Sexual harassment at work: issues and answers for health care administrators

Sexual harassment is not new to the health care industry. What is new is that recent media attention has heightened awareness that sexual harassment is illegal. This fact, coupled with the substantial liability that employers may incur if they fail to control sexual harassment, mandates the need for outlining the major issues relative to sexual harassment in today's health care setting. This article gives particular emphasis to the fact that sexual harassment can be prevented by taking a proactive stance.     

Modulation of N-methyl-d-aspartate (NMDA)-stimulated noradrenaline release in rat brain cortex by presynaptic α2-adrenoceptors

Summary Rat brain cortex slices and synaptosomes preincubated with [³H]noradrenaline were used to investigate whether the NMDA-evoked noradrenaline release is modulated by agonists or antagonists at presynaptic ₂-adrenoceptors.In experiments on slices, noradrenaline and the preferential ₂-adrenoceptor agonists talipexole (former B-HT 920) and clonidine inhibited the NMDA evoked tritium overflow whereas the selective ₁-adrenoceptor agonists cirazoline and methoxamine were ineffective. The ₂-adrenoceptor antagonists rauwolscine and idazoxan facilitated the NMDA-evoked tritium overflow whereas the preferential ₁-adrenoceptor antagonist prazosin was ineffective. The concentration-response curve of talipexole for its inhibitory effect on NMDA-evoked overflow was shifted to the right by idazoxan (apparent pA₂ = 7.5). The EC₅₀ of NMDA (97 mol/l) for its stimulating effect on tritium overflow was not substantially changed by blockade of ₂-autoreceptors with 1 mol/l rauwolscine (EC₅₀ of NMDA in the presence of the ₂-adrenoceptor antagonist, 155 mol/l), but the maximal overflow of tritium was increased 2.5 fold by this rauwolscine concentration. In experiments on synaptosomes, talipexole and noradrenaline inhibited the NMDA-evoked tritium overflow. The inhibitory effect of talipexole was abolished by idazoxan which, given alone, was ineffective, as was prazosin. Talipexole did also not produce an inhibition when tritium overflow was evoked by NMDA in the presence of -conotoxin GVIA 0.1 mol/l; the latter, by itself, decreased the response to NMDA by about 55%. It is concluded that the NMDA-evoked noradrenaline release in the cerebral cortex is modulated via presynaptic ₂-adrenoceptors on the noradrenergic neurones. Stimulation of these autoreceptors in slices by endogenous noradrenaline does not result in a decreased potency of NMDA, but in a decreased maximum effect, in stimulating noradrenaline release. The inhibitory effect of ₂-adrenoceptor agonists on the NMDA-evoked release is at least partially due to a functional interaction between the NMDA receptors and ₂-autoreceptors at the level of the same varicosities. The results obtained with -conotoxin GVIA suggest that Ca²⁺ influx via the N-type voltage-sensitive calcium channel (VSCC) occurs in response to NMDA receptor stimulation and contributes substantially to the induction of NMDA-evoked noradrenaline release. The inhibitory effect of ₂-adrenoceptor stimulation on this release appears to be ultimately due to an inhibition of the influx of Ca²⁺ via the N-type VSCC. Correspondence to: M. Göthert at the above address     

Involvement of presynaptic H3 receptors in the inhibitory effect of histamine on serotonin release in the rat brain cortex

Summary Rat brain cortex slices or synaptosomes preincubated with ³H-serotonin were superfused with physiological salt solution (which, in the case of slices, contained citalopram, an inhibitor of serotonin uptake), and the effects of histamine and related drugs on the evoked tritium overflow were studied.The electrically (3 Hz) evoked tritium overflow from slices was inhibited by histamine and the H₃ receptor agonists R-(–)--methylhistamine and N-methylhistamine (pIC_12.5 values: 6.41, 7.28 and 6.12, respectively), but not affected by the H₁ receptor agonist 2-(2-thiazolyl)ethylamine and the H₂ receptor agonist dimaprit (each at 10 mol/l). The concentration-response curve for histamine was shifted to the right by the H₃ receptor antagonists impromidine, burimamide and thioperamide (apparent pA₂ values: 7.45, 5.97 and 7.88, respectively); the concentration-response curve of serotonin for its inhibitory effect on the electrically evoked overflow was not affected by the three drugs (apparent pA₂ values: < 5.5, < 5.5 and < 6.5). Given alone, impromidine, thioperamide and a low concentration of burimamide facilitated the electrically evoked overflow. In slices superfused with K⁺-rich, Ca²⁺-free solution containing tetrodotoxin throughout and in synaptosomes superfused with Ca²⁺-free solution, histamine inhibited the overflow evoked by introduction of Ca²⁺ (in synaptosomes, simultaneously with an increased amount of K⁺). In either tissue, the effect of histamine was counteracted by thioperamide.The results provide evidence that exogenous and probably also endogenous histamine inhibits serotonin release in the rat brain cortex via presynaptic histamine H₃ receptors.Send offprint requests to E. Schlicker at the above address     

Evidence for the involvement of the 5-HT1A receptor in CCK induced satiety in rats

The present study was designed to examine possible interactions between exogenous CCK and the 5-HT_1A receptor subtype mediated serotonergic effects on feeding in rats. The somatodendritic 5-HT_1A receptor agonist 8-OH-DPAT (0.32 mg/kg sc) evoked feeding in freely feeding rats. This effect was attenuated by treatment with CCK-8 (1, 5 and 25 g/kg ip). In food deprived rats, CCK-8 (40 g/kg ip) significantly reduced the size of a test meal. Treatment with the 5-HT_1A receptor antagonist WAY-100135 (10 mg/kg ip) antagonized this anorectic effect of CCK-8. WAY-100135 on its own did not affect food intake. These results suggest the involvement of the 5-HT_1A receptor subtype in mediating 5-HT-CCK interactions in the control of food intake in rats.     

A new paradigm for alcohol use in older persons

BACKGROUND: Current paradigms for conceptualizing alcohol-related problems typically focus on persons who are abusing or dependent on alcohol. These paradigms may not apply to older drinkers whose alcohol use, regardless of consumption-level, can cause problems because of age-related changes in physiology and interactions with increased morbidity, medication use, and functional limitations. OBJECTIVE: We convened an expert panel# to develop clinical indications of harmful, hazardous, and nonhazardous drinking in persons 65 years of age and older. RESEARCH DESIGN AND SUBJECTS: Nine panelists with expertise in psychiatry, geriatrics, internal medicine, and alcohol research were provided with epidemiological data and a published explicit literature review of alcohol use in the elderly. The RAND/UCLA two-round panel method was used to develop the indications. After the second round, the authors wrote a draft statement that was circulated to the panelists whose comments were incorporated into a final document. RESULTS: Panelists agreed on 215 scenarios in which older peoples' use of alcohol either alone or in the presence of chronic medical conditions, medication use, symptoms, smoking, and functional limitations are hazardous or harmful. Panelists' ratings of risk did not differ significantly between persons aged 65 to 74 years and those aged 75 years and older. CONCLUSION: Alcohol use may be hazardous or harmful for older persons, particularly in conjunction with physical or emotional illnesses, medication use, functional limitations, smoking, and driving after drinking. When asking about alcohol use in older persons, clinicians need to be aware of these factors to assist in identifying and managing potential or actual alcohol-related problems.     

(+)-alpha-[11C]Dihydrotetrabenazine PET imaging in familial paroxysmal dystonic choreoathetosis

Clinical observations suggest a disturbance of striatal dopaminergic function in familial paroxysmal dystonic choreoathetosis (PDC). The authors used PET with [11C]dihydrotetrabenazine (DTBZ) to study striatal dopaminergic innervation in PDC. The results did not reveal abnormal DTBZ binding potential in PDC striatum. This suggests that dopaminergic abnormalities, if present, may be due to altered regulation of dopamine release or to postsynaptic mechanisms, rather than to an altered density of nigrostriatal innervation.     

Screening for somatization and hypochondriasis in primary care and neurological in-patients: a seven-item scale for hypochondriasis and somatization

The aim of this study was to investigate the internal and external validity of the Whiteley Index as a screening instrument for somatization illness. A 14-item version of the Whiteley Index for hypochondriacal traits was given to 99 of 191 consecutive primary care patients, aged 18-65 years, and to 100 consecutive patients, aged 18-60 years, admitted for the first time to a neurological ward. The primary care sample was, in addition, interviewed by means of the SCAN (Schedules for Clinical Assessment in Neuropsychiatry) psychiatric interview. The GPs and the neurologists were asked to rate various characteristics of the patients that might indicate somatization. The internal validity of the Whiteley Index was tested by means of latent structure analysis. On this basis, a reduced seven-item scale (Whiteley-7 scale) and two subscales (i.e., an Illness Conviction and Illness Worrying scale, each with three items) were constructed. All three had a high internal validity fitting into the very restricted Rasch statistical model (p>0.05) and an acceptable transferability between most of the subpopulations investigated. In the primary care population, the Whiteley-7 and the Illness Conviction scales at cut-point 0/1 showed 1.00 and 0.87 sensitivity and 0.65 and 0.87 specificity, respectively, using as "gold standard" the fulfillment of criteria for at least one ICD-10 somatoform disorder, and 0.71 and 0.63 sensitivity and 0.62 and 0.87 specificity, respectively, as gold standard for the fulfillment of criteria for at least one DSM-IV somatoform disorder, excluding the NOS diagnostic group. The Illness Worrying subscale showed less impressive performance in this respect. The agreement between the Whiteley-7 scale including the two subscales and neurologists' rating and the GPs' rating and the somatization subscale on the SCL-90 was modest or worse. It may be concluded that the Whiteley-7 scale and the Illness Conviction subscale had acceptable psychometric profiles, and both seem to be promising screening tools for not only hypochondriasis but also for somatoform disorders in general.     

Diagnosis and treatment of Wilson's disease

Wilson's disease is due to an inherited defect in copper excretion into the bile by the liver. The resulting copper accumulation and copper toxicity results in liver disease, and in some patients, brain damage. Patients present, generally between the ages of 10 and 40 years, with liver disease, neurological disease of a movement disorder type, or behavioral abnormalities, and often with a combination of these. Because Wilson's disease is effectively treated, it is extremely important for physicians to learn to recognize and diagnose the disease. Treatment options have evolved rapidly in the last few years, with zinc now being the drug of choice in most situations.