Testicular torsion represents a continuing source of morbidity among male patients. Early diagnosis and surgical exploration improve testis salvage but even this approach will result in orchiectomy if there is excessive delay in patient presentation. A 10-year retrospective review of testicular torsion was performed. The interval between onset of scrotal pain and presentation to the emergency department was determined. A specific age-related delay in presentation was identified between patients less than 18 years old (group 1, median delay 20 hours) and those greater than 18 years old (group 2, median delay 4 hours, p less than 0.001). At exploration 44 per cent of the group 1 patients required orchiectomy versus 8 per cent in group 2. Patients less than 18 years old are a high risk group for testicular loss after torsion and represent more than 90 per cent of the orchiectomies performed. We believe that this group should be targeted for improved health education, emphasizing early evaluation of scrotal pain to improve testicular salvage.

No abstract

Excitatory amino acid receptor activation and reactive oxygen species production are important mediators of neuronal death following acute brain injury and can lead to loss of membrane integrity. Poloxamer 188 (P188) is an amphiphilic, polyethylene-polypropylene-polyethylene copolymer that restores plasma membrane integrity of nonneuronal cells following membrane injury. Here, we demonstrate that P188 provides profound protection of hippocampal and cerebellar neurons following severe excitotoxic and oxidative injury in vitro, through membranetargeted mechanisms. Widespread death of cultured hippocampal neurons observed 48 h after Nmethyl-D-aspartate (NMDA) exposure was prevented by incubation of neurons in P188 following NMDA. P188 provided similar neuroprotection from kainate, menadione, and tertbutyl-hydroperoxide, but not from staurosporine. P188 application did not alter either NMDA receptor function or NMDA-induced [Ca 2+ ] i increases. Whole-cell capacitance measurements revealed that P188 application increased cell surface area, consistent with its insertion into the plasma membrane. Following plasma membrane electroporation, P188 arrested loss of intracellular contents, which demonstrated direct restoration of plasma membrane integrity following physical disruption. Measurements of oxidized C11-BODIPY 581/591 fluorescence demonstrated that P188 blocked lipid peroxidation. These observations demonstrate that amphiphilic tri-block copolymers provide strong, membrane-targeted neuroprotection and represent a novel approach to the treatment of acute neuronal injury.Key words: poloxamer • N-methyl-D-aspartate • excitotoxicity • lipid peroxidation • electroporation • capacitance ctivation of receptors for glutamate plays a central role in neuronal death following hypoxia-ischemia/reperfusion, hypoglycemia, or trauma (1). Activation of the N-methyl-D-aspartate (NMDA) receptor subtype is an important mediator of neuronal death, and this mechanism depends on receptor-linked increases in free intracellular Ca 2+ concentration ([Ca 2+ ] i ) 2 . In addition to depleting ATP as a result of energy-requiring Ca 2+ extrusion 3 , NMDAinduced [Ca 2+ ] i influx increases production of reactive oxygen species (4, 5), inducing cellular damage via single-strand DNA breaks, protein oxidation, and lipid peroxidation (6). Lipid

Lidocaine jelly offers no advantage over plain lubricant in regard to pain control during rigid cystoscopy in women. However, when used in adequate amounts and allowed to dwell in the urethra for 20 minutes before cystoscopy, lidocaine jelly can significantly decrease pain in men.

Congenital malformations have become a leading cause of infant mortality in the 1990s. Over the last several decades, this mortality declined more slowly in nonwhites than in whites.