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Biomedical subjects

U Sandbank

Publications and source records attributed to U Sandbank.

At least 19 recordsLinked to original sources
PubMed1992

Giant axonal neuropathy with predominant central nervous system manifestations.

The authors describe a 25-year-old woman with giant axonal neuropathy (GAN) and severe CNS involvement. She had been admitted to hospital with generalized seizures, and had gait disturbances followed by progressive mental deterioration since childhood. Neurological examination revealed mental retardation, scanning speech, cerebellar dysfunction, pyramidal signs, mainly in the lower extremities, and peripheral sensory neuropathy. Sensory nerve conduction velocity was decreased; brain CT and MRI showed diffuse demyelination. Sural nerve biopsy revealed characteristic signs of GAN. The patient's older sister had died at the age of 23, after having had similar neurological disturbances since childhood. This case illustrates an unfamiliar presentation of GAN, characterized by mild sensory neuropathy and serve CNS involvement, including seizures.

Adult↗
PubMed1991

The prognostic significance of glial fibrillary acidic protein staining in medulloblastoma.

Histologic and immunohistochemical properties of 53 medulloblastomas were analyzed with regard to clinical features and survival rate. No correlation was found between survival rate and histologic features of the tumor, such as desmoplastic reaction, number of mitoses, hemorrhages, necrosis, endothelial proliferation, glomerular arrangement, calcifications, rosettes, or oligodendroglial cells. However 82% of the patients with positive glial fibrillary acidic protein (GFAP) staining in numerous tumor cells survived more than 5 years; only 30% survived that long if their tumor cells were GFAP negative (P = 0.0093). This significant difference was not related to the mode of therapeutic protocol used. The authors suggest that GFAP staining may be a useful prognostic tool in medulloblastoma.

Adolescent↗
PubMed1991

Immunocytochemistry of epithelial markers in citral-induced prostate hyperplasia in rats.

Immunocytochemical characterization of several epithelial markers using the PAP technique was analyzed during different stages of induced prostatic hyperplasia in rats. Intact adolescent rats (42 days old) were treated with citral (3,7 dimethyl-2,6 octadienal) for 10, 30 and 100 days and their ventral prostate compared to untreated, matched-age animals. Among the epithelial markers studied the prostatic specific acid phosphatase was present in hyperplastic prostates of rats. The immunoreaction showed a fair correlation with the severity of lesion and duration of treatment. The prostatic specific antigen showed equally immunoreactive in both control and treated rats. The hyperplastic and normal rat prostates did not show immunoreactivity towards the other epithelial cell markers such as epithelial membrane antigen, carcinoembrionic antingen and alpha-fetoprotein antisera. It is concluded that prostatic specific acid phosphatase, and to a lesser extent prostatic specific antigen, might represent valuable markers for comparative studies of prostatic hyperplasia in rodents.

Acyclic Monoterpenes↗
PubMed1990

Familial myoedema, muscular hypertrophy and stiffness.

A father and son with muscular hypertrophy, stiffness and myoedema are described. The local swelling after tapping the muscle was not accompanied by electrical activity. Histological and histochemical studies of muscle biopsy showed no abnormalities. Electron-microscopy showed multiple vacuoles to be due to T-tubule dilatation. Further studies are necessary to determine the significance of this finding in the pathogenesis of muscle sensitivity to mechanical irritation in this rare syndrome.

Adolescent↗
PubMed1989

Lectin histochemistry of brains from a murine mutant carrying a storage disorder.

A strain of Balb/c mice with neurovisceral storage disorder exhibits metabolic and phenotypic manifestations similar to those found in Niemann-Pick type C and D patients. The storage material in the brain reacted positively with periodate-Schiff reagent. To identify the chemical nature of the storage material we applied lectin histochemistry on paraffin-embedded and frozen sections, using biotinylated lectins and avidin-biotin-peroxidase complex. Major abnormalities were noted in the neurons and glia cells. Swollen neurons were stained heavily by Con A and S-WGA, whereas glia cells, mainly astrocytes, which were abundant both in the cerebrum and cerebellum, were positive to RCA-I, GS-I, PNA, S-WGA and WGA. The myelin tracts reacted with PNA, SBA and RCA-I but to a lesser extent in affected animals when compared to normals. Frozen brain sections stained positively only after extraction with chloroform methanol prior to the lectin treatment and revealed a lectin binding pattern similar to that of the paraffin-embedded preparations. The data presented here show that the stored glucoconjugates in the neurons are of a different chemical composition than those found in glia cells. Since only paraffin embedded sections or lipid extracted frozen sections reacted with the lectins, we suggest that the stored glucoconjugates are glycoproteins or oligosaccharides rather than glycolipids.

Animals↗
PubMed1989

Massive pseudophakic pigment dispersion associated with an iris nevus.

A 67-year-old woman examined 12 months following extracapsular cataract extraction had a massive pseudophakic pigment dispersion associated with diffuse corneal epithelial edema, mild uveitis, and secondary glaucoma. She underwent penetrating keratoplasty following removal of a posterior chamber intraocular lens (IOL), anterior vitrectomy, capsulectomy, and iris biopsy. Histopathologic examination revealed a pigmented iris nevus and signs of iris erosion by the IOL loop. Because 3 months later the eye developed streptococcal endophthalmitis and had to be eviscerated, we had the opportunity to examine the eye contents; we found no evidence of phakoanaphylactic uveitis.

Aged↗
PubMed1988

Early and delayed neurotoxicity of mitoxantrone and doxorubicin following subarachnoid injection.

Doxorubicin (DXR) and Mitoxantrone (MXN) were administered into the subarachnoid space of mice or the ventricular system of rats. The maximal non-toxic systemic single dose (zero mortality = LDo) of DXR or MXN was used as reference for planning drug doses for CSF administration. LDo in mice were: 8 mg/kg DXR and 6 mg/kg MXN; in rats: 6 mg/kg DXR and 4.5 mg/kg MXN. Signs of neurotoxicity were remarkably similar in DXR or MXN treatment animals and included: head tremor, atactic-dystonic posture and circling behavior. The toxicity was dose dependent. Doses of greater than or equal to 10% the LDo caused early appearance of clinical signs: a dose of 10% LDo caused neurotoxicity in 90% of DXR treated mice and in only 15% of MXN-treated animals. Treatment with 25% LDo MXN caused neurotoxicity in 30% of treated animals. Doses of less than or equal to 5% the LDo caused a delayed onset of DXR neurotoxicity in one third of treated mice (after 60-90 days). In rats, neurotoxicity was of an early onset and augmented severity following doses of greater than or equal to 5% LDo. Abnormal histopathological findings were detected only in symptomatic animals with early toxicity and were usually restricted to superficial cortical layers in mice or the basal surface of the brainstem in rats. Brains of mice with delayed toxicity were unremarkable. The levels of monoamine neurotransmitters and their metabolites (DA, DOPAC, HVA, NE, 5HT) in the striatum, cortex and cerebellum of mice with early and delayed DXR neurotoxicity did not differ from normal brains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Indomethacin and dexamethasone treatment in experimental neoplastic spinal cord compression: Part 1. Effect on water content and specific gravity.

Water content and specific gravity were measured in the cervical, high thoracic, thoracic, and lumbar segments in an experimental model of neoplastic epidural spinal cord compression in rats harboring a thoracolumbar tumor. Increased content of water was observed only in the compressed lumbar cord segments of paralyzed rats (P less than 0.04). A progressive increase in specific gravity values of the compressed segments accompanied the increasing severity of neurological dysfunction (P less than 0.003 in paraplegic rats). Electron microscopy of the compressed cord revealed enlarged interstitial spaces, myelin breakdown, and extravasated blood cellular elements. Treatment with dexamethasone (10 mg/kg q 12 hr x 3) failed to reduce the increased content of water, but corrected specific gravity changes. Treatment with indomethacin (10 mg/kg q 12 hr x 3) reduced both elevated water content and specific gravity values back to normal levels. In untreated animals, the interval between the first neurological sign (limp tail) and paraplegia was 2.8 +/- 0.34 days (mean +/- SE). Treatment with dexamethasone lengthened this period by 28.6% (P less than 0.05); treatment with indomethacin lengthened it by 66.4% (P less than 0.005). We conclude that, because the specific gravity measurements in this model reflect complex pathophysiological processes, their translation into water content values is not advisable. Pharmacological intervention with indomethacin compares favorably with dexamethasone in reduction of spinal cord edema and in delaying the onset of paraplegia.

Animals↗
PubMed1987

Alteration of blood-brain-CSF barrier in experimental meningeal carcinomatosis. A morphologic and adriamycin-penetration study.

An experimental model of meningeal carcinomatosis has been produced by subarachnoid inoculation of B16 melanoma cells into C57BL mice. Injection of 10(3) viable cells was sufficient to cause 100% tumor incidence and death within a median survival time of 17 days. The tumor infiltrated diffusely the meninges of the brain and spinal cord and filled the ventricular system. Electron microscopic study of the leptomeningeal tumor revealed newly formed microvessels with fenestrated endothelium. The integrity of the blood-brain barrier was studied by the extravasation of the Evans blue and the Horseradish peroxidase tracers. Barrier disruption became evident from the seventh day on, using Evans blue. Electron microscopy study showed peroxidase activity in the luminal and abluminal sides of the meningeal microvessels, and within the tight junctions. Similar findings were noted in cortical capillaries adjacent to the meningeal tumor. Brain concentrations of Adriamycin (ADR) following administration of an intravenous dose of either 10 mg/kg or 50 mg/kg were measured on days 0 to 14 after tumor inoculation. A significant increase in mean +/- SEM content of whole brain ADR was observed only with the 50 mg/kg dose in days 7 to 14 (0.69 +/- 0.02 micrograms/g wet tissue weight) as compared to tumor-free controls (0.43 +/- 0.01, p less than 0.05). Our study suggests that barrier alteration in meningeal carcinomatosis allows extravasation of tracer solutes. Still, in order to achieve a significant increase in a water soluble drug penetration through the disrupted barrier, a high-dose drug regimen is required.

Animals↗
PubMed1987

Dysmyelination in NCTR-Balb/C mouse mutant with a lysosomal storage disorder. Morphological survey.

A morphological survey of the central nervous system of a NCTR-Balb/C mouse afflicted by neurovisceral storage disease was performed. It has been demonstrated that this mutant is characterized by primary dysmyelination, which is evident as early as 12 days of age. The failure of myelin formation in the CNS was shown by histochemical and ultrastructural methods. Inasmuch as neither lipid-containing macrophages nor infiltrating mononuclear cells were apparent, secondary demyelination could be excluded. The multiform ultrastructural appearance of the storage material in the various CNS cell types suggested heterogeneity of the accumulated substances. The storage materials which reacted positively with periodate-Schiff reagent, but not with other histochemical stains, are most likely the accumulated gangliosides and neutral glycosphingolipids identified previously in this mutant's brain. Considering the probable role of cholesterol ester in the early phases of myelinogenesis, in conjunction with the fact that the NCTR-Balb/C mouse carries a defect in the esterification of exogenously derived cholesterol, it is possible that the later metabolite is relevant to the impaired myelin formation.

Animals↗
PubMed1987

Acute pancreatitis in rats: a 31P nuclear magnetic resonance study.

High resolution 31P nuclear magnetic resonance (NMR) was used to evaluate the severity of acute pancreatitis in rats. Experimental pancreatitis was induced by intraparenchymal injection of 10% sodium taurocholate. pancreases were removed at various time periods and the NMR spectrum of the whole organ was recorded. Metabolic changes taking place during the progression of the disease were measured and correlated with the pathologic changes. Gradual depletion of the high energy compounds, adenosine triphosphate and phosphocreatine, was observed. The NMR spectral changes paralleled the extension of the pathologic lesions and were found to constitute a reliable indicator of the severity of acute pancreatitis. It is suggested that high resolution NMR may be used to evaluate the pathogenesis and therapy of various forms of experimental pancreatitis.

Adenosine Triphosphate↗
PubMed1987

Experimental neoplastic spinal cord compression: evoked potentials, edema, prostaglandins, and light and electron microscopy.

Spinal cord compression was induced in Fischer rats by percutaneous inoculation of 10(6) cells of malignant fibrous histiocytoma anterior to the T13 vertebral body. Paraplegia and incontinence occurred in all animals after 14-27 days (median, 23 +/- 3.0 days). Autonomic dysfunction and a measurable increase in tumor volume were documented with the use of computer tomography. The tumor penetrated the vertebral bone, invaded the epidural space, and gradually compressed the lumbar spinal segments. Electron-microscopic examination revealed dilated intermyelin spaces containing exuded homogenous material and extravasated leukocytes and erythrocytes. Myelin breakdown was accompanied by the presence of lipid-laden macrophages. Sequential recording of somatosensory evoked potentials (SEP) revealed a progressive increase in the latency of the cervical responses, which preceded the onset of clinical signs. In the presence of paraplegia, spinal cord conductivity was abolished. The levels of the prostaglandins TXB2, 6-keto-PGF1 alpha, and PGE2 were measured in the compressed and remote spinal cord segments during the presymptomatic and symptomatic periods. Only PGE2 was significantly elevated (P less than 0.001) in the paraplegic rats, all along the spinal cord segments. A significant increase in water content was measured in the compressed lumbar segments in the presymptomatic period, and when paralysis set in it was increased in the adjacent low thoracic area as well. Tissue specific gravity was significantly increased only in paraplegic rats in the compressed (P less than 0.01) and the adjacent low thoracic areas (P less than 0.05) but no significant change occurred during the presymptomatic period. Multiple mechanisms play a role in the pathogenesis of neurologic symptoms in neoplastic spinal cord compression.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Early stages of the pathogenesis of rat ventral prostate hyperplasia induced by citral.

Typical lesions of benign prostatic hyperplasia (BPH) were induced experimentally in the ventral prostate of adolescent (6 week old) male rats by citral, a nonsteroidal compound. Incipient BPH changes were already observed in the acinar glands 10 days after citral administration. A longer period of treatment (1 month) significantly enhanced epithelial hyperplasia, whereas the stromal elements were less reactive. Characteristic BPH lesions involving both prostatic compartments were found after 3 months of treatment. Castration prior to citral administration prevented such BPH changes; however, citral did not prevent the involutive lesions of castration. The mechanism of action of citral is yet unknown, various possibilities concerning the induction of BPH in rats are presented and discussed. The potential advantage of this model, especially as BPH is not necessarily linked to age or exogenous hormones, may offer new alternative pathways for understanding the complexity of BPH pathogenesis in animals and perhaps even in man.

Acyclic Monoterpenes↗
PubMed1985

Neurological mutation characterized by dysmyelination in NCTR-Balb/C mouse with lysosomal lipid storage disease.

Morphological and biochemical studies were performed on the CNS of neurologically affected NCTR-Balb/C mouse. Histological and electron microscopic techniques demonstrated severe myelin deficiency in the affected brains. Neither the presence of lipid-containing macrophages nor reactive gliosis was apparent. Analysis of myelin-associated lipids and proteins revealed prominent depletion of galactocerebroside, sulfatide, and proteolipid proteins. In contrast to the scarcity of myelin-specific constituents a marked accumulation of GM2 and GM3 gangliosides and several neutral glycolipids, i.e., glucocerebroside, lactosylceramide, gangliotriaosylceramide, and gangliotetraosylceramide were found in affected CNS. These abnormalities were already apparent in 12-day-old pups as well as in 65-day-old mice. A significant deficit in the proportion of long-chain fatty acids (C24), notable in both normal and alpha-hydroxy acids of cerebrosides from affected white matter, was measured. The lack of reactive gliosis, the observed depletion of galactocerebroside and sulfatide at the early age of 12 days, and the relative decrease in long-chain fatty acids in affected CNS strongly suggest a defect in myelinogenesis in this mutant rather than a secondary process of myelin breakdown.

Animals↗