Results of the search for inspiraling compact star binaries from TAMA300's observation in 2000-2004

We analyze the data of TAMA300 detector to search for gravitational waves from inspiraling compact star binaries with masses of the component stars in the range 1-3Msolar. In this analysis, 2705 hours of data, taken during the years 2000-2004, are used for the event search. We combine the results of different observation runs, and obtained a single upper limit on the rate of the coalescence of compact binaries in our Galaxy of 20 per year at a 90% confidence level. In this upper limit, the effect of various systematic errors such like the uncertainty of the background estimation and the calibration of the detector's sensitivity are included.Comment: 8 pages, 4 Postscript figures, uses revtex4.sty The author list was correcte

Observation results by the TAMA300 detector on gravitational wave bursts from stellar-core collapses

We present data-analysis schemes and results of observations with the TAMA300 gravitational-wave detector, targeting burst signals from stellar-core collapse events. In analyses for burst gravitational waves, the detection and fake-reduction schemes are different from well-investigated ones for a chirp-wave analysis, because precise waveform templates are not available. We used an excess-power filter for the extraction of gravitational-wave candidates, and developed two methods for the reduction of fake events caused by non-stationary noises of the detector. These analysis schemes were applied to real data from the TAMA300 interferometric gravitational wave detector. As a result, fake events were reduced by a factor of about 1000 in the best cases. The resultant event candidates were interpreted from an astronomical viewpoint. We set an upper limit of 2.2x10^3 events/sec on the burst gravitational-wave event rate in our Galaxy with a confidence level of 90%. This work sets a milestone and prospects on the search for burst gravitational waves, by establishing an analysis scheme for the observation data from an interferometric gravitational wave detector

SUMMARY Cerebral haemodynamics after cardiac resuscitation

Ventricular fibrillation was induced in fifteen monkeys by electric stimulation using a bipolar intracardiac pacemaker electrode which was inserted through a femoral vein. The monkeys were defibrillated and resuscitated after several minutes. Cerebral blood flow (CBF), intracranial pressure (ICP) and EEG were monitored continuously. CBF autoregulation was checked regularly before and after ventricular fibrillation to study the relation between it and other parameters such as CBF, ICP, EEG. Fifteen monkeys were divided into two groups, a burr-hole group and a no burr-hole group. ICP was measured in the burr-hole group (10 monkeys). The purpose of having two groups was to ascertain the effect of a burr-hole (artificial injury in the skull and dura) on the parameters CBF, EEG and autoregulation. CBF was measured with electromagnetic flowmeter at internal carotid artery. The conclusion of the experiment was as follows; (1) Autoregulation was lost in all monkeys after resuscitation. In the monkeys which had had autoregulation before cardiac arrest, the autoregulation recovered in three (no burr-hole group) to five (burr-hole group) hours after resuscitation, if resuscitation took place within five minutes. In the monkeys whose autoregulation had already been lost before cardiac arrest, it did not return despite successful cardiac resuscitation. (2) Immediately after resuscitation, BP, ICP and CBF increased for 20-60 minutes. In the monkeys who had no recovery of autoregulation after resuscitation, the rate of increase of ICP was much larger than those whose autoregulation recovered, and at the peak of ICP, the CBF decreased. Impairment of autoregulation itself, indicates that the ballance of circulatory dynamics of the brain is easily impaired by noxious stimulation such as hypoxia. (3) In the monkeys with recovery of autoregulation, general status was good after resuscitation but in the monkeys without recoverey, symptomes of increased ICP were seen and the prognosis was poor. (4) Six minutes of cardiac arrest would appear to be the upper limit for monkeys to survive after resuscitation. (5) Before ventricular fibrillation, corresponding changes in the CBF and the frequency of the EEG wave recorded, but after resuscitation the frequency of the EEG wave decreased despite an increase in CBF. This is probably the same mechanism as occures in the "luxury perfusion syndrome". There was no, relation between EEG and autoregulation, but when EEG showed dominant slow or flat waves, there was no autoregulation

Unique proximal tubular cell injury and the development of acute kidney injury in adult patients with minimal change nephrotic syndrome

Abstract Background Adult patients with minimal change nephrotic syndrome (MCNS) are often associated with acute kidney injury (AKI). To assess the mechanisms of AKI, we examined whether tubular cell injuries unique to MCNS patients exist. Methods We performed a retrospective analysis of clinical data and tubular cell changes using the immunohistochemical expression of vimentin as a marker of tubular injury and dedifferentiation at kidney biopsy in 37 adult MCNS patients. AKI was defined by the criteria of the Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for AKI. Results Thirteen patients (35.1%) were designated with AKI at kidney biopsy. No significant differences in age, history of hypertension, chronic kidney disease, diuretics use, proteinuria, and serum albumin were noted between the AKI and non-AKI groups. Urinary N-acetyl-β-D-glucosaminidase (uNAG) and urinary alpha1-microglobulin (uA1MG) as markers of tubular injury were increased in both groups, but the levels were significantly increased in the AKI group compared with the non-AKI group. The incidence of vimentin-positive tubules was comparable between AKI (84.6%) and non-AKI (58.3%) groups, but vimentin-positive tubular area per interstitial area was significantly increased in the AKI group (19.8%) compared with the non-AKI group (6.8%) (p = 0.011). Vimentin-positive injured tubules with tubular simplification (loss of brush-border of the proximal tubule/dilated tubule with flattening of tubular epithelium) were observed in the vicinity of glomeruli in both groups, suggesting that the proximal convoluted tubules were specifically injured. Two patients exhibited relatively severe tubular injuries with vimentin positivity and required dialysis within 2 weeks after kidney biopsy. The percentage of the vimentin-positive tubular area was positively correlated with uNAG but not with uA1MG in the non-AKI group. Conclusions Proximal tubular injuries with increased uNAG exist in MCNS patients without renal dysfunction and were more severe in the AKI group than they were in the non-AKI group. The unique tubular injuries probably due to massive proteinuria might be a predisposing factor for the development of severe AKI in adult MCNS patients