IMPORTANCESkin cancer is the most common malignancy occurring after organ transplantation. Although previous research has reported an increased risk of skin cancer in solid organ transplant recipients (OTRs), no study has estimated the posttransplant population-based incidence in the United States. OBJECTIVE To determine the incidence and evaluate the risk factors for posttransplant skin cancer, including squamous cell carcinoma (SCC), melanoma (MM), and Merkel cell carcinoma (MCC) in a cohort of US OTRs receiving a primary organ transplant in 2003 or 2008. DESIGN, SETTING, AND PARTICIPANTS This multicenter retrospective cohort study examined 10 649 adult recipients of a primary transplant performed at 26 centers across the United States in the Transplant Skin Cancer Network during 1 of 2 calendar years (either 2003 or 2008) identified through the Organ Procurement and Transplantation Network (OPTN) database. Recipients of all organs except intestine were included, and the follow-up periods were 5 and 10 years.MAIN OUTCOMES AND MEASURES Incident skin cancer was determined through detailed medical record review. Data on predictors were obtained from the OPTN database. The incidence rates for posttransplant skin cancer overall and for SCC, MM, and MCC were calculated per 100 000 person-years. Potential risk factors for posttransplant skin cancer were tested using multivariate Cox regression analysis to yield adjusted hazard ratios (HR).RESULTS Overall, 10 649 organ transplant recipients (mean [SD] age, 51 [12] years; 3873 women [36%] and 6776 men [64%]) contributed 59 923 years of follow-up. The incidence rates for posttransplant skin cancer was 1437 per 100 000 person-years. Specific subtype rates for SCC, MM, and MCC were 812, 75, and 2 per 100 000 person-years, respectively. Statistically significant risk factors for posttransplant skin cancer included pretransplant skin cancer (
Bone substitutes are being increasingly used in craniofacial surgery and craniomaxillofacial trauma. We will review the history of the biomaterials and describe the ideal characteristics of bone substitutes, with a specific emphasis on craniofacial reconstruction. Some of the most commonly used bone substitutes are discussed in more depth, such as calcium phosphate and hydroxyapatite ceramics and cements, bioactive glass, and polymer products. Areas of active research and future directions include tissue engineering, with an increasing emphasis on bioactivity of the implant.
Hollowing of the temple is an early sign of aging that, when corrected, can lead to significant patient and practitioner satisfaction. Proper anatomically knowledge is required to avoid potentially severe complications. In this study, the authors present a reliable technique to safely and effectively augment this often undertreated area of the aging face.
Severe hearing loss during early development is associated with deficits in speech and language acquisition. Although functional studies have shown a deafness-induced alteration of synaptic strength, it is not known whether long-term synaptic plasticity depends on auditory experience. In this study, sensorineural hearing loss (SNHL) was induced surgically in developing gerbils at postnatal day 10, and excitatory synaptic plasticity was examined subsequently in a brain slice preparation that preserves the thalamorecipient auditory cortex. Extracellular stimuli were applied at layer 6 (L6), whereas evoked excitatory synaptic potentials (EPSPs) were recorded from L5 neurons by using a whole-cell current clamp configuration. In control neurons, the conditioning stimulation of L6 significantly altered EPSP amplitude for at least 1 h. Approximately half of neurons displayed long-term potentiation (LTP), whereas the other half displayed long-term depression (LTD). In contrast, SNHL neurons displayed only LTD after the conditioning stimulation of L6. Finally, the vast majority of neurons recorded from control prehearing animals (postnatal days 9 -11) displayed LTD after L6 stimulation. Thus, normal auditory experience may be essential for the maturation of synaptic plasticity mechanisms.deafness ͉ long-term depression S evere hearing loss is known to affect auditory processing in humans. This loss includes impairments of signal detection in noise or in a multiple source environment, and disruption of intensity discrimination, frequency discrimination, and temporal resolution (1-4). Even transient bouts of conductive hearing loss can disrupt auditory processing, and months or years may be required for normal perception to resolve (5, 6). Because severe hearing loss during development is implicated in the deficient acquisition of auditory perceptual skills and language, which presumably require learning, we have examined whether synaptic plasticity is also affected.At a structural level, hearing impairments can lead to neuron death or atrophy and alter process outgrowth (7). Furthermore, direct examination of neuron function in brain slice preparations from deaf animals has revealed significant physiological changes to intrinsic and synaptic properties. In both the inferior colliculus and auditory cortex (ACx), early sensorineural hearing loss (SNHL) alters the balance of excitatory and inhibitory synaptic strength (8-10). A similar disruption in synaptic physiology and certain intrinsic properties also occurs in the auditory brainstem of the congenitally deaf mutant mouse (11,12).Both long-term potentiation (LTP) and depression (LTD) have been characterized in a series of studies on the rat ACx (13-18). For example, an NMDA receptor-mediated LTP in the ACx can be induced by stimulation of afferents innervating the ACx via the white matter (13), whereas thalamo-and corticocortical synapse activation can induce LTD (16). These cellular mechanisms may serve as a substrate for use-dependent alteration of coding properties in...
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