Asunto(s)
Neoplasias de la Mama/genética , Neoplasias de la Mama/terapia , Biología Computacional/tendencias , Medicina de Precisión/tendencias , Adulto , Neoplasias de la Mama/clasificación , Análisis Mutacional de ADN , Bases de Datos Factuales , Conjuntos de Datos como Asunto , Femenino , Regulación Neoplásica de la Expresión Génica/genética , Genoma Humano/genética , Humanos , Menopausia/genéticaAsunto(s)
Anuros , Conservación de los Recursos Naturales , Animales , Monitoreo del Ambiente , Maine , HumedalesAsunto(s)
Alopecia/terapia , Descubrimiento de Drogas , Cabello/crecimiento & desarrollo , Biotecnología , Ensayos Clínicos Fase II como Asunto , Cabello/citología , Humanos , Células Madre/metabolismo , Estados Unidos , United States Food and Drug Administration , Proteínas Wnt/genética , Proteínas Wnt/metabolismoRESUMEN
Athletes take anabolic steroids to increase strength, build muscle, and improve performance, even though the practice is banned by many athletic organizations and can cause serious adverse effects. State and federal laws regulate the sale and distribution of anabolic steroids to restrict their use, and yet, the Internet has become a world-flattening promoter of easy access to the drugs. While scientists continue to study the potential therapeutic and toxic effects of steroid drugs, prosecutors endeavor to uphold the laws in the slippery online environment. Here's the story of Albany County District Attorney's Office efforts to prosecute illegal online drug sales in 2000s. The discoveries of prosecutors and scientists alike should help inform policy makers of how best to manage the problem that anabolic steroids present to society.
Asunto(s)
Anabolizantes/administración & dosificación , Atletas/legislación & jurisprudencia , Comercio/legislación & jurisprudencia , Doping en los Deportes/legislación & jurisprudencia , Internet , Automedicación/métodos , Adolescente , Adulto , Anabolizantes/toxicidad , Doping en los Deportes/prevención & control , Femenino , Humanos , Masculino , New York , Adulto JovenAsunto(s)
Antihipertensivos , Biotecnología/tendencias , Industria Farmacéutica/tendencias , Hipertensión/terapia , Sistema Renina-Angiotensina/inmunología , Vacunas , Anticuerpos/sangre , Antihipertensivos/efectos adversos , Antihipertensivos/inmunología , Antihipertensivos/uso terapéutico , Biotecnología/economía , Industria Farmacéutica/economía , Humanos , Hipertensión/inmunología , Vacunas/administración & dosificación , Vacunas/efectos adversos , Vacunas/inmunologíaRESUMEN
Phospholipase A2 (PLA(2)) activation generates the release of arachidonic acid (AA) and platelet-activating factor (PAF), two compounds which may be involved in neuroplasticity. In previous studies, we found that PLA(2) activation is involved in the development of stimulant sensitization. In the present study, we have examined the roles of AA and PAF in the development of stimulant sensitization using agonists and antagonists selective for PAF receptors or the induction of various AA cascade-mediated eicosanoids. Sprague-Dawley rats were treated for 5 days with cocaine (30 mg/kg) or D-amphetamine (1 mg/kg) preceded 15 min earlier by various antagonists, and then tested following a 10-day withdrawal period for cocaine (15 mg/kg) or D-amphetamine (0.5 mg/kg)-induced locomotion. Consistent with our earlier work, pretreatment with the PLA(2) inhibitor quinacrine (25 mg/kg) blocked the development of cocaine and amphetamine sensitization. The lipoxygenase (LOX) inhibitors nordihydroguaiaretic acid (NDGA) (5-10 mg/kg) and MK-886 (1 mg/kg) had no effect on cocaine sensitization. The PAF receptor antagonist WEB 2086 (5-10 mg/kg) reduced the development of cocaine sensitization. The cyclooxygenase (COX) inhibitors indomethacin (1-2 mg/kg), piroxicam (0.5-1 mg/kg), 6-methoxy-2-napthylacetic acid (6-MNA; 0.5-1 mg/kg), and NS-398 (0.5-1 mg/kg) blocked the development of cocaine sensitization. The COX inhibitors indomethacin (2 mg/kg) and 6-MNA (1 mg/kg) also reduced the development of amphetamine sensitization. Rats were administered bilateral intraventral tegmental area (VTA) injections of D-amphetamine (5 microg/side) or saline coadministered with indomethacin (0.5 microg/side) or vehicle three times over 5 days and were then tested after a 10-day withdrawal for D-amphetamine (0.5 mg/kg ip)-induced locomotion. Intra-VTA amphetamine induced a robust form of amphetamine sensitization, which was blocked by coadministration of indomethacin. Unilateral intra-VTA injections of PAF (1 microg) did not significantly alter cocaine (15 mg/kg ip)-induced locomotion when tested after a 3-day withdrawal. These findings suggest that COX, and possibly PAF, activity is involved in the development of stimulant sensitization. Neuroanatomical studies demonstrate that this may occur at the level of the VTA.