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S C Phillips

Publications and source records attributed to S C Phillips.

At least 37 records · Page 2Linked to original sources
PubMed1991

Sequence and expression of a mouse U7 snRNA type II pseudogene.

The U7 snRNP functions in the 3' processing of histone pre-mRNAs of the replication variant class. The U7 snRNA is apparently the only RNA component of this minor snRNP particle. So far, the only U7 snRNA genes that have been isolated are a cluster of 5 from sea urchin. The function of the sea urchin U7 snRNP has been examined by microinjection experiments using Xenopus oocytes and the expression of these sea urchin U7 snRNA genes has been analysed by microinjection into sea urchin eggs. In our studies of U7 snRNA genes in mouse, we have isolated one of only 3 detectable U7 snRNA pseudogenes in the mouse genome and have determined its nucleotide sequence. Sequence comparisons and transcription analysis following microinjection of the gene into Xenopus oocytes supports our assignment of this isolate as a U7 snRNA type II pseudogene.

Animals↗
PubMed1990

The contribution of Wernicke's encephalopathy to alcohol-related cerebellar damage.

Mid-sagittal histological sections of the cerebellar vermis were prepared for light microscopy from six patients with Wernicke's encephalopathy, 13 alcoholics and 16 normal controls. From Nissl stained sections, the Wernicke's encephalopathy group was found to have a significant 29% lower Purkinje cell count relative to controls, while the alcoholic group had a non-significant 10% lower cell count. The degree of shrinkage of the molecular layer paralleled the degree of Purkinje cell loss. Damage to the medullary layer in the form of shrinkage in Nissl sections and torpedo formation in silver sections did not correlate as well with Purkinje cell loss. Thiamine deficiency would seem to be a significant contributing factor to the neuropathology of cerebellar damage seen in alcoholism. The presence or absence of cirrhosis of the liver was also found to influence the degree of Purkinje cell loss.

Journal Article↗
PubMed1990

Cerebellar white matter after long-term ethanol consumption in mice.

Although the cortex of the cerebellum has been studied in ethanol-treated rats and mice, the condition of the cerebellar white matter in such animals has not been described. We have maintained adult mice on a 9% ethanol nutritious diet for 4 months after which some were sacrificed while others were kept for a further 4 months on an ethanol-free diet. Convincing signs of axonal degeneration were not found in either of the ethanol-treated groups, nor could the groups be distinguished on the basis of neuroglial cell counts. The presence of degenerating Purkinje cells and cellular atrophy in the granule cell layer does however imply the existence of some degeneration in the medullary layer. Cellular degeneration was found to be occurring in the cerebellar cortex after 4 months of withdrawal from the alcoholic diet as well as immediately after 4 months of alcohol consumption. The medullary layer appears not to be a sensitive indicator of damage in long-term ethanol consumption in the mouse.

Alcoholism↗
PubMed1989

The threshold concentration of dietary ethanol necessary to produce toxic effects on hippocampal cells and synapses in the mouse.

A nutritionally complete liquid diet containing 0, 3, 5, or 7% ethanol was fed to C57 mice for 4 months and killed after a further 4 months on a standard food pellet diet. The number of pyramidal cells in Araldite sections of the hippocampus was not significantly reduced in any group relative to the zero alcohol intake group. Synaptic counts in the area occupied by the pyramidal cell basal dendrites showed the 7% alcohol group to have a reduced number of synaptic contacts, with no convincing differences between the other groups relative to the zero alcohol group. All measurements made collectively could not be used to distinguish 3 or 5% ethanol consuming animals from 0% ethanol consuming animals. Significant differences in body weight and dry brain weight were detected in the comparison of the group treated with 7% ethanol and 4-month recovery with the group receiving the 0% ethanol dose and 4-month recovery. It is concluded that maintaining mice on a diet containing not more than 5% ethanol has no adverse long-term structural effects on hippocampal pyramidal cells or synapses.

Alcoholism↗
PubMed1989

Cytoprotective value of lysine, penicillamine, and pyridoxal phosphate against the neurotoxicity of acetaldehyde.

Rats which received acetaldehyde by intraperitoneal injection on a single occasion sustained neural degeneration in the cerebral cortex detectable with both light and electron microscopy. The degeneration was more intense and included the hippocampus when acetaldehyde exposure was given on 5 consecutive days in the form of ethanol vapor inhalation and disulfiram injections. Pretreatment of animals with a combination 2.5 g lysine/kg plus 50 mg pyridoxyl phosphate/kg did not alter the degree of degeneration response to either a single injection of acetaldehyde or 5 days acetaldehyde treatment. Penicillamine injections (1.2 g/kg) did offer some (but not complete) cytoprotective value against the neurotoxicity of acetaldehyde. This cytoprotective action was effective at concentrations of acetaldehyde which are not distant from clinically observed concentrations.

Acetaldehyde↗
PubMed1988

Plasticity of postsynaptic density material in optic synapses of the suprachiasmatic nucleus in the senescent rat.

Optic synapses in the suprachiasmatic nucleus were studied in senescent rats after 2 weeks of constant light influence (light rats) or darkness (dark rats). The amount of postsynaptic density material was significantly greater in dark rats compared with light rats. Dark rats also showed a higher percentage of asymmetric synapses than light rats. The sizes of synaptic appositions and boutons were also compared. The phenomena observed may indicate supersensitivity and a higher number of excitatory synapses in dark rats and subsensitivity and lower number of excitatory synapses in light rats.

Aging↗
PubMed1988

Evaluation of excess colorectal cancer incidence among workers involved in the manufacture of polypropylene.

In response to reports of an unusually high number of colorectal cancers among employees on a unit devoted to the manufacture of polypropylene, we examined colorectal cancer incidence rates for 335 workers with at least 6 months employment on this unit from 1960 to 1985. Assuming a 10-year latent period, we found a significant 5.6-fold colorectal cancer excess (7 observed/1.26 expected, standardized incidence ratio (SIR) = 5.6, 95% confidence interval (CI) 2.2 to 11.5), concentrated among mechanical (5 observed/0.47 expected, SIR = 10.6, 95% CI 3.4 to 24.7) and process workers (2 observed/0.40 expected, SIR = 5.0, 95% CI 0.6 to 17.8). No colorectal cancer was found among administrative/office personnel on our study roster. All of the cancers occurred in employees who initially worked on the unit during its first 6 years of operation, and the minimum interval from start of employment to cancer development was 20 years. In addition, the ages of the cancer cases suggested a younger age distribution than would be expected based on general population rates. Since this study was descriptive in nature, we could not evaluate whether the cancer excess was related to occupational exposures, other environmental factors, or the random clustering of cancers in our worker populations (viz, "chance"). Further studies are currently ongoing to assess occupational and/or personal factors that may be related to this colorectal cancer excess.

Adenocarcinoma↗
PubMed1987

A cross-sectional survey of kidney function in refinery employees.

We examined sensitive biochemical and immunological markers of kidney function and damage in 53 male oil refinery workers exposed to hydrocarbons and compared their results with those of a control group of 61 age-matched nonexposed males. The mean duration of employment of exposed males was 11 years. The current levels of exposure to a variety of aliphatic and aromatic hydrocarbons, as determined by personal monitoring, were well below the current threshold limit values. No difference was found in the urinary tubular parameters beta-N-acetyl-D-glucosaminidase, beta 2-microglobulin (beta 2-m) and retinol-binding protein. Similar serum beta 2-m levels indicated no impairment of the glomerular filtration rate in the exposed workers. The levels of circulating immune complexes were also identical in both groups. The mean albuminuria was slightly higher (p less than .005) in the exposed group in a quantitative assay but was not dipstick-detectable. The mean urinary excretion of a renal antigen was also higher (p less than .05) in the exposed group and correlated with the excretion of albumin. Finally, slightly higher titers of anti-laminin antibodies were found in five exposed employees, but this was not accompanied by an increased albuminuria. We conclude that chronic low-level hydrocarbon exposure in these refinery workers does not lead to clinically significant renal abnormalities. Nevertheless, some findings are consistent with the possible role of hydrocarbon exposure in the induction of renal disturbances.

Adult↗
PubMed1987

Neuro-toxic interaction in alcohol-treated, thiamine-deficient mice.

Groups of adult male mice were either fed a thiamine-deficient diet for 10 weeks and thereafter treated with ethanol by making them inhale vapourized cane spirit for 10 weeks, or given both treatments simultaneously. The brains of these mice were then searched for degeneration using both light and electron microscopy. No degenerating nerve cells were observed in any animal in the cerebral cortex, hippocampus, cerebellum, olfactory bulbs, midbrain or hindbrain. However, axon terminal degeneration was seen in the olfactory bulbs and deep cerebellar nuclei in mice given the combined treatment. No cerebellar degeneration was found and only little degeneration was present in the olfactory bulbs of mice given the two treatments at different times. Thus, the combined treatment of alcohol and thiamine deficiency produced more brain damage than the sum of that produced by the two treatments given separately. This represents the first experimental in vivo demonstration of a biochemical interaction between these two factors in alcohol-related brain damage. The findings of long-term animal treatment with models using thiamine antagonists are compared.

Animals↗
PubMed1987

A search for degeneration in the circumventricular area of ethanol-treated mice.

Mice were treated with ethanol vapour for 6 weeks and the circumventricular area of the brains prepared for light and electron microscopy. No abnormalities were found in the subfornical organ, but degeneration was found in the medial preoptic area in 2 of the 6 ethanol-treated animals. There was no indication of functional impairment of brain or body water regulation mechanisms.

Alcoholism↗
PubMed1987

A quantitative histological study of the cerebellar vermis in alcoholic patients.

A quantitative histological study was made of the cerebellar vermis in 10 male alcoholic and 8 age-matched control cases. The mean Purkinje cell loss was 21% in the alcoholic group. The small rostral and caudal lobes were most severely affected. The mean Purkinje cell density per unit length of foliae showed similar changes. Histological measurements of the area of the molecular, granular and medullary layers of the cerebellar vermis showed that the molecular layer varied in the degree of shrinkage between lobes (from 11 to 39%) while the granular layer showed a consistent shrinkage (9 to 10%). The molecular layer appears to be the most vulnerable region in chronic alcoholics. Brains taken from patients with Wernicke's encephalopathy had particularly low Purkinje cell counts and a large pericerebral space. Nutritional deficiency would seem to be an important factor in the causation of the observed neuropathology, with liver disease playing a lesser role. Evidence that repeated alcohol withdrawal can lead to further brain disturbances is reviewed.

Aged↗
PubMed1987

Can brain lesions occur in experimental animals by administration of ethanol or acetaldehyde?

In a series of experimental studies involving ethanol vapour administration to rats, sustained blood alcohol levels in the range 89-115 mM for nine hours of each day over a two week period did not lead to neural degeneration detactable with either light or electron microscopy. A single nine hours exposure to ethanol and disulfiram giving rise to 20-41 mM alcohol and 52-76 microM acetaldehyde in the blood did lead to degeneration; and that with repeated exposures of this later type, the damage was found to be accumulative. The lowest levels of blood acetaldehyde which led to neural degeneration in the present study were not distant from clinically observed levels.

Acetaldehyde↗
PubMed1986

Does alcohol-induced blood cell agglutination cause brain damage?

After 3 weeks of alcohol intoxication, the brains of rats were searched with light- and electron microscopy for degenerating nervous tissue and agglutination of erythrocytes in the blood vessels. There was no sign of degeneration of nerve cells or synapses in the cerebral cortex, hippocampus, cerebellum, midbrain or hindbrain. No histological sections showed blood vessels with erythrocytes inside them. It is concluded that the agglutination of red blood cells seen in the conjunctivae of intoxicated human alcoholics is not necessarily an indication that vascular congestion is also occurring in the brain of such patients, nor that this is the primary mechanism of alcohol-related brain damage.

Alcoholism↗
PubMed1986

Assessment of clinical, metabolic, dietary, and occupational correlations with serum polychlorinated biphenyl levels among employees at an electrical capacitor manufacturing plant.

In order to assess the extent of polychlorinated biphenyl (PCB) exposure and potential health effects, a clinical-epidemiologic survey was initiated among 205 workers at a capacitor manufacturing plant. The geometric mean serum PCB level for workers was 18.2 ppb (SD 2.88), with a range of 0 to 424 ppb. Multiple regression analysis found duration of employment, cumulative occupational exposure, cumulative fish consumption, and cholesterol level to be significant predictors of log serum PCB levels. Of these predictors, duration of employment and cumulative occupational exposure were the strongest contributors to the regression model, indicating the dual importance of opportunity for dermal contact and respiratory exposure level in contributing to workers' serum PCB levels.

Diet↗
PubMed1985

Structural plasticity of developing optic synapses under different lighting conditions.

Four-month-old male hooded rats were reared from birth under constant light and darkness conditions. Changes in the amount of postsynaptic density material in the optic synapses in the suprachiasmatic nucleus of these rats were compared with animals maintained under routine light-dark (12 h) cycles. The thickness of postsynaptic density material was found to be significantly greater in dark-reared rats relative to light-reared animals. The plasticity of this structure may have functional implications in the sensitivity of postsynaptic response. There was no significant difference in the lengths of the synaptic apposition and the size of boutons.

Animals↗
PubMed1985

Qualitative and quantitative changes of mouse cerebellar synapses after chronic alcohol consumption and withdrawal.

For 4 months C57 mice were fed a nutritionally complete diet containing 9% alcohol or isocaloric sucrose and killed then or after 4 months recovery on standard food pellets. Electron microscopy was used to count synapses among the cerebellar Purkinje cell dendrites and a significant 13% reduction was found in the alcohol recovery group. The shape of the postsynaptic density material was studied and a significant 11% increase in length found in the alcohol group. The smaller thickness of the postsynaptic material in animals of the alcohol recovery group may be representative of new synaptic formation.

Alcoholism↗
PubMed1985

Age-dependent susceptibility of rat cerebellar Purkinje cells to ethanol exposure.

It is known that a proportion of cerebellar Purkinje cells do not complete development in the normal rat. In this study neonatal rat pups were treated at various stages of Purkinje cell development with ethanol vapour. We observed an increased rate of Purkinje cell loss at postnatal day 3, yet identically treated littermates had a normal complement of Purkinje cells compared to age-matched controls at 47 days of age. Single day ethanol exposures during Purkinje cell ontogenesis seems to accelerate a natural loss of Purkinje cells without a permanent loss persisting to adult life.

Aging↗