Healthcare disparities in adolescent idiopathic scoliosis: the impact of socioeconomic factors on Cobb angle.

STUDY DESIGN: Retrospective chart review. OBJECTIVES: The aim of this study is to assess the role of insurance type, geographic socioeconomic status, and ethnicity in AIS disease severity in a state with mandated scoliosis screenings. Early detection of adolescent idiopathic scoliosis (AIS) is associated with reduced curve progression, surgical treatment, and long-term sequelae. Type of insurance, ethnicity, and socioeconomic status are important determinants in healthcare access. METHODS: Data were obtained for 561 AIS patients aged 10-18 years, living within a single county, and presenting to a single healthcare system for initial evaluation of AIS between 2010 and 2016 that met inclusion criteria. Demographic data including gender, age, self-reported ethnicity, insurance, and zip code were collected. Outcome measures included Cobb angle, curve severity, and referral delay. A single fellowship-trained pediatric orthopedic surgeon calculated presenting Cobb angle for each case. Zip code was used as a proxy for household income level. Independent sample t tests, analysis of variance and covariance, and χ2 analysis were used to determine the significant differences and correlations. RESULTS: Female patients (n = 326, CA = 22.4°) had significantly greater Cobb angle measurements compared with male patients (n = 117, CA = 18.1°). Patients with government-supported insurance had significantly higher Cobb angles (CA = 22.1°) than privately insured patients (CA = 19.2°) but were both classified within the "mild" range clinically, and are likely not clinically significant. There was no correlation between income level and Cobb angle. Referral delay and Cobb angle severity did not vary by age, income, or insurance. A χ2 analysis showed no association between Cobb angle and race. CONCLUSIONS: Cobb angle severity was not influenced by SES factors, including ethnicity and household income. LEVEL OF EVIDENCE: Level-II.

A comparison of preoperative and intraoperative vein mapping sizes for arteriovenous fistula creation.

BACKGROUND: Duplex ultrasound (DUS) mapping of the veins and arteries of the upper extremity is a well-established practice in arteriovenous fistula creation for long-term hemodialysis access. Previous publications have shown that vein diameters varying from 2 to 3 mm are predictive of success. Regional anesthesia is known to result in vasodilation and thus to increase the diameter of upper extremity veins. This study compares the sizes of veins measured by preoperative DUS mapping with those obtained after regional anesthesia to determine whether intraoperative DUS results in increased vein diameters and thus changes in the operative plan. A second goal was to determine whether such changes resulted in functional access. METHODS: This was a prospective observational study conducted between July 2013 and December 2014. Consecutive patients were preoperatively mapped and then intraoperatively mapped after administration of a regional anesthetic. Comparison of vein mapping sizes and comparison of preoperative plan and operative procedure based on the preoperative and intraoperative DUS mapping, respectively, were analyzed with a repeated-measures linear model. Significance testing was two sided, with a significance level of 5%. RESULTS: Sixty-five patients with end-stage renal disease underwent placement of arteriovenous access with preoperative and intraoperative DUS mapping after regional anesthesia. Comorbidities were representative of the vascular population. After regional anesthesia, intraoperative mid forearm and distal forearm cephalic veins were significantly larger than their respective preoperative measurements. Average increase in diameter of the mid forearm cephalic vein and distal forearm was 0.96 mm (P < .001) and 0.50 mm (P = .04), respectively. There was a significant difference in the number and configuration of arteriovenous accesses (P < .0001). There was more than a twofold significant increase in radial artery-based access procedures concomitant with a significant reduction of brachial-based access procedures and a reduction in graft access procedures. Overall functional access rate was 63%, and patency rates were comparable to those reported in the literature. CONCLUSIONS: The routine use of intraoperative DUS mapping after regional anesthesia is recommended to determine the optimal access site for chronic hemodialysis access. Identifying additional access options not seen with physical examination and preoperative DUS mapping will provide end-stage renal disease patients with more fistula options and hence a longer access life span for a lifelong disease.

Denosumab Therapy for Giant Cell Tumor of Bone Pulmonary Metastasis.

CASE: A 68-year-old female was diagnosed with giant cell tumor of bone (GCTB) metastatic to her lungs. The patient was treated with IV denosumab for the course of 4.5 years for these metastases. The metastatic tumor burden decreased significantly after only 3 months of therapy. The size of the metastases has been stable for over 4 years. CONCLUSION: Denosumab therapy has promise in the treatment of GCTB, including pulmonary metastasis. However, the long-term role of denosumab for pulmonary metastases is yet to be determined.

Involvement of reactive oxygen species in cocaine-taking behaviors in rats.

Reactive oxygen species (ROS) have been implicated in the development of behavioral sensitization following repeated cocaine exposure. We hypothesized that increased ROS following cocaine exposure would act as signaling molecules in the mesolimbic dopamine (DA) system, which might play an important role in mediating the reinforcing effects of cocaine. The aim of this study was to evaluate cocaine enhancement of brain metabolic activity and the effects of ROS scavengers on cocaine self-administration behavior, cocaine-induced ROS production in the nucleus accumbens (NAc) and cocaine enhancement of DA release in the NAc. Metabolic neural activity monitored by temperature and oxidative stress were increased in NAc following cocaine exposure. Systemic administration of the ROS scavenger N-tert-butyl-α-phenylnitrone (PBN) or 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL), either pre- or post-treatment, significantly decreased cocaine self-administration without affecting food intake. Infusion of TEMPOL into the NAc inhibited cocaine self-administration. Increased oxidative stress was found mainly on neurons, but not astrocytes, microglia or oligodendrocytes, in NAc of rats self-administering cocaine. TEMPOL significantly attenuated cocaine-induced enhancement of DA release in the NAc, compared to saline controls. TEMPOL had no effect on the enhancement of DA release produced by the DA transporter inhibitor GBR12909. Taken together, these findings suggest that enhancement of ROS production in NAc neurons contributes to the reinforcing effect of cocaine.

Acute ethanol inhibits dopamine release in the nucleus accumbens via α6 nicotinic acetylcholine receptors.

Electrophysiology and microdialysis studies have provided compelling evidence that moderate to high ethanol concentrations enhance dopamine (DA) neurotransmission in the nucleus accumbens (NAc) through the mesolimbic DA system. However, with fast-scan cyclic voltammetry, short-term exposure to moderate to high doses of ethanol decreases evoked DA release at terminals in the NAc. The aim of this study was to evaluate the involvement of nicotinic acetylcholine receptors (nAChRs) in modulating the effects of ethanol on DA release in the NAc of C57BL/6 mice ex vivo and in vivo. Local stimulation evoked robust, frequency-dependent DA release in the NAc slice preparation, with maximal release at 40 Hz in the shell and 20 Hz in the core. Nicotine decreased DA release in a concentration-dependent (0.01-10 µM) manner in the shell and core, with an IC50 of 0.1 µM ex vivo and 0.5 mg/kg in vivo. Nicotine and ethanol inhibition of DA release was blocked by the α6*-nAChR antagonist α-conotoxins CtxMII and α-CtxMII [H9A; L15A] ex vivo (100 nM) in the core but not the shell. Furthermore, the nonspecific nAChR antagonist mecamylamine (2 mg/kg) blocked the effects of ethanol in the core in vivo. These findings suggest that DA release is inhibited by ethanol via nAChRs in the NAc and that DA modulation by nAChRs differs in the core versus the shell, with α6*-nAChRs affecting DA release in the core but not in the shell.