymphoid tissues plays an important role both in cell proliferation and cell death. Although many studies on cell proliferation have been reported, the cell death mechanism is not yet well understood. According to recent studies, apoptosis is the result of programmed, not pathological cell death, and it plays an important role in the maintenance, immunity and development of life. The present study showed that the tingible body was a mass of nuclear chromatin of dead cells, and that cells with a tingible body are macrophages, called tingible-body macrophages. The purpose of this study was to examine the relationship between tingible-body macrophages and apoptosis. The structure of tingible-body macrophages were observed by immunostaining methods.

Apoptosis↗

PubMed1995

Intracellular stability of alpha fragments of beta-galactosidase: effects of amino-terminally fused polypeptides.

Intracellular stability of alpha fragments of beta-galactosidase in Escherichia coli has been studied by pulse-chase/immunoprecipitation experiments. An alpha fragment encoded by the pUC118 vector was relatively stable with an estimated half-life of about 12 min at 37 degrees C, whereas another vector, pSTV28, encoded a less stable alpha fragment that had a different carboxy-terminal sequence. Stability of the fragment was found to be affected markedly by amino-terminal attachment of other sequences. An amino-terminal fusion of a sequence derived from cytoplasmic domain 4 of the SecY protein shortened the half-life of the alpha fragment to less than 1 min. In contrast, an amino-terminal sequence from the NusG protein had no apparent effect on the stability of the fragment. In a fusion protein in which the intact SecY protein was fused to the alpha fragment, stabilization of the SecY part by overproduction of the partner SecE protein resulted in an increased alpha complementation activity of beta-galactosidase. These results indicate that stability of alpha fragment can be dictated by the stability of the fused protein. The alpha fragment of beta-galactosidase, which is unique in that it is largely unstructured but can be "active" in alpha complementation, may be used as an in vivo indicator of stability of proteins attached to it.

Amino Acid Sequence↗

PubMed1995

Posterior migration of cervical spinal cord between split laminae as a complication of laminoplasty.

STUDY DESIGN: This is a case report. OBJECTIVE: To focus attention on a possible neurologic complication of laminoplasty. SUMMARY OF BACKGROUND DATA: An iatrogenic spinal cord lesion developed after laminoplasty as an operative complication of unknown cause. METHODS: Two patients had iatrogenic damage to the spinal cord from an unknown cause after laminoplasty of the cervical spine, but recovered soon after an additional laminectomy. They were evaluated with regard to the mechanism of damage and prevention. RESULTS: The spinal cord damage occurred when the spinal cord migrated posteriorly and deformed between the split laminae at the apex of the lordosis, where the maximum posterior displacement of the spinal cord was achieved. CONCLUSION: This damage was caused by a relatively narrower canal resulting from the split laminae of the apex of the adjacent laminae.

Aged↗

PubMed1995

Endothelin receptor subtype B mediates autoinduction of endothelin-1 in rat mesangial cells.

Autoinduction of endothelin-1 (ET-1) has been suggested to be involved in the profound and long-lasting effects of ET-1. We examined mechanisms that underlie autoinduction of ET-1 in cultured rat glomerular mesangial cells. Incubation of mesangial cells with ET-1 resulted in an immediate and dose-dependent stimulation of preproET-1 mRNA expression as assessed by polymerase chain reaction coupled with reverse transcription. Within 1 h of exposure to ET-1 (10(-7) M), preproET-1 mRNA expression was increased to a maximal level of 465 +/- 43% of the control value (p < 0.01), which was accompanied by significant stimulation of production of the immunoreactive ET-1 peptide. Nuclear run-off analysis revealed increases in the transcriptional rate of preproET-1 mRNA to 239 and 175% above the control values at 1 and 3 h of ET-1 stimulation, respectively. ET-1 also increased the stability of preproET-1 mRNA, resulting in an mRNA half-life of 60 min from 20 min seen in non-stimulated cells. Addition of an ETB-specific antagonist, RES701-1, at > 10(-9) M abolished ET-1 stimulation of preproET-1 mRNA (p < 0.001), whereas an ETA-specific antagonist, BQ123, was without effects (up to 10(-5) M). The ETB agonist, sarafotoxin S6c (10(-7) M), significantly stimulated preproET-1 mRNA expression to 201 +/- 14% above controls (p < 0.01), and effect that was lessened significantly by RES701-1 (p < 0.05). RES701-1 abolished the ET-1-induced production of the ET-1 peptide (p < 0.001). Taken together, we demonstrates that in mesangial cells, autoinduction of ET-1 occurs through the ETB receptor subtype via increases in both preproET-1 transcription and mRNA stability.

Animals↗

PubMed1995

Nitric oxide and endothelin in pathophysiological settings.

The role of the endothelium is now known to encompass the generation of many potent cytokines which impact endothelial cells, adjacent tissue such as smooth muscle cells, and distant sites in an autocrine, paracrine, and endocrine manner, respectively. This review addresses two of these cytokines, nitric oxide and endothelin, and describes how each effects the functions of endothelial cells, including regulation of platelet aggregation and coagulation, regulation of vasomotor tone, modulation of inflammation, and the regulation of cellular proliferation. The emphasis is on the increasingly recognized importance of the autocrine and paracrine mechanisms by which nitric oxide and endothelin act. In particular, autoinduction of endothelin is proposed as a central mechanism underlying endothelin's renowned effects. Additionally, specific nitric oxide/endothelin interactions are discussed by which each cytokine modulates the production and actions of the other. The net effect observed in a variety of physiological and pathophysiological settings, therefore, reflects a balance of these opposing functions.

Cell Division↗

PubMed1995

Role of cytochrome P-450 epoxygenase metabolites in EGF signaling in renal proximal tubule.

Epidermal growth factor (EGF) is a potent epithelial cell mitogen and induces eicosanoid production in many cell types. The present study examined signaling mechanisms for EGF in the renal proximal tubule, where high concentrations of cytochrome P-450 epoxygenase have been reported. In primary cultures of rabbit proximal tubule cells, EGF (30 nM) increased endogenous epoxyeicosatrienoic acid (EET) levels 5.3 +/- 1.4-fold within 10 min (n = 6). In these cells EGF-stimulated [3H]thymidine incorporation was significantly inhibited by the cytochrome P-450 inhibitors ketoconazole or clotrimazole but not by the cyclooxygenase inhibitor indomethacin. In fura 2-loaded proximal tubule cells, EGF caused a concentration-dependent increase in cytosolic Ca2+ concentration ([Ca2+]i), due to Ca2+ influx, which was inhibited by either ketoconazole or SKF-525A but not by indomethacin. Addition of 5,6-EET (0.5 microM) also induced Ca2+ influx in proximal tubule cells, whereas 8,9-11,12-, or 14,15-EET did not. In cells treated with bis(2-amino-5-methylphenoxy)ethane N,N,N',N'-tetraacetic acid tetraacetoxy-methyl ester to chelate [Ca2+]i, EGF-stimulated [3H]thymidine incorporation. These results indicate that EGF increases EET levels in proximal tubule and suggest that 5,6-EET or its metabolites may be a modulator of EGF-induced [Ca2+]i increases and involved in mitogenesis.

8,11,14-Eicosatrienoic Acid↗

PubMed1995

Modulation of muscle protein metabolism in disseminated intravascular coagulation.

Muscle protein degradation and intracellular protease activities were investigated in disseminated intravascular coagulation (DIC), which is frequently associated with severe catabolic states such as sepsis and multiple organ failure. DIC was introduced in rats by repeated intravenous thrombin injections. Saline was injected in control rats. In the 28 rats (14 with DIC and 14 controls), the bilateral soleus (SOL) muscles were incubated in an oxygenated medium without cycloheximide (CH) to determine the release of tyrosine (Tyr) into the incubated medium. From 24 rats (12 with DIC and 12 controls), the SOL and extensor digitorum longus (EDL) muscles were harvested to measure the activities of proteasome and of cathepsins L and B. The contralateral muscles were incubated in a medium with 0.5 mM CH to determine the release of Tyr and 3-methylhistidine (3-MH). The release of Tyr without CH (net proteolysis) from SOL muscles with DIC was greater than in controls (218 +/- 83.3 vs. 145 +/- 47.7 pmol/mg/h. However, the release of Tyr and 3-MH with CH (total proteolysis) and the activities of proteasome and cathepsins in DIC were nearly the same as those in controls. In both DIC and control rats, the total release of Tyr and proteasome activity were greater in SOL than in EDL muscles. These results suggest that reutilization of Tyr, reflecting protein synthesis, is suppressed in DIC and that the red slow muscle is more active in nonfibrillar proteolysis than the white fast muscle.

Animals↗

PubMed1995

Induction of heparin-binding epidermal growth factor-like growth factor mRNA in rat kidney after acute injury.

Previous studies have suggested that EGF or other members of the EGF family of mitogenic proteins are involved in proliferation of renal tubular epithelial cells occurring during recovery from injury to the kidney. The present studies examined whether expression of mRNA for the recently identified heparin-binding EGF-like growth factor (HB-EGF) is regulated in response to renal injury induced by either ischemia/reperfusion or mercuric chloride. Increased expression of HB-EGF mRNA was demonstrated in the post-ischemic kidney within 45 min of unilateral ischemia/reperfusion in the rat. Induction of HB-EGF mRNA occurred only when ischemia was followed by reperfusion, and was not eliminated by removal of blood cells from the post-ischemic kidney by saline perfusion. In situ hybridization with 35S-labeled antisense riboprobes of HB-EGF indicated that compared with control, there was increased HB-EGF mRNA expression in the 6 h post-ischemic kidney in the inner cortex and outer medulla in a patchy distribution, with the greatest expression in the inner stripe of the outer medulla. Expression occurred primarily in tubular epithelial cells. Recombinant human HB-EGF stimulated [3H]-thymidine incorporation in both primary cultures of rabbit proximal tubule cells and NRK 52E normal rat kidney epithelial cells, with potency similar to that of EGF. Induction of HB-EGF mRNA was observed in tubules freshly isolated from rat renal cortex or outer medulla when the tubules were subjected to reoxygenation after incubation in anoxic conditions. The nephrotoxin, mercuric chloride, also caused induction of HB-EGF mRNA both in vivo and in isolated rat cortical tubules. The anoxia/reoxygenation-induced expression of HB-EGF mRNA in isolated tubules was inhibited by the free radical scavengers, di- and tetra-methylthiourea, indicating involvement of reactive oxygen species. These findings indicate that HB-EGF mRNA is inducible in the kidney in vivo by acute tubular injury and suggest that HB-EGF may act as an autocrine/paracrine growth factor involved in proliferation of tubular epithelial cells and repair of the kidney.

Animals↗

PubMed1994

Effects of leukocyte and platelet depletion on ischemia--reperfusion injury to dog pancreas.

BACKGROUND/AIMS: Ischemia-reperfusion injury has been studied in various organs. Effects of leukocyte and platelet depletion on ischemia-reperfusion injury were evaluated using the isolated, perfused dog pancreas in vivo. METHODS: Pancreatic exocrine and endocrine functions were stimulated by an intra-arterial injection of cholecystokinin (10(-12) mol) and intravenous injection of glucose and arginine (1 g/kg body wt), respectively. The functions before and after 60 minutes of ischemia were evaluated in the no treatment and in the leukocyte and platelet depletion groups. RESULTS: Cholecystokinin increased prostaglandin I2 and thromboxane A2 production and stimulated exocrine pancreatic secretion. Glucose and arginine stimulated insulin and glucagon release from the pancreas. Sixty minutes of ischemia followed by 60 minutes of reperfusion damaged the pancreatic acinar and ductular cells. Ischemia of 60 minutes followed by 90 minutes of reperfusion damaged beta cells. Removal of leukocytes (97.6%) and platelets (99.4%) by using a filter throughout the experiment prevented the ischemia-reperfusion injury, reduced plasma lipid peroxide and thromboxane A2, and increased prostaglandin I2 levels. CONCLUSIONS: Leukocytes and platelets seem to damage the pancreas during ischemia-reperfusion by increasing the peroxidation of structurally important cell membrane lipids and reduced the thromboxane A2 prostaglandin I2 ratio, a predictor of cellular injury.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

Nutrient-induced thermogenesis (NIT) following amino acid infusion.

Nutrient-induced thermogenesis (NIT) induced by parenteral infusion of amino acid (AA) mixtures of different composition and of the same AA mixtures given via different routes (parenteral or intraportal infusion) were investigated in rats using a small animal indirect calorimeter. When 8 different AA solutions of differing composition but with the same total concentration were infused parenterally, both standard NIT (each AA is assumed to generate 3.28 kcal/g) and specific NIT (heat energy of each AA is calculated assuming that it is oxidized to carbon dioxide and water, and metabolised to urea and sulphuric acid) values of the leucine (Leu)-rich and the glycine (Gly)-rich solutions were significantly greater than those of the control solution. Removal of Leu or Gly from the respective AA solutions reversed the increase of both NIT values down to control levels. When the parenteral and portal infusion routes were used in one rat, both NIT values for parenteral infusion of the Leu-rich solution were again significantly greater than those of the control. Likewise, both NIT values for intrportal infusion of the Leu-rich solution were also significantly greater than those of the control. However, no difference in NIT values was found between parenteral and portal infusion of either solution. The result of this study indicated that Leu and Gly may be thermogenic AAs, and the thermogenic effect of Leu is not dependent upon the route of infusion.

Journal Article↗

PubMed1994

Comparative study of CA242 and CA19-9 for the diagnosis of pancreatic cancer.

A comparative study of a new tumour marker, CA242, and CA19-9 was conducted with special reference to their diagnostic usefulness in pancreatic cancer. CA242 showed sensitivity similar to that of CA19-9 for overall cases and early cases (stage I tumour) of pancreatic cancer. For other malignancies, the positive rates of CA242 were lower than those of CA19-9 except for colorectal cancer. An important characteristics of CA242 was that it was only slightly and infrequently elevated in the sera of patients with benign diseases such as chronic pancreatitis, chronic hepatitis and liver cirrhosis. This characteristic was more apparent in the patients with benign obstructive jaundice, indicating that the serum level of this marker was scarcely affected by cholestasis. Using cut-off levels corresponding to a 90% specificity, the clinical results obtained with CA242 in the diagnosis of pancreatic cancer were similar to those obtained with CA19-9, except that CA19-9 was falsely negative in some patients with early-stage pancreatic cancer. These findings suggest the usefulness of this marker for screening pancreatic cancer in patients on their first hospital visit. However, CA242 was found to be influenced by the Lewis blood group system. This unfavourable result is attributed to the C241 catcher antibody of this assay system, which has almost the same epitope specificity as the C50 and the NS19-9 monoclonal antibodies. In conclusion, CA242 is superior to CA19-9 in diagnosing pancreatic cancer by virtue of its higher specificity.

Antigens, Tumor-Associated, Carbohydrate↗

PubMed1994

Oxidants induce transcriptional activation of manganese superoxide dismutase in glomerular cells.

Cultured rat glomerular mesangial and epithelial cells and bovine glomerular endothelial cells were exposed to various concentrations of hydrogen peroxide (H2O2). Mesangial cells treated with 10 to 100 microM H2O2 for 24 hours showed a two- to ninefold increase in Mn-SOD mRNA expression associated with significantly (P < 0.005) increased Mn-SOD activity (22.2 +/- 1.2 and 12.2 +/- 0.7 mu/mg protein for H2O2 100 microM treated and untreated cells, respectively). In contrast, expression of Cu-Zn SOD and beta-actin mRNA was not affected by H2O2. Induction of Mn-SOD mRNA by H2O2 was inhibited by actinomycin-D (4 microM) treatment. Glomerular endothelial cells also showed an increase in Mn-SOD mRNA expression following 100 microM H2O2 treatment, as did glomerular epithelial cells following treatment with 500 and 1000 microM H2O2 but not with 100 microM. Transcriptional activity of the Mn-SOD gene was assessed with a fusion reporter gene consisting of a luciferase gene (pGL2P) and a 1.2 kb fragment from the rat Mn-SOD genomic DNA (-806 to +408 bp of the transcription initiation site, -806:+408). The construct was transfected into rat glomerular mesangial and epithelial cells. Mesangial and epithelial cells transfected with pGL2P (-806:+408) and treated with H2O2 (100 microM and 1 mM for mesangial and epithelial cells, respectively) demonstrated some threefold increase in luciferase activity, whereas cells transfected with pGL2P lacking the Mn-SOD fragment did not show changes in luciferase activity following H2O2 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Site specific regulation in the kidney of endothelin and its receptor subtypes by cyclosporine.

Endothelin (Et) has been suggested by us and others to play a role in glomerular dysfunction that characterizes cyclosporine (Cs)-associated nephrotoxicity. Since Et exerts its actions through at least two receptor subtypes, and because these receptor subtypes have particular distributions in the renal parenchyma, we investigated changes in mRNA expression for Et and its receptor subtypes in glomeruli and medulla of rats treated with Cs. Polymerase chain reaction coupled with reverse transcription (RT-PCR) method was used to assess prepro-Et-1, type A (EtA) and type B (EtB) receptor mRNA at 1, 3, 6, and 24 hours after Cs (20 mg/kg body wt i.v.). Results were normalized to the expression of beta-actin as an internal standard. Compared with control rats, glomerular mRNA expression for prepro-Et-1 was not affected by Cs. Similarly, Cs did not significantly change the glomerular mRNA expression of either EtA or EtB receptor subtypes. By contrast, in the medulla there was a marked and persistent increase in the expression for prepro-Et-1 and the EtB receptor subtype: prepro-Et-1 at 1, 3, 6, and 24 hours was 336 +/- 61, 295 +/- 65, 339 +/- 73, 440 +/- 123% of controls, respectively (P < 0.05 compared with controls at each time point). The EtB receptor mRNA at 1, 3, 6, 24 hours was 164 +/- 22, 157 +/- 15, 148 +/- 14, 116 +/- 18% (compared with controls, P < 0.01 at 3 hr and P < 0.05 at 1 and 6 hr), while the mRNA expression for EtA was not affected by Cs treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Spinal cord potential recordings from the extradural space during scoliosis surgery.

For monitoring spinal cord functions during corrective surgery of scoliosis, we have recorded percutaneously from the posterior extradural space at the C5-7 levels the ascending conducted spinal cord potentials (ASCP) in response to extradural stimulation of the cauda equina in 134 patients. The ASCP consists of three spike-like components (C1, C2 and C3) followed by slow components. The extradurally recorded ASCP were not affected by anaesthetic agents. There were no significant differential effects of spinal distractions on each of the three spike potentials. There were no post-operative neurological abnormalities in patients whose ASCP showed no changes, amplitude increases, amplitude decreases of less than 50% or latency increases (> 0.2 ms) during spinal manipulations (no false negatives, but some false positives). Five patients who suffered postoperative neurological damage exhibited more than 50% changes in amplitude of the ASCP during surgery. All these neurological sequelae occurred in the first 80 patients. In the last 54 patients, in whom the distraction forces on the spine were controlled rapidly by observation of the amplitude changes in ASCP, there were no postoperative neurological abnormalities, except for one patient in whom an accidental spinal cord injury was produced by a hook. The results suggest that the distraction force on the spine must be reduced immediately when the amplitudes of the ASCP decrease by more than 50% of control values with or without latency increases.

Adolescent↗

PubMed1994

Prostaglandin E1 protects dog pancreas from ischemia-reperfusion injury.

Effects of prostaglandin (PG) E1 on ischemia-reperfusion (I-R) injury to the pancreas was evaluated using isolated in vivo perfused dog pancreas. Pancreatic endocrine and exocrine functions were stimulated with 10(-12) M cholecystokinin octapeptide (CCK-8). This amount of CCK-8 promoted production of insulin, glucagon, PGI2, and thromboxane (Tx) A2 in the pancreas. Sixty minutes of ischemia and subsequent reperfusion induced damage to pancreatic ductular, acinar, and beta cells. Intra-arterial administration of PGE1 at a dose of 0.5 microgram/kg/min throughout the experiment prevented the I-R injury, reducing plasma lipid peroxides, and elevating PGI2 without changing TxA2 in the pancreas. PGE1 thus appears to protect pancreatic function from I-R injury both by depressing the effect of free-radicals and by decreasing TxA2/PGI2 which predicts cell injury.

6-Ketoprostaglandin F1 alpha↗