Compensation models of certified nurse-midwives in clinical practice.

Nurse-midwives have been recognized for decades as clinically effective health care providers for infants and women. Little information exists, however, as to how these clinically effective professionals are compensated for their services. The article presents five compensation models for certified nurse-midwives (CNMs), demonstrating the financial benefits and cost of each using a hypothetical case study format and composite data from current CNM practices in the United States. From these templates, CNMs can apply their own financial and productivity data to construct a financial analysis of their productivity against their current financial compensation.

Inhibition of human neutrophil elastase by bacterial polyanions.

We previously demonstrated that pneumococcal extracts contain a highly specific inhibitor of human neutrophil elastase (HNE). We now show that the active inhibitor in these extracts is a high-molecular-weight, heat-stable substance that appears to be RNA, since inhibitory activity of pneumococcal extracts is decreased by incubation with ribonuclease but not by incubation with deoxyribonuclease or proteinase K. Moreover, metabolically labeled ([3H]uridine) pneumococcal RNA, isolated by phenol extraction followed by ethanol precipitation, strongly inhibits HNE. Pneumococcal capsular polysaccharide, although polyanionic, is only weakly inhibitory toward HNE and is not a major source of elastase-inhibitory activity in pneumococcal extracts. On the other hand, the capsule of Haemophilus influenzae type b contains polyribosylribitol phosphate. This highly charged polyanion possesses HNE-inhibitory activity, but only under special circumstances to be discussed below. Pneumococci (type I, type II smooth, type II rough) and H. influenzae (type b) all release HNE-inhibitory activity into their culture medium during growth. By contrast, Klebsiella pneumoniae and Staphylococcus aureus release little (if any) stable HNE-inhibitory activity during growth. We propose that some bacterial pneumonias may spare host tissue because polyanions released by the invading microorganisms (e.g. RNA from autolysing pneumococci) inhibit elastase released from inflammatory neutrophils and thereby modulate accompanying tissue proteolysis. Pneumonias caused by microorganisms that do not release stable polyanionic inhibitors of HNE (e.g., Staphylococcus and Klebsiella) may be correspondingly more injurious to the lung.

Marketing to attract women.

Patient care and marketing programs sensitive to women can help Catholic facilities increase maternity care patient volumes. Four factors influence hospitals' ability to attract women. Women today are better educated and more sophisticated than ever before about health care needs, and they have more providers from which to choose. With limited resources, providers must be discriminating in the type of services they deliver and how. Finally, women make most of the health care decisions for the families. To attract women, providers should offer them personalized care, participation in decisions, information about treatment, attractive facilities, convenience, and affordable costs. Many providers believe Catholic facilities fail to attract maternity patients because they do not perform tubal ligations; however, parents generally see childbirth as a separate event from sterilization. Providers also believe that non-Catholic patients will not use their facilities, but today's patients choose a hospital because of what it offers, not sponsorship. Some patients may not choose Catholic facilities because they see them as less progressive, but this image can be corrected through marketing Catholic facilities' common strengths include their focus on care rather than profit, their compassionate, individualized care, the image of women caring for women, and their stability. Catholic facilities have built on their strengths to attract women patients by reinforcing positive perceptions with innovative programs, marketing directly to women, educating physicians in how to respond to women's needs, increasing linkages with all women in the community, ensuring that the mission of care is reflected in the physical plant, using a marketing program to help employees carry out compassionate care, and surveying patients for feedback on how their needs are met.

A new elastase inhibitor from Streptococcus pneumoniae protects against acute lung injury induced by neutrophil granules.

A neutrophil elastase-inhibitor isolated from lysed pneumococcal cells, as well as trypsin-digest peptides derived from this factor, were tested for their ability to suppress acute lung injury in mice treated with human neutrophil granule extracts. Injury was assessed by measuring pulmonary sequestration of circulating 125I-labeled albumin, lung water, and lung hemoglobin. Both the native inhibitor and the tryptic-peptides gave good protection when preincubated with granule extract for brief periods before intrapulmonary instillation. Lesser, but still significant, protection was observed in the absence of preincubation. Protection was not simply due to addition of exogenous proteins to the granule extract because substitution of goat immunoglobulin for pneumococcal fraction was ineffective. These results suggest that pneumococcal elastase-inhibitors, recently described by us, may play a role in minimizing lung injury during pneumococcal pneumonia.

Evaluation of the urinary desmosine radioimmunoassay as a monitor of lung injury after endobronchial elastase instillation in sheep.

Thirty male sheep were treated with varying doses of endobronchial elastase. Urinary excretion of elastin peptides was then measured by desmosine radioimmunoassay and compared with pre-enzyme values. Mean linear intercepts were measured in treated and untreated lobes 4 wk later, and in addition, lung perfusion, ventilation, and volume were measured before enzyme treatment and 4 wk later using radionuclide-imaging techniques. Most of the elevation in urinary desmosine excretion occurred in the first 48 h after elastase administration. The increase in desmosine excretion was positively correlated with: enzyme dose (r = 0.74, p less than 0.01), increase in mean linear intercept (r = 0.61, p less than 0.05), decrease in lung perfusion (r = 0.77, p less than 0.01), and decrease in ventilation (r = 0.58, p less than 0.05). These results demonstrate that the urinary desmosine radioimmunoassay is a reliable index of pulmonary elastin breakdown and of several resultant anatomic and physiologic stigmata of pulmonary emphysema.

Levels of elastase activity in bronchoalveolar lavage fluids of healthy smokers and nonsmokers.

Elastase activity was measured in concentrated, cell-free bronchoalveolar lavage (BAL), using the synthetic substrate butyloxycarbonyl-L-alanyl-L-alanyl-L-prolyl-L-valyl-amino-methylcoumarin. The BAL fluids obtained from young, asymptomatic smokers with normal urine desmosine concentrations 1 h after they had smoked 2 cigarettes showed significant increases in elastase levels compared with those in nonsmoking control subjects [nanomoles substrate hydrolyzed (3 h) per milligram lavage albumin = mean 2.7 +/- 1.9 SD (11 smokers) versus 0.5 +/- 0.4 (11 nonsmokers), p less than 0.01]. Repeated BAL samples were obtained at later times from one smoker with a high initial enzyme value and from one nonsmoking control subject. Elastase activity varied over time, but both subjects consistently remained within their respective group ranges. Inhibition studies on pooled BAL from smokers showed that the elastase activity present had properties of both serine and metalloenzymes, suggesting that neutrophils and/or monocytes (serine enzyme) as well as macrophages (metalloenzyme) contributed to the observed activity. Lung lavage cells obtained from 2 of the smokers and 2 of the nonsmokers were stained with both a chromogenic substrate and by indirect immunofluorescence for the serine enzyme. Positively stained neutrophils were readily found in smokers' lavages, but no, or only rare, positive mononuclear cells could be identified. By contrast, peripheral blood mononuclear cells from all 4 subjects stained positively with either method. These results show that some asymptomatic smokers have significantly more elastase activity in their bronchopulmonary secretions than do nonsmokers (as measured with a low molecular weight synthetic substrate). Furthermore, the enzyme activity recovered in smokers' BAL appears to be derived mainly from neutrophils (serine enzyme) and macrophages (metalloenzyme), rather than from monocytes.

Alpha 1-proteinase inhibitor is more sensitive to inactivation by cigarette smoke than is leukocyte elastase.

Aqueous solutions of gas phase cigarette smoke were incubated with pure human leukocyte elastase or with crude human leukocyte granule extract, and the effects on enzyme activity were determined using a synthetic amide substrate. Simultaneously, the same smoke solutions were incubated with 10% human serum under identical conditions, and the effects on serum inhibition of purified or crude leukocyte elastase were similarly measured. In addition, aqueous solutions of unfractionated cigarette smoke were incubated with leukocyte elastase or serum, and the abilities of the smoke-treated enzyme to digest elastin and of the smoke-treated serum to inhibit elastin digestion were determined. Both experimental protocols showed that serum elastase-inhibiting capacity (primarily caused by alpha 1-proteinase inhibitor) is more susceptible to inactivation by aqueous solutions of cigarette smoke than is leukocyte elastase, suggesting that elastase inhibition (rather than elastase activity) may be predominantly suppressed by cigarette smoke inhalation in vivo.

Partial purification and characterization of mouse peritoneal exudative macrophage elastase.

Mouse peritoneal exudate macrophage elastase can be significantly purified with 60% recovery of the starting activity by affinity chromatography against SDS-treated alpha-elastin covalently linked to agarose beads. The enzyme has an apparent Mr of 26 500 based on SDS-acrylamide gel electrophoresis. Molecular sieving chromatography on Sephadex gel gives a Mr for macrophage elastase of 21 000--28 000. The enzyme is not inhibited by chloromethyl ketone inactivators specific for pancreatic and leukocyte elastase nor by phenylmethylsulfonyl fluoride. Macrophage elastase also does not bind to tritiated diisopropylphosphorofluoridate. The enzyme is inhibited by EDTA and thus appears to be a metallo-protease. Macrophage elastase is resistant to human alpha 1-proteinase inhibitor and to human and mouse alpha 2-macroglobulin. In view of its lack of susceptibility to these endogenous serum proteinase inhibitors, macrophage elastase may play an important role in physiological and pathological remodeling of connective tissues.

Lung injury induced by leukocytic proteases.

Human polymorphonuclear neutrophilic leukocytes (PMNs) contain large amounts of neutral proteases that can degrade elastin, collagen, proteoglycan, and basement membrane. The instillation of one of the purified enzymes (elastase) into dog lungs in vivo causes degradation of elastic fibers and other alveolar septal components and results in anatomic changes similar to those of human pulmonary emphysema. Cigarette smoking is a major risk factor associated with pulmonary emphysema in man. One mechanism for this association may be interference with the regulation of PMN elastase activity by alveolar antiproteases. This possibility is supported by the observation that the oxidizing activity of tobacco smoke inactivates alpha 1-proteinase inhibitor in vitro. Macrophages also secrete an elastolytic protease, albeit at low levels. The short-term exposure of cultured mouse macrophages to cigarette smoke augments the rate of elastase secretion by these cells. Mouse macrophage elastase is not inhibited by alpha 1-proteinase inhibitor or alpha 2-macroglobulin. This unusual property of macrophage elastase may facilitate its attack upon elastin over prolonged intervals despite very low levels of macrophage elastase production. A unified hypothesis of lung injury in pulmonary emphysema is presented, involving both PMN and macrophage elastases and the actions of cigarette smoke. (Am J Pathol 97:111--136, 1979).

Parasexual interspecific plant hybridization.

Interspecific plant hybrids have been produced by parasexual procedures. Protoplasts of Nicotiana glauca and N. langsdorffii were isolated, fused, and induced to regenerate into plants. The somatic hybrids were recovered from a mixed population of parental and fused protoplasts by a selective screening method that relies on differential growth of the hybrid on defined culture media. The biochemical and morphological characteristics of the somatically produced hybrid were identical to those of the sexually produced amphiploid.