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Biomedical subjects

D Soffer

Publications and source records attributed to D Soffer.

At least 91 records · Page 5Linked to original sources
PubMed1988

Experimental closed head injury in rats: mechanical, pathophysiologic, and neurologic properties.

A model of closed head injury in rats was developed using a calibrated weight-drop device. The development of edema was studied in various brain regions (cerebral hemispheres, brain stem, cerebellum) using a linear specific gravity gradient column. Regional brain tissue density was measured within 1 min, at 15 and 60 min, 18 h, 4 and 10 days after injury to the left cerebral hemisphere, and was compared with values in sham-operated and control rats. Significant edema (i.e., reduced specific gravity) occurred only in the traumatized hemisphere and was maximal at 18 h. A neurologic severity score (NSS) was developed to evaluate the status of the rat after injury. Specific gravity was significantly correlated with NSS at 18 h after injury. The affected hemisphere displayed hemorrhagic lesions as early as one hour post head trauma (HT), which evolved into hemorrhagic necrosis at 18 h. A pathologic score, evaluated 18 h post HT based on size and severity of the lesion, was correlated with the NSS and evaluated for each rat at one hour and 18 h postimpact. This correlation was found to be highly significant. This model of brain injury may be useful in future studies on the effects of therapeutic agents.

Animals↗
PubMed1988

Chronic progressive myelopathy: its relation to the spinal progressive form of multiple sclerosis.

The causes and clinical features of chronic progressive myelopathy (CPM) were evaluated in a retrospective study of 107 patients. A special emphasis was put on those in whom no underlying cause for the myelopathy could be determined. Of 76 such, 39 (51%) had oligoclonal immunoglobulins (Ig) in the CSF and were therefore considered as possible MS, while the remainder, without oligoclonal Ig, were designated "myelopathy of unknown origin" (MUO). Our "possible MS" group was similar clinically to reported series of proven spinal MS, and it seems therefore, that the presence of oligoclonal Ig permits the recognition of a group of patients with myelopathy who might be at a greater risk for MS. Patients with MUO differed from possible MS patients in several clinical characteristics, but most significantly in disease course and levels of functional disability which were more benign in the former. Myelopathy in possible MS patients was also of a primary pyramidal and asymmetrical nature. It is therefore suggested that the segregation of patients with CPM of undetermined origin into 2 separate groups based on the presence or absence of oligoclonal Ig might be of prognostic significance.

Adult↗
PubMed1987

Effect of intrastriatal and intranigral administration of synthetic neuromelanin on the dopaminergic neurotoxicity of MPTP in rodents.

Previous studies showed that the neurotoxin MPTP and its toxic metabolites bind with high affinity to neuromelanin (NM). Therefore, the presence of NM in human and primate but not in rodent substantia nigra, theoretically may be responsible for the species-selective dopaminergic (DA) toxicity of MPTP. We measured DA levels in rodent striatum 7 days after an acute single challenge with MPTP (40 mg/kg, s.c.) given alone or 24 h following unilateral intrastriatal injections of synthetic DA-NM in mice and intrastriatal or intranigral pigment administration in rats. Ipsilateral striatal DA levels were unaffected in control rodents treated with unilateral intrastriatal or intranigral DA-NM. In mice, systemic MPTP produced marked striatal DA depletions which were mildly increased in the striata given prior DA-NM injections. In rats, a species resistant to MPTP, administration of toxin did not affect striatal DA levels. However, after pretreatment with unilateral intrastriatal DA-NM, MPTP induced mild DA falls in ipsilateral striata. By contrast, intranigral administration of DA-NM followed by MPTP, did not alter ipsilateral striatal DA in rats. The findings suggest that intrastriatal DA-NM in mice and rats may augment or initiate, respectively. MPTP-induced damage to sensitive DA-nerve-terminals perhaps by its action as a depot for binding and protracted release and action of the toxin. Lack of effect of intranigral DA-NM which is retained extraneuronally suggests that role of NM in the toxicity of MPTP may depend on its location within DA cell bodies in the nigra.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Chronic demyelinating peripheral neuropathy in cerebrotendinous xanthomatosis.

Three siblings with chemically proved cerebrotendinous xanthomatosis presented with typical neurological manifestations of dementia and spinocerebellar disorder. Electrodiagnostic tests revealed demyelinating neuropathy in all three. Sural nerve biopsies showed loss of myelinated large fibers, marked Schwann cell proliferation, and onion bulb formation. Teased-fiber preparations confirmed the occurrence of segmental demyelination and remyelination. We suggest that demyelinating neuropathy is part of the neurological spectrum of cerebrotendinous xanthomatosis and should be considered in the differential diagnosis of a recessively inherited motor and sensory neuropathy.

Adolescent↗
PubMed1986

Hemispheric brain damage in unilateral status epilepticus.

A 20-year-old woman with psychomotor seizures developed prolonged unilateral status epilepticus followed by coma, right hemiparesis, fever, liver failure, and eventually death. Neuropathological findings included severe neuronal ischemic cell change and massive brain edema, essentially restricted to the left cerebral hemisphere. Massive destruction of the hemisphere involved in epileptic activity with sparing of the contralateral hemisphere provides supportive evidence that in humans prolonged seizure activity can cause permanent brain damage.

Adult↗
PubMed1986

Immunocytochemical search for JC papovavirus large T-antigen in multiple sclerosis brain tissue.

The large T-antigens of papovaviruses JC (JCV) and BK share a C-terminal subsequence with myelin basic protein (MBP). Since this sequence functions as a phosphate acceptor site in MBP, expression of a competing T-antigen sequence in oligodendroglia might adversely affect their ability to post-translationally process MBP and thus to maintain myelin. We have used techniques which demonstrate JCV T-antigen in small oligodendroglial cells from progressive multifocal leukoencephalopathy tissue to search for a possible latent JCV infection expressing T-antigen in nine cases of multiple sclerosis (MS) and three normal brains. No cells expressing T-antigen were detected in plaque or periplaque regions of the MS brains or in control CNS tissue.

Adult↗
PubMed1986

Inhibition of binding of hamster antibody to myelin basic protein by a synthetic triproline-containing peptide from JC virus T-antigen.

Antisera raised against porcine myelin basic protein (MBP) in Syrian hamsters were assayed by an ELISA method. The specificity of a high-titered antiserum was probed with synthetic peptides representing a hexapeptide and a decapeptide of the JC virus (JCV) large T-antigen C-terminus which is homologous to the MBP triproline region, a decapeptide from MBP which is encephalitogenic in guinea pigs, and peptides unrelated to MBP, i.e., substance P and poly-L-lysine. In an ELISA inhibition assay, preincubation of the hamster antiserum to MBP with either the JCV T-antigen C-terminal decapeptide or the encephalitogenic determinant inhibited binding activity in a dose-dependent manner. In contrast, the T-antigen C-terminal hexapeptide, substance P, and poly-L-lysine were not inhibitory. These results suggest that the triproline region of MBP can be immunogenic in hamsters, and support the concept that a conformation of the MBP triproline region is shared with certain of its viral homologues. In an effort to detect similar cross-reactive specificities in hamster antisera to JCV T-antigen, sera of 50 hamsters bearing subcutaneous tumors induced by JCV-transformed glial cells were tested for ability to bind to MBP in the ELISA assay. While significant increases in response compared to prebleed levels were observed in about one-fourth of the sera, some of them showed similar increases in binding to other basic proteins such as histones, and the binding to MBP was not inhibited by the triproline-containing decapeptide.

Animals↗
PubMed1986

Autopsy findings of Serratia meningoencephalitis in infants.

Serratia meningoencephalitis is often a fatal disease that causes widespread destruction of brain tissue despite aggressive antibiotic treatment. The autopsy findings of 2 cases are described. In a case caused by S. liquefaciens, previously not reported as the causative organism of meningoencephalitis, suppurative meningitis, ventriculitis, vasculitis, and extensive necrotic process of the brain matter were found. In the other case, caused by S. marcescens, the findings were those of acute and subacute abscesses with hemorrhagic necrosis.

Bacterial Infections↗
PubMed1986

Amyloid tumor (amyloidoma) of a peripheral nerve.

We report a case of amyloidoma of a peripheral cervical nerve situated in the right anterior aspect of the neck. Such a localization has not been previously described, to the best of our knowledge.

Adult↗
PubMed1986

A new animal model for action myoclonus.

Morphine was injected into a catheter implanted chronically into the intrathecal space of rats. Three to eight minutes after drug administration, 80% of the rats developed arrhythmic stimulus-sensitive jerks that lasted up to 1 hr. The morphine-induced myoclonic activity was markedly reduced by naloxone. Methadone, pethidine, and etorphine failed to produce the syndrome. In spinally transected rats, morphine injected below the level of transection did not produce the syndrome. No significant changes in PaCO2 and PaO2 were produced by morphine before and throughout the period of myoclonic activity. Neither did induced hypoxia augment the effect of morphine. However, irreversible hypoxic-ischemic cell changes were noticed in some brain regions. The phenomenon described here resembles the human syndrome of action myoclonus and may serve as an animal model for studying the mechanism of that neurological disorder.

Animals↗
PubMed1985

Toxic and lethal effects of T-2 toxin upon intracerebral administration to rats.

T-2 toxin was given to rats in three ways: Subcutaneous or intracerebral injection of a solution in dimethyl sulfoxide (DMSO) and by implantation of toxin, adsorbed on talc, into various regions of diencephalon and brain stem. The latter method proved to be most effective. Within a few hours after administration of 10-20 micrograms toxin, the animals became restless, ataxic and dyspneic. These early symptoms were followed by depression and immobility. Prior to death, tachypnea and/or convulsions developed. The rats succumbed to implantation of toxin within 1 - 7 days; no fatalities occurred at later dates. Histologically, the toxin pellets caused necrosis a few days after implantation; at a later stage, the necrotic areas were surrounded by inflammatory infiltrates around small blood vessels. These morphological changes were limited to the application site and were insufficient to explain the lethal effect of intracerebral administration. After intracerebral injections of toxin solutions, the animals died within 24 h. No marked histological changes could be seen after such rapid fatalities.

Animals↗
PubMed1985

Neuronal intranuclear hyaline inclusion disease presenting as Friedreich's ataxia.

A case of neuronal intranuclear hyaline inclusion disease (NIHID) is described, and the literature on seven reported cases is briefly reviewed. The patient was a 24-year-old man who died of a chronic progressive neurologic disease starting at the age of 6 years. Clinically, the disease presented as Friedreichs's ataxia, and pathologically it was characterized by multisystem atrophy. An outstanding feature was the presence of widespread intranuclear hyaline inclusions in neurons of the brain, spinal cord, and myenteric plexus of the gut. The inclusions displayed yellow-green autofluorescence under ultraviolet (UV) light and were filamentous ultrastructurally. It seems that cases bearing such peculiar neuronal inclusions represent a distinct disease entity of unknown origin. The disease, which is sometimes familial, usually starts in childhood and affects both sexes. Clinically, it presents as multisystem degeneration with progressive ataxia as the prominent feature. Pathologically, it is characterized by neuronal loss, fiber tract atrophy, and intranuclear neuronal inclusions. In some cases such inclusions were found also in neurons of the myenteric plexus. Since these are accessible to biopsy it is recommended that rectal biopsy be made in every case of "atypical" system atrophy.

Adult↗
PubMed1985

Meningeal carcinomatosis due to basal cell carcinoma.

A case of meningeal carcinomatosis due to metastasizing basal cell carcinoma is reported. The patient was a 34-year-old woman who had a recurrent basal cell carcinoma of the upper eyelid with deep invasion. In spite of extensive surgery and radiotherapy, multiple bone metastases developed, and the patient eventually died of meningeal carcinomatosis. The possible pathogenic mechanisms of meningeal the present case, cancer cells reached the leptomeninges from adjacent vertebral metastases. It is suggested that the possibility of meningeal carcinomatosis should be considered in every patient with cancer and multiple vertebral metastases, particularly when neurologic signs involving the brain, cranial nerves, or spinal nerves are present.

Adult↗
PubMed1985

Treatment of experimental allergic encephalomyelitis in rabbits with alpha-fetoprotein.

We studied the ability of alpha-fetoprotein (AFP) to suppress experimental allergic encephalomyelitis (EAE) in rabbits. Animals were treated with daily injections of 50 micrograms of AFP following the onset of neurological signs. Clinical status, anti-myelin basic protein (MBP) antibody titers, and histopathological changes in the CNS were determined. Treatment with AFP significantly improved the clinical scores of the affected rabbits and inhibited the binding of anti-MBP antibodies to MBP in vitro. However, there was no significant difference in the titers of anti-MBP antibody, and no amelioration of histopathological changes between treated and control animals. We conclude that AFP is effective in improving the clinical status of animals with EAE, even after the appearance of clinical signs.

Animals↗
PubMed1984

Familial hemophagocytic lymphohistiocytosis in Israel. II. Pathologic findings.

Presented are the pathologic findings in familial hemophagocytic lymphohistiocytosis (FHLH), based on observation of 11 cases from four affected families. The outstanding morphologic feature was a multiorgan involvement with lymphohistiocytic cellular infiltrates. The organs most frequently affected were the bone marrow and lymph nodes and, less frequently, the liver and the brain. The histiocytes in the infiltrates were usually bland and displayed prominent hemophagocytosis. The differential diagnosis of FHLH and the difficulty in distinguishing it from malignant histiocytosis is discussed. In view of the focal distribution of lesions, it is suggested that histopathologic diagnosis of FHLH be made only after evaluation of combined findings in several organs and consideration of the patient's family history as well as the result of the clinical and laboratory investigations.

Bone Marrow↗
PubMed1984

Familial hemophagocytic lymphohistiocytosis (FHLH) in Israel. I. Description of 11 patients of Iranian-Iraqi origin and review of the literature.

Eleven patients with familial hemophagocytic lymphohistiocytosis (FHLH) are described. They all belonged to four Jewish families of Iranian and Iraqi origin. Parental consanguinity was found in three families. The age of onset of disease ranged from 6 weeks to 36 months. All patients had fever, wasting, and enlargement of the liver and spleen. In addition, lymph-node enlargement and neurologic complications were common. The most consistent laboratory findings were pancytopenia, atypical lymphomonocytoid cells in the peripheral blood, abnormal liver function test results, and increased cerebrospinal fluid protein. The course was fatal in all patients. Nine of the 11 patients died within 2 weeks to 3 months of presentation, and 2 patients achieved temporary remissions but died of disease within 8 and 24 months, respectively. Response to antibiotic therapy or to the administration of corticosteroids and cytotoxic drugs was unimpressive. Pancytopenia complicated by sepsis or bleeding, hepatic failure, or encephalopathy were the terminal events. This report draws attention to the existence of FHLH in Jews of Iranian-Iraqi origin in whom parental consanguinity is very common.

Child, Preschool↗
PubMed1983

Paraganglioma of cauda equina. A report of a case and review of the literature.

A case of a cauda equina paraganglioma in a 13-year-old boy is described. A review of literature revealed six similar reported cases. All were intradural extramedullarly tumors located in the cauda equina-filum terminale region. In all, the presenting and dominant symptom was low back pain, while neurologic deficit was mild or absent. Excessive CSF protein levels appeared to be a characteristic feature of the disease. Histologically, the tumor displayed the typical "Zellballen" pattern, however mild nuclear pleomorphism and some mitotic figures were noted. As it is impossible to predict the biological behaviour of paragangliomas from the histologic appearance, complete surgical resection with close follow-up is indicated in such cases.

Adolescent↗