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INTRODUCTION: The number of nontraumatic dental pain emergency department (ED) visits continues to substantially rise in frequency every year. While there are several methods for treating dental pain, an inferior alveolar nerve block (IANB) is a non-narcotic alternative that provides instantaneous relief of severe pain. CASE REPORT: A 59-year-old male presented to the ED from a dentist's office for evaluation of a right-sided headache with an associated episode of palpitations and near syncope that developed while receiving an inferior alveolar nerve block. Computed tomography of the patient's head revealed multiple small foci of air in the right temporalis muscle and in the intracranial venous drainage system. Given the patient's history of dental procedure, the intravascular introduction of air and local anesthetic was suspected. CONCLUSION: Inferior alveolar nerve block procedures can have complications, including hematoma formation, trismus, facial palsy, needle breakage, and in this case, intravascular injection and cerebral air embolism. To perform a successful IANB, it is critical for providers to be familiar with anatomical landmarks and to consistently perform aspiration to confirm that needle placement is not intravascular.
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The chemokine CCL27 has chemoattractant properties for memory T cells and has been implicated in skin allergic reactions. The present study reports the expression in the brain of two CCL27 splice variants localized in the cerebral cortex and limbic regions. CCL27-like immunoreactivity was identified mainly in neurons. Variant 1 was found elevated in the olfactory bulbs during allergic inflammation induced by intranasal challenge with allergen. This was accompanied by the presence of T cells in the olfactory bulbs. Intranasal administration of neutralizing antibodies against CCL27 reduced the presence of T cells in the olfactory bulbs suggesting a function in T cell activity in the brain.
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Encéfalo/metabolismo , Quimiocina CCL27/genética , Quimiocina CCL27/metabolismo , Regulación de la Expresión Génica/inmunología , Albúminas/efectos adversos , Albúminas/inmunología , Análisis de Varianza , Animales , Autorradiografía/métodos , Encéfalo/anatomía & histología , Encéfalo/citología , Complejo CD3/metabolismo , Recuento de Células/métodos , Hipersensibilidad/inmunología , Hipersensibilidad/metabolismo , Masculino , Ratones , Ratones Endogámicos BALB C , Neuronas/metabolismo , Isoformas de Proteínas/genética , ARN Mensajero/metabolismoRESUMEN
BACKGROUND: Interleukin 4 (IL-4) has been shown to suppress interleukin-1 (IL-1) induced expression of matrix metalloproteinase-3 (MMP-3) in human synovial and gingival fibroblasts, but the mechanism of suppression has not been determined. Activators of peroxisome proliferator-activated receptor-gamma (PPARgamma) have been shown to inhibit cytokine induced expression of MMPs in other cell types, and IL-4 has been shown to activate PPARgamma by stimulating production of ligands through the lipoxygenase pathway. It has been suggested that PPARgamma may inhibit expression of MMPs by competing with transcription factor AP-1 for binding to a putative composite binding element in the promoters. The objective of this study was to determine whether the suppressive effects of IL-4 on the IL-1 induced expression of MMP-3 involve activation of lipoxygenase and/or PPARgamma. RESULTS: Western blotting revealed the presence of PPARgamma in nuclear extract of HGF. IL-1 induced binding of nuclear extract to the putative composite PPRE/AP-1 site was diminished in the presence of pioglitazone, but there was no evidence of any change in the composition of the retarded complexes, and no evidence of PPARgamma binding to this site. Nordihydroguaiaretic acid (NDGA), a non-selective lipoxygenase inhibitor, and MK886, a specific inhibitor of 5-lipoxygenase, induced MMP-3 expression synergistically with IL-1. However IL-4 was still able to inhibit MMP-3 expression in the presence of NDGA or MK886 and IL-1. Activation of PPARgamma with pioglitazone not only failed to inhibit IL-1 induced expression of MMP-3 mRNA, but rather super-induced MMP-3 in the presence of IL-1. PPARgamma antagonist GW9662 failed to abolish the suppressive effects of IL-4. Another PPARgamma activator, 15-deoxy-Delta12,14prostaglandin J2 (15dPGJ2), also super-induced MMP-3 mRNA, and this was due at least in part to increased transcription. CONCLUSION: IL-4 suppression of IL-1-induced MMP-3 expression in HGF is independent of lipoxygenase activity and activation of PPARgamma. Super-induction of MMP-3 by pioglitazone may have important implications for patients using pioglitazone to treat type II diabetes in the presence of chronic inflammation.
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Encía/metabolismo , Interleucina-1/metabolismo , Interleucina-4/farmacología , Lipooxigenasa/metabolismo , Metaloproteinasa 3 de la Matriz/metabolismo , PPAR gamma/metabolismo , Sitios de Unión , Núcleo Celular/metabolismo , Células Cultivadas , Activación Enzimática , Fibroblastos/enzimología , Fibroblastos/metabolismo , Encía/citología , Encía/enzimología , Humanos , Metaloproteinasa 3 de la Matriz/genética , Pioglitazona , Regiones Promotoras Genéticas , ARN Mensajero/metabolismo , Tiazolidinedionas/farmacología , Factor de Transcripción AP-1/genética , TransfecciónRESUMEN
The expression of pro-thyrotropin-releasing hormone (pro-TRH) mRNA was analyzed in the hypothalamus of inflammatory susceptible LEW/N and resistant F344/N rats at baseline and in adrenalectomized and lipopolysaccharide-treated animals. In saline-treated control animals, increased pro-TRH transcription was detected in LEW/N with respect to F344/N rats. This increased LEW/N pro-TRH expression was stable regardless of condition in contrast to F344/N increased pro-TRH transcription post-adrenalectomy and decreased pro-TRH after lipopolysaccharide administration. The LEW/N increase in pro-TRH mRNA was independent of changes in hormonal status suggesting alteration of the thyroid axis at the central level in this strain.