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Biomedical subjects

J A Romano

Publications and source records attributed to J A Romano.

32 records · Page 2Linked to original sources
PubMed1975

Stereoacuity development in children with normal binocular single vision.

We made 344 stereoacuity determinations (Titmus Stereotest) on 321 children, ages 1 1/2 to 13 years, who had normal binocular single vision tested by other factors. The data showed a gradual improvement in stereoacuity scores with increasing age--up to age 9--when a normal stereoacuity of 40 seconds of arc was consistently found. The lower limits of stereoacuity compatible with normal binocular single vision were 3 1/2 years, 3,000 seconds; 5 years, 140 seconds: 5 1/2 years, 100 seconds; 6 years, 80 seconds; 7 years, 60 seconds; and 9 years, 40 seconds.

Adolescent↗
PubMedDate not supplied

In vitro and in vivo comparison of sulfur donors as antidotes to acute cyanide intoxication.

Antidotes for cyanide (CN) intoxication include the use of sulfane sulfur donors (SSDs), such as thiosulfate, which increase the conversion of CN to thiocyanate by the enzyme rhodanese. To develop pretreatments that might be useful against CN, SSDs with greater lipophilicity than thiosulfate were synthesized and assessed. The ability of SSDs to protect mice against 2LD50 of sodium cyanide (NaCN) administered either 15 or 60 min following administration of an SSD was assessed. To study the mechanism of action of the SSD, the candidate compounds were examined in vitro for their effect on rhodanese and 3-mercaptopyruvate sulfurtransferase (MST) activity under increasing SSD concentrations. Tests were conducted on nine candidate SSDs: ICD1021 (3-hydroxypyridin-2-yl N-[(N-methyl-3-aminopropyl)]-2-aminoethyl disulfide dihydrochloride), ICD1022, (3-hydroxypyridin-2-yl N-[(N-methyl-3-aminopropyl)]-2-aminoethyl disulfide trihydrochloride), ICD1584 (diethyl tetrasulfide), ICD1585 (diallyl tetrasulfide), ICD1587 (diisopropyl tetrasulfide); ICD1738 (N-(3-aminopropyl)-2-aminoethyl 2-oxopropyl disulfide dihydrochloride), ICD1816 (3,3'-tetrathiobis-N-acctyl-L-alanine), ICD2214 (2-aminoethyl 4-methoxyphenyl disulfide hydrochloride) and ICD2467 (bis(4-methoxyphenyl) disulfide). These tests demonstrated that altering the chemical substituent of the longer chain sulfide modified the ability of the candidate SSD to protect against CN toxicity. At least two of the SSDs at selected doses provided 100% protection against 2LD50 of NaCN, normally an LD99. All compounds were evaluated using locomotor activity as a measure of potential adverse behavioral effects. Positive hypoactivity relationships were found with several disulfides but none was found with ICD1584, a tetrasulfide. Separate studies suggest that the chemical reaction of potassium cyanide (KCN) and cystine forms the toxic metabolite 2-iminothiazolidine-4-carboxylic acid. An alternative detoxification pathway, one not primarily involving the sulfur transferases. may be important in pretreatment for CN intoxication. Although studies to elucidate the precise mechanisms are needed. it is clear that these newly synthesized compounds provide a new rationale for anti-CN drugs, with fewer side-effects than the methemoglobin formers.

Animals↗
PubMedDate not supplied

The effects of choline on soman-induced analgesia and toxicity.

The effects of acute choline (Ch) administration on the hot plate (HP) analgesia produced by soman and by morphine and on the toxicity produced by soman were examined in male rats. Morphine (9.0 mg/kg, IP) and soman (80 micrograms/kg, SC), but not Ch (60 mg/kg, IP), produced HP analgesia. Pretreatment with Ch (100 mg/kg, IP; given 20 min earlier) reduced morphine and soman analgesia by 68% and 38% respectively. Ch (LD50 = 405.8 mg/kg, IP) at doses above 200 mg/kg rapidly produced signs of cholinergic stimulation which disappeared by one hr. A fixed dose of Ch (100 mg/kg) altered neither the expression of toxic cholinergic signs produced by varying doses (from 75.9 to 151.4 micrograms/kg) of soman, nor the 24-hr LD50 (124.0 micrograms/kg, SC) of soman. Doses of Ch ranging from 213.8 to 269.2 mg/kg when given 40 min prior to a fixed dose (93.3 micrograms/kg) of soman resulted in persistent signs of cholinergic hyperstimulation, but again, did not affect the mortality produced by soman. The results demonstrate that acute Ch pretreatment increased the severity of cholinergic stimulation and reduced the HP analgesia, but were not accompanied by potentiation or antagonism of the lethal action of soman.

Analgesia↗
PubMedDate not supplied

Assessment of motor performance decrement following soman poisoning in mice.

A simple motor performance test, the inverted screen test, was used to assess the incapacitating effects of soman in mice and to evaluate the effectiveness of carbamate pretreatment and/or treatment with atropine plus 2-PAM on soman-induced debilitation. The test requires minimal equipment and personnel training, and can be done rapidly on untrained animals. Mice were placed individually on wire mesh screens which were horizontally mounted on a metal rod. The rod was rotated 180 degrees so that the mice were oriented upside down on the bottom of the screen. The animals were observed for their ability to climb to the top of the screen within one minute. Mice exhibited significant disruption of performance on the screen test 24 hours after soman doses of 0.71 LD50 or more. Treatment with atropine and 2-PAM i.m. 10 sec post-soman (1.1 x LD50) did not improve screen test performance when measured at 24 hours. Pretreatment with pyridostigmine or physostigmine in combination with post-soman therapy with atropine and 2-PAM significantly improved screen test performance as early as 2 hours after soman. The results suggest that the inverted screen test may be useful as a first-line assessment of the efficacy of pretreatment and treatment compounds against nerve agent-induced incapacitation.

Animals↗
PubMedDate not supplied

A comparison of physostigmine and soman using taste aversion and nociception.

The effects of a reversible (physostigmine) and an irreversible (soman) acetylcholinesterase inhibitor were compared in terms of nociception using the rat tail flick (TF), and hot plate (HP) tests. The conditioned taste aversion (CTA) procedure was employed to evaluate the stimulus properties of these drugs. In all procedures physostigmine salicylate was administered at doses of 0.20, 0.32, 0.45, or 0.65 mg/kg, IM. Soman was administered at doses ranging from 40 to 80 microgram/kg, IM. Using either TF or HP, physostigmine and soman were evaluated at 40 min following injection. Both physostigmine and soman produced dose-related effects on each measure of nociception. The median effective dose of physostigmine was 0.27 mg/kg on TF and 0.55 mg/kg on HP. For soman, the median effective dose was 54 micrograms/kg on TF and 52 micrograms/kg on HP. In the CTA procedure, a novel, saccharin sweetened solution was paired with either physostigmine or soman. Three days later rats were offered a choice of saccharin or tap water. Both soman and physostigmine produced dose-related CTAs over the range of doses studied. Whereas the ED50 for soman was 59 micrograms/kg with significant effects at doses of 60 micrograms/kg or more, physostigmine produced effects at doses of 0.45 mg/kg or greater (ED50 = 0.05 mg/kg) with no additional changes in saccharin preference beyond 0.45 mg/kg. The data suggest that these experimental procedures, TF, HP, and conditioned taste aversion may be employed to evaluate the behavioral toxicity of physostigmine and soman.

Animals↗
PubMedDate not supplied

Acute behavioral toxicity of the organophosphate sarin in rats.

Three experiments were performed to determine the behavioral effects of acutely administered isopropyl methylphosphonofluoridate, sarin (61-115 micrograms/kg, SC) to male rats. Dosages of 71 micrograms/kg or greater produced conditioned flavor aversions while spontaneous locomotor activity was increased at 61 micrograms/kg and significantly decreased at dosages of 84 to 115 micrograms/kg, when compared to vehicle control levels. Significant decrements in rotorod performance were observed at 98 and 115 micrograms/kg sarin. The LD50 of sarin was determined to be 165 micrograms/kg. Behavioral alterations were thus obtained at dosages that were between 37 and 59 percent of the LD50.

Animals↗