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Biomedical subjects

S Rothman

Publications and source records attributed to S Rothman.

31 records · Page 2Linked to original sources
PubMed1983

Attention deficit disorder: quantitative analysis of CT.

We compared the measurements of CTs in two groups of children: 35 satisfying DSM III criteria for attention deficit disorder (ADD) and 27 controls with other conditions. The groups were comparable in age, sex, and IQ. Measurements of the anterior horns of the lateral ventricles, bifrontal width, and right and left hemispheres did not differ. The ratio of ventricular size/bifrontal brain width (Evan's Index) averaged 0.237 in ADD and 0.263 in controls--results similar to those obtained in normal children by other investigators. Our findings suggest that when quantitative techniques, contrast populations, and "blind" analysis of CTs are employed, the results are indistinguishable in children with ADD and contrasts. If anatomic abnormalities are present in ADD, they are not discernible with current CT technology.

Adolescent↗
PubMed1981

A scanning electron microscope study of the in vitro development of dissociated hippocampal cells.

Cultures of dissociated hippocampal neurons from 18-day-old rat fetuses were examined by scanning electron microscopy after periods between one hour and 20 days following plating on a poly-L-lysine coated substrate. Cell attachment was virtually complete within one hour after plating, and at that stage many cells could be seen which had started to extend processes with broad growth cones. By four hours in culture, process formation was well advanced and some cells had already assumed a pyramidal configuration. After 16 hours in culture, numerous contacts were seen between neighboring growth cones, and this frequently led to fasciculation of the interacting fibers. During the next three weeks the cell bodies enlarged considerably and rounded-up, and two distinct types of processes became evident: large, rapidly tapering dendrite-like processes and finer, essentially uniform-diametered processes that resemble axons. In most of the older cultures a dense plexus of processes was formed, and many of the finer processes appeared to have "bouton-like" swellings as they traversed the upper surfaces of the neuronal perikarya. Non-neuronal elements, which comprised only about 5% of the cells initially plated, rapidly proliferated in our cultures and within three to six days formed a confluent monolayer beneath the neurons.

Animals↗
PubMed1981

Case report. Rapid development of cerebral atrophy due to perinatal herpes simplex encephalitis.

A case of neonatal herpes simplex virus (HSV) encephalitis is reported in which diffuse cerebral hemorrhagic lesions were seen in the neonatal period. Severe progressive cortical atrophy with parenchymal calcification developed over the subsequent 9 months, resulting in a striking computed tomography (CT) appearance. The range of CT findings in neonatal HSV encephalitis is reviewed, and differential diagnostic considerations in the present case are discussed.

Atrophy↗
PubMed1979

Unilateral cryptophthalmia.

Two patients had the variable clinical features of unilateral cryptophthalmia. A 5-month-old boy had isolated unilateral cryptophthalmia: a small boney orbit, deformed optic canal, and a small amorphous mass with no normal intraocular tissue representing the globe. No extraocular muscles or optic nerve were identified by B-scan ultrasound or by computed axial tomography x-ray techniques. The second patient, a 13-year-old girl, had unilateral cryptophthalmia, and numerous systemic abnormalities including a head circumference less than the third percentile, severe mental retardation, hypoplasia of the left side of the head, and a left facial cleft deformity. She also had contractures of hips, knees and ankles, and bilateral spasticity and jerky movements. The left boney orbit was contracted and deformed and contained a small amorphous tissue with no ocular detail, as revealed by B-scan and computed tomography scan.

Abnormalities, Multiple↗
PubMed1979

Role of clostridial toxin in the pathogenesis of clindamycin colitis in rabbits.

The pathophysiology of antibiotic-associated colitis was studied in rabbits with severe ileocolitis induced by oral administration of clindamycin. Cell-free, sterile filtrates of cecal contents of rabbits with clindamycin colitis contained a toxin that was lethal for mice and cytotoxic for HeLa-cell monolayers. The toxin was heat labile, was inactivated by pronase but not trypsin, and had a mol wt by gel filtration on Sephadex G-100 of 45,000. The toxin was neutralized by antiserum to Clostridium perfringens type E, but not by other clostridial antisera. The toxin also caused severe necrosis of rabbit rectal epithelium during 18-hr organ culture, which could be completely reversed by neutralization with C. perfringens type E antiserum. These studies indicate that clindamycin colitis in rabbits is caused by overgrowth of a clostridial species, which releases a heat-labile toxic protein of mol wt of 45,000 capable of necrosing colonic epithelial cells.

Administration, Oral↗
PubMed1978

Pathological involvement of primary sensory neurons in Werdnig-Hoffmann disease.

Seven patients with the typical clinical picture and muscle biopsy findings of classical Werdnig-Hoffmann disease showed Wallerian degeneration in their biopsied sural nerves. In dorsal root ganglia of one patient there were residual nodules and several chromatolytic neurons. By electron microscopy the changes of chromatolysis were confirmed and found to be consistent with an axonal reaction. Involvement of the primary sensory neuron is probably a regular pathologic feature of Werdnig-Hoffmann disease. The type of abnormality suggests in initial failure of the axon distal to the nerve roots.

Axons↗
PubMed1976

The childhood type of dermatomyositis.

The childhood type fo dermatomyositis, which occurs in children and young adults, shows a specific constellation of pathologic changes in muscle. Capillary necrosis leads to capillary loss, generally starting on the periphery of muscle fascicles. Electron microscopy discloses undulating tubules in endothelial cells, lymphocytes, pericytes, and pseudosatellite cells. The muscle fiber damage is coextensive with capillary damage and probably results from progressive ischemia. The muscle cells, before atrophying, show mitochondrial elongation, Z disk streaming, focal myofibrillary loss, and occassionally selective thick filament loss. Muscle cell necrosis is rare and limited to infarctlike lesions. Inflammatory infiltrates, if present, occur only in connective tissue septa. The cause of the capillary damage has not been determined.

Adult↗
PubMed1975

The syndrome of systemic carnitine deficiency. Clinical, morphologic, biochemical, and pathophysiologic features.

An 11-year old boy had had recurrent episodes of hepatic and cerebral dysfunction and underdeveloped musculature. Overt weakness developed at age 10. Lipid excess, especially in type I fibers, was found in muscle. Hypertrophied smooth endoplasmic reticulum and excessive microbodies were present in liver. Marked carnitine deficiency was shown in skeletal muscle, plasma, and liver. Ketogenesis was impaired on a high fat diet, but omega oxidation of fatty acids was enhanced. There was excessive glucose uptake and essentially no oxidation of labeled long-chain fatty acids by perfused forearm muscles in vivo. Oral replacement therapy restored plasma carnitine levels to normal, but not liver or muscle carnitine levels, and was accompanied by clinical improvement.

Adenosine Triphosphatases↗