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Purpose: To report a case of local transmission of invasive lobular carcinoma from a donor to a recipient in a keratolimbal allograft after cessation of systemic immunosuppressive therapy., Methods: This is a case report including the clinicopathologic findings. Sections of the donor breast tumor and recipient conjunctival lesions were stained with hematoxylin and eosin. Immunohistochemical studies were performed using pancytokeratin, CK7, CK20, CAM 5.2, CD138, TTF1, estrogen receptor, progesterone receptor, GATA-3, GCDFP-15, and mammaglobin. Polymerase chain reaction-based DNA profiling of tumor cells was performed., Results: Histopathologic examination revealed an infiltrate of atypical cells with large hyperchromatic nuclei consistent with carcinoma. Immunohistochemical analysis showed pancytokeratin, CK7, CAM 5.2, GATA-3, and estrogen receptor positivity and progesterone receptor absence, consistent with the previously determined phenotype of the donor's breast carcinoma. Results of polymerase chain reaction analysis were also consistent with the donor's tumor. After reduced dosing of tacrolimus and mycophenolate mofetil, 2 limbal tumors occurred in the recipient. The immunosuppressive treatment had been stopped completely before the appearance of the third lesion. The recipient had no history of malignancy, and she had routine screenings for breast cancer., Conclusions: We report a case of donor-derived breast carcinoma in a keratolimbal allograft recipient. The grafted tissue harbored donor-derived tumor cells for more than 4 years after surgery even after systemic immunosuppression was discontinued. Although no similar reports of tumor transfer could be found in the literature, this case suggests the need for increased stringency in donor selection and heightened surveillance for such tumor transmission.

Background: Closed reduction of pediatric fractures is commonly performed by orthopaedic residents using conscious sedation in the emergency department (ED). The purpose of this study was to determine the rate of satisfactory reductions as performed by residents, and to determine the outcomes of these procedures., Methods: A retrospective review was performed of all fractures that underwent closed reduction under conscious sedation in the ED of a level 1 pediatric trauma center between January 1, 2010 and November 30, 2014. Initial and subsequent radiographs were reviewed and a determination was made as to whether the initial reduction was satisfactory, based on predetermined criteria for angulation and displacement. If a second reduction attempt in the operating room was necessary, this was noted. Chart notes were reviewed until a documented endpoint was reached, such as uneventful healing, malunion, nonunion, or growth arrest., Results: A total of 838 subjects were identified. The upper extremity was involved in 85% of the fractures. Of the initial 838 fracture reductions performed, 39 (4.7%) were unsatisfactory. Residents on their first pediatric orthopaedic rotation had a higher unsatisfactory reduction rate compared with more experienced residents (7.0% vs. 3.4%, P=0.01). A second reduction was performed for 94 of 749 (12.6%) fractures. Of these, 35 (37.2%) required an open procedure to accomplish a satisfactory reduction. Fractures with initially satisfactory reductions were significantly less likely to require a second reduction attempt than those with initially unsatisfactory reductions (9.2% vs. 80.0%, P<0.01). The likelihood of a satisfactory reduction was significantly higher in the upper extremity than in the lower extremity. Overall, the vast majority (99.2%) of fractures had a satisfactory final outcome., Conclusions: Most attempts at closed reduction of pediatric fractures in the ED by orthopaedic residents are successful, and the likelihood of a satisfactory reduction was associated with increased levels of resident experience. Fractures with an initially successful reduction were far less likely to require remanipulation., Level of Evidence: Level IV-this is a therapeutic case series.

Background: Severe ischemia induces renal injury less frequently in women than men. In this study, cardiac arrest and cardiopulmonary resuscitation were used to assess whether estradiol is renoprotective via an estrogen receptor (ER)-dependent mechanism., Materials and Methods: Male and female C57BL/6 and ER gene-deleted mice underwent 10 min of cardiac arrest followed by cardiopulmonary resuscitation. Serum chemistries and renal stereology were measured 24 h after arrest., Results: Estrogen did not affect mean arterial pressure, regional renal cortical blood flow, and arterial blood gases. Hence, female kidneys were protected (mean +/- SEM: blood urea nitrogen, 65+/- 21 vs.149+/- 27 mg/dl, P = 0.04; creatinine, 0.14 +/- 0.05 vs. 0.73 +/- 0.16 mg/dl, P = 0.01; volume of necrotic tubules, 7 +/- 1% vs. 10 +/- 0%, P = 0.04). Estrogen also reduced renal injury. In intact females (n = 5), ovariectomized/vehicle-treated (n = 8), and ovariectomized/estrogen-treated (n = 8) animals, blood urea nitrogen was 65 +/- 21, 166 +/- 28, and 50 +/- 14 mg/dl (P = 0.002); creatinine was 0.14 +/- 0.05, 0.74 +/- 0.26, and 0.23 +/- 0.27 mg/dl (P = 0.014); necrotic tubules were 2.5 +/- 0.25%, 12.0 +/- 1.9%, and 5.0 +/- 1.6% (P = 0.004), respectively. In ER-[alpha] and ER-[beta] gene-deleted mice and controls estradiol-reduced functional injury (blood urea nitrogen: estradiol 117 +/- 71, vehicle 167 +/- 56, P = 0.007; creatinine: estradiol 0.5 +/- 0.5, vehicle 1.0 +/- 0.4, P = 0.013), but the effect of estradiol was not different between ER-[alpha] or ER-[beta] gene-deleted mice. Adding ICI 182,780 to estradiol did not alter injury., Conclusions: In women, kidneys were protected from cardiac arrest through estrogen. Estradiol-mediated renoprotection was not affected by ER deletion or blockade. Estradiol is renoprotective after cardiac arrest. The results indicate that estradiol renoprotection is ER-[alpha] and ER-[beta] independent.

Renal ischemia is a common complication in the perioperative period that leads to a high rate of morbidity and mortality. As in other forms of ischemia (i.e., cardiac, neurologic), the incidence and outcome of renal ischemia is strikingly sex-specific. Sexual dimorphism in response to renal injury has been noted for many years, but is now the subject of both clinical and experimental research. Clinically, women experience a lower incidence of perioperative acute renal failure, with the exception of cardiac surgery. Experimental science is now producing tantalizing clues that sex steroids, both male and female, play a role in the kidney's response to ischemia. In this review, we evaluated sex differences in perioperative renal failure and in the pathophysiology of renal ischemia/reperfusion injury. Although much work remains to characterize the biological mechanisms involved, the data are sufficient to support consideration of gender and the use of medications that impact steroid availability in the perioperative plan of care.

A case study describing an accident in Mexico caused by failure to de-energize an x-ray spectrometer prior to repair is presented. The evolution, medical management, and outcome of the radiation injury to the hand are briefly reviewed. A discussion follows, with radiation injury and thermal burns compared and contrasted. The anatomy and physiology of thick skin and the vascular system of the hand are reviewed so that the reader will have a better understanding of the role of vascular injury in the pathological process that leads to tissue atrophy and radiation necrosis. Hyperbaric oxygen therapy, sympathectomy, and other techniques for improving circulation in involved areas are reviewed.

The purpose of this study was to report the effects of spinal cord compression, ischemia, and distraction on clinical status, and somatosensory (SEP) and neurogenic-motor evoked potentials (NMEPs) in animals. The authors also reported their clinical experience with NMEPs elicited from humans undergoing surgery for spinal deformities. Results from the animal studies indicate that NMEPs are more sensitive and specific to the effects from spinal cord compression, ischemia, and distraction than SEPs. In every situation, NMEPs always correlated with the animal's post-surgical clinical status, while SEPs demonstrated an unacceptable false positive and false negative rate. In the 111 clinical cases in which NMEPs were administered, reliable NMEPs were easily elicited in more than 90% of the cases. In the remaining cases, no reliable NMEPs could be recorded because of procedural errors, which have been resolved. The results from this study suggest that the use of NMEPs should be considered as an adjunct to SEPs when monitoring spinal cord function during surgery.

Recent studies indicate that antagonism of calcium channels may not be the only mechanism whereby drugs such as verapamil alter myocardial function. We have examined the effect of verapamil on the binding of [3H]prazosin (alpha 1-adrenergic), [3H]quinuclidinyl benzilate (QNB, muscarinic) and [3H]dihydroalprenolol (DHA, beta-adrenergic) to membranes prepared from rat heart. Verapamil competed for the binding of these radioligands in the following rank order: [3H]prazosin greater than [3H]QNB greater than [3H]DHA (Ki for verapamil = 0.6 microM, 7 microM, and 72 microM, respectively). Verapamil (10 microM) competitively inhibited [3H]prazosin binding to rat ventricular membranes; the apparent dissociation constant (KD) of [3H]prazosin increased from 0.13 +/- 0.02 to 1.5 +/- 0.6 nM (SD) without change in maximal binding capacity (Bmax). The effect of verapamil on the affinity of [3H]prazosin was completely reversed by washing the membranes. The verapamil derivative D-600 also inhibited [3H]prazosin binding (Ki = 1.1 microM). Verapamil (30 microM) competitively inhibited [3H]QNB binding in both atria and ventricles and increased the apparent KD of [3H]QNB fivefold (from 0.07 nM to 0.32 nM) without decreasing Bmax. Verapamil was a less potent inhibitor of [3H]DHA binding and its effect was noncompetitive: the KD for DHA was unaltered by 100 microM verapamil while the Bmax decreased severalfold. We conclude that verapamil, at concentrations clinically achieved in the myocardium (approximately 1 microM), competitively inhibits binding to alpha 1-adrenergic and muscarinic receptors and that this inhibition may play a role in the effects of verapamil on the heart.