Bilateral Popliteal Artery Entrapment Syndrome in a Young Female NCAA Division-I Collegiate Basketball Player: A Case Report.

CASE: Popliteal artery entrapment syndrome (PAES) is rarely on the differential for exertional lower extremity pain in the young athlete. This article illustrates a case of a 20-year-old female National Collegiate Athletic Association (NCAA) Division-I college basketball player who was diagnosed with PAES after conservative treatment of medial tibial stress syndrome and comprehensive evaluation for chronic exertional compartment syndrome. She received bilateral popliteal artery releases through a posterior approach and made an asymptomatic return to Division-I collegiate basketball. CONCLUSION: PAES is a rare potentially limb-threatening disease that must be included on the differential of young athletes who present with exertional lower extremity pain.

A systematic review of opioid use after extremity trauma in orthopedic surgery.

BACKGROUND: The United States is in a prescription opioid crisis. Orthopedic surgeons prescribe more opioid narcotics than any other surgical specialty. The purpose of this study was to evaluate the state of opioid use after extremity trauma in orthopedic surgery. METHODS: A computerized literature search of PubMed/MEDLINE was conducted to evaluate the status of opioids after extremity fractures. Six articles were identified and included in the review. RESULTS: Patients who consume more opioids communicate greater pain intensity and less satisfaction with pain control. Intraoperative multimodal drug injection and nerve blockade are viable alternatives for postoperative pain control and can help decrease systemic opioid use. Orthopedic surgeons are overprescribing opioids. Compared to other countries, the United States consumes more opioids with no better satisfaction with pain control. CONCLUSION: Orthopedic trauma surgeons should tailor their postoperative opioid prescriptions to the individual patient and utilize alternative options in order to control postoperative pain. Patients should be counseled regarding narcotic addiction and dependence. Patients unable to manage pain postoperatively should be followed closely and receive the proper chronic pain management, mental and social health services referrals.

Role of GLUT1 in regulation of reactive oxygen species.

In skeletal muscle cells, GLUT1 is responsible for a large portion of basal uptake of glucose and dehydroascorbic acid, both of which play roles in antioxidant defense. We hypothesized that conditions that would decrease GLUT1-mediated transport would cause increased reactive oxygen species (ROS) levels in L6 myoblasts, while conditions that would increase GLUT1-mediated transport would result in decreased ROS levels. We found that the GLUT1 inhibitors fasentin and phloretin increased the ROS levels induced by antimycin A and the superoxide generator pyrogallol. However, indinavir, which inhibits GLUT4 but not GLUT1, had no effect on ROS levels. Ataxia telangiectasia mutated (ATM) inhibitors and activators, previously shown to inhibit and augment GLUT1-mediated transport, increased and decreased ROS levels, respectively. Mutation of an ATM target site on GLUT1 (GLUT1-S490A) increased ROS levels and prevented the ROS-lowering effect of the ATM activator doxorubicin. In contrast, expression of GLUT1-S490D lowered ROS levels during challenge with pyrogallol, prevented an increase in ROS when ATM was inhibited, and prevented the pyrogallol-induced decrease in insulin signaling and insulin-stimulated glucose transport. Taken together, the data suggest that GLUT1 plays a role in regulation of ROS and could contribute to maintenance of insulin action in the presence of ROS.

ATM and GLUT1-S490 phosphorylation regulate GLUT1 mediated transport in skeletal muscle.

OBJECTIVE: The glucose and dehydroascorbic acid (DHA) transporter GLUT1 contains a phosphorylation site, S490, for ataxia telangiectasia mutated (ATM). The objective of this study was to determine whether ATM and GLUT1-S490 regulate GLUT1. RESEARCH DESIGN AND METHODS: L6 myoblasts and mouse skeletal muscles were used to study the effects of ATM inhibition, ATM activation, and S490 mutation on GLUT1 localization, trafficking, and transport activity. RESULTS: In myoblasts, inhibition of ATM significantly diminished cell surface GLUT1, glucose and DHA transport, GLUT1 externalization, and association of GLUT1 with Gα-interacting protein-interacting protein, C-terminus (GIPC1), which has been implicated in recycling of endosomal proteins. In contrast, ATM activation by doxorubicin (DXR) increased DHA transport, cell surface GLUT1, and the GLUT1/GIPC1 association. S490A mutation decreased glucose and DHA transport, cell surface GLUT1, and interaction of GLUT1 with GIPC1, while S490D mutation increased transport, cell surface GLUT1, and the GLUT1/GIPC1 interaction. ATM dysfunction or ATM inhibition reduced DHA transport in extensor digitorum longus (EDL) muscles and decreased glucose transport in EDL and soleus. In contrast, DXR increased DHA transport in EDL. CONCLUSIONS: These results provide evidence that ATM and GLUT1-S490 promote cell surface GLUT1 and GLUT1-mediated transport in skeletal muscle associated with upregulation of the GLUT1/GIPC1 interaction.