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Biomedical subjects

J A Romano

Publications and source records attributed to J A Romano.

At least 19 recordsLinked to original sources
PubMed2001

Psychological casualties resulting from chemical and biological weapons.

This symposium addresses the complications encountered by medical planners when confronted by the use or threat of the use of weapons of mass destruction. The types of chemical warfare agents (CWA), their principal target organs, and physiological effects are discussed. We have reviewed the use of CWA in 20th century warfare and otherwise with emphasis on five cases: (1) use of sulfur mustard during World War I; (2) use by Italy against Ethiopia; (3) use in the Sino-Japanese War; (4) relatively well-studied use in the Iran-Iraq conflict; and (5) the use of sarin in the Tokyo subway terrorist incident. We reviewed the additional physiological and psychological consequences of their use and threat of use. Results from training and simulation are discussed. Finally, we present our conclusions derived from the analysis of these historical situations.

Biological Warfare↗
PubMed1995

A rapid in vitro assay of cellular chemomigration in an epithelial carcinoma cell line.

We have studied the chemomigration activity of an epithelial carcinoma cell line using a modified 96-well Boyden chamber apparatus consisting of upper and lower wells separated by an 8-microns pore polycarbonate filter. Cells from the malignant squamous carcinoma cell line A-431 were plated in the upper wells over a collagen IV-coated filter. In chemokinesis assays, the cells were allowed to migrate toward NIH 3T3 fibroblast-conditioned medium or control media in the lower wells for 6 hours at 37 degrees C with 10% CO2. A-431 cells preferentially migrate across the barrier toward conditioned media but not control media. Control normal keratinocytes showed no migration. A highly metastatic melanoma cell line and poorly metastatic melanoma cell line, in which chemomigration has been shown previously to correlate with metastatic potential, were used as positive and negative cellular controls. This system provides a rapidly quantifiable method by which the invasion characteristics of multiple cell lines can be studied simultaneously in a single assay using the 96-well format.

3T3 Cells↗
PubMed1991

Protection from lethality and behavioral incapacitation resulting from intoxication by soman (pinacolyl methylphosphonofluoridate) and treatment with atropine sulfate and 2-PAM chloride in the guinea pig, cavia porcellus.

The lethal and incapacitating effects of the toxic organophosphorus (OP) agent, soman were evaluated in guinea pigs. The protective effects of the standard therapies atropine sulfate (ATR) and pralidoxime chloride (2-PAM) in minimizing or reducing soman-produced lethality and incapacitation (evaluated using a modification of the rat conditioned avoidance procedure) were also studied. At 0.75 and 1.5 LD50 soman was extremely toxic and fast-acting; its effects appeared within five minutes, and its lethal effects occurred within the first three hours. Therapeutic combinations of ATR (64 or 128 mg/kg) and 2-PAM (25 or 100 mg/kg) protected animals from the lethality of soman, but not from its incapacitating effects. However, therapeutic treatment with ATR and 2-PAM also produced a behavioral toxicity in its own right, an effect which lasted for at least three hours in the guinea pig. This behavioral toxicity was lessened by reducing ATR dosage from 128 to 64 mg/kg, but 2-PAM dosage did not influence the behavioral toxicity of the treatment combinations within the range of dosages studied.

Animals↗
PubMed1990

Age-related differences in soman toxicity and in blood and brain regional cholinesterase activity.

The toxicity (lethality, acute toxic signs and body weight loss) of the irreversible ChE inhibitor soman was assessed in four groups of male rats differing in age: 30, 60, 120 and 240 days old. Plasma and brain regional ChE activity profiles were also studied in these groups. All measures of the toxicity of soman were found to increase with age. The calculated 24-hr LD50s were 110, 87, 66 and 59 micrograms/kg, IM, for 30-, 60-, 120- and 240-day-old rats, respectively. A significant and positive age-related effect on toxic sign rating scores was observed at one hr following soman injection. Furthermore, during a 14-day postsoman observation period, it was observed that young rats had less initial weight loss and more rapid, sustained recovery of growth than older animals. Survivors from the two oldest age groups did not recover to baseline body weights by the end of the 14-day observation period. Basal level of plasma ChE activity did not change significantly with age, while brain regional ChE showed two distinct age-dependent patterns: a linear decrease in the brainstem, midbrain and cerebellum and an inverted U-shaped change in the cortex, hippocampus and striatum. Our data suggest a relationship between soman toxicity and the aging process, but fails to demonstrate a definite relationship between soman toxicity and basal ChE activity in blood and brain of rats.

Aging↗
PubMed1988

Eccrine porocarcinoma.

Eccrine porocarcinoma is a rare malignancy of the eccrine sweat duct unit. This article brings to 79 the number of cases reported. Our report and a review of the literature illustrate the natural history and pathological findings of this disease. Patients' ages at the time of appearance for treatment range from 19 to 90 years. The lesions show no predilection for site; their location follows the distribution of sweat glands in the body. Thirty-nine percent of all patients had cutaneous, regional lymph node, or visceral metastases. Primary treatment is wide surgical excision. The value of adjunctive therapy has not been proved.

Adenocarcinoma↗
PubMed1987

Conditioned taste aversion and cholinergic drugs: pharmacological antagonism.

The effectiveness of drugs as unconditioned stimuli (UCSs) in the conditioned taste aversion (CTA) procedure may be influenced by specific pharmacological antagonism. The present studies examined the UCS effects of two carbamates, physostigmine salicylate (PS) and pyridostigmine bromide (PB), and three anticholinergic compounds, atropine methyl nitrate (AMN), atropine sulfate (AS), and benactyzine hydrochloride (BH). Individual drugs, as well as combinations of the carbamates and the anticholinergics, were studied in a two-bottle procedure in rats. The lowest effective doses for eliciting significant CTAs were PS, 0.32 mg/kg; PB, 1.00 mg/kg; AMN, 0.04 mg/kg; AS, 0.07 mg/kg and BH, 0.90 mg/kg, IP. Combinations of PS with either AMN or BH were mutually antagonistic as UCSs, whereas PS with AS was not. PB with AMN, but not with AS, also showed antagonism in the procedure. The present results suggest that the CTA procedure is well-suited for direct examination of cholinergic drug effects and may also be used to explore interactions of different classes of cholinergic drugs.

Animals↗
PubMed1986

Effects of the organophosphorus compound, O-ethyl-N-dimethyl-phosphoramidocyanidate (tabun), on flavor aversions, locomotor activity, and rotarod performance in rats.

An assessment of the behavioral effects of acutely administered anti-cholinesterase compound O-ethyl-N-dimethyl phosphoramidocyanidate (tabun), to male rats was performed in three studies across five dose levels (100-198 micrograms/kg, sc). Doses of 122 micrograms/kg or greater produced conditioned flavor aversions. Spontaneous locomotor activity was significantly decreased at doses of 122 micrograms/kg or greater when compared to vehicle control levels. When administered doses of 168 micrograms/kg or greater, rats exhibited significant decrements in rotarod performance. In addition, the LD50 of tabun was determined to be 240 micrograms/kg. Signs of cholinergic intoxication were not apparent until 144 micrograms/kg tabun or more were given. Behavioral effects were thus obtained at doses that were between 54 and 71% of the LD50.

Animals↗
PubMed1984

The effect of adrenalectomy and dexamethasone on the antinociceptive effects of physostigmine.

The tail-flick procedure was used to study the antinociceptive effects of physostigmine in adrenalectomized and sham-operated rats. At 5 days after surgery, they were tested 30 min after either 0.32 or 0.45 mg/kg IP physostigmine. Adrenalectomized animals showed significantly greater elevation of TF scores from predrug latencies than the sham controls at both doses of physostigmine. Following 3 days of dexamethasone replacement therapy on days 18, 19, and 20 post-surgery the antinociceptive effects of physostigmine were uniformly attenuated across doses or surgical groups. On the other hand, animals receiving saline injection instead of dexamethasone did not manifest any reduction of the physostigmine antinociceptive effect. The potentiation by adrenalectomy and the reduction following dexamethasone of the antinociceptive effects of physostigmine suggest that these effects may be mediated through hypothalamic-pituitary-adrenal mechanisms and are consistent with beta-endorphin-induced sensitization of opiate or cholinergic receptors.

Adrenalectomy↗
PubMed1983

Cholinergic mechanisms of analgesia produced by physostigmine, morphine and cold water swimming.

This study concerns the cholinergic involvement in three experimental procedures which produce analgesia. Rats were given one of seven treatments: saline (1.0 ml/kg, i.p.); morphine sulfate (3.5, 6.0 or 9.0 mg/kg, i.p.); physostigmine salicylate (0.65 mg/kg, i.p.); warm water swim (3.5 min at 28 degrees C); and cold water swim (3.5 min at 2 degrees C). Each rat was tested on a hot plate (59.1 degrees C) once prior to and 30 min after treatment. Immediately after the last test the rats were killed with focussed microwave radiation. Levels of acetylcholine (ACh) and choline (Ch) in six brain areas (brain stem, cerebral cortex, hippocampus, midbrain, cerebellum and striatum) were analyzed by gas chromatograph-mass spectrometer. Morphine (9.0 mg/kg), physostigmine and cold water swimming caused significant analgesia. Morphine elevated the levels of ACh in the cerebellum and striatum, cold water swimming--in the cerebellum, striatum and cortex, and physostigmine--in the striatum and hippocampus. Levels of choline were elevated by morphine in the cerebellum, cortex and hippocampus, while cold water swimming elevated levels of choline in the cerebellum, cortex, striatum and hippocampus. Physostigmine did not change levels of choline in any of the brain areas studied. These data suggest that the analgetic effects of morphine or cold water swimming may be mediated by components of the cholinergic system that differ from those involved in the analgetic effects of physostigmine.

Acetylcholine↗