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Biomedical subjects

J G Morris

Publications and source records attributed to J G Morris.

At least 109 records · Page 6Linked to original sources
PubMed1997

The minimum sodium requirement of growing kittens defined on the basis of plasma aldosterone concentration.

The minimum sodium requirement of growing kittens was measured using a 6 x 6 Latin square design. Twelve specific-pathogen-free short-hair growing kittens (six males, six females) were fed casein and lactalbumin-based purified diets supplemented with various levels of sodium (NaCI). Using six growing kittens (four males, two females), a sodium depletion and repletion study was conducted to define the variables associated with sodium deficiency. Sodium-deficient kittens exhibited anorexia, impaired growth, polydypsia, polyuria, hemoconcentration, reduced urinary sodium output and specific gravity, and elevated aldosterone concentration in plasma and output in urine. Plasma sodium concentration was not affected by dietary sodium intake. Urinary sodium output was positively related to (r = 0.818, P < 0.001), but fecal sodium loss was independent of sodium intake. These results suggest that sodium balance in kittens is essentially regulated by renal excretion. The recommended minimum sodium requirement of kittens for growth is 1.6 g Na/kg diet (energy density, 22 kJ ME/g diet), or 0.07 mg Na/kJ ME, or 34 mg Na x kg body wt(-1) x d(-1). A sodium requirement of adult cats for maintenance was estimated to be 21 mg Na x kg body wt(-1) x d(-1). These requirements are considerably greater than those recommended by the National Research Council in 1986.

Aldosterone↗
PubMed1997

The subthalamic nucleus in Parkinson's disease and progressive supranuclear palsy.

The subthalamus has become a promising target for the neurosurgical treatment of parkinsonian symptoms. We have used unbiased counting techniques to quantify the neuronal populations of the subthalamic nucleus in patients with idiopathic Parkinson's disease and progressive supranuclear palsy. In addition, the type of calcium binding proteins contained within these subthalamic neurons was established using immunohistochemistry. Most of the 550,000 subthalamic neurons contain either parvalbumin or calretinin calcium binding proteins, and patients with idiopathic Parkinson's disease sustained no damage to this nucleus. This is consistent with current theories of basal ganglia circuitry, which postulate that overstimulation of this excitatory nucleus contributes to the inhibition of the motor thalamus via the activation of inhibitory relays. In contrast, we found that there was substantial cell loss in the subthalamus in progressive supranuclear palsy (45 to 85% neuronal reduction) and that both cell types were equally affected. Extracellular neurofibrillary tangles as well as tau-positive glia were observed in the subthalamus of these cases. As the patients with Parkinson's disease and progressive supranuclear palsy all had overlapping parkinsonian symptoms, the loss of subthalamic stimulation within the basal ganglia of progressive supranuclear palsy cases is puzzling, unless their parkinsonian symptoms were generated by an alternate mechanism.

Aged↗
PubMed1997

Vibriocidal antibody responses in North American volunteers exposed to wild-type or vaccine Vibrio cholerae O139: specificity and relevance to immunity.

The emergence of a new agent of cholera, Vibrio cholerae O139, has prompted a reevaluation of the vibriocidal antibody assay. This assay, primarily directed to lipopolysaccharide, is an important correlate of O1 immunity. V. cholerae O139 strains are encapsulated, rendering them relatively resistant to killing by serum. Recent reports suggest that there is strain-to-strain variability in the sensitivity of the vibriocidal assay to fully encapsulated O139 strains. We have assessed a modified vibriocidal assay for fully encapsulated O139 strain AI-1837 and its unencapsulated mutant 2L in sera from 53 volunteers given wild-type AI-1837 or its attenuated derivative CVD 112 and from 48 controls challenged with V. cholerae O1 or strains of the family Enterobacteriaceae. Vibriocidal responses to the AI-1837 and 2L strains were seen in 67 and 89% of volunteers, respectively, following a single exposure to the wild-type strain. However, >50% of all controls had low-level vibriocidal responses to both strains. These nonspecific responses were transient and of the immunoglobulin G isotype. No binding activity against purified O139 lipopolysaccharide (LPS) by immunoblotting was seen in control sera. In contrast, vibriocidal assay and strain 2L LPS responses by immunoblotting were detectable in 91% of tested volunteers following a single exposure to O139. The presence of vibriocidal antibody to AI-1837 or 2L was not associated with protection in rechallenge studies with O139 strain AI-1837. The vibriocidal assay with unencapsulated strain 2L may be used to detect exposure to O139 strain AI-1837 in controlled research trials. However, its lack of specificity does not make it useful for determining exposure to V. cholerae O139 in the field.

Antibodies, Bacterial↗
PubMed1997

Release of tumor necrosis factor alpha in response to Vibrio vulnificus capsular polysaccharide in in vivo and in vitro models.

Vibrio vulnificus produces a severe septic shock syndrome in susceptible individuals. Virulence of the bacterium has been closely linked to the presence of a surface-exposed acidic capsular polysaccharide (CPS). To investigate whether CPS plays an additional role in pathogenesis by modulating inflammatory-associated cytokine production, studies were initiated in a mouse model and followed by investigations of cytokine release from human peripheral blood mononuclear cells (PBMCs). Mouse tumor necrosis factor alpha (TNF-alpha) could be detected in serum up to 12 h postinoculation in animals challenged with the encapsulated parent strain MO6-24/O. The unencapsulated strain CVD752 was quickly eliminated by the animals, thus preventing a direct association between serum TNF-alpha levels and the presence or absence of the CPS. Purified CPS from MO6-24/O when injected into D-galactosamine-sensitized mice was a more immediate inducer of TNF-alpha than an equivalent quantity of MO6-24/O lipopolysaccharide (LPS). Both V. vulnificus CPS and V. vulnificus LPS induced inflammation-associated cytokine responses from primary human PBMCs in vitro. CPS elicited TNF-alpha from PBMCs in a dose-dependent manner, with maximal induction at 6 to 10 h, and was not inhibited by polymyxin B. Expression of interleukin-6 (IL-6) mRNAs was also induced in the presence of CPS. Interestingly, while adherent PBMCs secreted high levels of TNF-alpha after stimulation with LPS, they secreted little TNF-alpha in response to CPS. These studies provide evidence that V. vulnificus CPS directly stimulates the expression and secretion of proinflammatory cytokines by murine and human cells and suggest that CPS activation of PBMCs operates through a cellular mechanism distinct from that of LPS.

Animals↗
PubMed1997

Pigmentary retinopathy associated with the mitochondrial DNA 3243 point mutation.

Fourteen patients from four unrelated families were studied to determine the prevalence of retinal pigmentary abnormalities associated with the MELAS A to G 3243 point mutation. Neurologic and ophthalmic examinations, retinal photography, pattern shift visual evoked potentials, and electroretinography were performed in all patients. Eight of the 14 patients had retinal pigmentary abnormalities characterized by symmetric areas of depigmentation involving predominantly the posterior pole and midperipheral retina. None of the patients had optic atrophy and only one patient with pigmentary retinal abnormalities had impaired visual acuity. None of the diabetic subjects (n = 6) had signs of diabetic retinopathy. Fluorescein angiography demonstrated mottled hyper- and hypofluorescent areas indicating multiple window defects in the retinal pigmentary epithelium. Visual evoked potentials showed delayed P100 responses in four of the eight patients with retinal pigmentary abnormalities. We conclude that there is a high prevalence of retinal pigmentary abnormalities in patients with MELAS A to G 3243 point mutation. These abnormalities are usually asymptomatic and best detected by retinal photography.

Adolescent↗
PubMed1996

Cloning and characterization of dnaE, encoding the catalytic subunit of replicative DNA polymerase III, from Vibrio cholerae strain C6706.

We report that Vibrio cholerae (Vc) contains a gene homologous to Escherichia coli dnaE, the structural gene for the alpha (catalytic) subunit of replicative DNA polymerase III (PolIII). Despite 24% amino acid (aa) differences in the encoded proteins, the Vc gene strongly complements an E. coli dnaE temperature sensitive (ts) mutant, indicating that all functional features essential for replication are conserved.

Amino Acid Sequence↗
PubMed1996

Brainstem myoclonus in a patient with non-dopa-responsive parkinsonism.

In the few reports where electrophysiologic techniques have been used to characterise stimulus-sensitive myoclonus in the setting of a parkinsonian syndrome, the origin of the myoclonus has usually been found to be cortical. We describe a patient with parkinsonism unresponsive to levodopa who had myoclonus that was both spontaneous and induced by somatosensory stimuli. In addition, autonomic symptoms and a marked sleep disturbance were present early in his illness. Results of electrophysiologic investigations including electromyography (EMG) studies, routine electroencephalography (EEG) recording, jerked locked back-averaging of EEG, and somatosensory evoked potentials were consistent with a brainstem origin for the myoclonic jerks. Following ipsilateral digital and supraorbital electrical stimulation, the earliest muscle activation occurred in the trapezius. An all-night sleep study showed frequent myoclonic jerks during sleep and markedly abnormal sleep architecture. We believe that this patient's myoclonus was related to pathologic changes in brainstem reticular nuclei that occurred as part of his disease process. To our knowledge, brainstem myoclonus has not been described as a feature of parkinsonian syndromes.

Brain Stem↗
PubMed1996

Acid-base balance affects dietary choice in cats.

The effect of acid-base status on self-selection of dietary protein was examined in three groups of adult male cats fed 20% soybean-protein and lactalbumin diets formulated to produce acidic, neutral or alkaline status. In two experiments, cats were offered a choice between the 20% protein diets or (1) the same diet with additional protein as casein (49% total crude protein) or (2) the same diet with added soybean-protein and lactalbumin (43% crude protein). Casein contained 0.63 mmol H+/g and caused all three groups to avoid the high casein diets by day 4. The high soybean-protein-lactalbumin diets did not contain added acid but would produce some extra acid upon catabolism of the sulfur-containing amino acids. Again, all three groups avoided the high protein diets by day 4. In a third choice trial, cats adapted to three low protein diets containing appropriate electrolytes to cause neutrality, acidemia or alkalemia, were offered a choice between: neutral vs. acidic; acidic vs. neutral or basic vs. acidic. The cats chose the neutral, neutral and basic diet respectively, restoring or maintaining acid-base homeostasis for each situation. The diets producing acidosis lowered serum sodium and potassium concentrations. We conclude that cats select appropriate diets in an attempt to maintain acid-base homeostasis.

Acid-Base Equilibrium↗
PubMed1996

Substantia nigra pars reticulata neurons in Parkinson's disease.

We have examined by immunohistochemistry the parvalbumin-containing neurons of the substantia nigra in patients with Parkinson's disease and in age-matched controls. Parvalbumin, a calcium binding protein, is involved in buffering intracellular calcium and in this study was localized within the majority of non-pigmented neurons of the human pars reticulata. Previous studies have shown that the parvalbumin-immunoreactive pars reticulata neurons are GABAergic and project to the motor thalamus and tectum. Their increased output, due to the loss of dopaminergic inhibition in Parkinson's disease, decreases cortical activation via thalamic pathways, causing parkinsonian symptoms. In Parkinson's disease there was a significant loss of parvalbumin-immunoreactivity from these neurons, though there was no evidence of actual cell loss. This loss of parvalbumin-immunoreactivity was detected only in those cases with end-stage Parkinson's disease.

Age of Onset↗
PubMed1996

Apomorphine can increase cutaneous inhibition of motor activity in Parkinson's disease.

We studied the effect of non-nociceptive ipsilateral digital stimulation on EMG recorded from a small hand muscle before and after the administration of subcutaneous apomorphine in 6 patients with Parkinson's disease. All were receiving the drug to control ¿on-off¿ fluctuations in motor performance. Averaged rectified EMG was recorded from tonically contracted abductor pollicis brevis (APB) following index finger stimulation using a brief stimulus train. In 5 patients motor evoked potentials (MEPs) were also recorded from APB during tonic contraction. A conditioning stimulus train was applied to the index finger at intervals between 15 and 65 msec prior to the transcranial magnetic stimulus. After apomorphine administration the patient group showed a significant increase in both EMG and MEP inhibition induced by digital stimulation. In patients with Parkinson's disease who have marked motor fluctuations, the inhibitory response of upper limb motor neurones to low level digital cutaneous stimulation can be altered by dopamine agonists.

Aged↗
PubMed1996

Antibodies that react with the capsular polysaccharide of Vibrio vulnificus are detectable in infected patients, and in persons without known exposure to the organism.

In serious infections with Vibrio vulnificus, IgG antibodies to the capsular polysaccharide of the infecting strain were demonstrable in patient serum. It was not possible to show that persons with probable increased exposure to V. vulnificus (shellfish industry workers) had increased levels of antibodies to any one of three capsular types tested when compared with persons who would be expected to have had minimal exposure to the organism (Seventh Day Adventists). Antibodies that reacted with the capsular polysaccharides were demonstrable in persons without a history of V. vulnificus infection, suggesting that cross-reacting antibodies are present in the general population.

Antibodies, Bacterial↗
PubMed1996

Cloning and sequence of a region encoding a surface polysaccharide of Vibrio cholerae O139 and characterization of the insertion site in the chromosome of Vibrio cholerae O1.

Vibrio cholerae serogroup O139 Bengal is the first documented serogroup other than O1 to cause epidemic cholera. The O139 Bengal strains are very similar to V. cholerae serogroup O1 biotype El Tor strains. The major differences between the two serogroups are that O139 Bengal contains a distinct O antigen and produces a polysaccharide capsule. We previously described three TnphoA mutants of O139 strain AI1837 which abolish both O antigen and capsule production. These TnphoA insertions were mapped to a 21.5 kb EcoRI fragment of the O139 chromosome. We describe here the cloning and mapping of this 21.5 kb EcoRI fragment and it was shown to complement each of the mutants in trans to produce O antigen and capsule. The EcoRI fragment contains 13 kb of DNA that is specific to O139 and 8.5 kb of DNA that is common to O1 and O139. Sequence analysis of the 13 kb of O139-specific DNA revealed that it contains 11 open reading frames all of which are transcribed in the same direction. Eight of the 11 open reading frames are homologous to sugar biosynthesis genes from other organisms. Using extended polymerase chain reactions, we show that the extent of the DNA region in O139 that is not present in O1 is approximately 35 kb. The site of insertion of this O139-specific DNA in the O1 chromosome was mapped to the rfbO1 region. We also demonstrate that O139 Bengal strain AI1837 contains a deletion of 22 kb that in serogroup O1 strains contains the rfb region. Therefore, O139 Bengal probably arose from an O1 strain that had undergone genetic rearrangements including deletion of the O1 rfb region and acquisition of a 35 kb region of DNA which encodes O139 surface polysaccharide.

Bacterial Capsules↗
PubMed1996

Vibrio cholerae O1 can assume a chlorine-resistant rugose survival form that is virulent for humans.

Vibrio cholerae can shift to a "rugose" colonial morphology associated with expression of an amorphous exopolysaccharide that promotes cell aggregation. Flow cytometric studies indicated that up to 3% of particles in rugose cultures represented aggregates of >5 bacterial cells. Rugose variants of our test strains displayed resistance to killing by chlorine, with viable cells persisting for >30 min in 2 mg/L free chlorine; strains also showed resistance to killing by complement-mediated serum bactericidal activity. Six volunteers fed 10(6) cfu of a rugose variant of V. cholerae O1 El Tor Inaba N16961 developed symptoms typical of cholera, with a mean diarrheal stool volume of 2.2 L (range, 1.4-4.3). Isolates recovered from the stool of infected volunteers retained the rugose phenotype. The data suggest that rugose strains cause human disease. The role of these strains in the epidemiology of cholera remains to be determined.

Adult↗
PubMed1996

Maillard reaction products in purified diets induce taurine depletion in cats which is reversed by antibiotics.

The effects of heat processing (Maillard reaction) and addition of antibiotics to diets on the metabolism of taurine in adult cats were studied. Groups of four cats were given daily 22 g/kg body weight one of four purified diets based on casein and starch. All diets contained the same major ingredients as the control (diet 1), except for starch substitutions. Diet 2 was autoclaved; in diet 3, 50 g glucose replaced 50 g starch before autoclaving; in diet 4, only the casein component was autoclaved with 50 g glucose before addition to the diet. Diets were fed for 5 wk, then a mixture of antibiotics was added to all diets and they were fed for a further 5 wk. In the first (no antibiotics) period, cats given the Maillard reaction products (diets 3 and 4) had a significant depletion of plasma and whole blood taurine and had twice the fecal, but less than half the urinary total taurine excretion of control cats. The addition of antibiotics to the diets restored plasma and whole blood concentration in cats given diets 3 and 4, reduced fecal and increased urinary taurine excretion, and decreased fecal cholyltaurine hydrolase activity. These results suggest that Maillard reaction products promote an enteric flora that favors degradation of taurine and decreases recycling of taurine by the enterohepatic route.

Amidohydrolases↗
PubMed1996

Dietary antibiotics decrease taurine loss in cats fed a canned heat-processed diet.

In a crossover design, cats were fed a canned heat-processed diet (18 g dry matter/kg initial body wt) either with (+) or without (-) antibiotics [a mixture of penicillin G, procaine (25 mg/18 g diet) and tetracycline (50 mg/18 g diet)]. The (-/+) group received no antibiotics during the first 5-wk period and received antibiotics during the second 5-wk period; the (+/-) group received the reverse. Plasma, whole blood, urinary and fecal concentrations of taurine, fecal bile acid excretion and cholyltaurine hydrolase activities were measured. Consumption of antibiotics for 5 wk resulted in a lower rate of depletion of plasma taurine. Taurine concentrations decreased more over the first 5 wk in cats in the (-/+) group than in cats in the (+/-) group [from 116 +/- 26 to 26 +/- 6 mumol/L (-/+) and from 109 +/- 6 to 77 +/- 7 mumol/L (+/-) for plasma, and from 546 +/- 8 to 292 +/- 29 mumol/L (-/+) and from 560 +/- 11 to 431 +/- 20 mumol/L (+/-) for whole blood]. Urinary total taurine excretions during the 5th week were 54 mumol/d for the (-/+) group and 135 mumol/d for the (+/-) group (pooled SEM, +/- 13). Fecal total taurine excretions during the 5th week were 184 and 53 mumol/d for the (-/+) and (+/-) groups, respectively, (pooled SEM +/- 9). Most of the fecal taurine was unconjugated (free). Fecal bile acid excretions during the 5th week were 235 +/- 18 and 106 +/- 11 mumol/d for the (-/+) and (+/-) groups, respectively. Dietary antibiotics suppressed fecal cholyltaurine hydrolase activity of cats. Fecal cholyltaurine hydrolase activities during the 5th week were 279 +/- 54 and 42 +/- 10 nmol cholic acid released.min-1.g dry feces-1 in the (-/+) and (+/-) groups, respectively. After the crossover, mean values for the groups were reversed, showing that the observed changes were due to the antibiotic treatment. These results support the hypothesis that the dietary taurine requirement of cats is largely determined by the extent of microbial degradation of taurine in the gastrointestinal tract.

Amidohydrolases↗
PubMed1996

Dietary crude protein increases slightly the requirement for threonine in kittens.

Previous work indicates that the essential amino acid requirements for kittens are not positively correlated with the concentration of dietary nitrogen as they are in other species. In the studies presented here, the interaction between graded levels of threonine and dietary crude protein was investigated. Dose-response curves were generated using six 4 x 4 Latin squares. Each square represented one concentration of threonine (4.0, 5.0, 6.0, 7.0, 9.0 or 12.0 g/kg diet) and four concentrations of crude protein (150, 200, 300 and 500 g/kg diet). Food intake, weight gain, nitrogen retention and plasma amino acids were measured. There was no strong positive relationship between the threonine requirement of kittens and dietary crude protein. Increasing crude protein when threonine was limiting in the diet increased growth and food intake under some conditions, whereas under other conditions food intake and growth were decreased in a manner consistent with an amino acid imbalance response. An additional experiment was done to verify some of these findings. The requirement for threonine was found to increase from 5.0 g/kg diet at 150 and 200 g crude protein/kg diet to 6.0 g/kg diet when crude protein was 300 or 500 g/kg diet. The requirement for crude protein in the kitten appears to be between 200 and 300 g/kg diet.

Amino Acids↗