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Biomedical subjects

S Hall

Publications and source records attributed to S Hall.

At least 181 records · Page 10Linked to original sources
PubMed1990

Lethal paralytic shellfish poisoning in Guatemala.

An outbreak of paralytic shellfish poisoning occurred in Champerico, on the Pacific coast of Guatemala, July-August 1987. Of 187 people affected with characteristic neurologic symptoms, 26 died. A case study implicated a species of clam, Amphichaena kindermani, harvested from local beaches as the vehicle of the neurotoxins (saxitoxins). Children less than 6 years old had a higher fatality rate (50%) than people greater than 18 years of age (7%). The minimum lethal dose for 1 child was estimated to have been 140 mouse units of toxin/kg body weight; thus children may be more sensitive to the saxitoxins than are adults. This is the first large outbreak of paralytic shellfish poisoning recognized in Guatemala.

Adolescent↗
PubMed1990

Takayasu's arteritis.

The cause of Takayasu's arteritis is still obscure. However, certain aspects of the disease have been greatly clarified over the past decade. The disease is worldwide in distribution, with no ethnic group being totally free from risk of the condition. The inflammatory and stenotic phases of the disease frequently coexist, and it is important that the condition be diagnosed before it has progressed to the phase of extensive, severe vascular occlusion. Corticosteroid therapy is effective in ameliorating both the more inflammatory aspects of the condition (fever, arthritis, myocarditis) and the hemodynamic problems of vascular stenoses, in some cases allowing return of previously absent pulses. The role of adjunctive cytotoxic therapy is less certain, although there is probably a place for it in cases characterized by corticosteroid resistance or severe consequences of hypercortisolism. Vascular reconstruction is safe and effective once the inflammatory phase of the disease has remitted or been controlled with drug therapy. Prognosis is related to specific disease complications associated with longer duration of disease. Therefore, treatment intervention may modify the natural history of the disease over the long term.

Adult↗
PubMed1990

Modulation of tartrate-resistant acid phosphatase expression by calcitriol in CSF-induced macrophage colonies.

The osteoclast is thought to be a hemopoietically derived cell, but questions exist about which hemopoietic growth factors are responsible for proliferation of osteoclast precursors. Experiments were thus performed to see if recombinant human colony-stimulating factors (CSFs) influenced the expression of tartrate-resistant acid phosphatase (TRAP), an osteoclast marker enzyme, by monkey bone marrow colonies in vitro. In addition, the effect of 1,25-dihydroxyvitamin D3 (calcitriol) on CSF-induced colony growth and TRAP expression was also determined. Bone marrow was obtained from a single Macaca nemestrina monkey, kept frozen in liquid nitrogen, and aliquots of frozen cells were thawed and placed at 10(5) cells per plate in a standard cell colony-forming unit (CFU-C) assay. The recombinant human CSFs (granulocyte-macrophage CSF, GM-CSF; macrophage CSF, M-CSF; interleukin 3, IL-3; and granulocyte CSF, G-CSF) were added to the cultures at 50 U/ml, and calcitriol was titrated for each CSF from 0.1 to 100 nM. Day-14 colonies were stained to demonstrate TRAP-positive cells in individual colonies. GM-CSF caused an increase (193%, p less than 0.0004) in total colony numbers that was only partially inhibited by calcitriol. IL-3 and M-CSF had less effect, and G-CSF had no effect. GM-CSF also caused a large increase in TRAP-positive macrophage (M) colonies (326%, p less than 0.0001) and changed the relative proportion of TRAP-positive M colonies from 39% to 62% of all M colonies. M-CSF caused less increase in numbers of TRAP-positive M colonies and had no effect on the proportion of TRAP-positive colonies. When GM-CSF was present, calcitriol caused a maximum number of TRAP-positive colonies to appear at 1 nM, and it caused a drastic decrease in TRAP-positive colonies at higher doses. Calcitriol at 10 nM caused TRAP-negative colonies to increase in number and proportion when GM-CSF was present, but in the presence of M-CSF, the same dose of calcitriol caused a decline in numbers of TRAP-negative colonies. These results suggest that GM-CSF may be important in the replication of TRAP-positive mononuclear cells that resemble osteoclast precursors and that myeloid cell development may be weighted toward TRAP-positive or TRAP-negative progeny depending on whether GM-CSF or M-CSF predominates. They further suggest that calcitriol concentration may be critical in this process.

Acid Phosphatase↗
PubMed1989

Rey-Auditory Verbal Learning and Rey-Osterrieth Complex Figure Design performance in Alzheimer's disease and closed head injury.

Performance on the Rey-Auditory Verbal Learning (R-AVL) and Rey-Osterrieth Complex Figure Design (R-O CFD) tests was examined in patients (N = 94) with dementia of the Alzheimer's type (DAT) and closed head injury (CHI). On the R-AVL, DAT patients demonstrated considerably greater impairment than CHI patients, along with a flat learning/retention curve that showed negligible improvement with repeated trials, recency effects only, and an excessive number of word intrusions (confabulation) on the recognition trial. CHI patients demonstrated both a recency and primacy effect along with improvement over repeated trials (positive slope learning curve). Both groups demonstrated impairment R-O CFD recall; the DAT group again displayed substantially greater copying and recall deficits. Clinical guidelines are given for the use of the R-AVL and R-O CFD for these two patient populations.

Adult↗
PubMed1989

Chronic progressive multiple sclerosis: serial magnetic resonance brain imaging over six months.

Eight patients in the chronic progressive stage of multiple sclerosis were studied prospectively with magnetic resonance imaging of the head and neurological examination every 2 weeks for 6 months. There were no clinical relapses and disability ratings did not change between the start and completion of the study. Despite the clinical inactivity, a total of 86 active events (new, reappearing, or enlarging lesions) were identified by magnetic resonance imaging over the 6 months, with 50 (51%) of 98 follow-up scans showing evidence of one or more active lesions. New and changing lesions were indistinguishable in appearance, distribution, and temporal pattern from those previously seen in patients who had relapsing and remitting multiple sclerosis. However, as noted previously, the patients in the chronic progressive stage had many more confluent lesions than did the group in relapse. These results strongly suggest that the frequently observed clinical evolution of multiple sclerosis into a chronic progressive course is not accompanied by a fundamental change in the disease process. In fact the chronic progressive stage seems associated with more active changes demonstrated by scans than does relapsing and remitting multiple sclerosis. This study also confirms our previous experience that serial magnetic resonance imaging is much more sensitive than clinical examination in detecting disease activity in multiple sclerosis.

Adult↗
PubMed1989

Defective myelination in the optic nerve of the Browman-Wyse (BW) mutant rat.

The Browman-Wyse (BW) rat displays a spectrum of ocular abnormalities which include myelination by Schwann cells of retinal ganglion cell (RGC) axons within the retina. Immunohistochemical and ultrastructural studies of the optic nerves of adult BW rats (30-60 days of age) with myelinated intraretinal axons were performed. Although individual nerves displayed considerable morphological variability, all were characterized by an initial dysmyelinated proximal segment which was separated from a normally myelinated distal segment by a transitional junctional zone. The proximal segment contained axons which were predominantly unmyelinated: where myelination occurred, almost all sheaths were Po-positive, proteolipid protein-negative, and the myelinating cell was a Schwann cell. In the distal segment the distribution of myelinated axons appeared to be normal, sheaths were PLP+, and the myelinating cell was an oligodendrocyte. Within the proximal segment, axons that were myelinated by Schwann cells were isolated by a basal lamina and expanded extracellular spaces from the bulk of other RGC axons within the optic nerve. Few carbonic anhydrase (CAII)+ or GalC+ oligodendrocytes were seen in proximal segments that contained Schwann cells: anti-CAII antibody stained atypical cells within the proximal segments which did not resemble CAII+ oligodendrocytes in the distal segment, and which were probably GalC-. Astrocytes appeared normal throughout the length of the nerve, and there was no morphological specialization at the junctional zone similar to that at the lamina cribrosa. The possible source(s) of the intraneural Schwann cells, and the pathogenetic mechanisms underlying the aberrant myelination of RGC axons within the BW optic nerve are discussed.

Animals↗
PubMed1989

Electron microscopic study of the interaction of axons and glia at the site of anastomosis between the optic nerve and cellular or acellular sciatic nerve grafts.

The interactions between retinal ganglion cell (RGC) axons and glia at the site of optic nerve section and at the junctional zone between optic nerve and cellular or acellular peripheral nerve (PN) grafts have been studied electron microscopically. After transection, RGC axons, accompanied by processes of astrocyte cytoplasm, grew out from the proximal optic nerve stump into the scar tissue that developed between proximal and distal stumps. However, axons failed to cross the scar, and none entered the distal stump. By 3 days post lesion (DPL), bundles of RGC axons, accompanied by astrocytes and oligodendrocytes, grew out from the proximal optic nerve stump into the junctional zone between optic nerve and either type of PN graft. The bundles of RGC axons and growth cones that grew towards acellular PN grafts degenerated within 10-20 DPL; by 30 DPL a small number of axons persisted within the end of the proximal optic nerve stump. No axons were seen within the acellular PN grafts. These results suggest that reactive axonal sprouting, axon outgrowth and glial migration from the proximal optic nerve stump are events that occur during an acute response to injury, and that they are independent of the presence of Schwann cells. However, it would appear that few axons entered either scar or junctional zone unless accompanied by glia. There was little evidence that axon outgrowth was laminin-dependent. The bundles that grew towards cellular PN grafts encountered cells that we have identified as Schwann cells within the junctional zone: the axons in these bundles survived and entered the cellular grafts. Schwann cells migrated into the junctional zone from the cellular PN graft. It is probable that Schwann cells facilitated RGC axon entry into the graft directly by both cell contact and the secretion of neuronotrophic factors, and indirectly by modifying the CNS glia in the junctional zone.

Anastomosis, Surgical↗
PubMed1989

Depression preceding choreiform movements in Huntington's Disease: a case study.

Huntington's Disease (HD) is a progressive neurological disorder whose cardinal features are involuntary movements and cognitive decline. Severe emotional and/ or psychiatric disturbances are common features of the mental deterioration. When the emotional disturbance precedes the development of the movement disorder, HD is often misdiagnosed as a psychiatric condition. The present case study taken from the University of Texas Neuropathology Museum illustrates these issues. The patient was diagnosed and treated for depression for over a decade before the behavioral and neurological deterioration progressed to the point that an HD diagnosis could be made. Only with the detection of a positive family history and the onset of the hallmark choreiform movements was the final diagnosis of HD made. The patient's behavioral features are presented and current pathological and neuropsychological findings in HD are reviewed and discussed.

Clinical Conference↗
PubMed1988

'Disengage' sensorimotor deficit following apparent recovery from unilateral dopamine depletion.

Sensorimotor behavior in Long-Evans rats was evaluated acutely and chronically after unilateral dopamine depletion caused by infusions of 6-hydroxydopamine into the nigrostriatal system. In each rat, control infusions were delivered to the opposite hemisphere and a noradrenaline uptake blocker was used as a pretreatment to help protect noradrenaline cells. During the first few postoperative weeks, head movement reactions to repetitive tactile-perioral stimulation contralateral to the dopamine-depleted hemisphere were delayed but not eliminated. With recovery, facilitated by special training, the rats were able to respond quickly. However, two lasting abnormalities were observed. First, the types of head-orienting movements directed toward contralateral stimulation were different from that directed toward ipsilateral stimulation. Second, when the animals were engaged in eating behavior there was a complete failure to orient to contralateral stimulation, whereas they instantly disengaged from eating to orient to ipsilateral stimulation. When not eating, orienting was rapid and reliable to stimulation of either side of the body. These data may have implications for the role of the striatum and connected structures in the organization and integration of sensorimotor and ingestive behavior.

Animals↗
PubMed1988

Response of axons and glia at the site of anastomosis between the optic nerve and cellular or acellular sciatic nerve grafts.

Axonal and glial reactions at the site of optic nerve section and at the junctional zone between optic nerve and normal or acellular peripheral nerve grafts have been studied. Following optic nerve section, no axons grew into the distal optic nerve stump. Similarly, no axons invaded the acellular peripheral nerve grafts, although in both instances fibres did regenerate into the junctional zone and a few remained there at least until 30 days post lesion (dpl, the duration of the experiments). Axons regenerated into normal peripheral nerve grafts by 3-5 dpl and by 10 dpl large numbers had penetrated deeply into the grafts. The glial response to injury appeared similar in both groups of grafted animals. Astrocytes and oligodendrocytes grew out into the junctional zone over the 5-7 day period and invaded the margins of the cellular grafts by 10 dpl. They did not penetrate the acellular nerves or distal optic nerve stumps. We were unable to determine whether Schwann cells invaded the junctional zone from the normal peripheral nerve grafts. Schwann cells are both GFAP+ and Vim+, especially when reacting after injury, and Lam- when not associated with axons: it is therefore possible that Schwann cells from the cellular grafts contributed to the population of GFAP+, Vim+ cells in the junctional zone of the cellular grafts. Anti-laminin immunoreactivity persisted in the basal lamina tubes of both the normal and acellular peripheral nerve grafts. Thus, the failure of axon regeneration into acellular peripheral nerve grafts can be correlated with the absence of Schwann cells and does not appear to be related to the presence of laminin.

Anastomosis, Surgical↗
PubMed1988

Evidence that fluoride-stimulated 3[H]-thymidine incorporation in embryonic chick calvarial cell cultures is dependent on the presence of a bone cell mitogen, sensitive to changes in the phosphate concentration, and modulated by systemic skeletal effectors.

In previous studies we have shown that clinically effective concentrations of fluoride (5 to 30 mumol/L) could also have direct effects in vitro on skeletal tissues to increase embryonic chick bone formation and bone cell proliferation (3[H]-thymidine incorporation into DNA). From these observations, we hypothesized that fluoride-stimulated bone formation might be mediated by a direct effect of fluoride to increase bone cell proliferation. The current studies were intended to investigate the mechanism of fluoride-stimulated 3[H]-thymidine incorporation, in chick calvarial cell cultures, by assessing mitogenic interactions between fluoride and inorganic phosphate, bone-derived growth factors, and systemic skeletal effectors. With respect to fluoride-phosphate interactions, the results of our studies indicate that the effect of fluoride was dependent on the phosphate concentration in the medium. Fluoride did not increase 3[H]-thymidine incorporation in BGJb medium containing 1 mmol/L (total) phosphate; but, in 1.6 mmol/L phosphate medium, fluoride caused a dose-dependent increase in 3[H]-thymidine incorporation, between 1 and 20 mumol/L (P less than .001). The action of fluoride was also dependent on the presence of a bone cell mitogen. Fluoride increased 3[H]-thymidine incorporation when added to calvarial cell cultures in the cell-conditioned medium, but had no effect in unconditioned (ie, fresh) medium. The action of fluoride could be restored by adding an exogenous growth factor (ie, concentrated cell-conditioned medium, bone-derived growth factors, or a systemic bone cell mitogen) to the unconditioned culture medium, P less than .05 for each effector.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Striatal dopamine and the interface between orienting and ingestive functions.

Recent lesion experiments have implicated forebrain catecholaminergic projections in a unique switching mechanism that enables sensory orientation to occur during ongoing feeding behavior. Unit recording studies indicate that there is a population of neurons in the striatum that respond to tactile stimulation only while an animal is eating. These sensory-related cells may serve as part of a system that diverts attention away from ingestive behavior. In the present study, 6-hydroxydopamine was infused directly into the striatum in rats to eliminate the dopaminergic input specifically to this region. The animals were tested for their reactions to tactile stimulation of the vibrissae during or in the absence of eating. During noneating trials, orienting was rapid and reliable to stimuli presented on either side of the body midline. While eating, contralateral orienting never occurred, even when the stimulation was intense, whereas ipsilateral orienting was unaffected. It was suggested that the capacity to disengage from ingestive behavior may depend importantly on the integrity of dopaminergic input to the striatum.

Animals↗