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Biomedical subjects

J Klein

Publications and source records attributed to J Klein.

At least 613 records · Page 34Linked to original sources
PubMed1988

Demystifying the patient dropout: a study of 122 brief-stay day-treatment center admissions.

Past studies examining the dropout from treatment phenomenon have failed to identify comparable populations or a standardized definition of the term "patient dropout." Although the phenomenon is widespread, few investigators have studied the problem within day-treatment programs serving subacutely disturbed clients in need of socialization or prevocational services. The primary purpose of the present study was to determine the reasons for brief Day Treatment Center (DTC) stays of 10 sessions or fewer and to ascertain implications of these findings for admission screening processes. Analysis of demographic information revealed that the average brief-stay patient was in his mid-thirties, was single (65%), was schizophrenic (39%) or suffering a mood disorder (27%), and had attended up to 4 days (63%) before leaving treatment. A retrospective review of 122 brief stay records revealed six categories of reasons for leaving the DTC: (1) a desire to return to work, (2) exacerbation of psychiatric symptoms, (3) resistance to treatment recommendations, (4) negative reaction to the treatment milieu, (5) a desire for less intense treatment, and (6) a belief that problems were resolved during the brief stay. The authors concluded that admission screening interviewers would benefit from complete past school and work records. Strategies for reducing dropout rates should include (1) longer transition periods for newly referred patients, (2) obligatory meetings with the patient and his family and therapist before inpatient discharge, and (3) improved orientation to the DTC program.

Day Care, Medical↗
PubMed1988

Enhancement of digoxin clearance by mannitol diuresis: in vivo studies and their clinical implications.

Because of its narrow margin of safety, digoxin toxicity may occur even during routinely prescribed doses. Due to its very large distribution volume (10 L/kg), only less than 1% of the body load is available for removal, making hemodialysis and hemoperfusion ineffective. Until recently it was assumed that most of the body load of digoxin is eliminated by glomerular filtration. It is now evident that substantial tubular reabsorption and secretion take place. As for the other drugs which are reabsorbed by the tubule (eg Aspirin), we wished to assess whether urine flow rate affect digoxin renal clearance. We studied anesthetized, ventilated dogs. They were preloaded with 25 micrograms/kg IV digoxin the day prior to the experiment. The dogs were infused initially with saline and after a urine collection for digoxin renal clearance 200 ml 10% mannitol were infused over 30 minutes. Digoxin renal clearance was increased 2-3 folds in all cases with a small increase in inulin clearance. Based on these results, the ability of mannitol diuresis to remove significant systemic amounts of digoxin should be tested in acute toxicity in animals. This may be an adjunct modality to FAB antibodies and activated charcoal.

Animals↗
PubMed1988

Effects of quinidine on the renal tubular and biliary transport of digoxin: in vivo and in vitro studies in the dog.

Quinidine is known to inhibit the renal clearance of digoxin without affecting glomerular filtration rate. The renal interaction between these drugs was investigated by a combination of in vivo and in vitro methods. The uptake of digoxin by brush border membrane vesicles was not affected by quinidine. Similarly, digoxin did not inhibit the uptake of the cation N-methylnicotinamide by these vesicles and did not alter the binding kinetics of digoxin to the Na+, K+-adenosine triphosphatase by the antiluminal membrane vesicles. By using the in vivo multiple indicator dilution technique transtubular transport of digoxin was documented; renal-artery infusion of quinidine did not affect the recovery of digoxin in the renal vein or urine. Clearance studies documented that the decrease in the renal clearance of digoxin is paralleled by a significant fall in renal blood flow evidenced by a decrease in p-aminohippuric acid clearance. It is concluded that quinidine inhibits the renal excretion of digoxin not by competition at the tubular cell membrane level, but rather by decreasing renal blood flow. A parallel decrease in biliary clearance of digoxin is documented and may suggest a similar mechanism.

Animals↗
PubMed1988

'Autoreactivity' of some hybridomas may be caused by a three-cell interaction.

We have produced hybridomas by the fusion of BALB/c (H-2d) bone marrow cells, bone marrow cells from BALB/c-nu/nu mice, BALB/c fetal liver cells, and BALB/c fetal thymocytes with the AKR (H-2k) thymoma BW5147. The hybridomas were selected for the expression of the Thy-1.2 antigen of the normal cell donor and for their ability to produce IL-2 upon co-culture with irradiated normal spleen cells. The hybridomas produce IL-2 when co-cultured with H-2k, H-2u, H-2j, or H-2v cells of some strains but not in mixtures with H-2p, H-2s, H-2f, H-2b, H-2q, or H-2d cells. An investigation into the nature of these differences revealed a novel type of interaction between hybridomas, mature T lymphocytes and class II-positive spleen or lymph node cells. The experiments described in this communication suggest that irradiated L3T4+, Ly-1 High T cells recognize syngeneic class II-positive spleen or lymph node cells, but only in some strains. The ability to recognize the syngeneic cells depends both upon the H-2 complex and on the non-H-2 genes. The recognition leads, in the absence of proliferation, to the secretion of an as yet unidentified and largely hypothetical factor which then acts on the hybridoma cells. Upon stimulation with the T lymphocyte-derived factor, the hybridoma cells begin to secrete IL-2, which can then be measured by the proliferation of the IL-2-dependent CTLL line. The IL-2 production by the hybridoma cells is independent of their proliferation. The described interaction apparently does not involve the T-cell receptor of the hybridoma cells. The interaction resembles the autoreactivity of thymocyte hybridomas described by other investigators, and therefore it is possible that this 'autoreactivity' may in fact be generated by a similar mechanism to the one described here.

Animals↗
PubMed1987

Endotoxin protection against pulmonary oxygen toxicity and plasma prostaglandin levels in the rat.

Exposure of rats to high concentrations of oxygen (greater than 95%) at 1 ATA pressure (101 kPa) is lethal within three days. Rats treated with a small dose of endotoxin are protected against these lethal effects of hyperoxia. Recently, we found that the lysine salt of acetylsalicylic acid antagonises this protective action of endotoxin. This suggests that prostaglandin metabolism plays an important role in the protective action of endotoxin against pulmonary oxygen toxicity. Therefore, we measured the plasma levels of 6KPGF1 alpha, a stable degradation product of prostacyclin (PGI2), PGE2 and thromboxane B2, the stable degradation product of thromboxane A2, in rats exposed to air or greater than 95% oxygen for 48 hours. We compared these with the plasma levels of rats treated with endotoxin (Salmonella typhimurium lipopolysaccharide 1 mg/kg) and exposed to air or greater than 95% oxygen for 48 hours. We found that exposure of rats to greater than 95% oxygen for 48 hours leads to a significant rise in the 6KPGF1 alpha levels. Rats exposed to greater than 95% oxygen for 48 hours and treated with endotoxin had significantly higher PGE2 and significantly lower 6KPGF1 alpha plasma levels than saline-treated rats exposed to greater than 95% oxygen for 48 hours.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

The influence of hypothermia on the disposition of fentanyl--human and animal studies.

The effect of hypothermia on the disposition of fentanyl was evaluated in 18 children undergoing corrective cardiac surgery. They received a bolus of fentanyl followed by a continuous infusion which was stopped when cardiopulmonary bypass was established and profound hypothermia was achieved (18 degrees C-25 degrees C). Fentanyl plasma concentration remained essentially unchanged during hypothermia (6.45 ng/ml 5 min into hypothermia and 5.26 ng/ml 100-140 min later; p greater than 0.1). In subsequent experiments, the effect of hypothermia on the pharmacokinetics of fentanyl was studied in 4 piglets serving as their own controls. Both distribution volume (Vz) and total body clearance (CL) were significantly smaller during hypothermia. Our studies indicate that being a drug with a large distribution volume and a high hepatic extraction ratio, both CL and Vz are significantly reduced by hypothermia-induced hypoperfusion. In addition, TBC is influenced by the temperature-dependent hepatic metabolism of fentanyl.

Adolescent↗