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Biomedical subjects

H Tada

Publications and source records attributed to H Tada.

At least 37 records · Page 2Linked to original sources
PubMed2001

Role of transisthmus conduction intervals in predicting bidirectional block after ablation of typical atrial flutter.

INTRODUCTION: Complete bidirectional cavotricuspid isthmus block is the endpoint for ablation of typical atrial flutter. The purpose of this study was to determine whether the extent of prolongation of the transisthmus interval after ablation predicts complete bidirectional block. METHODS AND RESULTS: Fifty-seven consecutive patients underwent 60 ablation procedures for isthmus-dependent atrial flutter. The clockwise and counterclockwise transisthmus intervals were determined before and after ablation during pacing from the low lateral right atrium and the coronary sinus. Bidirectional block was achieved with ablation in 55 (96%) of 57 patients. The transisthmus intervals before ablation and after complete transisthmus block were 100.3 +/- 21.1 msec and 195.8 +/- 30.1 msec, respectively, in the clockwise direction (P < 0.0001), and 98.2 +/- 24.7 msec and 185.7 +/- 33.9 msec, respectively, in the counterclockwise direction (P < 0.0001). An increase in the transisthmus interval by > or = 50% in both directions after ablation predicted complete bidirectional block with 100% sensitivity and 80% specificity. The positive and negative predictive values were 89% and 100%, respectively. The diagnostic accuracy of a > or = 50% prolongation in the transisthmus interval was 92%. CONCLUSION: Prolongation of the transisthmus interval by > or = 50% in the clockwise and counterclockwise directions is associated with a high degree of diagnostic accuracy and an excellent negative predictive value in determining complete bidirectional transisthmus block. This may be a useful and simple adjunctive criterion for assessment of complete transisthmus conduction block.

Aged↗
PubMed2001

Electrogram polarity and cavotricuspid isthmus block during ablation of typical atrial flutter.

INTRODUCTION: The atrial activation sequence around the tricuspid annulus has been used to assess whether complete block has been achieved across the cavotricuspid isthmus during radiofrequency ablation of typical atrial flutter. However, sometimes the atrial activation sequence does not clearly establish the presence or absence of complete block. The purpose of this study was to determine whether a change in the polarity of atrial electrograms recorded near the ablation line is an accurate indicator of complete isthmus block. METHODS AND RESULTS: Radiofrequency ablation was performed in 34 men and 10 women (age 60 +/- 13 years [mean +/- SD]) with isthmus-dependent, counterclockwise atrial flutter. Electrograms were recorded around the tricuspid annulus using a duodecapolar halo catheter. Electrograms recorded from two distal electrode pairs (E1 and E2) positioned just anterior to the ablation line were analyzed during atrial flutter and during coronary sinus pacing, before and after ablation. Complete isthmus block was verified by the presence of widely split double electrograms along the entire ablation line. Complete bidirectional isthmus block was achieved in 39 (89%) of 44 patients. Before ablation, the initial polarity of E1 and E2 was predominantly negative during atrial flutter and predominantly positive during coronary sinus pacing. During incomplete isthmus block, the electrogram polarity became reversed either only at E2, or at neither E1 nor E2. In every patient, the polarity of E1 and E2 became negative during coronary sinus pacing only after complete isthmus block was achieved. In 4 patients (10%), the atrial activation sequence recorded with the halo catheter was consistent with complete isthmus block, but the presence of incomplete block was accurately detected by inspection of the polarity of E1 and E2. CONCLUSION: Reversal of polarity in bipolar electrograms recorded just anterior to the line of isthmus block during coronary sinus pacing after ablation of atrial flutter is a simple, quick, and accurate indicator of complete isthmus block.

Adult↗
PubMed2001

Incidence and clinical significance of inducible atrial tachycardia in patients with atrioventricular nodal reentrant tachycardia.

INTRODUCTION: The purpose of this prospective study was to determine the prevalence and clinical significance of inducible atrial tachycardia in patients undergoing slow pathway ablation for AV nodal reentrant tachycardia who did not have clinically documented episodes of atrial tachycardia. METHODS AND RESULTS: Twenty-seven (15%) of 176 consecutive patients who underwent slow pathway ablation for AV nodal reentrant tachycardia were found to have inducible atrial tachycardia with a mean cycle length of 351+/-95 msec. The atrial tachycardia was sustained in 7 (26%) of 27 patients and was isoproterenol dependent in 20 patients (74%). The atrial tachycardia was not ablated or treated with medications, and the patients were followed for 9.7+/-5.8 months. Six (22%) of the 27 patients experienced recurrent palpitations during follow-up. In one patient each, the palpitations were found to be due to sustained atrial tachycardia, nonsustained atrial tachycardia, recurrence of AV nodal reentrant tachycardia, paroxysmal atrial fibrillation, sinus tachycardia, and frequent atrial premature depolarizations. Thus, only 2 (7%) of 27 patients with inducible atrial tachycardia later developed symptoms attributable to atrial tachycardia. CONCLUSION: Atrial tachycardia may be induced by atrial pacing in 15% of patients with AV nodal reentrant tachycardia. Because the vast majority of patients do not experience symptomatic atrial tachycardia during follow-up, treatment for atrial tachycardia should be deferred and limited to the occasional patient who later develops symptomatic atrial tachycardia.

Adult↗
PubMed2001

Relationship between serum potassium concentration and risk of recurrent ventricular tachycardia or ventricular fibrillation.

INTRODUCTION: Electrolyte abnormalities are considered a correctable cause of a life-threatening ventricular arrhythmia according to American Heart Association/American College of Cardiology Practice Guidelines, and ventricular tachycardia or ventricular fibrillation in the setting of an electrolyte abnormality is considered a class III indication for defibrillator implantation. However, there are little data to support this recommendation. The purpose of this study was to determine the risk of a recurrent sustained ventricular arrhythmia in patients with a low serum potassium concentration at the time of an initial episode of a sustained ventricular arrhythmia. METHODS AND RESULTS: One hundred sixty-nine consecutive patients who presented with a sustained ventricular arrhythmia and a serum potassium concentration determined on the day of the arrhythmia underwent defibrillator implantation. All patients had structural heart disease and left ventricular ejection fraction of 0.32+/-0.15. On the day of the index arrhythmia, 30% of the patients had a serum potassium concentration <3.5 or >5.0 mEq/L, including 7% who had a serum potassium concentration <3.0 or >6.0 mEq/L. For the entire cohort of patients, freedom from a recurrent sustained ventricular arrhythmia was 18% at 5 years and was not significantly different among patients with a serum potassium concentration <3.5 mEq/L (23%), between 3.5 and 5.0 mEq/L (16%), and >5.0 mEq/L (5%; P = 0.1). CONCLUSION: The results of the present study suggest that patients with structural heart disease and an abnormal serum potassium concentration at the time of an initial episode of sustained ventricular tachycardia or ventricular fibrillation are at high risk for a recurrent ventricular arrhythmia; therefore, implantable defibrillator therapy may be reasonable.

Aged↗
PubMed2001

Prevalence of central venous occlusion in patients with chronic defibrillator leads.

BACKGROUND: Many patients with previously implanted ventricular defibrillators are candidates for an upgrade to a device capable of atrial-ventricular sequential or multisite pacing. The prevalence of venous occlusion after placement of transvenous defibrillator leads is unknown. The purpose of this study was to determine the prevalence of central venous occlusion in asymptomatic patients with chronic transvenous defibrillator leads. METHODS: Thirty consecutive patients with a transvenous defibrillator lead underwent bilateral contrast venography of the cephalic, axillary, subclavian, and brachiocephalic veins as well as the superior vena cava before an elective defibrillator battery replacement. The mean time between transvenous defibrillator lead implantation and venography was 45 +/- 21 months. Sixteen patients had more than 1 lead in the same subclavian vein. No patient had clinical signs of venous occlusion. RESULTS: One (3%) patient had a complete occlusion of the subclavian vein, 1 (3%) patient had a 90% subclavian vein stenosis, 2 (7%) patients had a 75% to 89% subclavian stenosis, 11 (37%) patients had a 50% to 74% subclavian stenosis, and 15 (50%) patients had no subclavian stenosis. CONCLUSIONS: The low prevalence of subclavian vein occlusion or severe stenosis among defibrillator recipients found in this study suggests that the placement of additional transvenous leads in a patient who already has a ventricular defibrillator is feasible in a high percentage of patients (93%).

Adult↗
PubMed2001

Characteristics of experimental autoimmune hypophysitis in rats: major antigens are growth hormone, thyrotropin, and luteinizing hormone in this model.

We produced experimental autoimmune hypophysitis (EAH) in rats and investigated its characteristics. Female Lewis rats were immunized by two injections with homologous pituitary homogenate and complete Freund's adjuvant. Blood was collected serially from the rats, and serum antibodies to pituitary antigens were examined. The rats were sacrificed 2 or 4 weeks after the final immunization, and histological examinations of the endocrine organs were carried out. Histological examination revealed slight, focal infiltration of mononuclear cells in the pituitary gland only in the rats immunized with the pituitary homogenate. Infiltration of mononuclear cells was not observed in the thyroid gland, pancreas, adrenal gland, or ovary. In the serological examination, antibodies to both cytosolic antigens and cytoplasmic particle antigens from the pituitary gland were detected by enzyme-linked immunosorbent assay (ELISA), and these antibody levels increased with time. Western blotting using the serum antibodies identified an immunoreactive protein of approximately 21.5 kDa among these antigens, and we confirmed that this protein was rat growth hormone (GH). Furthermore, antibodies to GH, thyrotropin (TSH), and luteinizing hormone (LH) were detected by ELISA. Antibodies to follicule stimulating hormone, prolactin, or adrenocorticotropin were not detected. These data suggest that several antigens from the pituitary gland are involved in EAH in rats, and that GH, TSH, and LH are major antigens among the pituitary antigens in this model.

Animals↗
PubMed2001

Detection of E-cadherin expression after nerve repair in a rat sciatic nerve model.

The authors investigated E-cadherin expression during nerve regeneration after nerve suture using the rat sciatic nerve model. Five rats were used during each postoperative period. E-cadherin expression was detected by Western blot analysis and immunofluorescent staining with an anti-E-cadherin monoclonal antibody. The level of E-cadherin expression was calculated as the amount relative to that found in normal control nerve. The level of E-cadherin expression was decreased at first, and then gradually increased. The maximum level of E-cadherin was 1.92 +/- 0.07 fold in the sutured nerve. The level of E-cadherin expression in the sutured nerve was significantly greater (p < 0.0001) than that of the normal control nerve from postoperative day 3 to 21, and that of sutured nerve returned to the control level by postoperative day 28. The immunofluorescent staining results indicated that E-cadherin expression was almost negative or decreased immediately after the operation, but the degree of expression increased gradually in Schwann's cells. The degree of E-cadherin expression was significantly greater than that of normal control nerves from postoperative day 7 to 14, and returned to the control level by postoperative day 21. These results demonstrate that E-cadherin expression increases during nerve regeneration, and the expression was observed mainly in Schwann's cells. The degree of E-cadherin expression may affect the rate of nerve regeneration.

Animals↗
PubMed2001

The differential expression of N-cadherin in vascularized and nonvascularized nerve grafts: a study in a rat sciatic nerve model.

The authors investigated N-cadherin expression in vascularized and nonvascularized nerve grafts using a rat sciatic nerve model. The vascularized and nonvascularized nerve grafts were elevated, and then both nerves were sutured to the original site. At various periods after the operation, the entire graft was removed. N-cadherin expression was detected via Western blot analysis and histochemical staining using anti-N-cadherin antibody. In both grafts, the level of N-cadherin expression increased after the operation, but during postoperative weeks 6, 9, and 12, the level in the vascularized graft was significantly (p = 0.00023, 0.0018, and 0.0010, respectively) higher than that in the nonvascularized graft. At postoperative week 14, the level of both grafts returned to the control level. Histochemical findings showed that N-cadherin was expressed around the regenerated axons in both grafts, and the degree of regeneration was greater in the vascularized graft than in the nonvascularized graft. These results demonstrate that the expression of N-cadherin increases during the process of axonal regeneration in both grafts, and that the degree of the expression is augmented by vascularization of the nerve graft.

Animals↗
PubMed2001

Experience with surgical treatment of hidradenitis suppurativa.

The authors report their experience with 23 sites of hidradenitis suppurativa, including cases with musculocutaneous flap repair, and discuss the surgical methods applied. Twenty-three sites in 19 patients with chronic inflammatory skin lesions were reviewed. The lesions were divided into two groups: The limited group was comprised of mild lesions, which appear isolated and have limited abscesses without sinus tract formations. The severe group was compromised of severe lesions, which included diffuse, multiple abscesses with severe sinus tract formation and fibrosis. Nine sites were limited and 14 sites were severe. After resecting the lesion, the defect was covered with a split-thickness skin graft (four sites were limited, nine sites severe), a musculocutaneous flap (five sites severe), primary closure (four sites limited), and a local skin flap (one site limited). In six sites in 6 severe-group patients, local recurrence occurred. The local recurrence rate differed significantly between the limited and the severe groups. The reason for this may be because the lesions in the limited group could be resected completely, whereas the lesions in the severe group were diffuse and total resection was sometimes difficult for various reasons. The method of surgical repair did not affect the local recurrence rate. In recurrent cases, four sites treated with skin grafting required further surgical treatment, and two sites treated with musculocutaneous flaps were controlled with oral antibiotics. In conclusion, sufficient resection of the lesion is the most important issue in treating follicular occlusion triad disease. In lesions that can be resected completely, the surgical procedure to cover the lesions should be selected to suit the size and site of the defect. However, in cases that cannot be resected completely, a musculocutaneous flap is recommended instead of a skin graft for enhanced postoperative management of the recurring wound, and its contribution to aesthetic and functional improvement.

Adult↗
PubMed2001

Three-dimensional structure of human RNase 1 delta N7 at 1.9 A resolution.

Human pancreatic ribonuclease 1 (RNase 1) is considered to be the human counterpart of bovine pancreatic RNase A. Truncation of seven amino-acid residues from the amino-terminal sequence resulted in RNase 1 Delta N7, which has a reduced ribonucleolytic activity and a lower affinity for the human placental RNase inhibitor (PRI). This RNase 1 variant has been cloned, heterologously overexpressed, purified and crystallized. Its crystal structure has been determined and refined using data to 1.9 A resolution. The molecule displays the alpha + beta folding topology typical of members of the RNase A superfamily. The main distinct features found in RNase 1 Delta N7 are basically located in three loops affecting the fitting of the enzyme to the active site of subtilisin and the shape of the B2 subsite. These changes, taken with the lack of the catalytically active residue Lys7, may explain the reduced affinity of RNase 1 Delta N7 for PRI and the low ribonucleolytic activity of the protein when compared with the native enzyme.

Amino Acid Sequence↗
PubMed2001

Phage display cloning and characterization of monoclonal antibody genes and recombinant Fab fragment against the CD98 oncoprotein.

The Fab gene of anti-CD98 heavy chain (h.c.) monoclonal antibody (mAb) HBJ127 was cloned and expressed as a recombinant Fab (rFab) fragment by means of a phage display system. The variable heavy and light chain genes of HBJ127 were found to be derived from VOx-1 and IgVk8-30 germline, respectively. Extensive somatic mutation was found in the heavy chain complementarity determining region 2. rFab fragment was purified homogeneously from crude bacterial lysates by Ni-chelate chromatography in a yield of 71.4 mg from 100 ml of culture. rFab fragment was reactive with the cell surface of CD98-positive cells irrespective of tissues of origin, but not with CD98-negative cells. The recognition site of the rFab fragment was identical to that of mAb since the binding of rFab fragment to HeLaS(3) cells was completely inhibited by pretreatment with an excess of mAb. The relative affinity values of rFab fragment and mAb were found to be 0.11 x 10(8) and 0.35 x 10(8) M(-1), respectively. Three-fold lower affinity of rFab fragment may be due to the difference of valency of the antibody preparation. Cell growth inhibition in vitro by rFab fragment preincubated with anti-Fab suggests that the rFab fragment produced by cloned gene-bearing Escherichia coli was identical to the Fab part of HBJ127 mAb. These results show that a small fragment with antigen binding activity similar to that of the parent mAb can easily be prepared by using a phage display system. To our knowledge, this is a first report of the production of anti-CD98 h.c. rFab fragment.

Amino Acid Sequence↗
PubMed2001

Influence of breast-feeding on the production of cytokines.

PROBLEM: Recently, we reported increases in the production of interferon-gamma (IFN-gamma), interleukin-2 (IL-2), and IL-4 during the postpartum period. The present study was undertaken to investigate whether these increases might be explained by increased prolactin while breast-feeding. METHOD: Whole blood from 41 women who were breast-feeding, 13 women not breast-feeding, and 31 healthy non-pregnant women was stimulated with phorbol 12-myristate 13-acetate and ionomycin, and the levels of cytokines in the supernatant were measured by enzyme-linked immunosorbent assay. Their serum levels of prolactin were measured by enzyme immunoassay. RESULTS: Increases in IFN-gamma, IL-2, IL-4, and IL-10 production were observed in women who were breast-feeding but not in women who were not breast-feeding. Serum levels of prolactin correlated with the levels of IFN-gamma in culture supernatant. CONCLUSIONS: These results suggest that breast-feeding induces production of cytokines and that IFN-gamma production is enhanced by physiological concentrations of prolactin.

Breast Feeding↗
PubMed2001

Centrally administered neuropeptide Y delays gastric emptying via Y2 receptors in rats.

It has been shown that centrally administered neuropeptide Y (NPY) delays gastric emptying. To determine the receptor subtypes of NPY mediating the inhibitory effects on gastric emptying, effects of intracerebroventricular injection of NPY, [Leu31,Pro34]NPY (a Y1 agonist) and NPY-(3-36) (a Y2 agonist) on solid gastric emptying and postprandial antropyloric motility were studied in conscious rats. Intracerebroventricular injection of NPY and NPY-(3-36), but not [Leu31,Pro34] NPY, delayed solid gastric emptying in a dose-dependent manner (0.03-3 nmol). After the feeding (40 min), contractions with low frequency and high amplitude of the antrum were frequently observed, and the peak contraction of the antrum occurred most often 3-6 s before the peak contraction of the pylorus. Intracerebroventricular injection of NPY and NPY-(3-36) (3 nmol), but not [Leu31,Pro34]NPY, significantly reduced antral contractions and the number of antropyloric coordination events. It is suggested that centrally administered NPY impairs postprandial antral contractions and antropyloric coordination via Y2 receptors, resulting in delayed gastric emptying.

Animals↗
PubMed2001

Endothelial nitric oxide synthase plays an essential role in regulation of renal oxygen consumption by NO.

Nitric oxide (NO) regulates renal O2 consumption, but the source of NO mediating this effect is unclear. We explored the effects of renal NO production on O2 consumption using renal cortex from mice deficient (-/-) in endothelial (e) nitric oxide synthase (NOS). O2 consumption was determined polarographically in slices of cortex from control and eNOS-/- mice. NO production was stimulated by bradykinin (BK) or ramiprilat (Ram) in the presence or absence of an NOS inhibitor. Basal O2 consumption was higher in eNOS-/- mice than in heterozygous controls (919 +/- 46 vs. 1,211 +/- 133 nmol O(2). min(-1). g(-1); P < 0.05). BK and Ram decreased O2 consumption significantly less in eNOS-/- mice [eNOS-/-: BK -19.0 +/- 2.8%, Ram -20.5 +/- 3.3% at 10(-4) M; control: BK -29.5 +/- 2.5%, Ram -34 +/- 1.6% at 10(-4) M]. The NO synthesis inhibitor nitro-L-arginine methyl ester (L-NAME) attenuated this decrease in control but not eNOS-/- mice. An NO donor inhibited O2 consumption similarly in both groups independent of the presence of L-NAME. These results demonstrate that NO production by eNOS is responsible for regulation of renal O2 consumption in mouse kidney.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Systemic IFN-beta gene therapy results in long-term survival in mice with established colorectal liver metastases.

Most patients succumbing to colorectal cancer fail with liver-predominant metastases. To make a clinical impact in this disease, a systemic or whole-liver therapy may be required, whereas most cancer gene therapy approaches are limited in their ability to treat beyond local disease. As a preclinical model for cancer gene therapy, recombinant adenovirus containing the human IFN-beta (hIFN-beta) cDNA was delivered systemically in nude mouse xenograft models of human colorectal cancer liver metastases. The vector targeted hepatocytes that produced high levels of hIFN-beta in the liver, resulting in a profound apoptotic response in the tumors and significant tumor regression. hIFN-beta gene therapy not only resulted in improved survival and long-term cure in a micrometastatic model, but provided similar benefits in a clinically relevant gross disease model. A similar recombinant adenovirus containing the murine IFN-beta (mIFN-beta) cDNA also resulted in a therapeutic response and improved survival in syngeneic mouse models of colorectal cancer liver metastases. Depletion studies demonstrate a contribution of natural killer cells to this therapeutic response. The toxicity of an adenoviral vector expressing murine IFN-beta in a syngeneic model is also presented. These encouraging results warrant further investigation of the use of cancer gene therapy for targeting metastatic disease.

Adenocarcinoma↗
PubMed2001

Left ventricular epicardial outflow tract tachycardia: a new distinct subgroup of outflow tract tachycardia.

The present study investigated the incidence and ECG characteristics of ventricular tachycardias (VTs) originating from the left ventricular (LV) epicardium. Thirty-one consecutive patients with VT or premature ventricular contraction originating from the outflow tract (OT-VT) underwent catheter ablation. Twenty-one OT-VTs were ablated from the endocardium in the right ventricular (RV) OT and 3 were ablated from the endocardium in the LVOT. In the remaining 7 patients, 4 (13%) OT-VTs were LV epicardial in origin, and 1 of these was ablated from the left sinus of Valsalva. The ECG characteristics of OT-VT of epicardial origin included prominent tall R-waves in the inferior leads, an R-wave in V1 and an S-wave in V2, precordial R-wave transition in V2-4, a deep QS-wave in aVL, and no S-wave in V6. In addition, there was an atypical left bundle branch block morphology with an inferior axis. These findings were observed during pacing from several sites in the LV epicardium. Furthermore, pacing from the left sinus of Valsalva caused a relatively tall R in V1, deep S-wave in V2 and a tall R-wave with a shallow S-wave in V3, as well as tall R-waves in the inferior leads, which represented intermediate characteristics between RV endocardial OT-VT and LV endocardial OT-VT. In conclusion, OT-VT originating from the LV epicardium is not uncommon and has characteristic ECG findings. Some of them can be ablated from the left sinus of Valsalva.

Adult↗
PubMed2001

Role of nitric oxide in regulation of coronary blood flow in response to increased metabolic demand in dogs with pacing-induced heart failure.

The role of endothelium-derived nitric oxide (NO) in the metabolic control of coronary blood flow (CBF) in heart failure (HF) is poorly understood, so the present study investigated the effects of inhibitors of NO synthesis on the response of CBF to changes in myocardial oxygen consumption (MVO2) in dogs with HF produced by rapid ventricular pacing and in control dogs. The CBF, MVO2, and other hemodynamic parameters were measured in anesthetized animals. Before infusion of Nomega-nitro-L-arginine methyl ester (L-NAME), the increases in CBF and MVO2 during pacing tachycardia were not significantly different between the control and HF dogs. Intracoronary infusion of L-NAME did not alter the responses of CBF or MVO2 to pacing tachycardia in the control dogs, but in the HF dogs, it reduced the CBF response to pacing tachycardia without altering the tachycardia-induced changes in MVO2. Intracoronary infusion of L-arginine reversed the effect of L-NAME. These results suggest that in HF dogs NO contributes to the regulation of CBF in response to an increased metabolic demand.

Animals↗