Search PubMed⌕ Search

Biomedical subjects

M Fink

Publications and source records attributed to M Fink.

At least 217 records · Page 12Linked to original sources
PubMed1987

A family study of patients with temper outbursts.

To evaluate the heritability of a personality trait, "having temper outbursts," and of associated diagnoses, we obtained histories of first degree relatives on two groups: (1) patients with temper outbursts (N = 33), and (2) diverse psychiatric patients without temper outbursts (N = 12). Family interviews were conducted blind to patient (temper or not) status, using a modified version of the Family History RDC. Though Ns are relatively small, and results therefore require confirmation, the data indicate familial transmission of temper problems; an average of 18.2% of Group 1 relatives had temper problems, compared to 4.3% for Group 2. The trait of having temper outbursts was more strongly transmitted than were specific diagnoses (e.g. Intermittent Explosive Disorder, Antisocial Personality Disorder or Residual Attention Deficit Disorder) associated with temper outbursts. Patients with neurological conditions apparently related to their temper outbursts were less likely to have positive family histories.

Adult↗
PubMed1987

Optimal precision in ultrasound attenuation estimation and application to the detection of Duchenne muscular dystrophy carriers.

This paper deals with the measurement of the attenuation of ultrasound in muscle and its application to the detection of Duchenne Muscular Dystrophy (DMD) carriers. The precision obtained when measuring the attenuation is an important parameter to be considered. A statistical approach is taken on simulated data and compared to in vivo results. The results allow discussion for the minimum tissue volume needed for the estimation. Variations in muscle attenuation between normals were obtained from studies on 27 volunteers. These attenuation values were compared to those obtained from 19 carriers of DMD. Attenuation appears to be a potential clinical indicator of DMD carriers.

Biometry↗
PubMed1987

Diffraction correction for focused transducers in attenuation measurements in vivo.

Diffraction effects are a cause of error when estimating the frequency dependent attenuation of ultrasound in biological tissues in the reflection mode. Comparison of attenuation values estimated in vivo by different investigators using different types of transducers makes calibration and correction for diffraction necessary. In this paper, we present experimental results for in vivo calibration and correction for the diffraction effect for focused transducers. We also study numerically the diffraction filter in a time-frequency representation, and show that for a focused probe, there is a region in the time-frequency domain where the frequency slope of the diffraction filter does not vary with time. The main consequence for in vivo estimation is that for a given probe, it is possible to select both the distance between the region of interest and the probe, and the frequency limits, such that the attenuation thus estimated is unbiased by the diffraction effect. This result, obtained by numerical calculations, is confirmed by experimental calibration of a foam phantom and in vivo muscle.

Acoustics↗
PubMed1987

Experimental folic acid nephropathy.

In rats, single intravenous doses of folic acid induce damage to renal tubular epithelium, deposition of folic acid in tubular lumens, increase in wet kidney weight, oliguria and interstitial connective tissue proliferation. Separation of the nephrotoxic and obstructive effects of folic acid was attempted by pretreatment with NH4Cl or NaHCO3. These effects of folic acid were unaltered by pretreatment with NH4Cl and there was, in addition, accumulation of eosinophilic droplets in papillary collecting duct epithelium. After pretreatment with NaHCO3, folic acid deposition is decreased or absent; there is a smaller increase in wet kidney weight; the rats are polyuric rather than oliguric; interstitial connective tissue proliferation is reduced; and no droplets form in papillary collecting ducts, but lesions are still present in proximal convoluted tubule epithelial cells. These findings indicate that folic acid has direct nephrotoxic effects independent of intraluminal folic acid deposition, and that damage to renal epithelium, unlike that induced by many nephrotoxins, occurs at several levels of the nephron.

Ammonium Chloride↗
PubMed1986

Tissue fibrinolytic activity in different types of varicose veins.

The fibrinolytic activity of the venous wall was investigated by using Todd's technique in 92 patients with different types of varicosis. A control group consisted of 19 patients with apparently normal superficial veins who had had a saphenectomy prior to an aortocoronary bypass operation. Fibrinolytic activity was mainly localized in the adventitia of varicose and normal veins. It significantly decreased in the distal regions of all types of varicosis. The highest fibrinolytic activity was detected in the proximal part of the varicose vena saphena magna and the lowest values were observed in the perforating and side branch veins of the calf. Fibrinolytic activity is higher (p less than 0.077) in the normal vena saphena magna than in the varicose vena saphena of the calf. Older patients show a loss of fibrinolytic activity in their vena saphena magna. Obese patients have less fibrinolytic activity in varicose calf veins than patients with normal weight do.

Adult↗
PubMed1986

Predictors of benefit from art, movement, and poetry therapy: a pilot study.

No validated criteria exist for assigning patients to the creative arts therapies. This paper reports on a pilot study attempting to identify predictors of benefit from art, movement, and poetry therapy. Based on a priori hypotheses, selected psychological tests were administered to 31 patients who each received all three modalities of treatment. The relationships of these test scores and therapist prediction of benefit ratings to outcome were then evaluated statistically; outcome was measured by patient ratings and figure drawings. Results showed few significant predictors, though several findings requiring confirmation may provide a framework for future research. Implications and possible explanations of these results, as well as design and other research issues relevant to further work in this area, are discussed.

Art Therapy↗
PubMed1985

Effects of diazoxide-induced reversible diabetes on chemically induced autochthonous mammary carcinomas in Sprague-Dawley rats.

The effect of oral administration of diazoxide on rats bearing mammary carcinomas induced by dimethylbenzanthracene (7,12-DMBA) or methylnitrosourea (MNU) was investigated. Administration of 300 mg/kg diazoxide caused mild reversible diabetes with maximum glucose levels of 305 +/- 74 (control: 119 +/- 12) mg/dl and related insulin levels of 15 +/- 5 (control: 24 +/- 11) microU/ml after 4 hr in tumor-bearing animals. Following the same dose of diazoxide a more than 90% inhibition of tumor growth was observed in 7,12-DMBA- and MNU-induced autochthonous rat mammary carcinomas as well as remission of the median total tumor volume per group in 7,12-DMBA-induced lesions. Frequently, onset of remissions and median remission duration proved to be dose-dependent in 7,12-DMBA-induced mammary carcinoma and, with the exception of the median remission duration, in MNU-induced tumors too. After cessation of diazoxide application, 30% rebound responses were observed in 7,12-DMBA-induced tumors of animals that had had a first remission due to diazoxide. Application of insulin (2 IU per rat) together with diazoxide (300 mg/kg) reversed the tumor-inhibiting effect of diazoxide in MNU-induced tumors. The diazoxide effect might in part be due to a decrease in the percentage of proliferating cells caused by insulin depletion as indicated by a lower amount of cells in S-phase, as measured by DNA-flow cytometry. Marked toxicity was observed after effective doses of diazoxide; the experiments indicate that induction of reversible diabetes might be a useful tool in the treatment of hormone-dependent mammary carcinoma.

9,10-Dimethyl-1,2-benzanthracene↗