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1.
Clinical Pain ; (2): 36-39, 2019.
Artículo en Coreano | WPRIM | ID: wpr-785682

RESUMEN

Chronic postoperative inguinal pain (CPIP) is a major complication after inguinal herniorrhaphy. We report the treatment of CPIP using ultrasonography-combined with nerve stimulator for injection of the genitofemoral nerve (GFN). A 59-year-old man underwent laparoscopic herniorrhaphy and presented with numbness from the inguinal region to the scrotum after operation. In the pain clinic, ultrasonography-guided GFN block and pharmacological treatments had little effect. Six month after operation, patient was referred to the Department of Physical Medicine and Rehabilitation, and ultrasonography-combined with nerve stimulator for GFN injection underwent to enhance the accuracy of neural approach. The induction of scrotal contraction and paresthesia on the GFN distribution was monitored by nerve stimulator and local anesthetic was injected. After the block, pain relief lasted for 6 months without analgesic use. Ultrasonography-combined with nerve stimulator is an effective approach to treat CPIP as it enhances precise localization and injection of small peripheral nerve like GFN.


Asunto(s)
Humanos , Persona de Mediana Edad , Herniorrafia , Hipoestesia , Clínicas de Dolor , Parestesia , Nervios Periféricos , Medicina Física y Rehabilitación , Escroto
2.
Brain & Neurorehabilitation ; : e14-2018.
Artículo en Inglés | WPRIM | ID: wpr-716985

RESUMEN

We report a case of bilateral perisylvian polymicrogyria, which was evaluated using diffusion tensor imaging (DTI) and tractography. On DTI tractography, fibers of the arcuate fasciculus (AF), which connects the posterior inferior frontal region and superior temporal gyrus were absent. It indicates that in cases of bilateral perisylvian polymicrogyria, compromised language skills might be associated with the absence of AF.


Asunto(s)
Niño , Humanos , Imagen de Difusión Tensora , Polimicrogiria , Lóbulo Temporal
3.
Experimental & Molecular Medicine ; : e23-2013.
Artículo en Inglés | WPRIM | ID: wpr-159138

RESUMEN

Recent studies have documented that Janus-activated kinase (JAK)-signal transducer and activator of transcription (STAT) pathway can modulate the apoptotic program in a myocardial ischemia/reperfusion (I/R) model. To date, however, limited studies have examined the role of JAK3 on myocardial I/R injury. Here, we investigated the potential effects of pharmacological JAK3 inhibition with JANEX-1 in a myocardial I/R model. Mice were subjected to 45 min of ischemia followed by varying periods of reperfusion. JANEX-1 was injected 1 h before ischemia by intraperitoneal injection. Treatment with JANEX-1 significantly decreased plasma creatine kinase and lactate dehydrogenase activities, reduced infarct size, reversed I/R-induced functional deterioration of the myocardium and reduced myocardial apoptosis. Histological analysis revealed an increase in neutrophil and macrophage infiltration within the infarcted area, which was markedly reduced by JANEX-1 treatment. In parallel, in in vitro studies where neutrophils and macrophages were treated with JANEX-1 or isolated from JAK3 knockout mice, there was an impairment in the migration potential toward interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1), respectively. Of note, however, JANEX-1 did not affect the expression of IL-8 and MCP-1 in the myocardium. The pharmacological inhibition of JAK3 might represent an effective approach to reduce inflammation-mediated apoptotic damage initiated by myocardial I/R injury.


Asunto(s)
Animales , Masculino , Ratones , Apoptosis/efectos de los fármacos , Movimiento Celular/efectos de los fármacos , Quimiocinas/farmacología , Pruebas de Función Cardíaca/efectos de los fármacos , Inflamación/patología , Janus Quinasa 3/antagonistas & inhibidores , Macrófagos/efectos de los fármacos , Ratones Endogámicos C57BL , Daño por Reperfusión Miocárdica/tratamiento farmacológico , Miocardio/enzimología , Miocitos Cardíacos/efectos de los fármacos , Neutrófilos/efectos de los fármacos , Quinazolinas/farmacología
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