Hospitals.

Anticipating health care reform and seeking a marketing edge over competitors, hospitals are forming alliances with other providers.

Managed care organizations.

To prepare for health reform, HMOs are joining together, acquiring hospitals and provider groups, and developing data to demonstrate quality and cost effectiveness.

For mental health cost problems, see a specialist.

Separating mental health care from other benefits helps keep costs down while improving treatment, experts say.

Hospitals.

American hospitals are striving to improve both the quality of medical care and relationships with patients. Many have adopted TQM, an increasingly popular approach to improving the delivery of all services. A growing emphasis on making hospital facilities patient-friendly has resulted, for example, in women having birthing experiences that are far more pleasant they they were for those who gave birth in hospitals only a decade ago. Programs such as these are helping hospitals attract patients and stay competitive.

Urban health care.

Public hospitals are straining under the burden of having to care for many of the poorest and sickest people in America. The health care problems of the nation's most disadvantaged include infectious diseases such as AIDS and tuberculosis, as well as problems related to violence and lack of access to primary care. Urban hospitals are struggling to address the needs of the indigent, and to find alternatives for those who often rely on emergency rooms for routine care.

Rising to the challenge.

An overview of health care in America today. An estimated 37 million men, women, and children lack access to affordable health care. As the cost of medical care continues to rise, millions more face the possibility of joining the ranks of the uninsured. These problems must be addressed. But we also need to consider the many benefits that we derive from our health care system.

Biochemical analysis and electron microscopic study on intracellular virions in NIH/3T3 mouse cells chronically infected with Moloney murine leukaemia virus: effect of interferon.

Radioactively labelled virus particles of intracellular origin were isolated from the cytoplasmic fraction of disrupted NIH/3T3 cells chronically infected with Moloney murine leukaemia virus [NIH/3T3 (MLV)]. Interferon (IFN) treatment for 48 h, which arrested more than 90% of virus release, resulted in a remarkable accumulation of these intracellular virions. However, no major effect of such treatment was apparent on their structural properties. Transmission electron microscopic examination revealed that these intracellular virions were located within cytoplasmic vacuoles. IFN treatment resulted in a considerable increase in the number of virus-containing vacuoles, as well as the total number of vacuolar virions. It seems that IFN inhibits the final release of vacuolar virions from the cells, thus leading to their intracellular accumulation.

An effect of interferon on the uncoating of murine leukaemia virus not related to the antiviral state.

Adsorption of murine leukaemia virus (MLV) to NIH/3T3 cells, as determined by analysing its reverse transcriptase activity in the cell membrane, was found to be unaffected by interferon (IFN). Virus penetration and uncoating were followed by quantifying intracellular virions in terms of sedimentable reverse transcriptase activity in the cytoplasmic fraction. The penetrating virions were found to accumulate to a higher level in IFN-treated cells than in untreated controls. Intracellular virions were uncoated in untreated cells shortly after their penetration, whereas their uncoating was delayed in the IFN-treated cells for 2 to 3 h. Neither virus uncoating nor the effect of IFN on this process appeared to require new protein synthesis, since both were unaffected by cycloheximide (CH).

Effect of human fibroblast interferon on uncoating and release of murine leukaemia virus in NIH/3T3 mouse cells.

The effect of human fibroblast interferon (IFN), a heterologous IFN, on the uncoating of murine leukaemia virus (MLV) was investigated in exogenously infected NIH/3T3 mouse cells. Virus uncoating was determined by following the disappearance of the penetrating virus particles from the cytoplasm of the infected cells. Intracellular virus particles were estimated by sedimenting them at high speed from the cytoplasmic fraction of the infected cells and assaying their reverse transcriptase activity. In untreated control cells, uncoating started immediately after penetration, but in cells treated with human IFN, uncoating was delayed for 2 to 3 h. This delay led to prolongation of the infectious cycle, with delayed release of progeny virus. The delay in release did not result from inhibition by IFN of the process of release, since in NIH/3T3 cells chronically infected with MLV, treatment with IFN had no effect on virus release.

Adsorption, penetration, and uncoating of murine leukemia virus studied by using its reverse transcriptase.

A procedure using the virus-associated reverse transcriptase was developed for following the kinetics of adsorption, penetration, and uncoating of murine leukemia virus. Viral adsorption to cell membrane was determined by assaying this enzyme activity in isolated debris of mechanically disrupted cells after infection with murine leukemia virus in the presence of actinomycin D. At 37 degrees C, viral adsorption proceeded at a high initial rate, but after 5 min of incubation with the virus, it gradually slowed down. At 4 degrees C, viral adsorption was slower but proceeded at a linear rate. Intracellular virus was determined by centrifuging the cytoplasmic fraction of the disrupted cells at 105,000 x g for 45 min and assaying reverse-transcriptase activity in the high-speed pellet thus obtained. Sucrose gradient analysis of the enzyme activity recovered from the cytoplasm of infected cells indicated that this activity represented intact virus particles. No appreciable amount of such particles was recovered from the cytoplasm of cells infected at 4 degrees C. This indicates that the virions recovered from the cytoplasm of cells infected at 37 degrees C are indeed intracellular virus particles which penetrated into the cells and not just membrane-bound particles mechanically released to the cytoplasmic fraction during cell disruption. By this procedure intracellular virus was found to accumulate in the cytoplasm, reaching a maximal level within 20 min. The accumulated intracellular virus particles gradually disappeared from the cytoplasm, evidently due to their uncoating which was completed within 80 min.