Fox Chase Network: Fox Chase Cancer Center's community hospital affiliation program.

Fox Chase Cancer Center developed a format for affiliation with community providers in 1986. Fox Chase Network was formed to establish hospital-based community cancer centers to increase access to patients involved in clinical research. Under this program, the Fox Chase Network now contributes 500 patients per year to prevention and clinical research studies. As relationships with community providers form, patient referrals have increased at Fox Chase Cancer Center and for each Fox Chase Network member. A dedicated staff is required to operate the central office on a day-to-day basis as well as at each affiliate. We have found this to be a critical element in each program's success. New challenges in the cancer business-increasing volumes with declining revenue-have caused us to reconfigure the services offered to affiliates, while maintaining true to our mission: to reduce the burden of human cancer.

Pavlovian conditioning of the tickle response of human subjects: temporal and delay conditioning.

Previous studies of the human response to a tickle have demonstrated that subjects will respond to a gesture that signals the onset of a tickle in the same way as to a tickle. Researchers have described this anticipatory response as an "expectation." In the current study, we investigated, from the Pavlovian framework, the response to a verbal stimulus preceding the tickle stimulus. We exposed subjects to experimental phases which included the Neutral Stimulus Alone, 100% Pairing of the Neutral and Unconditioned Stimuli (tickle strokes to the foot), Random Presentation, Partial (75%) Reinforcement, and Temporal Conditioning. Pavlovian conditioning was observed in all phases, suggesting a parsimonious explanation for the expectation effect described by others.

Placental transfer and fetal deposition of hexachlorobenzene in the hamster and guinea pig.

Hexachlorobenzene (HCB) was administered at dose levels of 0, 1.0, 10.0, or 50.0 mg HCB/kg body wt by gavage to pregnant hamsters and guinea pigs for 6 days up to the time of liver development in the fetus. Samples of maternal fat, thymus, skin, liver, lung, brain, spleen, urinary bladder, muscle, plasma, and blood were analyzed for HCB concentration. Additionally, fetuses, placentas, and yolk sacs were analyzed for HCB content. HCB was found in all tissues assayed. The highest concentrations of HCB were found in hamster tissues, with the hamster fetuses having a fivefold greater concentration of HCB than the guinea pig fetuses. Comparisons were made of the hamster and guinea pig data with similar data in the mouse and rat.

Inhalation studies of Mt. St. Helens volcanic ash in animals. III. Host defense mechanisms.

The effects of inhalation exposure of mice or rats to 9.4 mg/m3 volcanic ash, 2.5 mg/m3 SO2, or both on host defense mechanisms were assessed. Cytologic changes in pulmonary lavage fluid included an increase in percentage polymorphonuclear leukocytes due to SO2 exposure and an increase in eosinophils due to ash. SO2 and ash also produced decreases in percentage alveolar macrophages. In the case of ash-exposed animals, this decrease was offset by an increase in lymphocytes. Total cell counts and viability were not affected by any of the exposures. Pulmonary clearance mechanisms were affected in that there were both decreased alveolar macrophage phagocytic capability following ash and ash + SO2 exposures and depressed ciliary beat frequency attributable to ash exposure. None of the inhalation exposures caused increases in susceptibility to an immediate or 24 hr postexposure aerosol challenge with Streptococcus. However, intratracheal instillation of both fine- and coarse-mode volcanic ash caused slight but significant increases in mortality due to bacterial challenge 24 hr after the instillation. The phytohemagglutinin-induced blastogenic response of splenic lymphocytes from exposed animals did not differ significantly from that of control lymphocytes, although the lipopolysaccharide-induced blastogenic response was enhanced. Ash exposure had no effect on susceptibility to murine cytomegalovirus. In summary, volcanic ash alone or in combination with SO2 had only minimal effects on certain host defense mechanisms.

Inhalation studies of Mt. St. Helens volcanic ash in animals: respiratory mechanics, airway reactivity and deposition.

Effects of fine volcanic ash aerosol on pulmonary mechanical properties of awake guinea pigs were evaluated during exposure by inhalation. Ash penetration into the lung as well as tissue response to ash were determined by transmission electron microscopy. The reactivity of airway epithelial irritant receptors following ash exposure was assessed using a histamine bronchoprovocation test. Results indicated that breathing 9,4 mg/m3 of ash for 2 hr did not cause a measurable change in pulmonary function of guinea pigs. Electron micrographs showed that ash particles in the lung below the hilus did not seem to produce any acute tissue reaction and were almost all phagocytized by macrophages. Airways of guinea pigs exposed to ash were significantly less responsive to histamine than were the airways of animals exposed only to air. It appears that even though Mt. St. Helens ash was well tolerated by the guinea pig during the exposure, its presence in the inhaled air did change the "histamine sensitivity" of airway epithelial irritant receptors.

Inhalation studies of Mt. St. Helens volcanic ash in animals : Respiratory mechanics, airway reactivity and deposition

This study was conducted to improve speculation of changes in breathing which might be expected while inhaling a dust like Mt. St. Helens volcanic ash. Effects of fine volcanic ash aerosol on pulmonary mechanical properties of awake Guinea pigs were evaluated during exposure by in halation. Ash penetration into the lung as well as tissue response to ash were determinated by transmission electron mycroscopy. The reactivity of airway epithelial irritant receptors following ash exposure was assessed using a histamine bronchoprovocation test. Airways of Guinea pigs exposed to ash were significantly less responsible to histamine tan were the airways of animals exposed only to air (AU)

Increased susceptibility to parathion poisoning following murine cytomegalovirus infection.

In mice treated with ordinarily sublethal doses of parathion 2 to 5 days postinfection with murine cytomegalovirus (MCMV) 50 to 100% mortality was observed. These mortalities appeared to be due to a decrease in the ability of infected mice to detoxify parathion. Pentobarbital-induced sleeping time was also enhanced 3 and 6 days postinfection and cytochrome P-450 concentrations were markedly depressed in mice tested 3 days after infection. MCMV-induced effects on sensitivity to parathion and pentobarbital did not appear to be directly attributable to liver infection since concentrations of virus in the liver persisted at maximum concentrations well beyond the time when sensitivity to these compounds returned to normal. The time frame during which enhanced sensitivity to parathion and pentobarbital was observed suggests that this sensitivity may have been caused by viral-induced interferon-mediated depression of cytochrome P-450.

Postnatal effects of hexachlorobenzene (HCB) on cardiac lactic dehydrogenase (LDH) and creatine kinase (CK) isozymes in CD-1 mice.

Pregnant CD-1 mice were treated with hexachlorobenzene (HCB) by gavage at doses of 0, 1, 10 and 50 mg HCB/kg body weight on days 6-17 of gestation and studied on day 1 or 21 postpartum (pp). Hearts of the dams and pups were assayed for lactic dehydrogenase (LDH) and creatine kinase (CK) activities and isozyme profiles. LDH and CK activities and CK isozyme profiles were not affected in the dams by HCB treatment, but isozyme LDH-5 was significantly depressed and isozyme LDH-3 significantly increased at the 50 mg/kg dose of HCB on day 1 pp. Hearts of the pups were studied on days 1, 8, 10, 15 and 21 pp. The 50 mg/kg dose level resulted in a statistically significantly increased mortality in the pups. The mortality at the other doses showed a dose-related effect. LDH and CK activities and CK isozyme profiles were not affected by HCB exposure in utero. The only isozyme affected was LDH-5 with a statistically significant increase in the 50 mg/kg dose group on day 21 pp.

Identification system for airways in lung models: a note.

A lobar notational system for the identification of airways in the mammalian lung is presented. This system was developed to identify uniquely the location of morphometric and deposition data within a lobe as well as within the lung, and to provide for easy and efficient data reduction. In addition, this notational system can be used to identify main stems like those found in the monopodial lung, and incorporates identification of terminal bronchioles in the airway identifier. The lobar notational system is composed of a two-character lobe code, followed by a third character identifying the branching structure as monopodial or symmetric. The fourth digit identifies the relative position of a branch within the lobe. Subsequent digits identify the airway's relative location within the branching.

An automated analysis of glutathione peroxidase, S-transferase, and reductase activity in animal tissue.

A centrifugal analyzer and a spectrophotometer were compared for routine analysis of xenobiotic metabolizing enzymes glutathione (GSH) peroxidase, GSH-S transferase, and GSH reductase. Lung, liver, and kidney from 60-day-old male rats were used as the source of enzymes. Linear regression analysis was used to assess the accuracy and precision of the centrifugal analyzer method in measuring enzyme activities. Biologically and statistically, the centrifugal analyzer proved to be acceptable for routine measurement of these GSH-dependent enzymes.