Rape-related services in federally funded community mental health centers.

Amendments to the Community Mental Health Centers Act (Public Law 94-63) required community mental health centers (CMHCs) to provide such rape-related services as rape prevention and control, and to assure service availability to rape victims and their families. A questionnaire designed to assess how rape-related services are delivered was mailed to directors of 107 federally funded comprehensive CMHCs in a seven-state region. Fifty-five responses were received, indicating that rape-related services were offered by approximately two-thirds of the centers, 65% of which considered their rape-related services to be less comprehensive than other services. The budget for rape services was less than $10,000 in 80% of responding centers, representing less than 0.5% of the average CMHC budget. Services provided, primarily clinical, involved crisis intervention, counseling, and psychotherapy with rape victims and their families. Prevention and educational activities accounted for less than 25% of all rape-related services at most CMHCs. The results of the study question the impact of federal mandates on local mental health services.

A kinetic investigation of the effects of adrenaline on 45Ca2+ exchange in isolated hepatocytes at different Ca2+ concentrations, at 20 degrees C and in the presence of inhibitors of mitochondrial Ca2+ transport.

The effects of adrenaline on 45Ca2+-exchange curves for isolated hepatocytes incubated under various steady-state conditions were investigated. Kinetic analysis showed that the simplest compartment configuration consistent with each set of data was a series configuration of a three-compartment closed system comprising compartment 1 (C1), the extracellular medium, and two kinetically distinct compartments of cellular exchangeable Ca2+, C2 and C3 (C1 = C2 = C3). Subcellular fractionation of hepatocytes labelled with 45Ca2+ at 0.1 mM-Ca2+ indicated that C3 includes exchangeable Ca2+ in the mitochondria and endoplasmic reticulum. The following results were obtained from experiments conducted at 37 degrees C at five different extracellular Ca2+ concentrations. For both untreated and adrenaline-treated cells, plots of the flux from C1 to C2 as a function of the extracellular Ca2+ concentration were best described by straight lines consistent with Ca2+ influx across the plasma membrane being a diffusion process. Adrenaline increased the value of the permeability constant for Ca2+ influx by 40%. For untreated cells, plots of the flux between C2 and C3 as a function of the concentrations of Ca2+ in these compartments approached a plateau at high Ca2+ concentrations. Adrenaline caused a 3-fold increase in the concentration of Ca2+ that gives half-maximal rate of Ca2+ transport from C2 to C3. At 1.3 mM extracellular Ca2+, a decrease in incubation temperature from 37 degrees C to 20 degrees C decreased the quantity of Ca2+ in C3 and the flux and fractional transfer rates for the transport of Ca2+ between C2 and C3. At 20 degrees C adrenaline increased the quantity of Ca2+ in C3 and the fractional transfer rates for the transfer of Ca2+ from C1 to C2, and from C2 to C3. At 37 degrees C and 2.4 mM extracellular Ca2+, antimycin A plus oligomycin decreased the quantity of Ca2+ in C3 and increased the fractional transfer rate for the transport of Ca2+ from C3 to C2. In the presence of antimycin A and oligomycin, adrenaline did not increase the quantity of Ca2+ in C2 or the flux and fractional transfer rate for the transport of Ca2+ from C1 to C2, whereas these parameters were increased in the absence of the inhibitors.

Delivery of rape-related services in CMHCs: an initial study.

A questionnaire designed to assess how rape-related services are delivered was mailed to directors of 34 federally funded comprehensive Community Mental Health Centers (CMHCs) in Missouri and Illinois. Responses were received from 18 CMHCs. Results indicated that rape-related services were offered by approximately three-quarters of the respondents, who reported delivering primarily clinical services.

Parathyrin and calcium homeostasis in the fetus.

The response of plasma parathyrin (PT) in cattle fetuses to changes in plasma calcium was investigated in utero. Resting plasma calcium levels for 4 fetuses averaged 3.1 mg/dl higher than for their mothers. Fetal PT levels (0.67 ng/ml) were half those of the mother (1.40 ng/ml). Hypocalcemia induced by EDTA infusion evoked a rise in plasma PT in 2 or 3 fetuses. The relationship between plasma PT and calcium levels in these fetuses was curvilinear, PT rising from about 0.7 ng/ml at 13 mg calcium/dl to a plateau of about 1.6 ng/ml below 10 mg calcium/dl. This contrasted with one of the mothers in which PT rose above 3 ng/ml when plasma calcium fell from 9 to 7 mg/dl. During infusion of EDTA to mother or fetus there were no changes in plasma calcium or PT levels in the respective fetus or mother.

A kinetic analysis of the effects of adrenaline on calcium distribution in isolated rat liver parenchymal cells.

1. The effects of adrenaline on Ca distribution in isolated rat liver parenchymal cells were studied using a (45)Ca exchange technique under steady-state conditions with respect to the net movement of Ca. (45)Ca was initially introduced into the extracellular medium. The amount of cellular (45)Ca was determined after separation of the cells from the medium by centrifugation through a solution which contained LaCl(3) (to displace (45)Ca bound to sites on the outside of the cell membrane) and silicon oil. At 1.3 and 2.4 mm-extracellular Ca, a stimulation of the initial rate of (45)Ca exchange was observed in the presence of 10(-7)m-adrenaline (or 10(-6)m-phenylephrine) with a 7% decrease, and no change, respectively, in the plateau of the exchange curve. The same degree of stimulation was observed when (45)Ca was added at 1, 15, 30 or 45 min after the adrenaline.2. No stimulation of the initial rate of exchange was observed at 0.1 mm-extracellular Ca, or at 2.4 mm-extracellular Ca in the presence of antimycin A and oligomycin. At 0.1 mm-Ca, a 60% decrease in the plateau of the exchange curve was observed in the presence of adrenaline. The concentration of adrenaline (10(-7)m) which caused half-maximal stimulation of the initial rate of (45)Ca exchange at 1.3 mm-Ca was similar to that (2 x 10(-7)m) which caused half-maximal decrease in the plateau at 0.1 mm-Ca.3. The addition of adrenaline to cells equilibrated with (45)Ca at either 2.4 or 1.3 mm-Ca caused a transient loss of (45)Ca followed by a return to a new steady state after 1 or 10 min, respectively. A loss of (45)Ca was also observed at 0.1 mm-Ca, but the (45)Ca content of the cells remained maximally depressed for at least 30 min.4. A non-linear least-squares iterative curve-fitting technique was used to demonstrate that (a) an equation which includes two exponential terms and (b) a parallel or series arrangement of three compartments of exchangeable Ca (the medium and two compartments associated with the cell) are consistent with each set of data obtained at 1.3 or 2.4 mm-Ca in the presence or absence of adrenaline (or phenylephrine). At 1.3 mm-Ca, the quantities of exchangeable Ca in the two kinetically defined cellular compartments were 0.04-0.07 and 0.34-0.37 nmol per mg wet weight with rate constants for Ca outflow of 1.2-1.5 and 0.06-0.08 min(-1), respectively.5. Analysis of the changes induced by adrenaline or phenylephrine showed that at 1.3 and 2.4 mm-extracellular Ca these agents caused a 75-150% increase in the quantity of exchangeable Ca in the small kinetically defined compartment and a 20% decrease in the quantity of exchangeable Ca in the large kinetically defined compartment. These changes were mediated by an 80-160% increase in the rate constant for the inflow of Ca from the medium to the small kinetically defined compartment, and either a 20-60% decrease in the rate constant for inflow to, or a 20% increase in the rate constant for outflow from, the large compartment.6. Replacement of the LaCl(3) in the solution used to separate the cells from the incubation medium with either 5 mm-EGTA or 5 mm-CaCl(2) did not alter the kinetics of (45)Ca exchange or the stimulation by adrenaline. This, together with the observation that at 1.3 mm-extracellular Ca, adrenaline increases the initial rate of exchange in the absence, but not in the presence, of antimycin A plus oligomycin, indicates that both cellular compartments of exchangeable Ca are intracellular.7. The addition of antimycin A plus oligomycin to cells equilibrated with (45)Ca at 2.4 mm-extracellular Ca in the presence or absence of adrenaline displaced 0.09 and 0.14 nmol (45)Ca. mg(-1), respectively.8. Subcellular fractionation of cells equilibrated with (45)Ca at 0.1 mm-extracellular Ca revealed that the mitochondria and microsomes contained significant amounts of (45)Ca. The amounts of (45)Ca in these fractions decreased by 50 and 40%, respectively, in the presence of adrenaline.9. In (45)Ca exchange experiments conducted with isolated mitochondria at 37 degrees C at 1.5 x 10(-7)m and 0.9 x 10(-7)m free Ca in the presence of 2 mm-Mg(2+), one kinetically defined compartment of exchangeable mitochondrial Ca was detected. The rate constants for Ca outflow were found to be 0.15+/-0.03 and 0.12+/-0.04 min(-1), respectively, in reasonable agreement with the value obtained for the rate constant for the outflow of Ca from the large kinetically defined compartment of exchangeable Ca observed in cells.10. It is concluded that adrenaline has two effects on Ca movement in the liver cell. These are to cause a loss of Ca from an intracellular compartment, which includes the mitochondria and microsomes, and to increase the transport of Ca from the extracellular medium to an intracellular site. This results in an increase in the amount of Ca in a small intracellular compartment which may represent cytoplasmic Ca, or Ca bound to sites on the inside of the plasma membrane.

The origin of lipoprotein in the intestinal and hepatic lymph of unsuckled new-born calves.

1. Experiments have been conducted to determine the origin and character of the lipid in thoracic duct lymph of new-born, unsuckled calves. This involved the collection and analysis of intestinal and hepatic lymph from two bile-fistulated and seven non-fistulated animals.2. The output of total esterified fatty acid in intestinal and hepatic lymph in the unfed calf after recovery from the anaesthetic was about 0.6 and 0.025 g/hr, respectively.3. Three lipoprotein fractions were obtained by ultracentrifugation of intestinal lymph samples. These appeared to correspond to very low- (d < 1.005), low- (1.2 > d < 1.005) and high- (d = 1.20) density lipoprotein of human serum. These lipoproteins contained approximately 40%, 50% and 10% respectively of the total lipid.4. Very low-density lipoprotein was not found in blood serum or hepatic lymph and it was evident that very low-density lipoprotein and most of the low-density lipoprotein in intestinal lymph were derived from sources other than the capillary filtrate.5. The output of total esterified fatty acid in intestinal lymph fell steadily during the course of an 11-16 hr period of bile deprivation to values 55% of those in comparable calves without bile fistulae. This was accompanied by a virtual disappearance of very low-density lipoprotein and a decrease in low-density lipoprotein of approximately 50%. These effects could not be attributed to starvation.6. There was a general resemblance in fatty-acid composition between biliary lipid and the triglyceride of the lipoproteins, the predominant fatty acids being 16:0 and 18:1. The presence of appreciable levels of odd carbon number and branched-chain fatty acids were consistent with the transfer of significant amounts of free fatty acid from maternal blood to the foetus.7. It is concluded that most of the lipid in thoracic-duct lymph of unfed, new-born calves is derived from the intestines and that the fatty acids of the very low-density lipoprotein in intestinal lymph arise from the absorption of biliary phospholipid.