The ventilator-assisted individual. Cost analysis of institutionalization vs rehabilitation and in-home management.

The purpose of this article is to present a cost analysis of in-home vs institutionalization for severely physically disabled ventilator-assisted individuals (VAIs). Following rehabilitation and adaptation to noninvasive methods of ventilatory support, 30 VAIs were maintained in the community for 12.9 +/- 1.1 years with personal care attendants organized by a home care vendor reimbursed by New York City Medicaid. The program permitted self-directed severely disabled clients, including these 30 exclusively nontracheostomized VAIs, to live in the community and direct their attendant care and personal affairs. Prior to discharge home, the 30 patients resided in the respiratory unit of a long-term care facility for a mean of 8.9 +/- 10.1 years. The unit is currently reimbursed at a mean rate of $718.80 per patient per day. The current mean total cost of maintaining these VAIs in the community is $235.13 +/- 56.73 per patient per day. The conversion to and/or maintenance on 24-h nontracheostomy ventilatory support permitted discharge to the community by allowing the VAI to be attended by trained but uncredentialed home care attendants, thus avoiding prohibitively expensive in-home nursing for tracheostomy care. This created a savings to the public of 77 percent or $176,137 per year per client. We conclude that conversion to and/or use of noninvasive methods of ventilatory aid can be a reasonable and cost-saving goal. More respiratory rehabilitation centers are needed to free up hospital beds and facilitate discharge of VAIs to the community. There is also evidence that trained attendants should be permitted to suction tracheostomized VAIs in the home.

Biological activity of region 65-102 of the myelin basic protein.

Region 65-102 of the myelin basic protein (MBP) houses a number of antigenic determinants known to induce delayed-type hypersensitivity, experimental allergic encephalomyelitis (EAE), suppressor cell function, and antibodies. In this report we describe the biological activity of synthetic peptides S53, S55, and S49 with sequence homology to region 69-84 of the rat, guinea pig, and bovine MBP. Peptide S53-A, defined by residues 75-84 of the guinea pig (SQRSQDEN) and of the rat (SQRTQDEN) MBP induced clinical signs of disease in Lewis rats. These included weight loss, flaccid tail, "muscle wasting," and hind-leg weakness. Histological examination of brain, spinal cord, and sciatic nerve sections of diseased rats revealed the complete absence of focal and perivascular lymphocytic infiltrates characteristics of demyelinating EAE lesions. Elongation of peptide S53 by three or six residues to residue sequences naturally found at its N-terminal end gave rise to peptides S55S (PQKSQRSQDEN) and S49S (GSLPQKSQRSDQDEN), respectively. Lewis rats challenged with either S55S or S49S developed classical clinical and histological signs of EAE. Severe hind-leg paralysis was accompanied by incontinence and sometimes death. Injected in the form of carrier-free peptide, S53 was a meager B cell immunogen. S53 conjugated with methylated-bovine serum albumin was also a potent immunogen and produced clinical signs of disease without CNS pathology. By comparison, carrier-free S55S and S49S were potent immunogens giving rise to antibodies that cross reacted completely and competitively with S55S but considerably less so with S53. The results show that the sequence of S53 defines an epitope responsible for the formation of anti-S53 antibodies. Elongation of the S53 sequence at its N-terminal end generated an additional epitope which induced cell-mediated immunity responsible for the concomitant development of pathological signs of EAE. It may be concluded that the induction of classical signs of EAE requires specific and defined sequences capable of expressing both B cell and T cell functions.