Biomedical subjects

K Kawamura

Publications and source records attributed to K Kawamura.

At least 19 recordsLinked to original sources

PubMed1997

Early detection of successful coronary reperfusion based on serum concentration of human heart-type cytoplasmic fatty acid-binding protein.

Both human heart-type cytoplasmic fatty acid-binding protein (H-FABPc) and myoglobin are low molecular weight proteins that are abundant in the cytoplasm of myocardial cells. Unlike myoglobin, H-FABPc content in the skeletal muscle is less than in cardiac muscle. To investigate the usefulness of the serum concentration of H-FABPc in the early detection of successful coronary reperfusion, we measured serum concentrations of H-FABPc and myoglobin in 45 patients with acute myocardial infarction treated with intracoronary thrombolysis or direct percutaneous transluminal coronary angioplasty. Coronary angiography was performed every 5 min for reperfusion therapy to identify the onset of reperfusion. Reperfusion, defined as a TIMI grade 2 or 3, was achieved within 60 min of the initiation of reperfusion therapy in 30 patients (the reperfused group), but was not achieved in 15 patients (the non-reperfused group). Blood samples were obtained before initiation of treatment and 15, 30 and 60 min after initiation of treatment in the non-reperfused group. In the reperfused group, samples were obtained before reperfusion and 15, 30 and 60 min after reperfusion. The H-FABPc ratio (the ratio of value after to value before the initiation of treatment or reperfusion) increased sharply after the onset of reperfusion, peaking at 41 +/- 18 min, and decreased rapidly thereafter. The predictive accuracy of an H-FABPc ratio of > 1.8 for the detection of reperfusion within 60 min of the initiation of treatment was 93% at 15 min after reperfusion, 98% at 30 min, and 100% at 60 min. Similar rates of predictive accuracy were observed for a myoglobin ratio > 2.4. The H-FABPc ratio detected successful reperfusion as early as 15 min after the onset of reperfusion and was highly accurate in detecting reperfusion within 60 min of the onset of reperfusion. The predictive accuracy of the H-FABPc ratio was similar to that of the myoglobin ratio for the early detection of successful coronary reperfusion.

Adult↗

PubMed1997

Immunohistochemical localization of neurocan and L1 in the formation of thalamocortical pathway of developing rats.

We used immunohistochemistry to examine possible molecular interactions between the subplate and growing thalamocortical axons in rat fetuses. In the cortical anlage of embryonic day 16 (E16), the subplate first appeared below the cortical plate. Among chondroitin sulfate proteoglycans, phosphacan was uniformly distributed throughout the cortical wall, whereas neurocan was localized only in the subplate at E16. Neural cell adhesion molecules, NCAM-H, TAG-1, and L1, were detected in the cortical anlage. Both cortical neurons and growing axons were diffusely immunopositive for NCAM-H, and TAG-1 immunoreactivity was found on immature neurons and cortical efferent axons but not on thalamocortical axons. L1 immunoreactivity was specifically localized on the growing thalamocortical axons. When the locations of neurocan and L1 were compared in the developing cortex, L1-bearing axons were found to extend to neurocan-immunopositive regions; neurocan immunoreactivity was intense in the subplate at E16, when small numbers of L1-immunoreactive thalamocortical axons began to invade the cortex. At E17, many L1-positive axons were observed in the subplate that expressed neurocan specifically. Double immunostaining showed that L1-positive axons and neurocan immunoreactivity overlapped in the subplate at E17. After E18, neurocan expression gradually extended to the lower part of the cortical plate; it extended to the entire cortex by E21, 1 day before birth. By E21, L1-bearing axons had invaded the lower part of the cortical plate. The present study demonstrated that the neurocan expression precedes growth of L1-bearing thalamocortical afferent fibers. Because neurocan can bind to L1 molecule in vitro, these results suggest that neurocan and L1 play some important roles in pathfinding of the thalamocortical afferent fibers during rat corticogenesis.

Animals↗

PubMed1997

Thrombopoietin enhances proliferation and differentiation of murine yolk sac erythroid progenitors.

Thrombopoietin (TPO), the ligand for the receptor proto-oncogene c-Mpl, has been cloned and shown to be the critical regulator of proliferation and differentiation of megakaryocytic lineage. Initially, TPO was not considered to have the activity on hematopoietic lineages other than megakaryocytes. Recently, however, TPO was reported to enhance the in vitro erythroid colony formation from human bone marrow (BM) CD34+ progenitors or from mouse BM cells in combination with other cytokines. We examined the effects of TPO on the colony formation of hematopoietic progenitors in mouse yolk sac. TPO remarkably enhanced proliferation and differentiation of erythroid-lineage cells in the presence of erythropoietin (Epo). This effect was observed even in the absence of Epo. Compared with adult BM, yolk sac turned out to have relatively abundant erythroid and erythro-megakaryocytic progenitors, which responded to TPO and Epo stimulation. TPO similarly stimulated erythroid colony formation from in vitro differentiation-induced mouse embryonic stem (ES) cells whose hematopoietic differentiation status was similar to that of yolk sac. These findings help to understand the biology of hematopoietic progenitors of the early phase of hematopoiesis. Yolk sac cells or in vitro differentiation-induced ES cells would be good sources to analyze the TPO function on erythropoiesis.

Animals↗

PubMed1997

Is CD36 deficiency an etiology of hereditary hypertrophic cardiomyopathy?

Hereditary hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease, but the genetic defects are still unclear in many cases. Reduced myocardial long-chain fatty acid (LCFA) uptake has been demonstrated in patients with some types of HCM. In addition, a possible relationship between a shift ofmyocardial substrate utilization and cardiac hypertrophy has been suggested by experimental studies. Myocardial uptake of LCFAs occurs via a specific transporter, which is homologous with human CD36. CD36 deficiency has also been reported in some individuals, and is transmitted as an autosomal dominant trait like HCM. In this study, we analyzed CD36 in 47 patients with HCM [29 with asymmetric septal hypertrophy (ASH) and 18 without ASH], 11 patients with dilated cardiomyopathy (DCM), and 26 patients with pressure-overload cardiac hypertrophy. Eleven patients (37.9%) who had HCM with ASH, one (9.1%) with DCM, and two (7.7%) with pressure-overload hypertrophy showed CD36 deficiency, while none of the HCM patients without ASH had CD36 deficiency. One patient who had HCM with ASH and CD36 deficiency showed no myocardial LCFA uptake, although myocardial perfusion was normal. Reduced myocardial LCFA uptake despite normal myocardial perfusion was demonstrated in the other HCM patients with ASH and CD36 deficiency. Based on the high prevalence of CD36 deficiency in HCM patients with ASH, we hypothesize that this deficiency might be one etiology of hereditary HCM.

Adult↗

PubMed1997

Iodine-123 metaiodobenzylguanidine myocardial scintigraphy for prediction of response to beta-blocker therapy in patients with dilated cardiomyopathy.

This study was performed to evaluate whether iodine-123 metaiodobenzylguanidine (MIBG) myocardial scintigraphy could predict the response to beta-blocker therapy in patients with nonischemic dilated cardiomyopathy (DCM). Beta-Blocker therapy is effective in some patients with DCM. MIBG myocardial scintigraphy has also been suggested to be useful in evaluating the severity of myocardial damage in DCM. However, no data exist on whether MIBG imaging can be used to predict which patients with DCM will respond to beta-blocker therapy. We prospectively evaluated whether MIBG myocardial imaging was useful in predicting responses to beta-blocker therapy in patients with DCM. MIBG imaging was performed in 45 patients with DCM (35 men, 10 women, aged 13 to 68 years) before the start of bisoprolol. The heart to mediastinum (H/M) MIBG uptake ratio was evaluated on initial and delayed images, and the percent washout rate of myocardial MIBG was also obtained from these data. Of the 45 patients, 30 (67%) responded to beta-blocker therapy, whereas 2 were resistant and 13 showed progression of heart failure or died of heart failure. By logistic regression analysis, the H/M uptake ratio on delayed images was seen to be a good predictor of the response to beta-blocker therapy with a threshold of 1.7 (sensitivity = 91%, specificity = 92%, accuracy = 91%, positive and negative predictive value = 97% and 80%, respectively). These results indicate that an H/M ratio > 1.7 on the delayed MIBG myocardial scintigraphic images provides a useful indication of whether patients with DCM will respond to beta-blocker therapy.

3-Iodobenzylguanidine↗

PubMed1997

Do repolarization abnormalities in hypertrophic cardiomyopathy represent impaired fatty acid utilization? An observation with QRST isointegral maps.

To identify the clinical significance of the isointegral body surface map of the QRST interval (QRST map) and the occurrence of repolarization abnormalities in patients with hypertrophic cardiomyopathy (HCM), the QRST map and signal-averaged electrocardiogram were evaluated in 50 patients with HCM, in 33 of whom the results were compared with nuclear images both for radioiodine-labeled fatty acid metabolism and for radiothallium perfusion. The QRST departure map was used to determine two parameters of difference between patient and control recordings: the subnormal area (the number of lead points at which the departure index values were negative and lay more than 2 SDs from the mean of the normal control group) and the subnormal minimum (the absolute value of the minimum in the departure map). Late potentials were detected in 6 (12%) of the 50 patients; they were observed in 3 of the 5 patients with dilated-phase HCM but in only 3 (7%) of the other 45 patients. The subnormal area and minimum values were lower in nonobstructive HCM than in dilated-phase HCM. Of the 33 patients examined by myocardial imaging, 28 (33%) had a filling defect or decreased uptake, as shown on fatty acid metabolic images, and 10 of the 28 also showed abnormal myocardial perfusion images, while the 18 others showed normal perfusion images. These 28 patients showed significantly larger values of the subnormal area and minimum than patients with normal results in both image tests, regardless of whether or not myocardial perfusion imaging abnormalities were present. The localization of filling defects or of decreased uptake presented in fatty acid metabolic images corresponded to the position of the minimum on the QRST departure map. These results suggest that the QRST map is useful for detection of repolarization abnormalities in HCM and that these abnormalities are highly related to impaired fatty acid utilization of the myocardium.

Adolescent↗

PubMed1997

Impaired expression of neural cell adhesion molecule L1 in the extrinsic nerve fibers in Hirschsprung's disease.

Immunohistochemical studies on the ganglionic and aganglionic segment in Hirschsprung's disease (HD) were carried out using antibodies against three neural membrane proteins, Thy-1, integrin alpha5, and L1. Enteric neural elements were immunostained with antibodies against neurofilament, which is the neuronal cytoskeletal protein. In ganglionic segments, neurofilament-immunoreactivity was detected in neuronal cell bodies and fine nerve fibers of the myenteric and submucosal plexuses. All of these neural elements were immunopositive for Thy-1, integrin alpha5, and L1. In aganglionic segments, no intrinsic neurons were detected, and instead, hypertrophied nerve bundles were observed in intermuscular space, in submucosa, and in circular muscle layer by immunochemistry for neurofilament. These hypertrophied nerve bundles were immunopositive with anti-Thy-1 and anti-integrin alpha5 antibodies. However, they were not immunostained with anti-L1 in all five cases. These findings indicate that the expression of L1 molecule, which plays an important role in cell adhesion, neural cell migration, and neurite outgrowth, is impaired in the extrinsic nerve fibers in aganglionic colon. And this may perturb neural crest migration and adequate neurite outgrowth, with resulting aganglionic segment and abnormal nerve bundles of extrinsic fibers in HD.

Antigens, CD↗

PubMed1997

Left ventricular Doppler filling pattern in dilated cardiomyopathy: relation to hemodynamics and left atrial function.

This study attempted to examine the relation of left ventricular filling patterns to hemodynamic status and left atrial function in dilated cardiomyopathy. Transesophageal echocardiography and cardiac catheterization were performed in 41 patients with dilated cardiomyopathy (six with an ischemic origin). Transmitral, left atrial appendage, and pulmonary venous flow velocities were recorded with the pulsed Doppler method. Left atrial systolic function was assessed by the peak velocity of the left atrial appendage emptying wave and pulmonary venous flow reversal during atrial systole. Patients were classified into three groups according to their left ventricular filling patterns. Group 1 showed an abnormal relaxation pattern (E wave/A wave ratio <1, n = 17), group 2 had a normal or pseudonormal pattern (1 < or = E/A < 2, n = 11), and group 3 had a restrictive pattern (E/A > or = 2, n = 13). No differences were found among the groups with regard to age, gender, heart rate, and M-mode echocardiographic indices of left ventricular function. Compared with patients in group 1, those in groups 2 and 3 had more symptoms (New York Heart Association functional class III or IV) and had higher left ventricular filling pressures. The sensitivity of an E/A ratio > or = 1 for predicting a pulmonary capillary wedge pressure > or = 15 mm Hg was 75% and the specificity was 94%. Despite a similar increase of filling pressures, group 3 patients had a lower left atrial appendage emptying velocity, pulmonary venous flow reversal velocity, and mitral A velocity than did group 2 patients. The sensitivity and specificity of an E/A ratio > or = 22 for detecting left atrial dysfunction (left atrial appendage emptying velocity < or = 40 cm/sec) was 85% and 86%, respectively. In conclusion, among patients with dilated cardiomyopathy, those who had a restrictive or pseudonormal filling pattern were in a higher functional class and had higher filling pressures. Further studies are needed to determine the therapeutic and prognostic significance of left atrial dysfunction, which was common in patients with a restrictive pattern.

Adult↗

PubMed1997

Unusual polyp-like structures in lobular panniculitis of a patient with Behçet's disease.

Unusual histopathologic structures were observed in lobular panniculitis of a patient with Behçet's disease. These were polyp-like in shape and protruded into cavities made of lysed fat cells. Various stages of development were observed. To determine the origin of cells making up these structures, we applied various histochemical and immunohistochemical techniques and found the cells to be histiocytes (macrophages) engaged in phagocytizing degenerated fat cells and cell membranes which had formed into membranocystic lesions.

Adipose Tissue↗

PubMed1997

Renal angiosarcoma: a case report.

We report the first case of angiosarcoma in the kidney occurring in a woman; the tumor was initially believed to be renal cell carcinoma. This malignant tumor was discovered in a patient with macrohematuria. The final diagnosis was confirmed by histologic and immunohistochemical findings. A review of the literature on this tumor is also included in the discussion.

Angiography↗

PubMed1997

Involvement of glucocorticoid-induced factor(s) in the stimulation of growth hormone expression in the fetal rat pituitary gland in vitro.

The mechanism by which glucocorticoids induce GH expression between embryonic days 18 and 19 (E18-19) in the fetal rat pituitary gland was examined with an in vitro organ culture system. Twenty-four hour incubation of E18 pituitary glands in serum-free medium containing either dexamethasone (DEX, 5-50 nM) or corticosterone (0.55 microM) resulted in a conspicuous accumulation of GH messenger RNA (mRNA), whereas no spontaneous expression of GH mRNA was noted without glucocorticoid. Triiodothyronine (1 nM) alone weakly induced GH mRNA but increased the effect of DEX 2-fold. The GH mRNA accumulation was not observed after 5 or 10 h incubation with DEX. However, a 10-h incubation with DEX followed by 14 h chase incubation without DEX resulted in apparent induction of GH mRNA. The induction of GH mRNA by DEX was completely inhibited by puromycin. These data, taken as a whole, suggest that the induction of GH mRNA by DEX in the fetal pituitary gland is not a direct effect of DEX on the GH gene but is mediated by a factor that is synthesized in the pituitary gland in response to DEX. Both immunoblot and RNase protection assays suggested that this factor is not pit-1, which is known to be required for GH mRNA expression.

Animals↗

PubMed1997

Comparison of immediate and long-term outcome of percutaneous transvenous mitral commissurotomy in patients who have and have not undergone previous surgical commissurotomy.

This study compared the immediate and long-term outcome of percutaneous transvenous mitral commissurotomy (PTMC) in patients who had (restenosis group, n = 9) or had not (de novo group, n = 27) previously undergone surgical mitral commissurotomy. The baseline echocardiographic score, which is an index of deformity of the mitral valve apparatus, was significantly higher in the restenosis group than in the de novo group (11 +/- 3 vs 7 +/- 2, p < 0.01), although age, left atrial diameter, and the prevalence of atrial fibrillation were similar. PTMC was performed by the Inoue technique, and was abandoned in 1 patient from the restenosis group because of failed trans-septal puncture. Including this patient, 3 patients (33%) in the restenosis group had a thickened atrial septum compared with only 1 (4%) in the de novo group. One patient in the de novo group developed cardiac tamponade during this procedure. In both groups, the mitral valve area increased significantly, but the success rate of PTMC was lower in the restenosis group (4/9 patients, 44%) than in the de novo group (22/27 patients, 81%) (p < 0.05). Twenty-six patients who had successful PTMC were followed up over 51 +/- 14 months. After 4 years of follow-up. 3 out of 4 patients (75%) in the restenosis group and 3 out of 22 patients (14%) in the de novo group demonstrated echocardiographic restenosis (p < 0.01). Stepwise multivariate analysis revealed that the echocardiographic score was the only significant predictor of both the immediate and long-term outcome. In conclusion, the immediate and long-term outcome of PTMC were worse in patients who had undergone previous surgical mitral commissurotomy than in those who had not. This was mainly attributable to the difference in the severity of the valvular lesions. In addition, our data suggested that a thickened atrial septum, possibly related to surgery as well as chronic rheumatic disease, may affect the performance of PTMC.

Adult↗

PubMed1997

Determining the optimum dose for the intravenous administration of nicardipine in the treatment of acute heart failure--a multicenter study. The Nicardipine Heart Failure Study Group.

Nicardipine is a potent arteriolar vasodilator with a negligible negative inotropic effect. Although intravenous administration of this drug has been reported to be effective in the treatment of heart failure, the optimal dose by this route is not clear. This study was designed to determine the optimum dose for the intravenous infusion of nicardipine in the treatment of heart failure. In Trial 1, nicardipine was administered intravenously at a dose of 0.5 microgram/kg per min to 14 patients with acute heart failure. The dose was increased to 1.0 microgram/kg per min in 13 cases with marked improvement at 2 h. In Trial 2, nicardipine was administered in a double-blind manner to 53 patients at 3 different rates of infusion for 2 h: 1.0 (Group 1, n = 19), 2.0 (Group 2, n = 15), and 3.0 (Group 3, n = 19) micrograms/kg per min. Neither heart rate nor mean right atrial pressure changed in any of the 3 groups. Favorable hemodynamic effects were evident in all groups beginning 30 min after the start of infusion, with an increase in cardiac index (control vs 2 h after infusion, L/min per m2) (Group 1: 2.2 +/- 0.4 vs 3.1 +/- 0.8, Group 2: 2.2 +/- 0.4 vs 2.9 +/- 0.5, Group 3: 2.3 +/- 0.3 vs 3.1 +/- 0.7, all p < 0.01 compared to the control) and a decrease in diastolic pulmonary artery pressure (Group 1: 26 +/- 10 vs 19 +/- 7, Group 2: 27 +/- 10 vs 20 +/- 8, Group 3: 26 +/- 7 vs 18 +/- 5 mmHg, all p < 0.01). The decrease in systolic pressure was greatest in Group 3 (Group 1: 141 +/- 31 vs 119 +/- 18, Group 2: 149 +/- 25 vs 118 +/- 17, Group 3; 147 +/- 27 vs 107 +/- 14 mmHg, all p < 0.01 compared to control, and p < 0.05 between Groups 1 and 3). The intravenous drip infusion of nicardipine is effective in the treatment of heart failure by inducing an increase in cardiac output and a decrease in pulmonary artery wedge pressure. The optimal dose in this study was 1.0 microgram/kg per min.

Acute Disease↗

PubMed1997

Studies on the novel antiallergic agent HSR-609: its penetration into the central nervous system in mice and guinea pigs and its selectivity for the histamine H1-receptor.

We studied the pharmacological characteristics of HSR-609 (3-[4-(8-fluoro-5,11-dihydrobenz[b]oxepino[4,3-b]pyridin-11- ylidene)- piperidino]propionic acid dihydrate), a novel amphoteric antiallergic agent, on the central nervous system (CNS). Its selectivity for the histamine H1-receptor and its ability to penetrate into the CNS were compared with those of typical antiallergic agents and the nonamphoteric basic compound PY-608 (8-fluoro-5,11-dihydro-11-(1-methyl-4-piperidylidene)benz[b]oxe pino- [4,3-b]pyridine), which has a chemical structure similar to that of HSR-609. In the in vitro study, HSR-609 had a high affinity for H1-receptors in the guinea pig cerebral cortex in comparison to affinities for muscarinic and serotonin 5-HT2-receptors in the rat cerebral cortex, while the selectivity of PY-608 for the H1-receptor was low. The inhibitory effects of these antiallergic agents on histamine-induced increase of vascular permeability in mice (ED50) were compared with the displacement of [3H]mepyramine binding to H1-receptors in mouse brain ex vivo (ID50). The ID50/ED50 ratio of HSR-609 was much larger than those of cyproheptadine, ketotifen and PY-608 and larger than those of terfenadine and cetirizine. HSR-609 was found to display selective displacement of the [3H]mepyramine binding to H1-receptors for lung vs cerebral cortex as found with terfenadine in guinea pigs ex vivo. These findings suggest that HSR-609 has high selectivity for the H1-receptor and poor ability to penetrate into the CNS in mice and guinea pigs due to its amphoteric chemical structure.

Administration, Oral↗

PubMed1997

Phorbol ester enhancement of IL-3-dependent proliferation of primitive hematopoietic progenitors of mice in culture.

Protein kinase C (PKC) is a Ca++- and phospholipid-dependent protein kinase activated by diacylglycerol that is either released from cell membranes in response to certain growth factors or mimicked by 12-O-tetradecanoyl phorbol-13-acetate (TPA). We studied the effects of TPA on interleukin-3 (IL-3)-dependent colony formation of mouse bone marrow cells from mice injected with 5-fluorouracil 2 days before examination in order to clarify the significance of PKC in the proliferation of primitive hematopoietic progenitors. Although TPA alone did not support colony formation, TPA in combination with IL-3 increased colony numbers from 1.5 to 2 times that formed with IL-3 and vehicle. TPA increased not only the granulocyte/macrophage colonies, but also the multilineage colonies. A sequential colony count showed that TPA, unlike IL-6, did not hasten the appearance of colonies. Because TPA enhanced IL-3-dependent colony formation derived from lineage-negative marrow cells obtained from mice that received 5-FU 2 days before, it is possible that it might act directly on primitive progenitors. Prolonged pretreatment of marrow cells with TPA prevented TPA-augmented colony growth. Calphostin C, a specific PKC inhibitor, and certain specific tyrosine kinase inhibitors, such as genistein and herbimycin A, abrogated the enhancing effects of TPA on IL-3-dependent colony formation. These data suggest that TPA had a direct effect on the primitive progenitors and enhanced IL-3-dependent colony formation via activation of PKC and certain tyrosine kinases.

Animals↗

PubMed1997

[Preservative effects of nitrous oxide on stored red cells].

While various additive solutions, containers and temperature have been shown to improve qualities of stored red cells, there are no reports on gas environment during blood storage. Nitrous oxide (N2O) showed a very high permeability through polyvinyl chloride membrane and high blood solubility. The whole blood with CPD was stored in N2 O (N2O-group) and compared with the control which was stored in air (Air-group). After storage (21 days at 5 degrees C and 35 days at 1 degree C), N2O-group showed significantly lower decreases of pH as well as significantly lower increases of Pco2 than Air-group. At both temperatures, glucose concentrations and ATP levels showed no differences between the two groups, but concentrations of lactate and 2, 3-DPG in N2O-group are significantly higher than those in Air-group. It is concluded that nitrous oxide gas environment can prevent decrease of pH by the suppression of increasing Pco2 in the stored blood due to high permeability and solubility into the cooled blood from ambient and can maintain functions of stored red cells, while neither oxidation toxicity nor antioxidation effects of N2O were demonstrated.

Adult↗

PubMed1997

Intracellular viral localization in murine coxsackievirus-B3 myocarditis. Ultrastructural study by electron microscopic in situ hybridization.

Group B Coxsackieviruses are a common cause of myocarditis. To detect the viral genome and its localization in the myocardium, we examined C3H/He mice with Coxsackievirus B3 (CVB3) myocarditis on days 5, 8, and 14 after inoculation by the reverse transcriptase polymerase chain reaction and by in situ hybridization. Sense and antisense CVB3 RNA were detected in the myocardium of all mice up to day 14 by reverse transcriptase polymerase chain reaction. Light microscopic in situ hybridization with a cDNA probe for CVB3 showed clusters of positive signals in the areas of myocardial necrosis and cell infiltration. With electron microscopic in situ hybridization, CVB3 RNA was detected in the cytoplasm of cardiocytes, between the myofibrils, near the mitochondria, and in tubular or vesicular structures. Viral RNA was also detected in necrotic debris, in the cytoplasm of macrophages, and in the cytoplasm of interstitial fibroblasts. These findings suggest that CVB3 RNA is replicated in the cytoplasm of cardiocytes, transferred into tubular or vesicular structures, released into the interstitium, and phagocytosed by macrophages. Some positive signals were also detected in the cytoplasm of cardiocytes showing close contact with infiltrating lymphocytes, suggesting that the lymphocytes recognized virus-infected cardiocytes and caused cell-mediated immune cardiocyte damage.

Animals↗

PubMed1997

Chromosome changes associated with growth potential of HTLV-I infected human lymphocytes.

The association between chromosomal changes and cellular growth potential was investigated in HTLV-I infected human lymphocytes. Cell lines studied include Coculture-5 (HTLV-I infected immortalized cells dependent of IL-2), Coculture-15 and -18 (semi-transformed Coculture-5 cells following cocultivation with transformed Coculture-5 cells), UV-5 (Coculture-5 cells transformed following UV irradiation), and MNNG-1 (Coculture-5 cells transformed following MNNG treatment). Immortalized cells were grown in IL-2 medium (IL-2+PHA+TPA), whereas semi-transformed and transformed cells were grown in RPMI medium. By G-band karyotyping, double band formation was seen in 3-33% of spreads at the centromeric region of chromosomes 1 and 7 to which structural abnormalities were found to cluster. The double band formation was also seen by FISH using alpha satellite DNA probe in Coculture-5 and -15 thus far examined. The ploidy of immortalized, semi-transformed, and transformed cell lines, was 4n, 4n to 2n, and 2n range, respectively. These findings suggest that chromosomal rearrangements cause abnormalities in cell division kinetics resulting in numerical and structural abnormalities of chromosomes, and render host cells growth advantage.

Cell Division↗