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Biomedical subjects

S Kennedy

Publications and source records attributed to S Kennedy.

At least 181 records · Page 10Linked to original sources
PubMed1996

Hysterosalpingo-contrast sonography (HyCoSy) using Echovist-200 in the outpatient investigation of infertility patients.

This study describes the introduction of hysterosalpingo-contrast sonography (HyCoSy) as a first line outpatient investigation of uterine and tubal factors in two fertility units. 136 infertile women had transvaginal scanning before and during the intrauterine injection of contrast medium (Echovist-200). HyCoSy was successfully completed in 132 cases (97%) within a mean time of 12.6 +/- 8.4 (4-50) min. The uterus and its cavity appeared normal in 108 (82%) women. Uterine abnormalities in the remaining 24 women (18%) included structural abnormality (n = 7), fibroids (n = 12) and endometrial polyps (n = 5). A total of 261 fallopian tubes in 132 women were assessed: 186 (71%) appeared patent and 55 (21%) blocked. The remaining 20 (8%) could not be assessed for technical reasons. Polycystic ovaries and ovarian cysts were diagnosed in eight women. The most common adverse effect was mild/moderate pain, similar to period pain, with 24 (18%) women requiring simple analgesia. HyCoSy is a simple and well tolerated outpatient procedure. The technique provides clinically valuable information about tubal patency, ovarian and uterine abnormalities.

Ambulatory Care↗
PubMed1996

Effects of low concentrations of dietary cobalt on rumen succinate concentration in sheep.

Sheep fed diets containing less than 70 micrograms Co per kg develop vitamin B12 deficiency. When sheep were fed diets containing 20 micrograms Co per kg or less, mean rumen succinate concentrations increased by more than one hundred-fold within 2 days. This increase was matched by an equimolar decrease in mean rumen propionate concentrations. When diets containing more than 20 micrograms Co per kg were fed to sheep, no such changes occurred. The synthesis of succinyl CoA from propionyl CoA in liver is impaired in ovine cobalt deficiency. We suggested that, paradoxically, accumulation of rumen succinate could reduce the effects of vitamin B12 deficiency on methylmalonyl CoA mutase and consequently result in lower plasma methylmalonic acid (MMA) concentrations than would arise by feeding diets that did not affect rumen succinate concentrations. This hypothesis was tested by feeding diets containing 4, 40 and 1000 micrograms Co per kg to sheep for 23 weeks. However, sheep fed 40 micrograms Co per kg did not have mean plasma MMA concentrations that were higher than those in the sheep fed 4 micrograms Co per kg, indicating that rumen succinate accumulation did not ameliorate the effects of Co deficiency.

Acyl Coenzyme A↗
PubMed1995

Post mortem investigations on cetaceans found stranded on the coasts of Italy between 1990 and 1993.

Detailed pathological and virological examinations were carried out on 25 cetaceans found stranded between 1990 and 1993 on the coasts of six Italian regions (Latium, Tuscany, Apulia, Abruzzo, Veneto and Sicily). There were 16 striped dolphins (Stenella coeruleoalba), three bottlenosed dolphins (Tursiops truncatus), three Risso's dolphins (Grampus griseus), one rough-toothed dolphin (Steno bredanensis), one fin whale pup (Balaenoptera physalus), and one minke whale (Balaenoptera acutorostrata). Apart from parasitic diseases (44 per cent), the most frequently detected lesions were pneumonia (68 per cent), enteritis (44 per cent), non-purulent hepatitis (40 per cent), interstitial nephritis (32 per cent) and encephalitis (32 per cent). Morbilivirus infection was diagnosed by immunocytochemistry in four striped dolphins, two stranded on the coasts of Latium in 1991 and two on the coasts of Tuscany in 1993. Despite the presence of lesions consistent with morbilliviral pneumonia in two other striped dolphins stranded on the coast of Apulia in 1991, no morbillivirus antigen was demonstrated in the tissues of these animals. Anticanine distemper virus antibodies were detected in the serum of the adult minke whale found stranded on the coast of Tuscany in 1993. However, no viruses were isolated from the tissues of any of the 25 cetaceans.

Animals↗
PubMed1995

Familial endometriosis.

PURPOSE: The study aimed to identify families with endometriosis and to document disease severity within the families and the clinical characteristics of the affected women. RESULTS: Two hundred and thirty women with surgically confirmed endometriosis in 100 families were identified. The families consisted of 19 mother-daughter pairs, 1 set of cousins and 56 sister pairs. There were 5 families with 3 affected sisters, 1 family with 5 affected sisters, and 18 families with > or = 3 affected members in more than one generation. The mean age at the onset of symptoms and the mean age at surgical diagnosis was 22.1 +/- 8.8 SD (range 10-46) and 31.8 +/- 7.9 SD (range 15-56) years respectively. Seventy-nine women (34.3%) had revised AFS Stage I-II disease, and 151 (65.7%) had revised AFS Stage III-IV disease. CONCLUSION: The study confirms a familial tendency for endometriosis and supports the hypothesis that endometriosis has a genetic basis.

Australia↗
PubMed1995

An abnormal methylation ratio induces hypomethylation in vitro in the brain of pig and man, but not in rat.

1. The ratio of the methyl donor, S-adenosylmethionine, to the co-product, S-adenosylhomocysteine (the methylation ratio) is known to control the activity of methyltransferases in tissues. Inactivation of the vitamin B12-dependent enzyme, methionine synthase, reduces the methylation ratio in rats and pigs in vivo. 2. We have determined the effect that such alterations have on neural protein 'O' and 'N' methyltransferases using an in vitro assay in rats, pigs and humans in the presence of the normal methylation ratio and the abnormal methylation ratios found experimentally in vivo in rats and pigs. 3. The methylation ratio found in the neural tissues of vitamin B12-inactivated pigs significantly inhibits the protein methyltransferases of pigs and humans. 4. By contrast, the altered methylation ratio found in vitamin B12-inactivated rats only marginally inhibits the equivalent rat methyltransferases. 5. This is consistent with the induction of a myelopathy by such treatment in pigs and humans, but not in the rat. 6. Dietary supplements of methionine given to vitamin B12-inactivated pigs have been shown to prevent the myelopathy in vivo by both elevating the neural S-adenosylmethionine level and resetting the methylation ratio. We find in our in vitro assay that these events reinstate the methyltransferase activity to near normal levels, thus explaining its protective effect in vivo.

Animals↗
PubMed1995

Demonstration of hypomethylation of proteins in the brain of pigs (but not in rats) associated with chronic vitamin B12 inactivation.

1. Pigs treated with nitrous oxide for periods of 1, 2 and 4 months demonstrated markedly reduced levels of methionine synthase and concomitant reduction in the ratio of S-adenosylmethionine to S-adenosylhomocysteine, the methylation ratio, at all time intervals. 2. Both 'O' and 'N' methylations were significantly reduced in pigs after 4 months in nitrous oxide but not after shorter periods. 3. Hypomethylation correlated with the development of clinical ataxia, but was absent when the pigs were clinically normal. It also only occurred when the S-adenosylmethionine level fell. 4. Rats maintained in nitrous oxide for 4 months showed a marked reduction of methionine synthase but no reduction in the methylation ratio or in brain hypomethylation. None of the rats became clinically ataxic. 5. Using an exogenous protein as a methyl group acceptor, it was demonstrated in an in vitro assay that the methyltransferase enzymes responsible for brain 'O' and 'N' methylation were not affected per se by nitrous oxide treatment. 6. It is concluded that reduction of the methylation ratio in the brain of pigs as a consequence of methionine synthase inhibition leads to brain hypomethylation. This hypomethylation could affect critical components of nerve tissue, inducing the vacuolar myelopathic changes seen in the spinal cord of these animals, which mimic those of subacute combined degeneration in man.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1995

Lipid peroxidation, prostacyclin and thromboxane A2 in pigs depleted of vitamin E and selenium and supplemented with linseed oil.

In a 2 x 2 balanced factorial experiment the biochemical effects on pigs of two dietary factors were investigated. The first factor was alpha-tocopherol and Se supplementation and the second factor was supplementation with alpha-tocopherol-stripped linseed oil. In pigs fed on diets depleted of alpha-tocopherol and Se, increases in concentrations of markers of lipid peroxidation (4-hydroxynonenal and hexanal) were observed. However, skeletal myopathy was only observed in those pigs fed on diets depleted of alpha-tocopherol and Se and supplemented with oil. In those pigs, increased lipid peroxidation was observed in heart and supraspinatus muscle. The plasma concentration of thromboxane B2 was increased in pigs fed on diets depleted of alpha-tocopherol and Se, suggesting an increased tendency towards platelet aggregation. However, this change was reversed in pigs depleted of alpha-tocopherol and Se, but supplemented with oil. This may have been a consequence of loss of arachidonic acid, the substrate for thromboxane formation, as a result of lipid peroxidation.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Toxicity of Streptococcus pneumoniae in neurons, astrocytes, and microglia in vitro.

The toxicity of pneumococci and endotoxin in primary cultures of rat neurons, astrocytes, and microglia and in a human astrocyte and two human glial cell lines was determined. Heat-inactivated, rough pneumococci (up to 10(8) cfu/mL) or their cell wall (up to 50 micrograms/mL) produced dose-dependent toxicity after 48 h in microglial cells and to a lesser extent in astrocytes but not in neurons. Toxicity was similar for equivalent doses of heat-inactivated organisms and pneumococcal cell wall, but time-course experiments showed significant differences between the two stimuli. Endotoxin at concentrations of up to 5 micrograms/mL did not induce significant toxicity in any of the cells. Thus, pneumococci can induce toxicity in two brain cell types, microglia and astrocytes, and the pneumococcal cell wall appears to mediate toxicity. Direct toxic effects of bacteria on brain cells may in part be responsible for brain injury during meningitis.

Animals↗
PubMed1995

Bulimia nervosa in a Canadian community sample: prevalence and comparison of subgroups.

OBJECTIVE: Previous epidemiological studies of bulimia nervosa have generated differing estimates of the incidence and prevalence of the disorder. These differences are attributable, in part, to varying definitions of the illness and a range of methodologies. The authors sought to define the prevalence of bulimia nervosa in a nonclinical community sample, examine the clinical significance of DSM-III-R threshold criteria, and examine comorbidity. METHOD: Subjects across Ontario (N = 8,116) were assessed with a structured interview, the World Health Organization Composite International Diagnostic Interview, with specific questions added for bulimia nervosa. Subjects who met DSM-III-R criteria for bulimia nervosa were compared with those who were missing only the frequency criterion (two or more binge-eating episodes per week for 3 months). RESULTS: In this sample, the lifetime prevalence of bulimia nervosa was 1.1% for female subjects and 0.1% for male subjects. The subjects with full- and partial-syndrome bulimia nervosa showed significant vulnerability for mood and anxiety disorders. Lifetime rates of alcohol dependence were high in the full-syndrome group. Rates of parental psychopathologies were high in both bulimic groups but tended to be higher in the subjects with full-syndrome bulimia nervosa. Both bulimic groups were significantly more likely to experience childhood sexual abuse than a normal female comparison group. CONCLUSIONS: This study confirms other prevalence estimates of bulimia nervosa and its comorbid diagnoses from studies that were based on sound methodologies. It also points to the arbitrary aspects of the frequency of binge eating as a diagnostic threshold criterion for the disorder.

Adolescent↗
PubMed1995

Experimental vitamin A deficiency in mallards (Anas platyrhynchos): lesions and tissue vitamin A levels.

Captive mallards (Anas platyrhynchos), fed an all-grain diet for up to 5 months during the winters of 1991 to 1992 and 1992 to 1993, developed lesions of squamous metaplasia; some had no detectable hepatic vitamin A. Vitamin A deficiency in mallards was defined as hepatic levels of retinyl palmitate < 2 micrograms/g liver. Lesions were found only in ducks with low levels of hepatic vitamin A, but not all ducks with these low levels of hepatic vitamin A had histological lesions. The prevalence of lesions in the esophagus was greatest cranially and caudally and less common in the central region. Palatine salivary glands rarely were affected. Mallards with liver stores > 600 micrograms of hepatic retinyl palmitate per g liver, fed a diet deficient in vitamin A were unlikely to become deficient over a 5 month period. Birds fed an all-grain diet had significantly lower vitamin A concentrations in their liver compared to those fed an all-grain diet with vitamin A added. Liver weight, when corrected for body size, did not affect vitamin A concentration. Serum retinol levels were conserved over a large range of hepatic vitamin A levels but levels below 300 micrograms retinol/l were useful in detecting vitamin A deficiency in captive mallards. Based on the findings, the presence of lesions provides a conservative measure of vitamin A status in ducks and tissue levels should be measured in instances when mallards have questionable vitamin A status.

Animals↗
PubMed1995

Vitamin A status of wild mallards (Anas platyrhynchos) wintering in Saskatchewan.

Vitamin A status of wild male mallards (Anas platyrhynchos) overwintering in Saskatchewan, Canada was determined. Vitamin A levels < 0.2 micrograms hepatic retinyl palmitate/g liver, occurred in 6% and 25% of male mallards sampled in 1991 to 1992 and 1992 to 1993, respectively. There was no temporal trend in vitamin A levels over either winter. Squamous metaplastic lesions, commonly associated with vitamin A deficiency in domestic animals, were not observed in any bird; hence, they were not a good indicator of vitamin A status in wild mallards. Serum retinol was not a good indicator of vitamin A status in wild mallards. Many mallards in good body condition had low vitamin A levels; thus, we propose that good body condition and ample fat stores are not indicative of overall health of the bird.

Animal Nutritional Physiological Phenomena↗
PubMed1995

Postmortem diagnosis of morbillivirus infection in bottlenose dolphins (Tursiops truncatus) in the Atlantic and Gulf of Mexico epizootics by polymerase chain reaction-based assay.

Lung tissue from 39 bottlenose dolphins (Tursiops truncatus) found dead off the U.S. Atlantic and Gulf of Mexico coasts from 1987 to 1994 was examined for the presence of morbillivirus using a reverse transcriptase polymerase chain reaction (RT-PCR) technique. Of the Atlantic cases examined, six of six were positive using this assay; 18 of 25 Gulf of Mexico cases with amplifiable RNA also were found to be positive, and eight additional specimens had no amplifiable RNA. The RT-PCR allowed the diagnosis of morbillivirus infection to be made from either sections of paraffin-embedded formalin-fixed material or from unfixed tissue. Conformation of diagnosis was made by subsequent hybridization of the amplified products with a dolphin morbillivirus specific probe using the Southern blot technique. Application of this method to autolyzed post-mortem tissues allows diagnoses of morbillivirus infection to be made in specimens which cannot be evaluated by histologic and immunocytochemical techniques.

Animals↗
PubMed1995

Experiments in transgenic mice show that hepatocytes are the source for postnatal liver growth and do not stream.

One hypothesis is that postnatal liver growth involves replication of mature hepatocytes, which have an unlimited proliferative potential. An alternative viewpoint is that only certain periportal cells can replicate extensively and that daughter cells stream slowly from the periportal to the pericentral region of the liver. Transgenic mice expressing the beta-galactosidase (beta-gal) gene from the human alpha 1 antitrypsin promoter were used to examine the proliferative potential of hepatocytes. Surprisingly, only 10% of hepatocytes in two different transgenic lines stain blue with X-gal. In neonatal animals, singlets or doublets of expressing cells are randomly scattered throughout the liver. Although the overall frequency of blue cells is similar in older animals, these cells are present in much larger clusters, suggesting that individual expressing cells have replicated to form a clonally derived cluster. Expression patterns are not altered by the administration of an acute phase stimulus or by the performance a partial hepatectomy, suggesting that the expression state cannot be easily altered, and making it more likely that the expression state is indeed fixed. These results suggest that the clusters of blue cells are clonally derived in the transgenic mice. They argue that the parenchymal hepatocyte is responsible for growth in the postnatal liver and that streaming of liver cells does not occur.

Acute-Phase Proteins↗
PubMed1995

Cobalt-vitamin B12 deficiency and the activity of methylmalonyl CoA mutase and methionine synthase in cattle.

Cobalt deficiency was induced in cattle by feeding two groups of animals either a basal diet that was very low in Co (12.9-17.6 micrograms Co per kg), or the same diet supplemented with cobalt, for a total of 64 weeks. Vitamin B12 deficiency was induced, as judged by hepatic concentrations of vitamin B12 and plasma concentrations of MMA. However, the activity of holo-methylmalonyl CoA mutase was significantly reduced only in brain. This was reflected in very minor alterations in the tissue concentrations of branched chain- and odd numbered-fatty acids. The activity of holo-methionine synthase was significantly reduced in liver and brain, but there were no consequent alterations in the concentrations of phosphatidyl choline and phosphatidyl ethanolamine. This study confirms that cattle are less susceptible to the effects of cobalt deficiency than sheep, and concludes that prolonged cobalt deficiency had little significant effect on tissue metabolism.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗