The use of P-aminobenzoic acid and chromic oxide to confirm complete excreta collection in a carnivore, Felis silvestris catus.

Complete excreta collection is a pre-requisite for several protocols in protein metabolism, and lack of confidence in achieving this may be increased when working with carnivores. Recovery of p-aminobenzoic acid (PABA) as a check for complete urine collection and chromic oxide for complete faeces collection were assessed in the cat. A single oral dose of PABA (4 mg/kg BW) was excreted more slowly than has been reported in the human (82% recovery at 6 h). A daily dose of PABA proved a useful method for confirming complete urine collection in the cat, and was 99% excreted in 72 h. Chromic oxide (500 mg/cat) was administered orally and recovery of chromium in the faeces was 90% after 96 h. A HPLC method for the analysis of PABA in cat urine was developed, and from the application of the techniques to a nitrogen balance study, it was concluded that PABA and chromic oxide are useful checks for complete excreta collection in the cat.

Maillard reaction kinetics in model preservation systems in the vicinity of the glass transition: experiment and theory.

Rates of reactant consumption for the Maillard reaction between lysine and glucose were measured for a noncrystallizing trehalose-sucrose-water matrix in the glass transition region. At temperatures above the glass transition temperature (T(g)), the consumption rates showed Arrhenius temperature dependence with activation energies of 135 and 140 kJ mol(-1) for lysine and glucose, respectively. Finite reaction rates were observed for glassy samples that were faster than that of one of the nonglassy samples. A comparison of experimental results with predicted diffusion-controlled reaction rate constants indicated that the reaction was reaction-controlled at temperatures above T(g) and approached the diffusion-influenced regime in the glassy state. The needs for further research on reactant diffusivity, the theory of the orientation dependence of reactivity, and a detailed understanding of the reaction mechanism and kinetics were identified.

Sudden death in the dysphagic stroke patient--a case of airway obstruction caused by a food bolus: a brief report.

The clinical events leading up to the sudden death of a dysphagic stroke patient with dementia is described. A 63-yr-old man sustained right thalamic and mid-brain infarctions. On the inpatient stroke rehabilitation ward, he exhibited significant impulsivity and dementia, the latter felt to be premorbid. The patient frequently coughed, and modified barium swallow testing showed dysphagia, with aspiration occurring only when consuming greater than teaspoon amounts of liquid. He subsequently died at home while eating a meal. Autopsy showed an intact large cheese ball (bocconcini) occluding the airway. Sudden death in the impulsive stroke patient secondary to airway occlusion by a food bolus has not previously been reported, although such patients seem to be at greater risk. New eating-related interventions are warranted for dysphagic patients who exhibit impulsivity. It is proposed that food particle size be limited to 1 cm2 and that such patients be closely monitored while eating.

CT scanning as an adjunct to screening for medullary carcinoma of the thyroid.

CT scanning of the thyroid following oral administration of potassium iodate was performed on two sisters in whom raised calcitonin levels had been found at a pentagastrin stimulation test undertaken to screen for medullary carcinoma of the thyroid. Three histologically proven, clinically occult C-cell carcinomas measuring 2 mm or less were detected by CT scanning. This technique may be useful prior to surgery in patients in whom medullary carcinoma of the thyroid is suspected but not proven.

Responses of isolated guinea pig pulmonary venules to hypoxia and anoxia.

Because small pulmonary arteries are believed to be the major site of hypoxic pulmonary vasoconstriction (HPV), pulmonary venular responses to hypoxia have received little attention. Therefore the responses of isolated guinea pig pulmonary venules to hypoxia (bath PO2, 25 Torr) and anoxia (bath PO2, 0 Torr) were characterized. Pulmonary venules [effective lumen radius (ELR), 116 +/- 2 microns] with an adherent layer of parenchyma responded to hypoxia and anoxia with a graded sustained contraction (hypoxia, 0.03 +/- 0.01; anoxia, 0.26 +/- 0.03 mN/mm), whereas paired femoral venules (ELR, 184 +/- 7 microns) contracted to anoxia only (0.05 +/- 0.02 mN/mm). Repeated challenges with hypoxia and anoxia continued to elicit sustained pulmonary venular contractions; femoral venule contractions to anoxia were not repeatable. Hypoxia- and anoxia-induced pulmonary venular contractions were calcium and pH dependent. Dissection of the parenchyma from pulmonary venules did not alter contractions to decreased PO2. Anoxic contractions of pulmonary venules were variably reduced by replacement of the bath fluid; however, the release of a contractile mediator(s) from pulmonary venules during hypoxia or anoxia was not demonstrated. Pulmonary venular responses to hypoxia and anoxia are similar to those induced by hypoxia in vivo, and results obtained from this model may be useful in predicting mechanisms of HPV.

Effect of endothelial injury on the responses of isolated guinea pig pulmonary venules to reduced oxygen tension.

The influence of the endothelium on pulmonary venular responses to reduced oxygen tension has not been defined. To examine this question, endothelial injury was induced in small guinea pig pulmonary artery and venule segments (effective lumen radius, 174 +/- 5 and 122 +/- 2 microns, respectively) by perfusion with either a mixture of hypoxanthine (5 mM) and xanthine oxidase (0.05 U/ml) (HX/XO) or collagenase (2 mg/ml). HX/XO significantly (p less than 0.05) reduced the relaxation of precontracted pulmonary arteries by acetylcholine (ACH), bradykinin (BK), and A-23187, and the relaxations were restored by including superoxide dismutase (40 micrograms/ml) in the HX/XO solution. However, neither HX/XO nor collagenase affected vasodilation induced by ACH, BK, and A-23187 in precontracted pulmonary venules. In contrast, HX/XO significantly (p less than 0.05) augmented the sustained contraction of pulmonary venules to hypoxia (HX/XO, 3.2 +/- 1.0 mg/mm; control, 1.0 +/- 0.5 mg/mm) and anoxia (HX/XO, 35.1 +/- 6.6 mg/mm; control, 20.3 +/- 4.0 mg/mm). Collagenase also significantly (p less than 0.05) enhanced the anoxic contractions (collagenase, 36.0 +/- 3.7 mg/mm; control, 20.9 +/- 6.8 mg/mm). Superoxide dismutase (40 micrograms/ml) and catalase (323 micrograms/ml) abolished HX-XO-induced augmentation of the hypoxic and anoxic contractions of pulmonary venules. Collagenase removed 54 +/- 8% of the venular endothelium (control, 5 +/- 1%), whereas HX/XO-exposed endothelial cells contained numerous craters. Neither gossypol (5 microM) nor methylene blue (10 microM) affected pulmonary venular contractions to reduced PO2. Endothelial damage augments the PO2-dependent contractions of the pulmonary venule, and this augmentation does not appear to be due to decreased release of endothelium-derived relaxing factor.

Efficacy of tetroxoprim/sulphadiazine in the treatment of Pneumocystis carinii pneumonitis in rats.

Pneumocystis carinii pneumonitis was induced using dexamethasone in male Sprague-Dawley rats. After the first death due to Pn. carinii occurred, nine rats received 50 mg/kg/day tetroxoprim and 120 mg/kg/day sulphadiazine. Four additional rats were given no therapy and served as a positive control. All the surviving rats including five negative controls were sacrificed four weeks after the last positive control rat died. All four rats in the positive control group and two of nine in the treated group developed Pn. carinii pneumonitis, whereas none of the five negative controls had evidence of Pn. carinii infection. The difference between the treated and untreated rats was significant (P = 0.05). These results suggest that combination therapy with tetroxoprim/sulphadiazine is effective in the treatment of Pn. carinii pneumonitis in this animal model.

Possible spread of bronchogenic carcinoma to the chest wall after a transthoracic fine needle aspiration biopsy. A case report.

Spread of tumor along the needle tract following aspiration biopsy with the so-called "fine" needles (thinner than 18 gauge) is recognized to be an extremely uncommon complication of this technique. A case is presented in which such a spread appears to have occurred to the chest wall 13 months after a transthoracic aspiration biopsy of a bronchogenic tumor.

Interstitial pneumonitis in myasthenia gravis.

Both myasthenia gravis and interstitial pneumonitis are associated with various autoimmune phenomena and can coexist with other immune disorders, but the two have not been described together. We present a woman with such a concurrence whose clinical picture improved following plasmapheresis and thymectomy.

Choriocarcinoma metastatic to the lung. A cytologic study with identification of human choriogonadotropin with an immunoperoxidase technique.

A case of choriocarcinoma metastatic to the lung following a previous hydatidiform mole is presented. It was possible to make definitive identification of trophoblastic elements on a needle aspiration biopsy using an immunoperoxidase staining technique, thus avoiding diagnostic thoracotomy prior to therapeutic intervention. A method of immunoperoxidase staining of previously fixed and Papanicolaou-stained needle aspiration biopsy specimens is also described, and other uses of the immunoperoxidase technique on needle biopsy specimens are discussed.

Giant-cell carcinoma of the lung. A cytologic study.

A case of giant-cell carcinoma of the lung, confirmed at autopsy, is presented. The cytologic features seen in sputum samples, bronchial washings and brushings and fine needle aspiration biopsy material as well as the histologic findings are described. The possible relationship to bronchioloalveolar carcinoma is discussed. The cytologic features of giant-cell carcinoma of the lung, when seen in the context of the clinical and radiologic setting, should allow the cytologic identification of the tumor prior to surgical intervention.

Inactivation by alveolar macrophages of slow-reacting substance of anaphylaxis released from pig lung cells.

The influence of alveolar macrophages on the release of slow-reacting substance of anaphylaxis (SRA-A) and histamine from dispersed pig lung cells was studied. The addition of alveolar macrophages to lung cells (1:3) decreased SRS-A release by 62% +/- 7% without a significant decrease in histamine release. Increased numbers of alveolar macrophages (1:1) decreased both SRS-A release (by 90% +/- 5%) and to a lesser extent histamine release (by 59% +/- 18%). The decrease in released SRS-A was not caused by prostaglandin release from macrophages, and kinetic data indicated that in contrast to histamine the decrease was predominantly the result of SRS-A inactivation rather than inhibition of its release. When alveolar macrophages were incubated with SRS-A, inactivation (191 units/10(7) cells/30 min) was confirmed. SRS inactivation was not reproduced by glutaraldehyde-treated macrophages or by granulocyte and mononuclear populations obtained from peripheral blood. Alveolar macrophages may limit the consequences of SRS-A release in the peripheral air spaces.

Release of slow-reacting substance of anaphylaxis from dispersed pig lung cells: effect of cyclo-oxygenase and lipoxygenase inhibitors.

Study of the release of slow-reacting substance of anaphylaxis (SRS-A) from lung cells has been hampered by the lack of suitable animal model. Using both immunologic and pharmacologic stimuli, we have obtained histamine and SRS-A release from dispersed pig lung cells containing 6% mast cells (with a histamine content of 1.9 pg/cell). Lung cells dispersed from actively sensitized (with intratracheal Ascaris antigen) but not unsensitized pigs released both histamine (mean net release 33%) and SRS-A (mean release, 47 units/10(7) cells) when challenged with Ascaris antigen. Greater release of histamine (mean net release 52%) and of slow-reacting substance (SRS) (mean release 701 units/10(7) cells) was induced by challenge with the calcium ionophore A23187. The pharmacologic and physicochemical characteristics of the SRS together with its profile of enzymatic inactivation resembled those described for SRA-A released from human lung. Both antigen-induced and A23187-induced SRS(-A) release were enhanced by indomethacin, a cyclo-oxygenase inhibitor, but inhibited by both phenidone (IC50 35 microM) and eicosatetraenoic acid (IC50 15 microM), inhibitors of both cyclo-oxygenase and lipoxygenase, confirming that generation of SRS(-A) by either stimulus required an intact lipoxygenase pathway of arachidonic acid metabolism.

Tubular aggregates in murine dystrophy heterozygotes.

Heterozygous dystrophic mice (strain 129 ReJ dy/+) were studied to determine the morphological changes that are characteristic of the heterozygote state. The morphology of the muscle in 35 heterozygotes (+/?) was compared with that of 35 homozygotes (dy/dy) and 20 normal controls (+/+). Muscle was examined with light microscopy, standard histochemical techniques, and electron microscopy. Few abnormalities were detected with light microscopy or with histochemistry. With electron microscopy, some slight nonspecific evidence of muscle damage in the form of focal myofibrillar degeneration was seen in all of the heterozygotes. The striking abnormality, however, was the presence of tubular aggregates in type 2 fibers in 60% of the heterozygotes. Tubular aggregates were not found in homozygous dystrophic mice or in normal controls. The significance of this finding is discussed and it is suggested that tubular aggregates may represent lateral sac dilatation and infolding.