Abnormal motor blockade after epidural analgesia caused by pneumorrhachis and the role of hyperbaric oxygen treatment: a case report.

INTRODUCTION: Pneumorrhachis is a rare clinical entity that is usually asymptomatic. Previous reports have associated such events with epidural insertion using a loss of resistance (LOR) to air technique. This report describes a case of symptomatic epidural pneumorrhachis following epidural anaesthesia using LOR to saline. CASE REPORT: A 32-year-old American Society of Anesthesiologists (ASA) Classification II female patient was admitted for unplanned caesarean section. Epidural anaesthesia was performed at the L3-4 space using LOR to saline. The procedure, including delivery of the neonate, was uneventful. In the recovery room, a local anaesthetic infusion via an elastomeric pump (infusion 'balloon') was started. Two hours after initiation of the infusion the patient complained of motor blockade, so it was stopped. Two hours later she remained paraparetic, and a neurologist assessment was required. A computed tomography scan showed epidural pneumorrhachis at the L2-3 level. The patient was referred for emergent hyperbaric oxygen treatment (US Navy Treatment Table 5) and following one session the patient recovered completely. DISCUSSION: Anaesthetists should be aware of this rare complication, which is easily overlooked. Hyperbaric oxygen treatment is a first line treatment for gas-associated lesions with neurological impairment. Timely referral is essential to prevent irreversible deficits.

Cdk5 and GSK3ß inhibit fast endophilin-mediated endocytosis.

Endocytosis mediates the cellular uptake of micronutrients and cell surface proteins. Fast Endophilin-mediated endocytosis, FEME, is not constitutively active but triggered upon receptor activation. High levels of growth factors induce spontaneous FEME, which can be suppressed upon serum starvation. This suggested a role for protein kinases in this growth factor receptor-mediated regulation. Using chemical and genetic inhibition, we find that Cdk5 and GSK3ß are negative regulators of FEME. They antagonize the binding of Endophilin to Dynamin-1 and to CRMP4, a Plexin A1 adaptor. This control is required for proper axon elongation, branching and growth cone formation in hippocampal neurons. The kinases also block the recruitment of Dynein onto FEME carriers by Bin1. As GSK3ß binds to Endophilin, it imposes a local regulation of FEME. Thus, Cdk5 and GSK3ß are key regulators of FEME, licensing cells for rapid uptake by the pathway only when their activity is low.

Training Experience and Maturational, Morphological, and Fitness Attributes as Individual Performance Predictors in Male and Female Under-14 Portuguese Elite Basketball Players.

ABSTRACT: Ramos, S, Volossovitch, A, Ferreira, AP, Fragoso, I, and Massuça, LM. Training experience and maturational, morphological, and fitness attributes as individual performance predictors in male and female under-14 Portuguese elite basketball players. J Strength Cond Res 35(7): 2025-2032, 2021-The association of the biological maturation, morphological attributes, and fitness attributes of 13- to 14-year-old players selected to regional basketball teams, which participated in the Portuguese Festival of Youth Basketball, was analyzed in the study. A total of 416 under-14 Portuguese elite basketball players (male, n = 224; female, n = 192) were evaluated in this cross-sectional study. Maturational parameters (maturity offset and predicted age at peak height velocity), morphological attributes (body mass, stature, skinfolds, and lengths), and fitness (sprint, agility, jump, and upper-body strength) attributes were measured. In addition, basketball game performance was assessed using technical statistics (rebounds and point averages) and the performance index rating (PIR). Correlation analyses indicated that male players with better PIR/minute were taller, had a longer hand span, had more free-fat mass, and demonstrated better results in all jumping tests, upper-body strength tests, 20-m speed test, and agility T-test. Female players with better PIR/minute were significantly older, more matured, heavier, taller, and had longer arm and hand span. They also demonstrated better results in jumping tests, medicine ball throw, had greater practice experience, and were subjected to higher training loads. Multiple regression analysis showed that combined stature, handgrip strength, agility, and countermovement jump (with arm swing power) can be considered strong predictors of PIR per time played for male players. The prediction model for female players indicated that maturity offset, practice experience, and agility were the strongest predictors of basketball performance. In conclusion, the results of this study indicate that around puberty, physical fitness attributes of elite basketball players of both sexes are associated with game performance parameters. Two regression models have been estimated to predict the performance of youth basketball players of both genders.

Differences in Maturity, Morphological, and Fitness Attributes Between the Better- and Lower-Ranked Male and Female U-14 Portuguese Elite Regional Basketball Teams.

Ramos, S, Volossovitch, A, Ferreira, AP, Barrigas, C, Fragoso, I, and Massuça, L. Differences in maturity, morphological and fitness attributes between the better- and lower-ranked male and female U-14 Portuguese elite regional basketball teams. J Strength Cond Res 34(3): 878-887, 2020-During a national championship, the anthropometric, physiological, and maturation attributes of 13-14-year-old players of regional selection basketball teams and their association with team's final classification were analyzed. Body parameters (body mass, height, skinfolds, and lengths) were measured and physiological capacities assessed by sprint (20 m), agility, jump, and upper-body strength tests. Chronological age, maturity offset (years from age at peak height velocity; YAPHV), and predicted age at peak height velocity were calculated. In both sexes, no significant differences were found for maturity. Anthropometric and physiological analysis indicated that male players from finalist's teams were significantly faster, were more agile, threw the medicine ball longer, and showed lower percentages of body fat than players from lower-ranked teams. Further, semifinalists were faster than lower-ranked players. In the same sense, female players from semifinalist teams demonstrated to be significantly faster, more agile, and threw the medicine ball longer than female players from lower-ranked teams. In addition, discriminant analysis showed that speed (in boys) and the combination of speed and upper limb strength (in girls) could successfully discriminate players with different performances in a championship. In conclusion, speed and upper limb strength appear to be the physical attributes associated with better team performance in youth basketball. Coaches should be aware of the relationship between the improvement of these physical attributes and the teaching-learning process of the basketball game.

Publisher Correction: FBP17 and CIP4 recruit SHIP2 and lamellipodin to prime the plasma membrane for fast endophilin-mediated endocytosis.

In the version of this Letter originally published, the name of co-author Safa Lucken-Ardjomande Häsler was coded wrongly, resulting in it being incorrect when exported to citation databases. This has been corrected, though no visible changes will be apparent.

FBP17 and CIP4 recruit SHIP2 and lamellipodin to prime the plasma membrane for fast endophilin-mediated endocytosis.

Endocytosis mediates the cellular uptake of micronutrients and the turnover of plasma membrane proteins. Clathrin-mediated endocytosis is the major uptake pathway in resting cells1, but several clathrin-independent endocytic routes exist in parallel2,3. One such pathway, fast endophilin-mediated endocytosis (FEME), is not constitutive but triggered upon activation of certain receptors, including the ß1 adrenergic receptor4. FEME activates promptly following stimulation as endophilin is pre-enriched by the phosphatidylinositol-3,4-bisphosphate-binding protein lamellipodin4,5. However, in the absence of stimulation, endophilin foci abort and disassemble after a few seconds. Looking for additional proteins involved in FEME, we found that 20 out of 65 BAR domain-containing proteins tested colocalized with endophilin spots. Among them, FBP17 and CIP4 prime the membrane of resting cells for FEME by recruiting the 5'-lipid phosphatase SHIP2 and lamellipodin to mediate the local production of phosphatidylinositol-3,4-bisphosphate and endophilin pre-enrichment. Membrane-bound GTP-loaded Cdc42 recruits FBP17 and CIP4, before being locally deactivated by RICH1 and SH3BP1 GTPase-activating proteins. This generates the transient assembly and disassembly of endophilin spots, which lasts 5-10 seconds. This mechanism periodically primes patches of the membrane for prompt responses upon FEME activation.

Mechanisms of Carrier Formation during Clathrin-Independent Endocytosis.

Clathrin-independent endocytosis (CIE) mediates the cellular uptake of many extracellular ligands, receptors, and pathogens, including several life-threatening bacterial toxins and viruses. So far, our understanding of CIE carrier formation has lagged behind that of clathrin-coated vesicles. Impediments have been the imprecise definition of some CIE pathways, the lack of specific cargoes being transported and of exclusive cytosolic markers and regulators. Notwithstanding these limitations, three distinct molecular mechanisms by which CIE carriers form can be defined. Cargo capture by cytosolic proteins is the main mechanism used by fast endophilin-mediated endocytosis (FEME) and interleukin 2 receptor (IL-2R) endocytosis. Acute signaling-induced membrane remodeling drives macropinocytosis. Finally, extracellular lipid or cargo clustering by the glycolipid-lectin (GL-Lect) hypothesis mediates the uptake of Shiga and cholera toxins and receptors by the CLIC/GEEC pathway. Here, we review these mechanisms and highlight current gaps in knowledge that will need to be addressed to complete our understanding of CIE.

Endophilin marks and controls a clathrin-independent endocytic pathway.

Endocytosis is required for internalization of micronutrients and turnover of membrane components. Endophilin has been assigned as a component of clathrin-mediated endocytosis. Here we show in mammalian cells that endophilin marks and controls a fast-acting tubulovesicular endocytic pathway that is independent of AP2 and clathrin, activated upon ligand binding to cargo receptors, inhibited by inhibitors of dynamin, Rac, phosphatidylinositol-3-OH kinase, PAK1 and actin polymerization, and activated upon Cdc42 inhibition. This pathway is prominent at the leading edges of cells where phosphatidylinositol-3,4-bisphosphate-produced by the dephosphorylation of phosphatidylinositol-3,4,5-triphosphate by SHIP1 and SHIP2-recruits lamellipodin, which in turn engages endophilin. This pathway mediates the ligand-triggered uptake of several G-protein-coupled receptors such as α2a- and ß1-adrenergic, dopaminergic D3 and D4 receptors and muscarinic acetylcholine receptor 4, the receptor tyrosine kinases EGFR, HGFR, VEGFR, PDGFR, NGFR and IGF1R, as well as interleukin-2 receptor. We call this new endocytic route fast endophilin-mediated endocytosis (FEME).

Analysis of the virulence of an atypical enteropathogenic Escherichia coli strain in vitro and in vivo and the influence of type three secretion system.

Atypical enteropathogenic Escherichia coli (aEPEC) inject various effectors into intestinal cells through a type three secretion system (T3SS), causing attaching and effacing (A/E) lesions. We investigated the role of T3SS in the ability of the aEPEC 1711-4 strain to interact with enterocytes in vitro (Caco-2 cells) and in vivo (rabbit ileal loops) and to translocate the rat intestinal mucosa in vivo. A T3SS isogenic mutant strain was constructed, which showed marked reduction in the ability to associate and invade but not to persist inside Caco-2 cells. After rabbit infection, only aEPEC 1711-4 was detected inside enterocytes at 8 and 24 hours pointing to a T3SS-dependent invasive potential in vivo. In contrast to aEPEC 1711-4, the T3SS-deficient strain no longer produced A/E lesions or induced macrophage infiltration. We also demonstrated that the ability of aEPEC 1711-4 to translocate through mesenteric lymph nodes to spleen and liver in a rat model depends on a functional T3SS, since a decreased number of T3SS mutant bacteria were recovered from extraintestinal sites. These findings indicate that the full virulence potential of aEPEC 1711-4 depends on a functional T3SS, which contributes to efficient adhesion/invasion in vitro and in vivo and to bacterial translocation to extraintestinal sites.