A Case of Peritoneal Tuberculosis Mimicking Ovarian Cancer in a Young Female.

Background: Tuberculosis causes significant morbidity and mortality globally. Peritoneal tuberculosis can have a similar presentation to ovarian cancer. Case: We present a case of a 42-year-old female referred to gynecology oncology with imaging findings of enlarged right ovary, omental caking, and elevated CA-125 (1289 U/mL). A diagnostic laparoscopy revealed diffuse studding of intraperitoneal surfaces. Histopathological examination of omental and abdominal wall biopsies showed granulomas, but stains and cultures for mycobacteria were negative. Antimicrobial treatment for tuberculosis was initiated. Within eight weeks, there was clear clinical and radiographic improvement, consistent with a diagnosis of peritoneal tuberculosis. Conclusion: This case highlights the importance of including peritoneal tuberculosis in the differential diagnosis when evaluating for ovarian cancer in women with epidemiologic risk factors for tuberculosis.

Reduced soma size of the M-neurons in the lateral geniculate nucleus following foetal alcohol exposure in non-human primates.

Visual impairment is commonly reported as a consequence of heavy prenatal ethanol exposure in humans. Children generally display characteristic cranio-facial dysmorphology and represent typical severe cases of foetal alcohol syndrome. Binge-like rodent model systems have concluded that third trimester equivalent ethanol exposure results in widespread apoptosis in the visual system from the retina to the visual cortex. Neither clinical nor animal studies address the consequences of more moderate prenatal ethanol exposure on the visual system. The current study uses a naturalistic and voluntary consumption approach in non-human primates (Chlorocebus sabeus) in order to more closely model prenatal ethanol consumption patterns in humans. Pregnant vervet monkeys voluntarily drank on average 2.418 +/- 0.296 g etoh/kg/day four times a week during the third trimester. Using unbiased stereology, we estimated the neuronal and glial population of the parvocellular (P) and magnocellular (M) layers of the lateral geniculate nucleus (LGN) following foetal alcohol exposure (FAE) in infant subjects. Layer volume and total number of neurons and glia in the LGN of the FAE subjects were not significantly different from age-matched control subjects. The M neuronal soma size of FAE subjects, however, was significantly reduced to resemble the size of the P-neurons. These results suggest that alterations at the level of morphology and anatomy of the M-neurons may lead to behavioural deficits associated with the integrity of the dorsal visual pathway.

A primate model for Alzheimer's disease: investigation of the apolipoprotein E profile of the vervet monkey of St. Kitts.

The apolipoprotein E4 allele has been previously associated with late onset Alzheimer's disease (AD). The major neuropathology of AD, senile (amyloid) plaques, and neurofibrillary tangles, has been observed in the vervet monkey (Chlorocebus aethiops). To further assess the suitability of the vervet as a model for AD, we undertook to determine the sequence of the vervet apoE exon 4 and to genotype an unrelated group of 30 aged animals raging from 15 to 28 years of age. All 30 animals were homozygous for the E4 allele.

Ibogaine: complex pharmacokinetics, concerns for safety, and preliminary efficacy measures.

Ibogaine is an indole alkaloid found in the roots of Tabernanthe Iboga (Apocynaceae family), a rain forest shrub that is native to western Africa. Ibogaine is used by indigenous peoples in low doses to combat fatigue, hunger and thirst, and in higher doses as a sacrament in religious rituals. Members of American and European addict self-help groups have claimed that ibogaine promotes long-term drug abstinence from addictive substances, including psychostimulants and opiates. Anecdotal reports attest that a single dose of ibogaine eliminates opiate withdrawal symptoms and reduces drug craving for extended periods of time. The purported efficacy of ibogaine for the treatment of drug dependence may be due in part to an active metabolite. The majority of ibogaine biotransformation proceeds via CYP2D6, including the O-demethylation of ibogaine to 12-hydroxyibogamine (noribogaine). Blood concentration-time effect profiles of ibogaine and noribogaine obtained for individual subjects after single oral dose administrations demonstrate complex pharmacokinetic profiles. Ibogaine has shown preliminary efficacy for opiate detoxification and for short-term stabilization of drug-dependent persons as they prepare to enter substance abuse treatment. We report here that ibogaine significantly decreased craving for cocaine and heroin during inpatient detoxification. Self-reports of depressive symptoms were also significantly lower after ibogaine treatment and at 30 days after program discharge. Because ibogaine is cleared rapidly from the blood, the beneficial aftereffects of the drug on craving and depressed mood may be related to the effects of noribogaine on the central nervous system.

An amino acid mixture deficient in phenylalanine and tyrosine reduces cerebrospinal fluid catecholamine metabolites and alcohol consumption in vervet monkeys.

An amino acid mixture devoid of tryptophan, given orally, was previously shown to reduce cerebrospinal fluid levels of tryptophan and 5-hydroxyindoleacetic acid in vervet monkeys, as compared to a control mixture containing all essential amino acids. In the present study, we tested the possibility that a similar amino acid mixture containing tryptophan, but devoid of phenylalanine and tyrosine (the amino acid precursors of catecholamine neurotransmitters), would influence dopamine and noradrenaline metabolism. Five hours after the administration of this mixture to vervet monkeys, cerebrospinal fluid levels of homovanillic acid and 3-methoxy-4-hydroxyphenylethylene glycol were reduced by 27.4% and 26.9%, respectively. Both effects were statistically significant. Plasma tyrosine (-30%) and the ratio of tyrosine to the sum of other large neutral amino acids (sigmaLNAA) were also significantly reduced. The behavioral efficacy of phenylalanine/tyrosine depletion was compared with that of tryptophan depletion in a primate model of voluntary alcohol consumption. All three drinks lowered alcohol consumption, but the effects of the tryptophan-deficient amino acid mixture were not different from those of the balanced amino acid control. The phenylalanine/tyrosine-deficient drink differentially lowered alcohol consumption, consistent with other data in this species and elsewhere implicating dopamine in the rewarding effects of alcohol.

Strategic business planning for internal medicine.

The internal medicine generalist is at market risk with expansion of managed care. The cottage industry of Academic Departments of internal medicine should apply more business tools to the internal medicine business problem. A strength, weakness, opportunity, threat (SWOT) analysis demonstrates high vulnerability to the internal medicine generalist initiative. Recommitment to the professional values of internal medicine and enhanced focus on the master clinician as the competitive core competency of internal medicine will be necessary to retain image and market share.

Altered dopamine transporter densities in alcohol-preferring vervet monkeys.

Altered dopamine (DA) transporter densities have been implicated in mechanisms of vulnerability and relapse in human alcoholics. The regional distribution and density of the DA transporter was studied in alcohol-preferring vervet monkeys to investigate baseline status and regulation of the DA transporter at different stages of chronic alcohol drinking. Combined ligand binding and in vitro autoradiography of the cocaine congener [125I]RTI-55 (beta-CIT) demonstrated a significant increase in DA transporter densities in abstinent alcohol-preferring monkeys over those in alcohol-avoiding monkeys. Chronic alcohol consumption down-regulated DA transporter densities, and this effect was reversed by acute withdrawal. These results demonstrate that the DA transporter is regulated by alcohol exposure and suggest that increased DA transporter densities may be a phenotypic marker of alcohol preference in vulnerable monkeys.

Acute effect of altered tryptophan levels and alcohol on aggression in normal human males.

Normal males received amino acid mixtures designed to raise or lower tryptophan availability, and thus to raise or lower brain serotonin synthesis. They also received alcoholic or non-alcoholic drinks. The subjects were tested in the Taylor Competitive Reaction Time Task in which they competed against a (non-existent) partner in a reaction time task. The magnitude of electric shocks that the subjects were willing to give to their bogus partner was used as a measure of aggression. Lowered tryptophan levels and ingestion of alcohol were associated with increased aggression. Our data support the idea that low serotonin levels may be involved in the etiology of aggression. They suggest that subjects with low brain serotonin levels may be particularly susceptible to alcohol-induced violence.

A contribution to the differential diagnosis of the "group of schizophrenias": structural abnormality of chromosome 4.

A structural abnormality of chromosome 4 [inv 4 (p15.2; q21.3)] is reported in a male presenting with DSM-III-R schizophrenia, undifferentiated type (295.94) and in his mother, who displayed symptoms associated with schizotypal personality disorder (DSM-III-R 301.22). The proband had a performance IQ of 91, poor motor coordination, stature in the lowest quartile and an impaired sense of time. There were no diagnostic physical or neurological abnormalities. Mild ventricular enlargement and prominent sulci were found on computed tomography. Both he and his chromosomally normal father had strabismus which required surgical correction. This case joins the long list of chromosomal abnormalities previously reported to confer an increased risk of mental illness and emphasizes the importance of a sophisticated differential diagnosis in evaluating patients who present with symptoms of schizophrenia. The implications for recent initiatives which attempt to localize genes conferring susceptibility to schizophrenia and other major mental illnesses are discussed.

Homicidal somnambulism: a case report.

A case of a homicide and an attempted homicide during presumed sleepwalking is reported in which somnambulism was the legal defense and led to an acquittal. Other possible explanations including complex partial seizures, dissociative state, rapid eye movement sleep behavior disorder and volitional waking behavior are discussed. The evidence supporting the probability that this act occurred during an episode of somnambulism and sleep-related confusional arousal is reviewed and weighed. This evidence includes personal and family history of somnambulism and related disorders; neurological, psychiatric and psychological assessments; presence of possible precipitating factors; and polysomnographic data.

Voluntary alcohol consumption in vervet monkeys: individual, sex, and age differences.

The patterns of voluntary alcohol consumption were studied in 35 vervet monkeys (Cercopithecus aethiops), classified into four groups. Each monkey showed a fairly steady rate during the studied period, resulting in individual differences that became more evident as the treatment evolved. Females showed higher alcohol intake frequencies than males. This sexual difference was maintained among adults and juveniles. Age differences were also observed: juveniles showed higher frequencies of intake than adults, both in general and in each sex group. Intake frequency was not related to age in prepubertal subjects, neither in general nor in each particular sex. The origin of these sex and age alcohol consumption differences remains to be studied, but differences in alcohol metabolism and factors related to puberty are possible influences.

Long-term protective effects of human recombinant nerve growth factor and monosialoganglioside GM1 treatment on primate nucleus basalis cholinergic neurons after neocortical infarction.

Neocortical infarction induces biochemical and morphological retrograde degenerative changes in cholinergic neurons of the rat nucleus basalis magnocellularis [Sofroniew et al. (1983) Brain Res. 289, 370-374]. In the present study, this lesion model has been reproduced in the non-human primate (Cercopithecus aethiops) to investigate whether degenerative changes affecting the cortex surrounding the lesioned area and the ipsilateral basal forebrain are prevented by the early administration of recombinant human nerve growth factor alone or in combination with the monosialoganglioside GM1. Six months after surgery and treatment, the monkeys were processed either for biochemistry (choline acetyltransferase assay) or immunocytochemistry. In lesioned vehicle-treated animals, choline acetyltransferase activity significantly decreased by 28% in the cortex surrounding the injured area and by 31% in the ipsilateral nucleus basalis of Meynert when compared with values of sham-operated monkeys. These biochemical changes were fully prevented with the administration of nerve growth factor alone or in combination with the monosialoganglioside GM1. The morphometrical analysis revealed a significant shrinkage of cholinergic neurons (61 +/- 1.4% of sham-operated cell size) and loss of neuritic processes (59 +/- 10% of sham-operated values) within the intermediate nucleus basalis region of lesioned vehicle-treated animals. Although a protection of the cholinergic cell bodies within the nucleus basalis was found with both treatments, a significant recovery of the neuritic processes (84 +/- 7.2% of sham-operated values) was assessed only in the double-treated monkeys. These results indicate that the early administration of nerve growth factor alone or in combination with the monosialoganglioside GM1 induces a long-term protective effect on the nucleus basalis cholinergic neurons in cortical injured non-human primates.

Primate nucleus basalis of Meynert p75NGFR-containing cholinergic neurons are protected from retrograde degeneration by the ganglioside GM1.

The effects of unilateral devascularizing lesions of the neocortex in primates (Cercopithecus aethiops) on the immunoreactivity of choline acetyltransferase and the low-affinity nerve growth factor receptor (p75NGFR) were investigated in cell bodies of the nucleus basalis of Meynert. Choline acetyltransferase enzymatic activity was measured in the dissected ipsi- and contralateral nucleus basalis of Meynert as well as in the remaining cortex adjacent to the lesion. Cortically lesioned animals displayed a shrinkage of p75NGFR-immunoreactive cholinergic cell bodies in only the intermediate portion of the nucleus basalis of Meynert as well as a depletion of choline acetyltransferase activity in this cellular complex. In contrast, cortically lesioned monkeys treated with monosialoganglioside did not reveal a significant loss of choline acetyltransferase activity or shrinkage of nucleus basalis of Meynert cholinergic neurons, but rather a modest hypertrophy. These results are discussed in relation to a possible use of putative trophic agents in the repair of the damaged central nervous system.

The cholecystokinin hypothesis of panic and anxiety disorders: a review.

It has been suggested that cholecystokinin, a neurotransmitter found in high density in mammalian brain, might be implicated in the neurobiology of panic and anxiety disorders. Cholecystokinin-tetrapeptide induces panic attacks analogous to spontaneous panic attacks in patients suffering from panic disorder and to a much lesser degree in healthy volunteers, suggesting an enhanced sensitivity to cholecystokinin-tetrapeptide in panic disorder. In animal models of anxiety, pre-treatment with cholecystokinin antagonists significantly decreases the anxiogenic effects of cholecystokinin agonists. This paper reviews clinical and basic studies supporting an involvement for cholecystokinin in panic and anxiety disorders.

Effect of sucrose consumption on alcohol-induced impairment in male social drinkers.

Two studies were conducted to examine the interaction between sucrose and ethanol in normal young fasting adult males. The first experiment employed a 3 (100 g sugar, 35 g sugar, 0 g sugar) x 3 (alcohol, placebo and sober) factorial design, which was carried out double-blind using aspartame to ensure that all the drinks were equally sweet. Subjects were tested for mood, memory, subjective intoxication and psychomotor performance at baseline and at times up to 3.5 h after ingestion of the drinks. An alcohol by sugar interaction was seen at 0.5 after drinking. Sugar attenuated alcohol intoxication at this time without influencing blood alcohol levels. Contrary to previous reports, the combination of alcohol and sugar failed to produce significant hypoglycemia, or any of the adverse behavioral effects associated with hypoglycemia, at later times after drink ingestion. The second experiment involved a simpler design, carried out single-blind in which the subjects receiving no sugar did not get aspartame. This was to rule out the possibility that aspartame was exacerbating alcohol intoxication instead of sugar attenuating it. The second experiment also showed that sugar can attenuate alcohol intoxication in fasting humans without altering blood alcohol levels significantly.

Lead and cadmium levels in violent criminals.

Two groups of violent incarcerated male criminals and 30 nonviolent criminals were compared for element content of hair by atomic absorption spectroscopy. Groups did not differ in age, socioeconomic status, or months institutionalized. The groups did differ significantly in lead and cadmium levels. The importance of cadmium in affecting reactivity to stimuli is discussed.