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Biomedical subjects

R M Rubin

Publications and source records attributed to R M Rubin.

At least 37 records · Page 2Linked to original sources
PubMed1995

Change in expenditure patterns of retirees: 1972-1973 and 1986-1987.

This study presents a comparative analysis of changes over time in expenditure patterns of retirees. Tobit regressions reveal significant differences in expenditure patterns in health care, leisure, necessities, and philanthropy. Over the past two decades, health care became more of a necessity, and its budget share increased. The marginal propensity to consume (MPC) leisure activities more than doubled. Retirees allocated lesser budget shares to the necessity areas of food and apparel, but single females had increased housing shares. The budget share and MPC for charitable contributions declined. Over time, the average propensity to consume (APC) increased greatly from 94 to 103 percent, a potential problem if elderly persons dissave at unsustainable rates. The spending of older retirees now differs substantially from younger retirees, with the APC declining with age, an apparent contradiction of the life cycle hypothesis. Apparently, the retired are more cautious about spending in the latter stages of the life cycle.

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PubMed1995

Out-of-pocket health expenditures by elderly households: change over the 1980s.

This study compares out-of-pocket health expenditures of elderly and nonelderly households over the past decade, using descriptive statistics and two-stage least squares analysis of Consumer Expenditure Survey data for 1980-1981 and 1989-90. This empirical analysis provides a basis for discussion of both efficiency and equity issues in health policy. We find that increases in out-of-pocket medical care expenditures over the last decade were mainly for insurance premiums rather than medical goods and services, which indicates potential inefficiencies in health care markets. We also find that Medicare promoted equity of out-of-pocket expenditures on health care among elderly persons over the 1980s, which implies that universal national health insurance would enhance distribution equity.

Aged↗
PubMed1993

Out-of-pocket health expenditure differentials between elderly and non-elderly households.

Regression analysis was used to compare out-of-pocket health expenditures between lower and higher income elderly and non-elderly households. Race and housing tenure were significant determinants for both age groups, but assets, education, and family size were significant only for the non-elderly. Analysis of out-of-pocket health costs indicated greater equity among elderly persons, probably due to Medicare, but income elasticities revealed that health spending is a luxury for lower income elderly households.

Adult↗
PubMed1992

Reduction of endotoxin-induced vascular permeability by monoclonal antibodies against lipopolysaccharide determinants.

Endotoxin, a bacterial lipopolysaccharide implicated in the pathogenesis of septic shock, markedly alters vascular permeability following intravenous injection in rabbits. We investigated the ability of murine monoclonal antibodies to confer protection against endotoxin-induced increases in a rabbit model of ocular vascular permeability. Four monoclonal antibodies of differing specificities as well as polymyxin B were compared for their effects on endotoxin from either Escherichia coli or Pseudomonas aeruginosa. Preincubation of endotoxin with antibodies directed against Pseudomonas O side chain or core glycolipid resulted in marked attenuation of vascular permeability due to Pseudomonas endotoxin, but not E. coli endotoxin. Antilipid A antibodies were not significantly effective in neutralizing either endotoxin with in vitro preincubation. Low avidity of the antilipid A antibody, low density of lipid A binding sites, or inaccessibility of the lipid A may have prevented more marked interactions. When administered intravenously prior to endotoxin challenge, none of the antibodies demonstrated the ability to provide specific protection to subsequent endotoxin in this model. They did provide partial nonspecific protection against endotoxins regardless of epitope specificity. When administered prophylactically, polymyxin B, an antibiotic that binds to lipid A, was highly effective in neutralizing the toxic effects of endotoxin. Since antibodies to lipid A reduce mortality in septic shock, the failure to demonstrate efficacy in this study may be due to the marked sensitivity of the rabbit eye to endotoxin. Alternatively, beneficial effects from antiendotoxin antibodies in septic shock may be unrelated to the inhibition of vascular permeability. Some protection from antiendotoxin antibodies may be due to enhancement of nonspecific mechanisms.

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PubMed1989

Private long-term care insurance. Simulations of a potential market.

Long-term care is now the most common cause of catastrophic illness costs for the elderly. Although acute care health insurance represents a mature market, private long-term care insurance is in its infancy and poised for development. This study presents a comparative analysis of simulation data, generated from the Brookings-ICF Long-Term Care Financing Model, for five alternative private long-term care insurance models. The simulation results indicate 1) the potential market for private long-term care insurance is substantial, 2) moderately comprehensive long-term care policies are affordable by a significant minority of the elderly, 3) policies are considerably more affordable to those under age 65, and 4) long-term care insurance has somewhat less potential to pay for nursing home costs for high risk groups than for other elderly.

Adult↗
PubMed1989

The potential impact of private long-term care financing options on Medicaid: the next thirty years.

This study analyzes the potential effect on the Medicaid program of private sector financing mechanisms for long-term care. The data are from the Brookings-ICF Long-Term Care Financing Model and include projections over the next thirty years. While private financing alternatives have some modest impacts on Medicaid expenditures and the number of Medicaid long-term care recipients, the data suggest relatively little change in the need for Medicaid. There will be substantial increases in Medicaid long-term care expenditures over time, and private sector options cannot change this much.

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PubMed1988

A platelet-activating factor antagonist inhibits interleukin 1-induced inflammation.

Treatment with a platelet-activating factor receptor antagonist, SRI 63-441, inhibited interleukin 1-induced increases in vascular permeability and leukocyte infiltration in the rabbit eye following the intravitreal injection of human interleukin 1-alpha. Treatment with the prostaglandin-synthetase inhibitor, flurbiprofen, or the corticosteroid, prednisolone, resulted in comparable attenuation of the increase in vascular permeability. In contrast to the effect of flurbiprofen, SRI 63-441 did not reduce interleukin 1-induced increases in prostaglandin E2 levels. Combined treatment with the platelet-activating factor antagonist and inhibitors of prostaglandin synthesis nearly prevented interleukin 1-induced increases in vascular permeability or cellular infiltration. These findings suggest a role for platelet-activating factor in interleukin 1-induced inflammation. Platelet-activating factor and prostaglandins may act synergistically as mediators of interleukin 1-induced vascular permeability.

Animals↗
PubMed1988

Prostaglandin-independent inhibition of ocular vascular permeability by a platelet-activating factor antagonist.

Platelet-activating factor (PAF), a lipid mediator of inflammation, may markedly increase vascular permeability. We assessed the ability of the PAF antagonist SRI 63-441 to inhibit ocular vascular permeability induced by the intravenous injection of endotoxin or anterior chamber paracentesis. The PAF antagonist SRI 63-441 significantly blocked ocular vascular permeability following either intravenous endotoxin or anterior chamber paracentesis as determined by the reduction in accumulation of 70,000-molecular-weight fluorescein isothiocyanate-conjugated dextran or serum proteins into the anterior chamber. SRI 63-441 did not reduce increases in aqueous humor prostaglandin E2 levels. The efficacy of the PAF antagonist was additive in combination with either topical indomethacin or topical corticosteroid. Combined therapy almost completely prevented increases in ocular vascular permeability. These data support the conclusion that multiple mediators contribute to ocular vascular permeability and that combinations of pharmacologic agents may be superior to a single drug.

Animals↗
PubMed1988

Effects of a fish oil dietary supplement on endotoxin-induced ocular inflammation.

We compared the effects of fish oil versus corn oil dietary supplements on two rabbit models of uveitis induced by either intravenous (IV) or intravitreal (IVT) Escherichia coli endotoxin. Addition of fish oil to a standard diet consistently diminished the rise in aqueous humor prostaglandin E2 levels 24 hours after IVT endotoxin injection or 3 hours following IV endotoxin injection. Aqueous humor thromboxane B2 levels following IV or IVT endotoxin injection were also lower in rabbits fed a fish oil supplemented diet. However, the fish oil diet resulted in only a modest attenuation of increases in ocular vascular permeability following either IVT or IV endotoxin injection. Fish oil supplementation inconsistently reduced leukocyte infiltration into the anterior chamber following IVT endotoxin. In contrast to the reported ability of fish oil dietary supplements to reduce corneal inflammation, these models of anterior uveal inflammation do not seem to be altered in a clinically significant manner.

Animals↗
PubMed1988

Ocular inflammatory effects of intravitreally-injected tumor necrosis factor.

Many of the pathophysiologic effects of bacterial endotoxin have recently been attributed to a monokine, tumor necrosis factor (TNF). The rabbit eye is extremely sensitive to locally injected endotoxin. The authors have investigated the possible contribution of TNF to ocular inflammation in a rabbit model. The intravitreal injection of 10(5) to 5 X 10(5) units of recombinant human TNF produced a sustained disruption of the blood-aqueous barrier as manifested by elevated aqueous humor protein levels. In addition, 83% of rabbits receiving this dose of TNF developed hyperemia of limbal vessels and early neovascularization of the cornea. Many developed posterior synechiae (fibrous adhesions between the iris and the lens). TNF induced only a slight cellular response in the anterior chamber. Histologic studies confirmed the presence of new vessels and demonstrated a marked mononuclear infiltrate within and beneath the epithelium of the iris and ciliary body. Lower doses of TNF produced inconsistent results. Heating TNF completely destroyed its inflammatory effects. The time course of the ocular response to TNF and the quantity of recombinant protein needed to produce consistent effects were vastly different from effects observed with interleukin-1. For example, 24 hours after an intravitreal injection, 2.2 X 10(4) ng of TNF (5 X 10(5) units) produced significantly less protein extravasation and polymorphonuclear leukocyte infiltration than 4 ng of recombinant interleukin-1. Similarly, 24 hours after intravitreal injection, 1 ng of Escherichia coli endotoxin tended to be a more potent inflammatory stimulus than this quantity of TNF. These observations indicate that the ocular pathophysiologic effects of TNF can be readily distinguished from changes induced by either endotoxin or another endotoxin induced monokine, interleukin-1.

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