Prevention of diabetes in BioBreeding/Worcester rats with monoclonal antibodies that recognize T lymphocytes or natural killer cells

Diabetes-prone BioBreeding/Worcester (BB/Wor) rats received thrice weekly injections of mAb against antigens expressed on the surface of all T cells (OX19), cytotoxic/suppressor, and NK cells (OX8), helper/inducer cells (W3/25, OX35, OX38), and Ia+ cells (OX6, 3JP, OX17). Treatment with OX8 or OX19 achieved stable reductions of splenic and peripheral blood NK cells and helper/inducer T lymphocytes, respectively, and protected against diabetes. OX19 injections also prevented lymphocytic insulitis, thyroiditis, and the synthesis of autoantibodies to thyroid colloid and smooth muscle antigens. OX8 injections reduced splenic NK-mediated YAC-1 cell lysis, but did not prevent insulitis, thyroiditis, or autoantibody synthesis. Injections of mAb specific for antigens on the surface of helper/inducer cells, and for cells expressing IaE antigens provided marginal protection against diabetes without reductions of phenotypic subsets. These findings suggest that pancreatic beta cell destruction in the spontaneously diabetic BB/Wor rat is mediated by the combined action of NK and helper/inducer cells.     

MR imaging of cavernous hemangioma of the face and neck

Four patients with cavernous hemangioma of face and neck were evaluated with magnetic resonance imaging. Pathologically, soft tissue cavernous hemangiomas are characterized by small feeding arteries and large blood poolings. Arteriography usually fails to demonstrate the extent of the lesion. Computed tomography does not allow differentiation between these lesions and surrounding normal tissues. Magnetic resonance clearly demonstrates hemangiomas with good contrast between lesion and normal tissues. Spin-echo technique with long echo time appears to be particularly useful to delineate these lesions.     

Congenitally corrected transposition of the great arteries associated with the pre-excitation syndrome

A case with congenitally corrected transposition of the great arteries associated with the pre-excitation syndrome is presented. A gated-blood-pool study and Tl-201 myocardial imaging were performed using SPECT. The tomographic gated-blood-pool images showed the shapes of the right ventricle (RV) and left ventricle (LV), i.e., anatomically LV and RV respectively, to be reversed from that of normal patients. The relationships of the great vessels and ventricles also were easily visualized. RV hypertrophy (anatomical LV) was visualized on the Tl-201 images. Phase analysis showed the earliest excitation was in the anteroseptal region near the base of the LV, which was consistent with the site of the accessory conduction pathway. The gated-blood-pool and Tl-201 tomographic studies were helpful for demonstrating the corrected transposition of the great arteries and the pre-excitation syndrome.     

Neuronal development of the chick cerebral cortex. A Golgi study

The neuronal morphological development of the avian telencephalic cortex (DMC) is studied in Golgi-stained brain sections. The neuronal types at embryonic days 10, 13, 16, as well as of newborn chick are identified. The immature neurons are characterized by the presence of hair-like processes, growth cones and dendritic varicosities. These characteristics are absent in neuronal types of newborn chick. There are five patterns of differentiation, which produce six neuronal types in the newborn chick: horizontal neurons, pyramidal neurons, bipyramidal neurons, short axon multipolar neurons, long axon multipolar neurons and periventricular neurons. The morphological features of migrating embryonic cells are described. The dendritic spines appear in 16-day embryos in the majority of neuronal types.     

Release of [3H]norepinephrine: alteration by early developmental exposure to diazepam

The effect of prenatal exposure to diazepam (over gestational days 13-20) on the release of tritiated norepinephrine [( 3H]NE) from selected brain regions was analyzed to determine mechanisms whereby such exposure could disrupt functioning in specific NE neurons, as previously observed. Pregnant rats were administered diazepam (DZ) once daily at doses of 1.0, 2.5 or 10.0 mg/kg and the offspring studied as adults at 70-90 days of age and during development at 14, 21, 35 and 56 days of age. Release of [3H]NE was measured during in vitro incubation using 25 mM potassium as the depolarizing stimulus. As noted previously, prenatal exposure to DZ induced an effect only on NE neurons innervating the hypothalamus, sparing the NE innervation to the hippocampus and cerebellum. Prenatal exposure to DZ had no effect on the depolarized release of [3H]NE in the hypothalamus until after 35 days of age, a developmental pattern previously observed with respect to endogenous NE levels. In adult rat offspring, however, the depolarization-induced release of [3H]NE from the hypothalamus decreased 28%, 32% and 64% (relative to uninjected control values) in animals prenatally exposed to DZ at 1.0, 2.5 or 10 mg/kg/day respectively. Concurrent exposure of the pregnant dam to benzodiazepine antagonists (Ro 15-1788 or ethyl-beta-carboline-3-carboxylate) prevented the effects of DZ (2.5 mg/kg/day) on [3H]NE release, demonstrating again the importance of the benzodiazepine binding site to the effects induced by the early DZ exposure. The initial accumulation of the [3H]NE was not altered by the prenatal exposure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Respiratory symptoms and bronchial reactivity: identification of a syndrome and its relation to asthma

Two postal questionnaire surveys were carried out among the adult population of Southampton aimed at clarifying the diagnostic criteria for asthma (study 1) and at testing the validity of symptoms so identified as diagnostic of bronchial hyper-reactivity (study 2). The questionnaires asked about respiratory symptoms and included three questions thought likely to disclose increased bronchial reactivity. Laboratory measurements on subsamples of respondents included spirometry and bronchial challenge with increasing doses of histamine till a concentration was reached provoking a fall of more than 20% (PC greater than 20) in forced expiratory volume in one second. In the first study no normal subject (that is, one who did not report shortness of breath or wheezing on the questionnaire) had a PC greater than 20 below 0.5 g/l. Of 51 subjects who reported shortness of breath or wheezing, or both, nine had a cluster of abnormalities consisting of one or more symptoms of bronchial irritability, nocturnal dyspnoea, and prolonged morning tightness together with PC greater than 20 values of 0.5 g/l or less. These symptoms in conjunction with a low PC greater than 20 were termed the bronchial irritability syndrome. In the second study bronchial challenge confirmed the close association of these symptoms with bronchial hyper-reactivity, all other subjects being less reactive to histamine. Only 27% of subjects with symptoms of the bronchial irritability syndrome had been diagnosed as asthmatic by their general practitioners. The bronchial irritability syndrome is a definable entity for epidemiological study and patient care.