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Biomedical subjects

H Kitamura

Publications and source records attributed to H Kitamura.

At least 397 records · Page 22Linked to original sources
PubMed1990

Excess purine degradation caused by an imbalance in the supply of adenosine triphosphate in patients with congestive heart failure.

To evaluate purine degradation in patients with congestive heart failure concentrations of serum hypoxanthine, lactate, and noradrenaline were measured before and after submaximal treadmill exercise in 12 patients with chronic congestive heart failure and nine healthy volunteers. In four patients the concentration of hypoxanthine was significantly higher than in the controls or in the remaining eight patients with congestive heart failure. Venous lactate and noradrenaline in the four patients with high concentrations of hypoxanthine were also significantly higher than those in the eight patients with normal concentrations of hypoxanthine. Patients who responded normally were also more likely to have been treated with vasodilators and angiotensin converting enzyme inhibitors. Exercise induced arrhythmias were more common in the patients with high concentrations of hypoxanthine. These results suggest that the excess purine degradation in patients with congestive heart failure might be the result of a "relative" disturbance in the supply of adenosine triphosphate caused by the shift of cellular metabolism from aerobic glycolysis to anaerobic glycolysis during submaximal exercise and that hypoxanthine (a substrate for xanthine oxidase and a source of free radicals) was increased after submaximal exercise in some patients with congestive heart failure.

Adenosine Triphosphate↗
PubMed1990

A new complement factor B variant (BF S075) in Japanese.

A new slow-moving variant of the complement factor B, named BF S075, was found in a Japanese patient with cerebral thrombosis and urticaria. The variant was inherited in a codominant manner. The protein concentration and functional hemolytic activity of the complement factor B in the patient's serum were within normal limits. The BF S075 is the fourth rare BF variant found in the Japanese population.

Complement Factor B↗
PubMed1990

Effect of glycerol on cell kinetics and tumorigenesis in mouse lung following urethan administration.

Extending previous studies, we hypothesized that glycerol modulates pulmonary tumorigenesis in mice through metabolic activation in bronchiolar cells. To test this, we examined the effects of glycerol on pulmonary cell kinetics and tumorigenesis induced by urethan. Male ddY mice were given 1 mg/g urethan and/or 5% glycerol solution for a fixed period. [3H]Thymidine autoradiography revealed that glycerol administration significantly suppressed the urethan-induced facilitation of cell kinetics of the bronchiolar cells (p less than 0.05), but not that of the alveolar wall cells. Furthermore, glycerol did not affect urethan-induced pulmonary tumorigenesis. These findings suggest that glycerol modifies the metabolism of carcinogens in the bronchiolar epithelium.

Animals↗
PubMed1990

Diagnostic value of R-wave amplitude increase during treadmill exercise testing for detecting coronary artery disease.

To evaluate the diagnostic value of an exercise-induced increase in R-wave amplitude (RWA) for detecting coronary artery disease (CAD), treadmill testing using the modified Bruce protocol was performed on a CASE II computerized system (Marquette) in 10 healthy young men, 35 patients (pts) with CAD, 22 subjects with normal coronary arteries, and 11 pts with aortic or mitral regurgitation. Based on the analysis of the patterns of serial changes in RWA in lead V5, we proposed new RWA criteria for detecting CAD. (1) During exercise, RWA increases in stage 1 and subsequently increases further or remains unchanged. (2) During exercise, RWA decreases in the early phase of exercise and subsequently increases. (3) In the recovery period, RWA shows a gradual and excessive increase. A combination of the above RWA criteria showed a sensitivity, specificity and accuracy of an equal value of 86%. We conclude that an exercise-induced RWA increase is a useful indicator for detecting CAD, especially when taking the patterns of serial changes into consideration, and that the abnormal RWA increase may be related to an increase in left ventricular (LV) end-diastolic volume due to exercise-induced LV dysfunction.

Adult↗
PubMed1990

Morphological studies of the cardiac lymphatic system.

The distribution and structure of the mammalian cardiac lymphatic system have been investigated by puncture injection, intra-arterial injection of silver nitrate, hydrogen peroxide immersion, and light and electron microscopy. The cardiac lymphatic system consists of drainage vessels and lymphatic capillaries. The drainage vessels contain many valves and are mainly situated subepicardially following branches of the coronary artery. The lymphatic capillaries are composed of a thin layer of endothelial cells, and form relatively dense networks in a fishnet arrangement. These lymphatic networks are richer in the ventricles than in the atria, being present in the subepicardial myocardial and subendocardial regions. In addition, networks are found in all cusps of the atrioventricular valves, and in the sinuatrial node and atrioventricular system. The lymphatic system maintains cardiac homeostasis by receiving proteins, electrolytes and excess fluid from the interstitial tissue and returning them to the venous system.

Animals↗
PubMed1990

[Chronic subdural hematoma with a markedly fibrous hypertrophic membrane. Case report].

A 40-year-old female, who had taken low-dose oral contraceptives for 2 months before onset, developed transient dysarthria, left hemiparesis, and left hemihypesthesia. One month later, a computed tomography (CT) scan revealed a uniformly enhanced, convex-shaped, hypertrophic membrane with a lobulated lumen in the subdural space of the right parietal region. A right parietal craniotomy was performed. The membrane, consisting of elastic-hard, hypertrophic granulation tissue and yellowish, sticky fluid in the lumen, was readily freed and totally extirpated. Subsequently, the patient recovered without persistent symptoms. Light microscopic examination detected the sinusoidal channel layer and the fibrous layer in an alternating configuration, along with intramembranous hemorrhagic foci. Such hypertrophy must have been caused by repeated intramembranous hemorrhages and reactive granulation. Such findings of hematoma membrane have never previously been reported. Thus, this is an interesting case, clearly distinguished from typical chronic subdural hematoma.

Adult↗
PubMed1990

[Long-term follow-up of electrocardiographic changes in patients with asymmetric apical hypertrophy].

The serial electrocardiographic (ECG) changes of 20 patients with asymmetric apical hypertrophy (AAH) were retrospectively reviewed relative to their clinical symptoms, echocardiography and Doppler echocardiography, and thallium-201 perfusion scintigraphy. These patients were followed 4-18 years (mean 8 years). Patterns of the serial ECG changes were as follows: Seven patients (group Ia) had an increase of 10 mm or greater in the highest R wave amplitude in the precordial leads, with newly-developed giant T wave inversion. Five patients (group Ib) had relatively stable ECGs and the changes in the R wave amplitudes of less than 10 mm. Six patients (group IIa) had a decrease of 10 mm or greater in the highest R wave amplitude with mild decreases of negative T wave amplitudes. In the remaining two patients (group IIb) right bundle branch block developed. At the last follow-up study, group IIa had lower R wave amplitudes and longer QTc than did those in group I. The follow-up periods and their mean age did not differ among the groups. At the initial evaluation, exercise limitation was rare in group I; whereas, most of the patients in group II presented symptoms such as palpitation, chest pain or exertional dyspnea. These cardiac symptoms developed slowly but progressively during the follow-up period, and their incidence increased both in groups I and II at the final observation. Left ventricular (LV) wall thickness at the chordal level showed normal values and did not differ between the two groups, but apical wall thickness was greater in group II than in group I. Two-dimensional echocardiography showed a spade-like deformity of the LV in group II. In group I, the LV deformity was less marked and was not noted at the initial examination. Color Doppler echocardiography frequently revealed "paradoxical flow" expelled from the obliterated apex to the base in the early diastolic filling period in group II. Left ventriculography confirmed asynchronous contraction, hyperkinesis in the basal segment and dyskinesis at the apical segment, resulting in this abnormal intraventricular blood flow profiles. Serial studies by thallium-201 (TL) perfusion scintigraphy disclosed that four of the eight patients in group II developed localized hypoperfusion at the apex where a high and homogeneous uptake of TL was previously noted.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

[Clinical significance of serum cardiac myosin light chain I in patients with muscular dystrophy].

We examined serum cardiac myosin light chain I (LCI), serum creatine kinase (CK) levels and left ventricular function in patients with muscular dystrophy and secondary cardiac involvement. LCI levels were determined by a two-site immunoradiometric assay method in 25 patients with muscular dystrophy and 10 normal subjects. This study included 15 patients with Duchenne muscular dystrophy (DMD), 8 patients with Fukuyama type congenital muscular dystrophy (FCMD) and 2 sisters with non-Fukuyama type congenital muscular dystrophy (nFCMD). We measured the value of left ventricular fractional shortening (FS) using echocardiography. All patients with DMD and FCMD showed moderate or severe skeletal muscle weakness. The mean values of LCI were significantly higher in patients with DMD (11.0 +/- 8.3 ng/ml, p less than 0.01) and in patients with FCMD (1.6 +/- 1.4 ng/ml, p less than 0.05) than in normal subjects (0.3 +/- 0.2 ng/ml). In patients with DMD, LCI level correlated closely with CK level (r = 0.81, p less than 0.01) but not with FS (r = 0.35, n.s.). In patients with FCMD, LCI level correlated significantly with CK level (r = 0.75, p less than 0.05) but not with FS (r = 0.44, n.s.). Close correlation between LCI and CK levels was thought to result from the cross reaction between cardiac LCI and myosin light chains of skeletal muscle in the assay method we used. Two siblings with nFCMD showed mild skeletal muscle weakness. A 22-year-old sister with mild left ventricular dysfunction (FS = 0.41) showed high level of CK (4794/U/L) and mild elevation of LCI (7.3 ngml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Long-term maintenance of human distal airway epithelial cells in nude mice: a potentially useful model for the study of pulmonary carcinogenesis and lung cell biology.

We investigated whether the normal morphology of distal airway epithelial cells from adult human lungs could be maintained for long periods of time as xenografts in nude mice. Peripheral lung tissue obtained from normal regions of lungs resected for lung cancer was transplanted subcutaneously into nude mice. The implants were then retrieved at intervals from 2 to 26 weeks for light and electron microscopy, and for immunohistochemical examination. At 2 weeks, revascularization of the implants and replication of immature epithelial cells were observed. At 4 weeks and thereafter, the epithelium formed in the implants was almost mature and normal in appearance. Pseudostratified columnar epithelium composed of ciliated, mucus, and basal cells lined the larger airspaces, whereas the smaller airspaces including alveolar structures were generally lined with type II pneumocytes and occasionally with Clara cells. Normal alveoli with type I pneumocytes and capillary networks were rarely observed. The implants were maintained in the nude mice for as long as 26 weeks. Cytokinetic studies of the epithelial cells in the implants using immunocytochemical detection of incorporated bromodeoxyuridine revealed that an inverse relationship existed between the degree of maturation and the replicative capacity of the epithelial cells. It was also found that, even in the mature epithelium, a small fraction of the cells were undergoing DNA synthesis. Peripheral lung tissue xenografts in nude mice may provide an excellent in vivo model for the study of pulmonary carcinogenesis and also for the study of both the function and differentiation of human epithelial cells of the distal airways.

Animals↗
PubMed1990

Growth and differentiation of human distal airway epithelial cells in culture. Effects of small amounts of serum in defined medium.

We herein describe a new simple method for culturing primary epithelial cells derived from the distal airway of adult human lung. Peripheral lung tissue obtained from surgical materials was cultured as explants in Ham's F12 medium supplemented with hormones and growth factors. From days 10 to 14, outgrowth of epithelial cells started on the dish surface, and even after removal of explants at days 14 to 16, these cells continued to replicate during the 3rd and 4th week of culture, and eventually formed epithelial cell foci (10 to 20-fold increase in population). They then ceased to replicate and terminally differentiated in the 5th week. Addition of 1% serum to the culture medium enhanced the initial outgrowth of epithelial cells, whereas small amounts of serum had no effect on proliferation of cells after explant removal. On the other hand, serum modulated the differentiation phenotypes of epithelial cells. In the presence of 1% serum, numerous ciliated and secretory cells appeared, whereas the cells underwent epidermoid differentiation in the absence of serum. When replated onto 3T3 fibroblast feeder layers, the epithelial cells from earlier cultures showed a great replicative capability and formed colonies at higher frequencies (colony-forming efficiency, 8 to 27% at days 14 to 21), but the replicative capability was significantly reduced at the confluent stage (colony-forming efficiency, 0.44 to 2.0% at day 28). Morphologic examinations of explants strongly suggested that the primary cells were derived from the bronchiolar epithelium. We conclude that this new culture system provides an excellent model for studying the growth, differentiation, and function of human bronchiolar epithelial cells in vitro.

Bronchi↗
PubMed1989

The endocrine pancreas of alloxan-diabetic rats: microangiopathy as revealed by electron microscopy.

We studied the microvasculature of the pancreatic islet with an electron microscope using 15 alloxan-diabetic and 16 control rats. These animals were morphologically examined at 2 weeks, 1, 2, and 4 months after alloxan injection (diabetic rats) or at comparable times (control rats). Control rats were non-diabetic, either sequentially treated with glucose and alloxan (injected controls) or not subjected to any medication (non-treated controls). Body weights, plasma glucose levels, and erythrocyte glycosylated hemoglobin (HbA1c) concentrations were also measured at intervals. All the diabetic rats exhibited retarded growth, hyperglycemia, and increases in HbA1c concentrations. The primary changes in diabetic islet capillaries can be grouped into four categories: (1) narrowing and closing of capillaries and occurrence of possible acellular capillaries, (2) formation of perivascular edema, (3) bulging and projection of endothelial cytoplasm, and (4) perivascular proliferation of collagen-like fibrils together with thickening of the basement membrane. These changes tended to worsen with diabetic duration. They are regarded as pathognomonic for diabetic microangiopathy. It is presumed that the present microvascular lesions of the islet play an important role in the pathogenesis and advancement of the diabetic state.

Animals↗
PubMed1989

Probing the C4-binding site on C1s with monoclonal antibodies. Evidence for a C4/C4b-binding site on the gamma-domain.

The catalytic site for C4 of C1s has been presumed to consist of a C4-binding domain and a proteolytic domain. A mAb to C1s, M81, blocked C4 activation and C4 binding to C1s. M81 recognized the H chain of C1s. Using M81 as a probe, we tried to define C4-binding site on C1s. Plasmin digestion of C1s generated four products of Mr 58,000 (P1), 48,000 (P2), 37,000 (P3), and 27,000 (P4). These products, except for P2, all possessed a 26,000-Da H chain fragment (26k-HF) connected to variable-sized L chain pieces. 26k-HF alone had an ability to interact with M81. Amino-terminal amino acid analysis of 26k-HF mapped the epitope for M81 to domain IV and/or V of gamma-domain of C1s. The gamma-domain therefore contains the C4-binding site. The confirm and further elucidate the role of the C4-binding site for C4, we used a substrate-blotting technique in which labeled C4 was incubated with nitrocellulose membrane-fixed C1s and its fragments. C4 was successfully blotted onto C1s and P1, but not P2-P4; i.e., further degradation of the L chain led to the loss of C4-binding. During the incubation, most of the added C4 was converted to C4b. The binding was augmented, if the proteolytic activity of C1s and P1 was blocked, so that the added C4 remained intact. Although C4b also bound to C1s and P1, its binding was less effective and abolished by the addition of cold C4. Based on these results, the gamma-domain and the L chain constitute the catalytic site of C1s to activate C4 to C4b. Moreover, the generated C4b, although it still has weak affinity for C1s, can be replaced by newly coming C4.

Antibodies, Monoclonal↗
PubMed1989

Comparative effects of isosorbide dinitrate, prednisolone, indomethacin, and elastase on the development of monocrotaline-induced pulmonary hypertension.

The pathogenesis of monocrotaline-induced pulmonary hypertension is not clear. Progressive pulmonary arteritis leading to vascular sclerosis, narrowing of the lumina, and thrombosis is the suspected sequence. To investigate this, we examined the effect of isosorbide dinitrate (ISDN), prednisolone, indomethacin, and elastase in 100 SD male rats, 4 weeks after the injection of monocrotaline (MCT) by cardiac catheterization, right ventricle-to-left ventricle plus septum weight ratio (RV/LV + S), histology, and electron microscopy. ISDN, a vasodilator, reduced the elevation of right ventricular (RV) pressure, RV/LV + S, and also pulmonary vascular remodeling; the characteristic histological feature was dilatation of small pulmonary arteries. Both prednisolone and indomethacin reduced RV pressure, RV/LV + S, and pulmonary vasculitis. Elastase, a protease which controls the metabolism of elastin in the arterial wall, likewise reduced RV pressure, RV/LV + S, and pulmonary vascular remodeling, with a significant decrease in elastosis of the small pulmonary arteries histologically. We concluded that all of the pathological processes resulting from arteritis are important in the development of MCT-induced pulmonary hypertension. In all experimental groups, decreased histopathologic changes correlated with decrease in the pressure. Elastase, which reduces pulmonary arterial sclerosis, is suggested as a new agent to treat pulmonary hypertension.

Animals↗
PubMed1989

Granulocytosis associated with malignant neoplasms: a clinicopathologic study and demonstration of colony-stimulating activity in tumor extracts.

We studied seven cases of malignant neoplasms, taken from various sites in the body, that were associated with marked granulocytosis. The seven cases were characterized clinically by marked granulocytosis with mature neutrophils, nonspecific inflammatory signs, and a rapid and progressive fatal course of the disease. The elevation of granulocyte count generally paralleled the increase in tumor size. Postmortem examination revealed no evidence of extensive bone marrow metastases or significant suppuration in any case. The bone marrows showed varying degrees of granulocytic hyperplasia with or without a shift to the left in the maturation series. Erythroid cell hyperplasia was observed in some cases, and in one instance there was an increase in immature eosinophils. The spleen showed various degrees of infiltration by neutrophils, from minimal to extremely marked; some spleens had foci of extramedullary hemopoiesis. Colony-stimulating activity was demonstrated in tumor extracts from three of these cases and from the serum in another case. Thus, it is suggested that marked granulocytosis in these patients was caused, at least in part, by colony-stimulating factor produced by the neoplastic cells.

Adult↗
PubMed1989

Acceleration of site-to-site transfer of C1- by a monoclonal antibody to C1-s.

A monoclonal antibody to human C1-s (a subcomponent of C1-), M365 blocked the complement-mediated lysis of C1(-)-coupled IgM-sensitized sheep erythrocytes (EAIgMC1). However, M365, via its binding to C1-s, did not inhibit C2 activation and only partially inhibited C4 activation, both attributable to the proteolytic action of C1s. Therefore, the inhibition of lysis of EAIgMC1 is not due to the direct effect of antibody binding to C1-s in the C1- molecule. M365, when added to the pre-formed EAIgMC1, deprived the whole C1 molecule from the cells. It was also found that M365-bound C1 could not bind to EAIgM. These phenomena were induced only when M365, one of seven monoclonal antibodies to C1-s, was employed and when IgM antibody-sensitized E was used. The observed C1- liberation and C1 binding inhibition by M365 were found to be less effective when the C4b bearing cells, EAIgMC4, were used. But the addition of M365-bound C1- to EAIgMC4 promoted the formation of the C3 convertase, C4b2a, which caused an incremental lysis of the C4b bearing cells. The results are interpreted to mean that C1-, once complexed with M365, still remains active and acquires the ability to transfer from one C1 binding site on IgM to another to activate the convertases. C4b must be a prerequisite on the cells to induce the effective C1- transfer and resulting increase of C3 convertase sites. We hypothesize that the M365-C1-s association alters the conformation of C1q and thereby leads to the dissociation of whole C1- from IgM. The M365-C1- complex, therefore, can move from site to another.

Animals↗