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Biomedical subjects

C Tamminga

Publications and source records attributed to C Tamminga.

At least 19 recordsLinked to original sources
PubMed2002

An observational clinic-based study of diarrheal illness in deployed United States military personnel in Thailand: presentation and outcome of Campylobacter infection.

Campylobacter is a leading cause of traveler's diarrhea in Thailand. Since resistance to quinolones is high among Campylobacter isolates, empiric therapy with quinolones for traveler's diarrhea may be ineffective in this region. We conducted an observational study among 169 U.S. military personnel with acute diarrhea and compared their microbiologic findings to those of 77 asymptomatic personnel deployed to Thailand in May 1998. Of 146 pathogenic bacterial isolates, the most common were nontyphoidal Salmonella (n = 31), enterotoxigenic Escherichia coli (n = 24), and C. jejuni/coli (n = 23). Campylobacter was strongly associated with disease (odds ratio = 5.9; 95% confidence interval = 1.3-37.3), with a more severe clinical presentation, and with a reduced functional ability at presentation (P = 0.02). In vitro resistance to ciprofloxacin was observed in 96% of the Campylobacter isolates. Sub-optimal treatment response to ciprofloxacin was observed in 17% of the cases of Campylobacter infection versus 6% due to other causes. These results highlight the importance of Campylobacter as a cause of severe traveler's diarrhea in Thailand and illustrates the ongoing problem with antibiotic-resistant strains and associated treatment problems.

Adult↗
PubMed1999

Glutamatergic aspects of schizophrenia.

Almost all the neurons in the brain are influenced by the excitatory amino acid glutamate. Glutamatergic neurotransmission has been associated functionally with a number of physiological processes and with certain pathophysiological processes, including schizophrenia. Imaging studies provide indirect evidence that glutamate may be involved in schizophrenia. Positron emission tomography scanning has shown a correlation between positive symptoms of schizophrenia and abnormalities of glucose metabolism in components of the limbic system with the highest concentration of glutamate receptors. Studies with ketamine, an anaesthetic that antagonises the N-methyl-D-aspartate (NMDA) glutamate receptor, show an exacerbation or worsening of positive symptoms when this drug is administered to patients with schizophrenia. Regional cerebral blood flow studies with ketamine show that the drug produces increased blood flow in the anterior cingulate cortex, the area where high concentrations of NMDA receptors exist and where alterations in glucose metabolism seem to occur in people with schizophrenia. Diminished glutamatergic neurotransmission in the hippocampal glutamate-mediated efferent pathways and cerebral dysfunction in the hippocampus and its target areas, particularly the anterior cingulate cortex, may underlie some of the clinical manifestations of schizophrenia.

Cerebrovascular Circulation↗
PubMed1993

Strong inference, theory testing, and the neuroanatomy of schizophrenia.

Failure to address the putative etiologic and pathophysiologic heterogeneity of the schizophrenia syndrome and problems in definitive assessment of human brain function have impaired progress in schizophrenia research. New approaches to psychopathology and converging evidence from antemortem and postmortem study can now result in more decisive study of the neuroanatomy and neuropathology of schizophrenia.

Brain↗
PubMed1993

Changes in psychopathology and dyskinesia after neuroleptic withdrawal in a double-blind design.

The goal of this study was to assess the time course of change in psychopathology and dyskinesia after neuroleptic withdrawal. Fifteen DSM-III schizophrenic patients were abruptly withdrawn in a double-blind fashion from stable haloperidol treatment. Weekly ratings of dyskinesia and psychopathology were performed for 4 weeks post-withdrawal. There was an overall increase in dyskinesia ratings over the 4-week period (p < 0.05) beginning in week 2, with dyskinetic movements of the fingers showing the most significant increase (p < 0.001). There were no overall changes in psychopathology, though the group appeared to be bimodal with 6 of the 15 patients showing a significant relapse in psychotic symptoms. Neither baseline TD nor psychotic relapse significantly interacted with change in TD over time. These schizophrenic patients showed an increase in global dyskinesia rating early within four weeks of neuroleptic withdrawal. This time course did not appear to be associated with reemergence of psychopathology which occurred later. A significant minority of patients relapsed within this time period. This suggests the relative safety of brief periods of neuroleptic withdrawal for carefully selected patients in a controlled setting with specific goals (e.g., for evaluation or in preparation for clozapine) and the need to further understand who is at risk for rapid relapse.

Adolescent↗
PubMed1991

Expression of acidic and basic fibroblast growth factors in the substantia nigra of rat, monkey, and human.

The distribution of acidic (aFGF) and basic (bFGF) fibroblast growth factor mRNA and protein were examined in mesencephalon by immunohistochemistry, immunoblot analysis, in situ hybridization histochemistry, and RNA analysis. Coexistence of aFGF or bFGF with tyrosine hydroxylase protein in nigral cells was observed with immunohistochemistry. Both aFGF and bFGF mRNAs were found in the substantia nigra. Unilateral 6-hydroxydopamine lesions of nigrostriatal neurons resulted in a loss of aFGF and tyrosine hydroxylase [L-tyrosine, tetrahydropteridine: oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] mRNA-positive neurons on the lesioned side. The distribution of aFGF mRNA in monkey brain was similar to that seen in the rat. RNA and immunoblot analysis confirmed the presence of both aFGF and bFGF mRNAs and proteins in the substantia nigra of rat, monkey, and human.

Animals↗
PubMed1991

Tobacco smoking increases square-wave jerks during pursuit eye movements.

Smooth-pursuit eye-movement (SPEM) abnormalities have been consistently observed in schizophrenia. The SPEM changes in schizophrenia are not thought to be an artifact of voluntary attention or medication, although a number of nondisease factors are known to affect SPEM. However, cigarette smoking has recently been reported to deteriorate SPEM in both smokers and nonsmokers. This finding is particularly relevant to schizophrenia, because schizophrenic patients smoke cigarettes considerably more than do normals, and none of the previous studies in this patient group have controlled for smoking. The current study was initiated to examine the effects of smoking on a number of oculomotor measures, including SPEM in smoker and nonsmoker normal volunteers. The results of this study suggest that cigarette smoking induces or significantly increases square-wave jerks, especially during smooth pursuit in normals. However, the effect is small and the global qualitative SPEM score is not affected. Other eye movements such as latencies for reflex and volitional saccades and saccadic distractibility are also unaffected by smoking. No differences were apparent between chronic smokers and nonsmokers under nonsmoking conditions in any of the eye-movement measures.

Adult↗
PubMed1989

Oculomotor abnormalities and their clinical correlates in schizophrenia.

Smooth pursuit eye movements (SPEMs) have been consistently found to be abnormal in the majority of schizophrenic patients. The traditional SPEM measurement technique, however, fails to inform us about the underlying oculomotor deficit in these patients, since it remains a non-specific and a global oculomotor measure. A number of diverse clinical features such as tardive dyskinesia (TD) or negative symptoms correlate with the SPEM abnormality. Other eye movement abnormalities such as fixation difficulties, increased "volitional" saccadic latency and saccadic distractibility in anti-saccade paradigm have also been noted in schizophrenic patients. Still, it remains unclear how these different eye movement measures relate with each other and with the traditional SPEM measure, the presence of which is so widely described in schizophrenia. The advantage of some newer oculomotor paradigms is their functional specificity and the degree to which their biology is known. To further address these issues and to search for clinical correlates of various eye movement abnormalities found in schizophrenia, we have developed a battery of oculomotor measures to be administered to a large number of clinically well described schizophrenic patients and normal controls. The results from a preliminary analysis of a relatively small number of subjects are presented here, thus limiting the scope of possible conclusions. But, these results do indicate that this technique of studying multiple paradigms for oculomotor control in schizophrenia may prove to be fruitful.

Eye Movements↗
PubMed1987

Increased growth hormone response to clonidine in 6-hydroxydopamine-treated rats.

Alpha 2-adrenergic receptors mediate adrenergic stimulation of growth hormone (GH) secretion in the rat. The GH response to the alpha 2-adrenergic agonist clonidine has thus been used as an index of alpha 2-adrenergic receptor responsiveness. Pharmacologic manipulations known to upregulate alpha 2-adrenergic receptor sensitivity would then be expected to result in an enhancement of the GH response to clonidine. To test this hypothesis, rats were injected in the lateral ventricle with either 6-hydroxydopamine or sterile saline. One month following the lesion, urethane-anesthetized rats from each group were administered clonidine or saline. Venous samples for plasma GH were drawn prior to or following the clonidine or saline administration. Rats administered clonidine had greater GH responses than those administered saline within either the lesioned or nonlesioned groups. The GH response to clonidine was significantly greater in the lesioned group than in the nonlesioned group. As 6-hydroxydopamine pretreatment upregulates alpha 2-adrenergic receptors, these results support the validity of the use of the GH response to clinidine as an index of alpha 2-adrenergic receptor responsiveness.

Animals↗
PubMed1986

GABA-agonist therapy for Alzheimer's disease.

Evidence suggesting a reduction of cerebral gamma-aminobutyric acid (GABA) neurons in Alzheimer's disease has been reported. To evaluate the possible contribution of GABA system dysfunction to the intellectual decline associated with this disorder, a controlled therapeutic trial of a potent and specific GABA agonist, THIP [4,5,6,7-tetrahydroisoxazolo(5,4,-c)pyridin-3-ol], was undertaken. Six Alzheimer patients with mild to moderately severe dementia and low spinal-fluid GABA levels received THIP at maximum individually tolerated dosage. No significant change in cognitive function could be discerned, despite attainment of dose levels that produced centrally mediated adverse effects similar to those of other GABA agonists. The results support the views that pharmacologic attempts to stimulate central GABA-mediated synaptic function may not confer therapeutic benefit to patients with Alzheimer's disease and that a GABA system deficit may not serve as a critical determinant of the dementia that characterizes this disorder.

Alzheimer Disease↗
PubMed1985

Failure of chronic haloperidol to affect prolactin secretion due to acute haloperidol administration.

Withdrawal from chronic haloperidol exposure was associated to unaltered circulating levels of prolactin (PRL), decreased 3H-spiperone binding sites in the anterior pituitary and increased 3H-spiperone binding sites in the striatum of male rats. Haloperidol (0.1 mg/kg ip) induced similar rises in plasma PRL in haloperidol-or saline-treated rats and the dose of 0.01 mg/kg was ineffective in both groups. These findings illustrate the poor relatedness existing at the pituitary D2 receptor between biochemical and functional indices.

Animals↗
PubMed1983

Behavioral, physiological, and neuroendocrine responses to arecoline in normal twins and "well state" bipolar patients.

Cholinergic supersensitivity has been postulated to be an etiologic factor in affective disorder. After several pilot dose-response studies, we administered 8 mg of the cholinergic agonist arecoline subcutaneously to eight pairs of normal volunteer identical twins and eight bipolar patients currently euthymic and unmedicated. During the hour following arecoline administration, the Profile of Mood States (POMS) showed an increase in total mood disturbance in both patient and control groups. Mean systolic blood pressure, pulse, plasma cortisol, prolactin, and growth hormone also increased. Anger and elation scores on the POMS showed significant concordance in identical twins, as did change in prolactin, implying that these are the components of drug response possibly influenced by genetic factors. None of these responses differentiated well state patients from controls. Thus, mood, behavioral, and neurochemical responses to arecoline, which appears to have nonspecific neurochemical effects at the dose employed, are not markers of vulnerability to affective illness.

Arecoline↗
PubMed1977

Effect of apomorphine on schizophrenic symptoms.

The effects of apomorphine on psychotic symptoms were evaluated in chronic schizophrenic patients using double-blind placebo controlled procedures. Although on the basis of dopamine theory of schizophrenia, apomorphine was expected to increase schizophrenic symptoms, in this study apomorphine substantially reduced psychotic symptoms in some chronic schizophrenic patients. No patient showed the substantial increase in psychotic symptoms previously demonstrated after the administration of IV methylphenidate. These clinical effects of apomorphine in schizophrenia may be relevant to recent pharmacological research which has indicated that apomorphine also has potent effect on presynaptic dopamine neurons, in addition to its previously described postsynaptic receptor stimulation.

Apomorphine↗
PubMed1977

Postsynaptic supersensitivity in schizophrenia.

In the context of the dopamine hypothesis of schizophrenia, the authors examined postsynaptic dopamine (DA) receptor sensitivity in schizophrenic patients by means of a neuroendocrine strategy using the DA receptor agonist apomorphine and growth hormone (GH) release as the measurable postsynaptic event. The activity of platelet adenylate cyclase, an enzyme intimately associated with catecholamine receptor activity, was also studied following stimulation by prostaglandin E1 (PGE1). Patients diagnosed as having acute schizophrenia had significantly higher GH responses and adenylate cyclase activity than normal control subjects and patients diagnosed as having chronic schizophrenia. Chronic schizophrenic patients with and without tardive dyskinesia showed GH responses slightly lower than but not significantly different from those of control groups.

Acute Disease↗