‘Sex’ – it’s not only women’s work: a case for refocusing on the functional role that sex plays in work for both women and men

Mention of the term sex work often invokes images of marginalized women at risk for HIV infection. Such images, however, are counterintuitive to the functional role intended by the movement that spawned use of the terms ‘sex work’ and ‘sex worker.’ This article looks at the sexual practices of men in urban China to argue for a return to a functional definition of ‘sex work’, which was originally meant to legitimize the role sex plays in work. The progenitors of this movement intended to use ‘sex work’ as a means to legitimize sex as an income-generating activity for women involved in prostitution. I show that sex can also serve a functional role in the work-related duties of men seeking economic and political success in contemporary urban China. Men in China utilize sex as one way for demonstrating the loyalty necessary to access state-owned and controlled resources in a market economy governed under a Leninist system. Overall, the article demonstrates that reclaiming perception of sex work as a functional rather than behavioral category can expand its use for preventing HIV among the broad subset of people who engage in sex as part of their work.     

Interaction of permanently charged chlorpromazine and dopamine analogs with the striatal D-1 dopaminergic receptor

Although a structural feature common to all dopaminergic agonists and antagonists is a side-chain basic amino group, it is unclear whether this moiety binds to the D-1 dopamine (DA) receptor in the charged or uncharged form. To obtain information on this point, we synthesized permanently charged dimethylsulfonium and quaternary ammonium analogs of chlorpromazine and DA and determined whether these compounds can bind to the D-1 receptor by measuring their abilities to inhibit the binding of SCH 23390, a D-1 receptor antagonist. Chlorpromazine and the dimethylsulfonium and trimethylammonium analogs of chlorpromazine were found to inhibit the binding of [3H]SCH 22390, which was maximally inhibited to the same extent by all three compounds. In addition, inhibition curves for the compounds fit a one-site binding model, indicating binding to a single class of sites. However, while the permanently charged chlorpromazine analogs were able to inhibit [3H]SCH-23390 binding, they were considerably less potent than chlorpromazine. DA and dimethyl DA were also able to inhibit [3H]SCH 23390 binding. However, the permanently charged dimethylsulfonium and trimethylammonium analogs of DA were ineffective in inhibiting [3H]SCH 23390 binding. In addition, the permanently uncharged methylsulfide analog did not inhibit binding. These studies show that permanently charged analogs of chlorpromazine can bind to the striatal D-1 receptor, which is consistent with an anionic recognition site on the D-1 receptor that interacts with antagonists in the cationic form. In addition, it appears that a nitrogen atom is not required for binding to the D-1 receptor, since the sulfonium analog of chlorpromazine bound to the receptor to the same extent as chlorpromazine. However, since the permanently charged or uncharged analogs of DA did not bind to the D-1 receptor, it is still unclear as to whether the charged form of a dopaminergic agonist can bind. The lower potency or ineffectiveness of the permanently charged analogs compared to the parent amines (chlorpromazine, DA, dimethyl DA) in binding to the D-1 receptor may reflect the inability of the permanently charged analogs to undergo hydrogen binding with the anionic site of the receptor.     

Primary Prevention of Sudden Cardiac Death in Heart Failure: Will the Solution Be Shocking?

Sudden cardiac death (SCD) may occur in as many as 40% of all patients who suffer from heart failure. This review describes the scope of the problem, risk factors for SCD, the effect of medications used in heart failure on SCD and the potential effect of the implantable cardioverter-defibrillator in primary prevention.     

Antagonism of the hypermotility response induced by excitatory amino acids in the rat nucleus accumbens

Summary Several compounds have been shown to antagonize the excitation of single neurons produced by excitatory amino acids. This study was designed to determine the effectiveness of these compounds in antagonizing the hypermotility response to excitatory amino acids after intraaccumbens administration. Of the putative antagonists tested, D-aminoadipic acid, diaminopimelic acid and glutamic acid diethyl ester all showed significant inhibitory effects on excitatory amino acid-induced hypermotility while 2-amino-5-phosphonovaleric acid, -D-glutamylglycine, 2-amino-4-phosphonobutyric acid and cis-2,3-piperidine dicarboxylic acid were ineffective. D-Aminoadipic acid decreased N-methyl-aspartic acid-induced hypermotility while having no significant effect on the hypermotility responses induced by kainic or quisqualic acids. Diaminopimelic acid markedly decreased N-methyl-aspartic acid- and kainic acid-induced hypermotility but was totally ineffective on quisqualic acid-induced hypermotility. In contrast to D-aminoadipic acid, glutamic acid diethyl ester antagonized the increase in motility produced by kainic and quisqualic acids but not that produced by N-methyl-aspartic acid. The above data suggests that N-methyl-aspartic acid and quisqualic acid may produce their motor effects through the activation of two different receptors in the nucleus accumbens while kainic acid may mediate its hypermotility response through both N-methyl-aspartic acid and quisqualic acid receptors. However, a third receptor type activated solely by kainic acid cannot be excluded at this time.     

Sensitization of stereotyped behavior to amphetamine is context and response dependent.

The present study was designed to determine whether the environmental context in which amphetamine is administered plays a role in the development of sensitization to the stereotyped behavioral effects of amphetamine in mice. In male CF-1 mice, the dose-response curve for stereotyped behavior elicited by amphetamine was shifted 1.9-fold to the left 48 h after pretreatment with 14 mg/kg amphetamine. Behavioral sensitization only developed in mice that were pretreated in the same or a similar environment as that of the test environment. In addition, when mice were placed in an environment that attenuated the acute expression of stereotyped behavior elicited by the pretreatment dose of amphetamine, sensitization never developed. A further experiment showed that 96% of the mice that expressed stereotypy after the ED50 pretreatment dose of 10 mg/kg amphetamine showed a stereotyped behavioral response to the lesser dose of 7 mg/kg 48 h later, indicating sensitization. In contrast, mice that did not express stereotypy after the ED50 dose of amphetamine failed to show a significant stereotyped behavioral response to amphetamine challenge compared to vehicle-pretreated controls. Therefore, the results indicate that preexposure to a single high dose of amphetamine produces context- and response-dependent sensitization to amphetamine-induced stereotyped behavior.     

Effects of morphine in the nucleus accumbens on stimulant-induced locomotion.

This study assessed the effects of morphine in the nucleus accumbens on motility elicited by dopaminergic and other classes of drugs, using locomotor activity as the measured response. Dopaminergic stimulants, d-amphetamine (10 micrograms) or dopamine (20 micrograms, 2 hours after nialamide, 200 mg/kg, IP) induced large increases in locomotor activity when injected into the nucleus accumbens. This response was blocked by coadministration of morphine (5 micrograms). The hypermotility response elicited by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA; 0.5 micrograms), an excitatory amino acid agonist, was also abolished by coadministration of morphine. Increasing the dose of AMPA to 1.5 micrograms partially overcame the morphine block, while increasing the dose of amphetamine to 50 micrograms did not. In other experiments, morphine (5 micrograms) injected into the nucleus accumbens blocked the hypermotility elicited by systemic caffeine (10 mg/kg, SC) or scopolamine (0.5 mg/kg, SC) or intra-accumbal MK-801 (5 micrograms). However, picrotoxin (0.15 or 0.5 microgram) injected into the nucleus accumbens elicited a hypermotility that was not attenuated by coinjection of morphine (5 or 10 micrograms). These data demonstrate that opiate and dopaminergic pathways have competing actions on the regulation of locomotion in the nucleus accumbens. Furthermore, the results with combinations of picrotoxin and morphine suggest the presence of two distinct locomotor pathways or a GABA receptor site "downstream" from the morphine site in a single pathway.     

Effects of acute alterations in left ventricular loading conditions on peak filling rate in the denervated (transplanted) ventricle

Peak filling rate is an indicator of left ventricular (LV) diastolic function. It is influenced by heart rate, loading conditions, sympathetic nervous system activity, ejection fraction and other factors. To determine the effect of altered loading conditions on peak filling rate, independent of heart rate and sympathetic nervous system activity, 12 patients were studied 3 weeks after orthotopic heart transplantation. Plasma catecholamine level, heart rate and ejection fraction were not changed by any maneuver. Nitroglycerin caused a decrease in pulmonary artery wedge pressure (9 +/- 2 to 6 +/- 1 mm Hg, p less than 0.001) and in absolute peak filling rate (46.0 +/- 3.0 to 42.8 +/- 2.5 kcts/s, p less than 0.01), but no change in normalized peak filling rate. Volume infusion increased pulmonary artery wedge pressure (9 +/- 2 to 12 +/- 2 mm Hg, p less than 0.001) and absolute peak filling rate (46.0 +/- 3.0 to 51.5 +/- 5.3 kcts/s, p less than 0.01), but peak filling rate normalized to stroke volume was unchanged. During nitroglycerin and volume infusions, there was a high correlation between changes in pulmonary artery wedge pressure and absolute peak filling rate (r = 0.82, p less than 0.001). With normalization of peak filling rate, these variables correlated less well. With methoxamine, 4 patients demonstrating systolic dysfunction had a decrease in absolute and normalized peak filling rate despite a large increase in pulmonary artery wedge pressure. The other 8 patients without systolic dysfunction had an increase in pulmonary artery wedge pressure with increased absolute but unchanged normalized peak filling rate.(ABSTRACT TRUNCATED AT 250 WORDS)