Patient referrals to a multispecialty asthma clinic. Asthma Care Center Clinical Consortium.

A total of 656 patients with asthma have been referred to a multispecialty pediatric asthma clinic for evaluation; 52 (7.9%): mild; 406 (61.9%): moderate; 177 (27%): severe; and 21 (3.2%): incomplete data. No significant differences in demographics or payer source were observed across disease severity levels. Only 25% of the patients with primary care providers were referred by these practitioners. Over 20% of the mild asthmatics were using inhaled bronchodilators regularly. Only 40% and 50% of the moderate and severe asthmatics, respectively, were using inhaled bronchodilators regularly, and only 19% and 36%, respectively, were on maintenance inhaled corticosteroids. Pressures to reduce subspecialty services may place some of these asthma patients at increased risk for complications from this chronic lung disease.

A multifaceted intervention for infants with failure to thrive. A prospective study.

OBJECTIVE: To determine whether a multifaceted intervention decreased the incidence of failure to thrive (FTT) in a group of preterm infants with low birth weights and improved the 3-year intelligence, health, growth, and behavior status of the children with FTT. DESIGN: Three-year, prospective, randomized, clinical trial. SETTING: Eight large university hospital sites throughout the United States. SAMPLE: Nine hundred fourteen preterm infants with low birth weights who were born at the sites and met study criteria. INTERVENTION: Home visits weekly during the first year of life and biweekly thereafter until the age of 3 years to provide family support and implement two curricula; and attendance at a child development center from 12 months until 3 years of age, 5 days a week, to deliver an early childhood educational intervention. RESULTS: The incidence of FTT did not differ between the treatment and control groups (20% vs 22%). Overall, children with FTT in the treatment group were not different from children with FTT in the follow-up group on any of the outcome variables. However, after controlling for other factors, treatment group membership significantly contributed to the prediction model of 36-month IQ (P = .005) for the children with FTT. In addition, children with FTT in the intervention group with higher compliance demonstrated higher 3-year IQ and better behavior scores than the children with FTT in the low-compliance group. CONCLUSIONS: The intervention did not change the incidence of FTT or the 3-year outcomes in this low-birth-weight, preterm cohort. After controlling for multiple independent variables, marked effects on 3-year IQ were noted. In addition, these beneficial effects were most pronounced in families that were most complaint with the intervention.

Pulmonary metastasis from histologically benign giant cell tumor of bone. Report of a case diagnosed by fine needle aspiration cytology.

The cytologic features of pulmonary metastasis from a histologically benign giant cell tumor of bone are reported. The patient had undergone curettage of a benign giant cell tumor of the humerus two years earlier. Aspiration of a pulmonary mass yielded a cellular population of mononuclear stromal cells admixed with a smaller population of binucleate forms and occasional giant cells. Vacuolation and granulation of the stromal cells are cytologic features seen commonly in giant cell tumors of bone, but in the lung these features may deceptively mimic the appearance of pulmonary macrophages. Video thoracoscopic wedge resection of the metastatic lesion was performed subsequently.

Toxicity of low and moderate multiplicities of Chlamydia psittaci for mouse fibroblasts (L cells).

When mouse fibroblasts (L cells) were infected in suspension or in monolayer with 10 to 100 50% infectious doses (ID(50)) of Chlamydia psittaci (6BC) per host cell, they showed signs of damage 24 to 48 h later. Host-cell injuries were termed multiplication dependent when both the ingestion and subsequent reproduction of C. psittaci were required; when only ingestion but not replication was needed, the injuries were considered to be multiplication independent. The time that the injury was first apparent, as well as its final magnitude, was proportional to the multiplicity of infection. When L cells ingested infectious or ultraviolet-inactivated C. psittaci, damage was manifested by failure to exclude trypan blue, by leakage of lactic dehydrogenase, by inhibition of reproduction as measured by ability to form colonies, by inhibition of protein and deoxyribonucleic acid synthesis, and eventually by cell disintegration. Infectious, but not ultraviolet-killed, chlamydiae stimulated host-cell glycolysis. Heat-killed chlamydiae were without measurable toxicity. The time of appearance of host-cell injury was always earlier, and its terminal magnitude always greater, with infectious inocula than with ultraviolet-inactivated ones. The multiplication-independent toxicity of ultraviolet-killed C. psittaci disappeared with inocula of less than 10 ID(50) per L cell, but an inoculum of only a single ID(50) of infectious chlamydiae per host cell injured most of the cells it infected, as evidenced by increased trypan blue staining and decreased efficiency of colony formation. The toxicity of multiplicities of infection between 10 and 100 ID(50) of infectious C. psittaci per host cell was the sum of both multiplication-dependent and -independent components. The effects of chloramphenicol and isoleucine deficiency on the ability of C. psittaci to injure L cells suggested that some synthesis of protein by both parasite and host may be essential for expression of multiplication-independent chlamydial toxicity. The failure of infectious chlamydiae to stimulate host-cell glycolysis in the presence of cycloheximide suggested that this multiplication-dependent consequence of chlamydial infection was also dependent on protein synthesis by the host.

Immediate toxicity of high multiplicities of Chlamydia psittaci for mouse fibroblasts (L cells).

One hour after suspensions of mouse fibroblasts (L cells) were exposed to 500 to 1,000 L-cell 50% infectious doses of Chlamydia psittaci (6BC), the L cells failed to attach to and spread out on solid substrates, phagocytosed polystyrene latex spheres at reduced rates, incorporated less [14C]isoleucine into protein, and had smaller soluble pools of nucleoside triphosphates. The infected L cells began to die at 8 h and were all dead by 20 h. Lower multiplicities of infection took correspondingly longer to kill the L cells. These effects of high multiplicities of C. psittaci on L cells will be referred to collectively as immediate toxicity. Similar effects were obtained with other strains of C. psittaci and C. trachomatis and with other cell lines. Ultraviolet-inactivated C. psittaci retained the ability to cause immediate toxicity, but heat-inactivated chlamydiae did not. C.psittaci cells had to be ingested by L cells before they were immediately toxic but, once they were phagocytosed, they did not need to multiply or to synthesize macromolecules in order to cause immediate injury to their hosts. Immediate toxicity was not the result of depression of energy metabolism, changes in the levels of intracellular cyclic nucleotides, or release of hydrolases from lysosomes. It was suggested that a lesion is produced in the plasma membrane of the L cell every time it ingests a chlamydial cell, that each act of ingestion produces an independent lesion, and that their injurious effects are additive. Thus, the more ingestion lesions there are, the faster the host cell dies. It was also suggested that induced phagocytosis, inhibition of lysosomal fusion, and death of mice and of cells in culture may all depend on a single activity of C. psittaci.

Thermochemical remanent magnetization and thermal remanent magnetization: comparison in a basalt.

Recent studies have shown that the remanent magnetization carried by an extrusive igneous rock may not be entirely thermal remanent magnetization (TRM). Some may be thermochemical remanent magnetization (TCRM) acquired by the rock at temperatures at least as low as 300 degrees C during oxidation of the contained titanomagnetite grains. Results from a study of a set of basaltic samples from one locality indicate that the intensity of TCRM acquired by a sample in a known magnetic field is equal to that of TRM subsequently produced in the same sample in the same field. On the assumption that the samples we studied are not magnetically unique, we tentatively conclude that paleointensity studies are valid in spite of the presence of TCRM, as long as the rock acquired the magnetization during the initial cooling.