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Renal artery injury from blunt abdominal trauma is a rare condition that is typically managed nonoperatively in hemodynamically stable patients. Revascularization can be achieved by stenting or surgical reconstruction of the renal artery. All attempts at revascularization should minimize warm ischemic time. Here, we discuss a patient postmotor vehicle accident who presented to Ryder Trauma Center with intra-abdominal bleeding. He underwent emergency exploratory laparotomy with splenectomy and abdominal packing. Postoperative CT scan revealed a contrast nonenhancing left kidney. The patient then returned to the operating room and underwent in situ renal artery reconstruction after >4 hours of warm ischemia. The patient survived a 2-month hospital course and was discharged home after prolonged in-hospital stay and intensive care treatment. Nuclear medicine scan showed scarring and atrophy of the reattached kidney with 16.3% of overall function attributed to the affected kidney. This case shows that patients with renal artery injury can be managed operatively with arterial reconstruction. Reducing warm ischemic time is critical in preserving kidney function.

The sequence and predicted membrane topology of pannexin1 (Panx1) places it in the family of gap junction proteins. However, rather than forming gap junction channels, Panx1 forms channels in the nonjunctional membrane. Panx1 operates in two distinct open states, depending on the mode of stimulation. The exclusively voltage-gated channel has a small conductance (2+ and the currents through the voltage-activated channel were not altered by Ca2+, Zn2+, Ba2+, or Gd3+. In contrast, the Panx1 channel activated to the large channel conformation by extracellular K+, osmotic stress, or low oxygen was inhibited by the multivalent cations in a dose-dependent way. Thus, monovalent cations activated the Panx1 channel from the closed state to the “large” conformation, while di- and trivalent cations exclusively inhibited this large channel conformation.

Introduction: Boron compounds are being investigated as therapies for dermatologic conditions. Several features of boron chemistry make this element an ideal component in dermatologic treatments. We review the published dermatologically-relevant clinical trials and case studies pertaining to boron compounds.Methods: PubMed was utilized to query terms boron, chemistry, drug, development, dermatology, atopic dermatitis, psoriasis, onychomycosis, tavaborole, AN 2690, crisaborole, and AN 2728. Clinical trials, case studies, animal studies and in vitro studies. Pertaining to atopic dermatitis, psoriasis and onychomycosis were included.Results: Crisaborole 2% topical solution reduced atopic dermatitis lesions by ∼60% when compared to pretreatment baseline. Crisaborole maintains its dose-dependent effect in treatment of psoriasis and significantly reduces psoriatic plaques when compared to controls. Adverse effects were mild, frequency of events varied between studies. Crisaborole was well tolerated when applied to sensitive skin. Topical tavaborole significantly reduced or eliminated onychomycosis with minimal side effects compared to placebo. Tavaborole was effective in treating recalcitrant onychomycosis.Discussion: Boron-based compounds form stable interactions with enzyme targets and are safe medications for the treatment of atopic dermatitis, psoriasis, and onychomycosis. The mild and rare side effects of topical boron-based compounds may make them ideal treatments for individuals with sensitive skin and pediatric populations.

Changes in the mRNA and protein expression of renin-secreting cells in the juxtaglomerular apparatus (JGA) were examined in the rat following administration of ZENECA ZD8731, an angiotensin II receptor antagonist. Doses of 0 or 90 mg/kg were administered daily by gavage for 26 wk. JGA hypertrophy was apparent in histological sections. Immunohistochemistry demonstrated an increase in the number of renin-containing cells in both the afferent arterioles and the interlobular arteries. Similarly, renin mRNA expression, demonstrated by in situ hybridization, had extended to more proximal segments of the afferent arterioles and was also present in efferent arterioles and interlobular arteries. In conclusion, JGA hypertrophy occurred as a result of antagonism of the angiotensin II receptor. Associated with JGA hypertrophy was increased expression of both renin and renin mRNA, indicative of stimulated renin synthesis caused by an exaggerated pharmacological response of renin-secreting cells to the loss of feedback inhibition by angiotensin II.