Depressive disorders lack objective physiological measurements to characterize the affected population and facilitate study of relevant mechanisms. The melanopsin-mediated light signaling pathway may contribute to seasonal variation and can be measured non-invasively by pupillometry. We prospectively studied changes in melanopsin-mediated pupillary constriction in 19 participants with major depressive disorder (MDD) and 10 control across the summer and winter solstices. The melanopsin-mediated response, as measured by the pupil's sustained constriction six s after a high intensity blue light stimulus, was marginally attenuated in those with MDD relative to controls (p=0.071). The participants with MDD unexpectedly showed a significantly reduced transient pupillary response to low intensity red (p=0.011) and blue light (p=0.013), but not high intensity red and blue light. Sustained pupillary constriction in response to high intensity blue light was more pronounced with increasing daylight hours (p=0.037) and was more strongly related to objectively measured versus estimated light exposure. Melanopsin-mediated impairments in pupil response may serve as a biological marker for vulnerability to depression in low light conditions. Assessment of these and other responses to light stimuli, such as response to low intensity light, may be useful for the study of the neurobiology of MDD and related mood disorders.

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Purpose Instability of the proximal tibioibular joint (PTFJ) can be treated with bicortical suspension (BCS) ixation. However, the ideal location, orientation, and coniguration to apply one or two BCS devices are not clear. Methods A inite-element model of the PTFJ was created from a female adult's CT dataset. Anterior and posterior ligaments at the PTFJ were modeled and suppressed to simulate stable and unstable joints. Fifty-six models simulated 56 device placements along guiding tunnel lines that connect eight entry locations on the ibular head to seven exit points on the anteromedial tibia. Doubling device stifness created 56 more models. Combing any two placements created 1176 double-device conigurations which were categorized to be crossed, divergent or parallel. Displacement of the ibular head relative to the ixed tibia under 100 N anterolateral and posteromedial forces was assessed. Results Diferent placements had 2.1-27.9 mm translation with 0.7-8.9° internal rotation under anterolateral loading, and 1.8-5.2 mm translation with 6.1-7.9° external rotation under posteromedial loading. More transverse and superior orientations were associated with smaller anterolateral translation; more posterior and superior entry locations were associated with smaller internal rotation. The median (IQR) reductions in anterolateral translation by doubling device stifness and by adding a second device were 0.8 (IQR 0.5-1.0) and 0.8 (IQR 0-6.1) mm, respectively. The type of double-device conigurations had no signiicant efect on ibular motion. Conclusion Surgeons should drill the guiding tunnel superiorly and transversely to ensure the optimal restoration of the PTFJ anterolateral stability.

Fracture-related infections (FRIs) remain a significant problem. Many approach FRI cases in a staged fashion, focusing on infection eradication initially and fracture union during subsequent procedures. The literature quotes high success rates with this strategy. However, associated patient morbidity and economic impact are noteworthy. A single-stage FRI treatment, using an antibiotic-coated locked intramedullary nail, also exists. This video details low-cost, antibiotic-coated locked intramedullary nail fabrication in the operating room alongside preliminary results using this technique for acute FRI and septic nonunion treatment.

Background Neonatal growth restriction (nGR) leads to leptin deficiency and increases the risk of hypertension. Previous studies have shown nGR-related hypertension is normalized by neonatal leptin (nLep) and exacerbated by psychological stress. With recent studies linking leptin and angiotensin signaling, we hypothesized that nGR-induced nLep deficiency increases adult leptin sensitivity; leading to leptin- or stress-induced hypertension, through a pathway involving central angiotensin II type 1 receptors. Methods We randomized mice with incipient nGR, by virtue of their presence in large litters, to vehicle or physiologic nLep supplementation (80 ng/g/d). Adult caloric intake and arterial pressure were monitored at baseline, during intracerebroventricular losartan infusion and during systemic leptin administration. Results nGR increased leptin-triggered renal sympathetic activation and hypertension with increased leptin receptor expression in the arcuate nucleus of the hypothalamus; all of those nGR-associated phenotypes were normalized by nLep. nGR mice also had stress-related hyperphagia and hypertension, but only the stress hypertension was blocked by central losartan infusion. Conclusion nGR leads to stress hypertension through a pathway that involves central angiotensin II receptors, and nGR-associated leptin deficiency increases leptin-triggered hypertension in adulthood. These data suggest potential roles for preservation of neonatal growth and nLep supplementation in the prevention of nGR-related hypertension.