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OBJECT Transfer of the triceps motor branch has been used for treatment of isolated axillary nerve palsy in the adult population. However, there are no published data on the effectiveness of this procedure in the pediatric population with traumatic injuries. The authors reviewed demographics and outcomes in their series of pediatric patients who underwent this procedure. METHODS Six patients ranging in age from 10 to 17 years underwent triceps motor branch transfer for the treatment of isolated axillary nerve injuries between 4 and 8 months after the inciting injury. Deltoid muscle strength was evaluated using the modified British Medical Research Council (MRC) grading system. Shoulder abduction at last follow-up was measured. RESULTS The mean duration of follow-up was 38 months. The average postoperative MRC grading of deltoid muscle strength was 3.6 ± 1.3. The median MRC grade was 4. One patient who did not achieve an MRC grade of 3 suffered multiple injuries from high-velocity trauma. Unlike in the adult population, age, body mass index of the patient, and delay from injury to surgery were not significant factors affecting the outcome of the procedure. CONCLUSIONS In the pediatric population with traumatic injuries, isolated axillary nerve injury treated with triceps motor branch transfer can result in good outcomes.

New Findings What is the central question of this study? Hyperoxia blunts hypoglycaemia counterregulation in healthy adults. We hypothesized that this effect is mediated by the carotid bodies and that: (i) hyperoxia would have no effect on hypoglycaemia counterregulation in carotid body‐resected patients; and (ii) carotid body‐resected patients would exhibit an impaired counterregulatory response to hypoglycaemia. What is the main finding and its importance? Our data indicate that the effect of hyperoxia on hypoglycaemic counterregulation is mediated by the carotid bodies. However, a relatively normal counterregulatory response to hypoglycaemia in carotid body‐resected patients highlights: (i) the potential for long‐term adaptations after carotid body resection; and (ii) the importance of redundant mechanisms in mediating hypoglycaemia counterregulation. Hyperoxia reduces hypoglycaemia counterregulation in healthy adults. We hypothesized that this effect is mediated by the carotid bodies and that: (i) hyperoxia would have no effect on hypoglycaemia counterregulation in patients with bilateral carotid body resection; and (ii) carotid body‐resected patients would exhibit an impaired counterregulatory response to hypoglycaemia. Five patients (three male and two female) with bilateral carotid body resection for glomus tumours underwent two 180 min hyperinsulinaemic, hypoglycaemic (∼3.3 mmol l−1) clamps separated by a minimum of 1 week and randomized to either normoxia (21% fractional inspired O2) or hyperoxia (100% fractional inspired O2). Ten healthy adults (seven male and three female) served as control subjects. Hypoglycaemia counterregulation in carotid body‐resected patients was not significantly altered by hyperoxia (area under the curve expressed as a percentage of the normoxic response: glucose infusion rate, 111 ± 10%; cortisol, 94 ± 6%; glucagon, 107 ± 7%; growth hormone, 92 ± 10%; adrenaline, 89 ± 26%; noradrenaline, 79 ± 15%; main effect of condition, P > 0.05). This is in contrast to previously published results from healthy adults. However, the counterregulatory responses to hypoglycaemia during normoxia were not impaired in carotid body‐resected patients when compared with control subjects (main effect of group, P > 0.05). Our data provide further corroborative evidence that the effect of hyperoxia on hypoglycaemic counterregulation is mediated by the carotid bodies. However, relatively normal counterregulatory responses to hypoglycaemia in carotid body‐resected patients highlight the importance of redundant mechanisms in mediating hypoglycaemia counterregulation.

SummaryBackground/ObjectivesLow‐grade inflammation is an underlying feature of obesity and identifying inflammatory markers is crucial to understanding this disease. Therefore, the purpose of this study was twofold: (i) to perform a global microarray analysis and (ii) to investigate the role of lactoferrin (LTF), one of the most altered genes, in relation to obesity in Latino youth.MethodsNon‐diabetic Latino youth (71 males/92 females; 15.6 ± 3.2 years) were studied. A subset of 39 participants was randomly selected for global microarray analysis profiling from the whole blood sample. Serum LTF was compared between lean (n = 78) and overweight/obese (n = 85) participants.ResultsMicroarray analysis revealed that a total of 1870 probes were altered in expression ≥1.2‐fold and P < 0.05 in overweight/obese participants compared with lean. KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis revealed significant enrichment for pathways including toll‐like receptor (TLR) and B cell receptor signalling pathways. LTF and TLR5 were increased in expression by 2.2 and 1.5 fold, respectively, in the overweight/obese participants. Increased LTF concentrations were significantly associated with high risk of obesity‐related phenotypes (all P < 0.05).ConclusionsOur data suggest that increased LTF is associated with obesity risk among Latino youth. This finding is discordant to what has been shown in adults and suggests that age may modulate the association between LTF and obesity‐related health.

Key Points High-throughput RNAi screening identified lenalidomide sensitizer genes, including RSK2, RAB, peroxisome, and potassium channel family members. Knockdown or inhibition of RSK2 synergized with lenalidomide to induce myeloma cytotoxicity and downregulation of interferon regulatory factor 4 and MYC.

The 2001 Bethesda system recommends further classifying atypical glandular cells (AGCs) as either endocervical or endometrial origin. Numerous studies have investigated the clinical significance of AGC. In this study, we investigated the incidence of clinically significant lesions among women with liquid-based Papanicolaou cervicovaginal (Pap) interpretations of atypical endometrial cells (AEMs) or AGC favor endometrial origin (AGC-EM). More importantly, we correlated patients of AEM or AGC-EM with their clinical presentations to determine if AEM/AGC-EM combined with abnormal vaginal bleeding is associated with a higher incidence of significant endometrial pathology. All liquid-based Pap tests with an interpretation of AEM and AGC-EM from July, 2004 through June, 2009 were retrieved from the database. Women with an interpretation of atypical endocervical cells, AGC, favor endocervical origin or AGC, favor neoplastic were not included in the study. The most severe subsequent histologic diagnoses were recorded for each patient. During this 5-year period, we accessioned 332,470 Pap tests of which 169 (0.05%) were interpreted as either AEM or AGC-EM. Of the 169 patients, 133 had histologic follow-up within the health care system. The patients ranged in age from 21 to 71 years old (mean 49.7). On follow-up histology, 27 (20.3%) had neoplastic/preneoplastic uterine lesions. Among them, 20 patients were diagnosed with adenocarcinoma (18 endometrial, 1 endocervical, and 1 metastatic colorectal), 3 with atypical endometrial hyperplasia, and 4 with endometrial hyperplasia without atypia. All patients with significant endometrial pathology, except one, were over 40 years old, and 22 of 25 patients reported abnormal vaginal bleeding at the time of endometrial biopsy or curettage. This study represents a large series of women with liquid-based Pap test interpretations of AEM and AGC-EM with clinical follow-up. Significant preneoplastic or neoplastic endometrial lesions were identified in 20.3% of patients. Patients with Pap test interpretations of AEM or AGC-EM and the clinical presentation of abnormal vaginal bleeding should be followed closely.

Key Points Dinaciclib is a novel cdk inhibitor that demonstrates single agent activity in myeloma. Dinaciclib has a safety profile that is easily manageable.

The formation of amyloid β (Aβ) peptide aggregates, oligomers, and fibrils is a dynamic process; however, the kinetics of their formation is not well understood. This study compares the time course of aggregate/fibril formation by transmission electron microscopy (TEM) analyses with that of oligomer/fibril formation by Western blot analysis under native and denaturing conditions. Efforts to deaggregate/defibrillate these peptides by using hexafluoroisopropanol, ammonium hydroxide, or dimethylsulfoxide did not change the nondenaturing polyacrylamide gel electrophoresis (PAGE) footprints or drive the peptides to a monomeric species. Regardless of the pretreatment protocol, TEM analyses reveal that all Aβ peptides (Aβ40, Aβ42, Aβ39E22Δ [Osaka], Aβ40E22G [Arctic], Aβ40E22Q [Dutch], and Aβ40A2T [Icelandic]) immediately formed nonfibrillar, amorphous aggregates when first placed into solution with the Osaka mutation, quickly forming early‐stage fibrils. The extent of fibril formation for other Aβ peptides is time dependent, with the Arctic mutation forming fibrils at 1 hr, the Dutch and Icelandic at 4 hr, Aβ42 at 8 hr, and Aβ40 at 24 hr. In contrast, nondenaturing PAGE revealed unique footprints for the different Aβ species. The rapidity of aggregate formation and the rapid transition to fibrils, particularly for the Osaka deletion, suggest an important role for aggregates/fibrils of Aβ in the development of neuronal degeneration. © 2014 Wiley Periodicals, Inc.

AbstractRationale, aims and objectivesThis study was undertaken to assess the frequency of lipid screening in comparison with the United States Preventive Services Task Force guideline in a sample of family medicine patients. In addition, we sought to determine the association between testing frequency and achievement of lipid targets.MethodsA random sample was extracted from 271 patients from among all patients cared for in our Department of Family Medicine for whom lipid screening was ordered from March to September 2012 and who had ≥2 well‐defined cardiovascular risk factors. Lipid testing frequency was classified in three ways: semi‐annual or less often (0–12 tests over 6 years), annual or less often (0–6 tests), or biennial (0–3 tests).ResultsMultiple logistic regression analysis revealed that the predictors of lipid screening more often than semi‐annually were age ≥60 years [odds ratio (OR) = 3.7] and diabetes mellitus (DM) (OR = 30.6). Predictors of screening more often than annually were DM (OR = 4.3), hypertension (OR = 2.1), family history of premature coronary artery disease (OR = 5.6) and statin treatment (OR = 3.5). Lipid goal attainment was not associated with testing frequency except with regard to low‐density lipoprotein levels (P = 0.043, P < 0.001, P = 0.005, by semi‐annual, annual and biennial, respectively) and total cholesterol levels (P = 0.015, P = 0.025 by semi‐annual and annual, respectively).ConclusionsQuestionable high frequency of lipid testing was detected even when the more conservative approach of annual monitoring was assumed. Frequency of testing was not associated with goal attainment for most parameters. Physicians should request the lipid testing based on overall risk assessment and person variability in accordance with published guidelines.