RESUMEN
RATIONALE: Neuroleptic malignant syndrome (NMS) is a life threatening neurologic emergency associated with neuroleptic or antipsychotic agent use. NMS is rarely related to thyroid disease. PATIENT CONCERNS: We report a case of NMS in a 66-year-old male with past medical history of paranoid schizophrenia on chlorpromazine, diabetes, hypertension and asthma, who presented with a humeral fracture after a fall. Patient developed hyperpyrexia, altered consciousness, autonomic instability, elevated serum creatine kinase (CK) without rigidity. DIAGNOSES: CT head and workup for infection were negative. Electroencephalogram (EEG) showed generalized slow wave activity. Ultrasound revealed a large goiter with nodules. INTERVENTIONS: Chlorpromazine was stopped due to concern of NMS. Patient was treated with cooling, fluid and electrolyte maintenance. OUTCOMES: Patient slowly improved and CK level normalized. Thyroid-stimulating hormone (TSH) level trended down from 10.2âmIU/L to 0.02âmIU/L. Patient was discharged with aripiprazole. LESSONS: Hypothyroidism predisposes patients to NMS by altering central dopaminergic systems. The typical symptoms may be masked by hypothyroidism. Thyroid dysfunction should be excluded in all patients with NMS. Discontinuing antipsychotic agents decreases TSH levels which maybe due to the negative feedback of dopaminergic activity. This is the first case report describing dramatic changes in TSH after discontinuing chlorpromazine in NMS.
Asunto(s)
Aripiprazol , Clorpromazina , Hipotiroidismo , Síndrome Neuroléptico Maligno , Esquizofrenia Paranoide , Nódulo Tiroideo/diagnóstico por imagen , Anciano , Antipsicóticos/administración & dosificación , Antipsicóticos/efectos adversos , Aripiprazol/administración & dosificación , Aripiprazol/efectos adversos , Clorpromazina/administración & dosificación , Clorpromazina/efectos adversos , Creatina Quinasa/análisis , Diagnóstico Diferencial , Sustitución de Medicamentos/métodos , Fluidoterapia/métodos , Humanos , Hipotiroidismo/complicaciones , Hipotiroidismo/diagnóstico , Hipotiroidismo/terapia , Masculino , Síndrome Neuroléptico Maligno/diagnóstico , Síndrome Neuroléptico Maligno/etiología , Síndrome Neuroléptico Maligno/fisiopatología , Síndrome Neuroléptico Maligno/terapia , Esquizofrenia Paranoide/complicaciones , Esquizofrenia Paranoide/tratamiento farmacológico , Tirotropina/análisis , Resultado del TratamientoRESUMEN
Photoswitching in densely packed azobenzene self-assembled monolayers (SAMs) is strongly affected by steric constraints and excitonic coupling between neighboring chromophores. Therefore, control of the chromophore density is essential for enhancing and manipulating the photoisomerization yield. We systematically compare two methods to achieve this goal: First, we assemble monocomponent azobenzene-alkanethiolate SAMs on gold nanoparticles of varying size. Second, we form mixed SAMs of azobenzene-alkanethiolates and "dummy" alkanethiolates on planar substrates. Both methods lead to a gradual decrease of the chromophore density and enable efficient photoswitching with low-power light sources. X-ray spectroscopy reveals that coadsorption from solution yields mixtures with tunable composition. The orientation of the chromophores with respect to the surface normal changes from a tilted to an upright position with increasing azobenzene density. For both systems, optical spectroscopy reveals a pronounced excitonic shift that increases with the chromophore density. In spite of exciting the optical transition of the monomer, the main spectral change in mixed SAMs occurs in the excitonic band. In addition, the photoisomerization yield decreases only slightly by increasing the azobenzene-alkanethiolate density, and we observed photoswitching even with minor dilutions. Unlike in solution, azobenzene in the planar SAM can be switched back almost completely by optical excitation from the cis to the original trans state within a short time scale. These observations indicate cooperativity in the photoswitching process of mixed SAMs.
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We show that diamagnetic particles can be remotely manipulated by a magnet by the reversible adsorption of dual-responsive, light-switchable/superparamagnetic nanoparticles down to their surface. Adsorption occurs upon exposure to UV light, and can be reversed thermally or by ambient light. The dynamic self-assembly of thin films of the dual-responsive nanoparticles induces attractive interactions between diamagnetic particles. We demonstrate that catalytic amounts of the dual-responsive nanoparticles are sufficient to magnetically guide and deliver the diamagnetic particles to desired locations, where they can then be released by disassembling the dynamic layers of superparamagnetic nanoparticles with visible light.
Asunto(s)
Compuestos Azo/química , Compuestos Férricos/química , Magnetismo , Nanopartículas/química , Adsorción , Rayos UltravioletaRESUMEN
Obesity is a chronic medical condition that is expected to become an indirect but leading cause of mortality and morbidity. Obesity results in type 2 diabetes mellitus, insulin resistance, hypertension, dyslipidemia, coronary heart disease. These factors contribute to cardiovascular disease that is a leading cause of death. Therefore, the approach to obesity therapy should be designed to reduce cardiovascular disease risk and mortality. Diet and lifestyle changes remain the cornerstones of therapy for obesity, but the resultant weight loss is often small. For more effective weight loss, individuals have shown to benefit from anti-obesity medications. Anti-Obesity therapy is considered for individuals with a body mass index greater than 30 kg/m2 or ranging from 25 to 30 kg/m2, or individuals with co-morbid conditions. Recent anti-obese medications affect biological mechanisms that suppress appetite and absorb nutrients to regulate body weight. In this review, we discuss the FDA approved anti-obesity drugs and recent patents which include phentermine/topiramate, pramlintide, lorcaserin, AOD9604, oleoyl-estrone, trk-beta antagonists and melanin concentrating hormone that can reduce adiposity at the molecular level.