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Houston, TX, United States

Narang S.,UTHSC Houston | Clarke J.,University of Texas Health Science Center at San Antonio
Journal of Child Neurology

Abusive head trauma has a robust and interesting scientific history. Recently, the American Academy of Pediatrics has endorsed a change in terminology to a term that is more general in describing the vast array of abusive mechanisms that can result in pediatric head injury. Simply defined, abusive head trauma is "child physical abuse that results in injury to the head or brain." Abusive head trauma is a relatively common cause of childhood neurotrauma, with an estimated incidence of 16 to 33 cases per 100 000 children per year in the first 2 years of life. Clinical findings are variable; AHT should be considered in all children with neurologic signs and symptoms, especially if no or only mild trauma is described. Subdural and retinal hemorrhages are the most common findings. The current best evidence-based literature has identified some features-apnea and severe retinal hemorrhages-that reliably discriminate abusive from accidental injury. Longitudinal studies of outcomes in abusive head trauma patients demonstrate that approximately one-third of the children are severely disabled, one third of them are moderately disabled, and one third have no or only mild symptoms. Abusive head trauma cases are complex cases that require a rigorous, multidisciplinary team approach. The clinician can establish this diagnosis with confidence if he/she maintains a high index of suspicion for the diagnosis, has knowledge of the signs, symptoms, and risk factors of abusive head trauma, and reasonably excludes other etiologies on the differential diagnosis. © The Author(s) 2014. Source

Faro S.,UTHSC Houston | Faro J.P.,UTHSC Houston
Clinical Obstetrics and Gynecology

For the clinician, necrotizing soft-tissue infections have remained a daunting opponent since the first writings on the subject over 2000 years ago. Early disease may be incorrectly diagnosed as cellulitis, and this delay in correctly diagnosing and expeditiously proceeding to radical surgical debridement may lead to a high degree of mortality. Although several inciting events and risk factors have been described that allow for the development and progression of this disease, the diagnosis is still made clinically. Only aggressive surgical management in combination with broad-spectrum antibiotics will offer a chance at improving patient outcomes. © 2012, Lippincott Williams & Wilkins. Source

Cao Y.,UTHSC Houston | Cao Y.,University of Texas Health Science Center at Houston | Yang W.,UTHSC Houston | Tyler M.A.,UTHSC Houston | And 12 more authors.

Objective: To investigate the role of bone morphogenetic protein (BMP) signaling in acute pancreatitis (AP) by administration of noggin, an endogenous BMP antagonist, in a cerulein-induced AP model. METHODS: Acute pancreatitis was induced by 9 hourly intraperitoneal injections of cerulein (50 μg/kg). Control mice received phosphate-buffered saline injections. In a separate group, noggin (0.5 mg/kg) was given intraperitoneally at 1 hour before and 2, 4, and 6 hours after AP induction. The mice were euthanized at 1 hour after completion of AP induction. The blood samples and the pancreas were harvested for analysis. Isolated pancreatic acini from normal mice and AR42J cells were treated with BMP2 and cerulein. AR42J cells were also treated with noggin. Phosphorylation of Smad1/5/8 was measured. RESULTS: Bone morphogenetic protein signaling was up-regulated in AP mouse pancreas. Bone morphogenetic protein 2 and cerulein-induced phosphorylation of Smad1/5/8 in the acinar cells in vitro, which was blocked by noggin.Noggin administration in vivo attenuated AP induction, decreased vacuole formation in acinar cells, blocked LC3-II levels, and partially restored Beclin-1 and lysosomal-associated membrane protein 2 levels. CONCLUSIONS: Bone morphogenetic protein signaling seems to promote AP induction and autophagy, as suggested by our study showing that noggin ameliorates AP and partially restores autophagic homeostasis. Copyright © 2013 Lippincott Williams & Wilkins. Source

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