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Biomedical subjects

H Takano

Publications and source records attributed to H Takano.

At least 109 records · Page 6Linked to original sources
PubMed2000

Effects of reduced pulse pressure to the cerebral metabolism during prolonged nonpulsatile left heart bypass.

We investigated changes in the cerebral metabolism with long-term reduced pulse pressure. Nine goats underwent pulsatile left heart bypass (LHB) for 2 weeks while awake, and nonpulsatile LHB was subsequently conducted for 4 weeks. The average pulse pressure during nonpulsatile LHB (13, 10, 11, and 11 mm Hg at the 1st, 2nd, 3rd, and 4th nonpulsatile LHB week, respectively) was significantly lower than that during pulsatile LHB (36 mm Hg). There were no significant differences in either arterio-jugular venous oxygen differences (AJDO2) and cerebral oxygen extraction ratio between the 2nd pulsatile LHB week and the 1st, 2nd, 3rd, and 4th nonpulsatile LHB weeks. The arterio-jugular venous glucose differences, jugular venous-arterial lactate differences (JAD Lactate), and lactate oxygen indexes (JAD Lactate/AJDO2) also remained unchanged during the entire course of the experiments. In conclusion, the cerebral metabolism during nonpulsatile LHB did not change compared to that during pulsatile LHB.

Analysis of Variance↗
PubMed2000

Potassium-adsorption filter for RBC transfusion: a phase III clinical trial.

BACKGROUND: Within the past 2 years, three cases of cardiac arrest just after rapid transfusion of RBCs preserved for over 7 days after 15-Gy irradiation were found. This severe complication caused transient hyperkalemia. To prevent potassium (K(+)) overload by RBC transfusion at the bedside, a K(+)-adsorption filter made of sodium polystyrene sulfonate was developed. STUDY DESIGN AND METHODS: After in vitro and animal safety and efficacy tests, a Phase III clinical trial was conducted with 65 patients given transfusions via the newly developed filter (filter group) and 37 patients in whom the filter was not used (control group) and transfusions were given at twice the usual flow rate (20 mL/min). RESULTS: More than 85-percent (94.4+/-3.8%) removal of K(+) in RBCs in mannitol-adenine-phosphate (MAP) that had been preserved for more than 14 days or that were used 3 days after 15-Gy irradiation (calculated K(+): 3.8+/-1.3 mEq/bag) was achieved in 82 of 83 bags of MAP RBCs in the filter group, with 79.6 percent removed in the other, even in rapid transfusions. RBC recovery 1 day after transfusion, determined by increments in RBCs, Hb, and Hct, were 24 and 0.4 x 10(4) per microL, 0.7 and 0.3 g per dL, and 1.6 and 0 percent, respectively, in the filter and control groups. No adverse transfusion reactions, such as hypotension, anaphylactoid reactions, or asthma-like attacks, were observed, except for one case of urticaria in the filter group. Mild fever (within 1 degrees C) after transfusion was observed in both groups. Serologic markers of hemolysis rose slightly in both groups, but there was no significant difference between the two groups. CONCLUSION: The newly developed K(+)-adsorption filter is useful, especially in a rapid transfusion setting.

Adenine↗
PubMed2000

Angiotensin II-induced cardiomyocyte hypertrophy and cardiac fibrosis in stroke-prone spontaneously hypertensive rats.

Angiotensin-converting enzyme inhibitors (ACEIs) cause regression of hypertensive left ventricular hypertrophy (LVH) by reducing angiotensin II, increasing bradykinin, or both. The mechanisms of these cardioprotective effects remain controversial. The aims of this study were to determine whether the cardioprotective effects of ACEIs are mediated by reducing angiotensin II and whether ACEIs ameliorate the morphologic, physiologic, and biochemical changes in the hearts of stroke-prone spontaneously hypertensive rats (SHRSPs). Male SHRSPs were treated with hydralazine, captopril, or candesartan, an angiotensin II type 1 receptor (AT1R) antagonist, from age 12 to 24 weeks. We measured systolic blood pressure (SBP), left ventricular weight (LVW), left ventricular (LV) myocyte cross-sectional area (myocyte size), LV Interstitial collagen volume fraction (ICVF), perivascular collagen area/luminal area ratio (PVCA/LA), the medial area to luminal area ratio (MA/LA), the relative amount of V3 myosin heavy chain (MHCV3), and coronary reserve maximum (coronary flow max/ventricular weight (CFmax/VW)). These parameters were compared with those of untreated SHRSPs and Wistar-Kyoto rats (WKYs). SHRSPs exhibited decreased coronary reserve and LVH with an increase in myocyte size, PVCA/LA, MA/LA, and MHCV3 at 12 weeks of age. In addition to these changes, 24-week-old SHRSPs showed an increase in ICVF. The LVW, coronary reserve, myocyte size, PVCA/LA, ICVF, and MHCV3 of SHRSPs treated with captopril or candesartan all approached control values. In contrast, hydralazine decreased only ICVF. These results suggest that ACEIs regress LVH and normalize coronary reserve by modulating the effects of angiotensin II via AT1R on the induction of cardiomyocyte hypertrophy, perivascular fibrosis, and medial thickening of intramyocardial coronary arteries in SHRSPs. We concluded that these effects, in addition to the reduction of SBP, are important in causing the regression of LVH.

Angiotensin Receptor Antagonists↗
PubMed2000

Complex phenotype of mice lacking occludin, a component of tight junction strands.

Occludin is an integral membrane protein with four transmembrane domains that is exclusively localized at tight junction (TJ) strands. Here, we describe the generation and analysis of mice carrying a null mutation in the occludin gene. Occludin -/- mice were born with no gross phenotype in the expected Mendelian ratios, but they showed significant postnatal growth retardation. Occludin -/- males produced no litters with wild-type females, whereas occludin -/- females produced litters normally when mated with wild-type males but did not suckle them. In occludin -/- mice, TJs themselves did not appear to be affected morphologically, and the barrier function of intestinal epithelium was normal as far as examined electrophysiologically. However, histological abnormalities were found in several tissues, i.e., chronic inflammation and hyperplasia of the gastric epithelium, calcification in the brain, testicular atrophy, loss of cytoplasmic granules in striated duct cells of the salivary gland, and thinning of the compact bone. These phenotypes suggested that the functions of TJs as well as occludin are more complex than previously supposed.

Animals↗
PubMed2000

Changes in the surface structure of the hamster sperm head associated with maturation, in vitro capacitation and acrosome reaction: an atomic force microscopic study.

Structural changes of the hamster sperm head surface associated with maturation, capacitation and acrosome reaction were examined by atomic force microscopy. Spermatozoa were taken from the initial segment and distal cauda of the epididymis, washed in a modified Tyrode solution and fixed by glutaraldehyde. Some sperms taken from distal cauda epididymides were incubated with the capacitation medium before fixation. All samples were attached on the glass slide, dried in a critical point drier and observed by atomic force microscopy. The sperm head surface was characterized by the presence of numerous round particles, approximately 40 and 60 nm in diameter. The distribution and density of these particles on the sperm surface were significantly different between the equatorial segment and post-acrosomal region in each sperm, and also between sperms under different conditions. The surface of the equatorial segment was rather smooth in sperms from the initial segment of the epididymis, but had many large (60 nm) particles in sperms from the distal cauda epididymides, suggesting that the large particles were glycoproteins which were secreted from the epididymis and attached to the sperm surface during maturation. The number of these particles dramatically decreased in both capacitated acrosome-unreacted and acrosome-reacted sperms. This finding supports the idea that glycoproteins are removed from the sperm surface during capacitation. Atomic force microscopic studies of the sperm head surface are expected to be used for future molecular studies on the cell surface components involved in the mechanism of maturation, capacitation and acrosome reaction.

Acrosome Reaction↗
PubMed2000

Transcription factor decoy for NFkappaB inhibits cytokine and adhesion molecule expressions in synovial cells derived from rheumatoid arthritis.

OBJECTIVE: Numerous cytokines are expressed in lesions of synovial hyperplasia of patients with rheumatoid arthritis (RA), and their pathophysiological contributions have been the subject of speculation. These genes are regulated by the transcription factor NFkappaB which in turn is activated by tumour necrosis factor-alpha (TNF-alpha) and cytokines. In this study we examined the inhibition of the production of pro-inflammatory cytokines, adhesion molecule and matrix metalloproteinase (MMP) from synovial tissue of patients with RA by the introduction of synthetic double-stranded DNA with high affinity for the NFkappaB binding site. METHOD: NFkappaB decoy oligonucleotides (ODN) were introduced with the aid of the haemagglutinating virus of Japan (HVJ)-liposome method into synovial tissue or synovial cells derived from patients with RA. The levels of interleukin-1beta (IL-1beta), IL-6, TNF-alpha, intercellular adhesion molecule-1 (ICAM-1) and MMP-1 were determined by means of enzyme-linked immunosorbent assay (ELISA) and Northern blotting analysis. A cell counting kit was used to study the effect of NFkappaB decoy ODN on synovial cell proliferation. RESULTS: The production of these mediators was significantly inhibited by the introduction of NFkappaB decoy ODN compared with the effect of scrambled decoy ODN. Transfection of NFkappaB decoy ODN resulted in a significant inhibition of synovial cell proliferation as compared with that of scrambled decoy ODN. CONCLUSION: The results demonstrated in this study suggest the potential usefulness of NFkappaB decoy ODN for gene therapy of inflammatory synovitis of RA.

Arthritis, Rheumatoid↗
PubMed2000

Increased gene expression of components of the renin-angiotensin system in glomeruli of genetically hypertensive rats.

OBJECTIVE: The renin-angiotensin system (RAS) is implicated in the development of hypertensive glomerulosclerosis. However, no experimental evidence exists that clearly demonstrates activation of glomerular RAS in hypertensive nephropathy. We used stroke-prone spontaneously hypertensive rats (SHRSP) to examine whether RAS components are increased in glomeruli of SHRSP and whether this increase leads to an increase in mRNA levels for transforming growth factor-beta1 (TGF-beta1). METHODS: We examined the sequential changes of urinary albumin excretion (UAE), morphology, and glomerular mRNA expression for TGF-beta1 and fibronectin (FN) in relation to glomerular mRNA expression for angiotensinogen (ATN), angiotensin converting enzyme (ACE), angiotensin II type 1a (AT1a), and type 1b (AT1b) receptors, and intervention with angiotensin II type 1 receptor antagonist candesartan and equihypotensive hydralazine. RESULTS: In SHRSP, UAE was normal at 9 weeks of age, but became higher, beginning at 12 weeks of age, than that in the age-matched Wistar-Kyoto (WKY) rats, while SHRSP showed no glomerulosclerosis until 14 weeks of age; it was marked at 24 weeks. Plasma renin activity and plasma angiotensin II level was equivalent in the 9- and 12-week-old SHRSP and the WKY rats; both parameters, however, were elevated in 24-week-old SHRSP as compared with age-matched control. RNase protection assays showed that glomerular levels of ATN, ACE, and AT1a and AT1b receptors mRNA were significantly increased in 9-, 12-, and 14-week-old, but not in 24-week-old SHRSP, compared with age-matched WKY rats. Northern blot analysis showed that glomerular levels of TGF-beta1 and FN mRNA were higher in SHRSP than in WKY rats at all time points. Candesartan reduced UAE to control levels, whereas hydralazine reduced UAE but not to control levels. Candesartan administration for 12 weeks virtually prevented the progression of glomerulosclerosis. While candesartan reduced mRNA levels for RAS components, TGF-beta1, and FN to control levels, hydralazine was not effective in this respect. Conclusion Results suggest that increases in glomerular RAS components that occur independently of circulating RAS alter glomerular permselectivity and increase the glomerular expression of TGF-beta1 and FN in young SHRSP. Findings in old SHRSP suggest that altered glomerular permselectivity and an increased glomerular expression of TGF-beta1 and FN may be associated with the activation of systemic RAS.

Albuminuria↗
PubMed2000

Differential role of K(ATP) channels in late preconditioning against myocardial stunning and infarction in rabbits.

The role of ATP-sensitive potassium (K(ATP)) channels in the late phase of ischemic preconditioning (PC) remains unclear. Furthermore, it is unknown whether K(ATP) channels serve as end effectors both for late PC against infarction and against stunning. Thus, in phase I of this study, conscious rabbits underwent a 30-min coronary occlusion (O) followed by 72 h of reperfusion (R) with or without ischemic PC (6 4-min O/4-min R cycles) 24 h earlier. Late PC reduced infarct size approximately 46% versus controls. The K(ATP) channel blocker 5-hydroxydecanoic acid (5-HD), given 5 min before the 30-min O, abrogated the infarct-sparing effect of late PC but did not alter infarct size in non-PC rabbits. In phase II, rabbits underwent six 4-min O/4-min R cycles for 3 consecutive days (days 1, 2, and 3). In controls, the total deficit of systolic wall thickening (WTh) after the sixth reperfusion was reduced by 46% on day 2 and 54% on day 3 compared with day 1, indicating a late PC effect against myocardial stunning. Neither 5-HD nor glibenclamide, given on day 2, abrogated late PC. The K(ATP) channel opener diazoxide, given on day 1, attenuated stunning, and this effect was completely blocked by 5-HD. Thus the same dose of 5-HD that blocked the antistunning effect of diazoxide failed to block the antistunning effects of late PC. Furthermore, when diazoxide was administered in PC rabbits on day 2, myocardial stunning was further attenuated, indicating that diazoxide and late PC have additive anti-stunning effects. We conclude that K(ATP) channels play an essential role in late PC against infarction but not in late PC against stunning, revealing an important pathogenetic difference between these two forms of cardioprotection.

Adenosine Triphosphate↗
PubMed2000

Biphasic response of cardiac NO synthase isoforms to ischemic preconditioning in conscious rabbits.

In conscious rabbits, a sequence of six 4-min coronary occlusion/4-min reperfusion cycles, which elicits late preconditioning (PC), caused rapid activation of calcium-dependent nitric oxide (NO) synthase (NOS) [cNOS; endothelial NOS (eNOS) and/or neuronal NOS (nNOS)], whereas calcium-independent NOS [inducible NOS (iNOS)] activity remained unchanged. The enhanced cNOS activity was associated with increased myocardial levels of NO(2) and/or NO(3) (NO(x)). Twenty-four hours after ischemic PC was induced, the opposite pattern was observed, i.e., there was a pronounced increase in cytosolic iNOS activity but no change in cNOS activity. The initial burst of ischemia-induced cNOS activity was not affected by pretreatment with the antioxidant N-2-mercaptopropionyl glycine (MPG), the protein kinase C (PKC) inhibitor chelerythrine, or the tyrosine kinase inhibitor lavendustin A, indicating that it is independent of the generation of oxidant species and the activation of PKC and tyrosine kinases. In contrast, the delayed upregulation of iNOS 24 h after PC was prevented by pretreatment with N(omega)-nitro-L-arginine, MPG, or chelerythrine before the PC ischemia, indicating that it is triggered by a signaling mechanism that involves the generation of NO, the formation of oxidant species, and the activation of PKC. Taken together, these results demonstrate that, in conscious animals, ischemic PC elicits a biphasic response in cardiac NOS activity, i. e., an immediate activation of cNOS (most likely eNOS) followed 24 h later by a delayed upregulation of iNOS. To our knowledge, this is the first study to directly measure NOS activity after brief myocardial ischemia in vivo. In conjunction with previous functional studies, the data support a distinctive role of NOS isoforms in late PC, with eNOS serving as the trigger on day 1 and iNOS as the mediator on day 2.

Animals↗
PubMed2000

Late preconditioning enhances recovery of myocardial function after infarction in conscious rabbits.

It is unknown whether late preconditioning (PC) enhances the recovery of left ventricular (LV) function after a myocardial infarction. Thus 25 conscious rabbits were subjected to a 30-min coronary occlusion followed by 28 days of reperfusion after PC 24 h earlier with either ischemia or nitric oxide donor administration [S-nitroso-N-acetylpenicillamine (SNAP)]. The recovery of wall thickening (WTh) after reperfusion was significantly improved in the ischemic PC and SNAP PC groups compared with controls, both at rest and during dobutamine stress. Interestingly, neither ischemia- nor SNAP-induced late PC attenuated myocardial stunning from day 1 through day 14. Infarct size was smaller in the ischemic PC and SNAP PC groups compared with controls. In all groups, WTh at 28 days was positively and linearly related to the percentage of viable tissue in the region underlying the ultrasonic crystal (r = 0.90), indicating that the improvement in LV function after both ischemia-induced and NO donor-induced late PC can be fully explained by the reduction in infarct size; a separate effect of late PC on LV remodeling or LV contractility need not be invoked. In conclusion, in conscious rabbits late PC, induced either by ischemia or pharmacologically, not only limits infarct size but also enhances the recovery of LV function after myocardial infarction. This finding has important clinical implications and provides triphenyltetrazolium chloride-independent evidence that late PC limits myocellular death after sustained ischemia.

Animals↗
PubMed2000

Circulating hepatocyte growth factor as a marker of thrombus formation in unstable angina pectoris.

A new enzyme-linked immunosorbent assay can detect 10 pg/ml of human hepatocyte growth factor (HGF). Circulating HGF was significantly higher in patients with unstable angina (296+/-184 pg/ml, mean+/-SD, n=36) than in healthy volunteers (201+/-64 pg/ml, n=250, p<0.0001). Individual concentrations exceeded the mean control value +2 SD (329 pg/ml) in 12 of the 36 (33%) patients with unstable angina. The present study indicates that this new, sensitive HGF assay can successfully detect thrombosis in patients with unstable angina.

Adolescent↗
PubMed2000

Mutational analysis of X-linked adrenoleukodystrophy gene.

X-linked adrenoleukodystrophy (ALD) is an inherited peroxisomal disorder characterized by progressive neurological dysfunction, occasionally associated with adrenal insufficiency. The clinical phenotypes of ALD are quite variable, and include childhood ALD, adult-onset ALD, adrenomyeloneuropathy, and Addison's disease only. Although the causative gene for ALD has been identified, the physiological role of the gene product remains to be clarified. Despite many mutations having been identified in patients with these clinical phenotypes, the genotype-phenotype correlations have not been clarified. The authors investigated genotype-phenotype correlations in ALD by analyses on 29 unrelated Japanese patients with ALD and by a review of the literature. All the phenotypes were associated with mutations leading to protein truncation, as well as those resulting in subtle amino acid changes. Furthermore, there were no differences in phenotypic expression among the natures of the subtle amino acid changes. All these data indicate that no obvious correlations exist between the phenotypes of ALD patients and their genotypes, suggesting that other genetic or environmental factors may also be involved in determining phenotypic expression in ALD.

Adrenoleukodystrophy↗
PubMed2000

Properties of spontaneous electrical activity in smooth muscle of the guinea-pig renal pelvis.

In the guinea-pig renal pelvis, most smooth muscle cells examined (>90%), using a conventional microelectrode, had a resting membrane potential of about -50 mV and produced spontaneous action potentials with initial fast spikes and following plateau potentials. The remainder (<10%) had a resting membrane potential of about -40 mV and produced periodical depolarization with slow rising and falling phases. Experiments were carried out to investigate the properties of spontaneous action potentials. The potentials were abolished by nifedipine, suggesting a possible contribution of voltage-gated Ca(2+) channels to the generation of these potentials. Niflumic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), inhibitors of Ca(2+)-activated Cl(-) channels, showed different effects on the spontaneous action potentials, and the former but not the latter inhibited the activities, raised the question of an involvement of Cl(-) channels in the generation of these activities. Depleting internal Ca(2+) stores directly with caffeine or indirectly by inhibiting Ca(2+)-ATPase at the internal membrane with cyclopiazonic acid (CPA) prevented the generation of spontaneous activity. Chelating intracellular Ca(2+) by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) increased the amplitude of the spike component of spontaneous activity. Indomethacin inhibited the spontaneous activity, whereas prostaglandin F(2 alpha) enhanced it. The results indicate that in smooth muscle of the renal pelvis, the generation of spontaneous activity is causally related to the activation of voltage-gated Ca(2+) channels through which the influx of Ca(2+) may trigger the release of Ca(2+) from the internal stores to activate a set of ion channels at the membrane. Endogenous prostaglandins may be involved in the initiation of spontaneous activity.

Animals↗
PubMed2000

NADPH/quinone oxidoreductase is a priority target of glioblastoma chemotherapy.

We attempted to determine a target of chemotherapy specific to glioblastoma cells to ensure a favorable response to anticancer drugs, through comparison in biologic nature related to drug resistance with other types of cancer cells. Using 13 human cancer cell lines including 3 glioblastoma lines, gene expression analysis and biochemical quantitative assay were performed for a total of 12 properties, which have been linked to drug action. Although most of genes related to drug resistance, such as MDR1, MRP, MGMT and GSTpi, were overexpressed in T98G, U-373MG, and U-251MG glioblastoma cells, Topo I (topoisomerase I) expression was relatively low and alpha- and beta-TUB (tubulin) expression was comparable to other types of 10 cell lines. The glioblastoma cell lines also showed an increased expression of NADPH/quinone oxidoreductase gene (NQO1), but the respective enzyme NQO activated MMC. Among the drugs targeting such properties, MMC was more active than Topo I inhibitors and docetaxel (TXT) due to the lack of other sensitivity (resistance) determinants. Differing from MMC, MGMT was shown to participate in the resistance of Topo I inhibitors (CPT-11, SN-38 and DX-8951f), while GSTpi and MDR1 were involved in docetaxel (TXT) resistance. MMC was also more active than ACNU and CDDP in the three glioblastoma cells. NQO may be a priority target of glioblastoma chemotherapy suitable for biochemical nature of the cells, and expression analysis of NQO1, alpha-TUB, beta-TUB, MGMT, MDR1 and GSTpi may help to seek a truly active drug against glioblastomas.

Antineoplastic Agents↗
PubMed2000

[Monitoring of the cryptococcus count in the cerebrospinal fluid with negative cultures in two cases of serious cryptococcal meningitis].

We monitored the cryptococcus count in the cerebrospinal fluid(CSF) using the filter technique in two cases of serious cryptococcal meningitis during the course of treatment with antifungal agents. Lumbar puncture was performed once a week, and 1 ml of CSF was filtered through a Millipore filter(5.0-micron pore for cells), followed by staining of the filters with Alcian blue. All of the cryptococci on the filter were counted under a light microscope at a magnification of x 100. More than 500/ml and 2,000/ml of cryptococci were still observed in the CFS in Cases 1 and 2, respectively, in whom CFS cultures for Cryptococcus neoformans became negative after 4 weeks of treatment. Even though the treatment with antifungal agents were continued in these cases, cryptococci could still be observed for 5 weeks and 60 weeks on the filter preparations of Cases 1 and 2, respectively, after the CSF cultures became negative. The cryptococcal antigen could also be detected in the CSF during the positive filter preparations in these cases. At autopsy in Case 2, patchy lepromeningeal inflammatory lesions with the characteristic capsules of cryptococci were observed in the subarachnoid space. These observations suggest that cryptococci, which persisted in the CSF despite the negative cultures, were responsible for the lesions in the subarachnoid space and protracted clinical course in the two cases of cryptococcal meningitis.

Aged↗
PubMed2000

[Spinal anesthesia for a patient with epidermolysis bullosa hereditaria dystrophica].

A 39-year-old male with epidermolysis bullosa hereditaria dystrophica was scheduled for surgical excision of squamous cell carcinoma in the lower leg. Spinal anesthesia was chosen, because the skin of the puncture site for spinal anesthesia appeared to be dry and scarred, and to have less chance of infection. To avoid shear stress to the skin, we carefully performed anesthetic management including attachment of equipments associated with anesthesia, monitoring and surgery. However, we experienced some troubles and complications associated with anesthetic technique, such as pain on removing a dressing sheet, burning sensations induced by alcoholic stimuli for cold sign test and tent-like traction of the punctured skin on withdrawing the spinal needle.

Adult↗
PubMed2000

[Preliminary report on the efficacy and safety of brief-pulse ECT in depression].

Because there is no report on the use of brief-pulse devices in Japan, we have examined the efficacy and safety of brief-pulse electroconvulsive therapy (ECT) on four treatment-resistant depressive patients (three males and one female, 55.0 +/- 17.8 years of age). The ethical committee of the National Center of Neurology and Psychiatry approved this study and written informed consent was obtained from all of the patients. ECT was administered bilaterally twice a week using atropine, propofol, and succinylcholine (or vecronium) as anesthetic medications. The Hamilton rating scale for depression scores decreased from 30.5 +/- 11.0 to 14.8 +/- 11.5 following a course of 5-12 treatments. Memory and cognitive functioning, evaluated using the Mini-Mental State Examination, Short-Memory Questionnaire and so on, had not changed a week after the last ECT. These results further support the view that brief-pulse ECT is efficacious and safe for the treatment of depression.

Adult↗