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In partnership with the Southern California Regional Transit Training Consortium (SCRTTC), the California State University at Long Beach (CSULB) expanded potential audiences and offered program support for the Electric Vehicle Transit Bus High Voltage Safety Awareness class, which was previously developed under the National Center for Sustainable Transportation (NCST). CSULB expanded both the number of online offerings and the geographic reach by opening the class to transit agencies and campus fleet operators within the NCST network. The course was designed to enhance a technician's basic electrical skills and 2-circuit diagnosis, while teaching students how to work with a Digital Volt-Ohm Meter (DVOM). The effort supports the broader goal of building the workforce needed to support the transition to alternative energy and zero emission bus fleets.View the NCST Project Webpage

Compromised heat loss due to limited convection and evaporation can increase thermal strain. We aimed to determine the effectiveness of ice slurry ingestion to reduce thermal strain following hyperthermia in a state of compromised heat loss. Twelve healthy males (age: 25 ± 4y) underwent hot water immersion to elevate rectal temperature (Trec) by 1.82 ± 0.08°C on four occasions. In the subsequent 60-min of seated recovery, participants ingested either 6.8 g·kg-1 of ice slurry (-0.6°C) or control drink (37°C) in ambient conditions (21 ± 1°C, 39 ± 10% relative humidity), wearing either t-shirt and shorts (2 trials: ICE and CON) or a whole-body sweat suit (2 trials: ICE-SS and CON-SS). Trec and mean skin temperature (Tsk) were recorded and a two-compartment thermometry model of heat storage was calculated. Heat storage was lower in ICE compared with CON at 20-40min (p ≤ 0.044, d ≥ 0.88) and for ICE-SS compared with CON-SS at 40–60 min (p ≤ 0.012, d ≥ 0.93). Trec was lower in ICE compared with CON from 30-60min (p ≤ 0.034, d ≥ 0.65), with a trend for a reduced Trec in ICE-SS compared with CON-SS at 40min (p = 0.079, d = 0.60). A greater Tsk was found in ICE-SS and CON-SS compared with ICE and CON (p < 0.001, d ≥ 3.37). A trend for a lower Tsk for ICE compared with CON was found at 20-40min (p ≤ 0.099, d ≥ 0.53), no differences were found for ICE-SS vs CON-SS (p ≥ 0.554, d ≤ 0.43). Ice slurry ingestion can effectively reduce heat storage when heat loss through convection and evaporation is compromised, relevant to those wearing personal protective equipment or those with compromised sweat loss. Compromised heat loss delays the reduction in heat storage, possibly related to ice slurry ingestion not lowering Tsk. [ABSTRACT FROM AUTHOR]

Purpose: To examine the efficacy of per-cooling via ice slurry ingestion (ICE) in wheelchair tennis players exercising in the heat. Method: Eight wheelchair tennis players undertook sprints (4 sets of 10 × 5 s over 40 min) in a hot environment (∼32 °C), interspersed by 3 boluses of 2.67 g·kg (6.8 g·kg total) ICE or drinking temperate water (control condition). Athletes performed an on-court test of repeated sprint ability (20 × 20 m) in temperate conditions immediately before and 20 minutes after the heat exposure, and time to complete each sprint as well as intermediate times were recorded. Gastrointestinal and weighted mean skin and forehead temperatures were collected throughout the heat exposure, as were thermal sensation, heart rate, and blood lactate concentration. Sweat rate was calculated from body mass changes and fluid/ice intakes. Results: Compared with the control condition, ICE resulted in a significantly lower gastrointestinal temperature (95% CI, 0.11–0.17 °C; P <.001), forehead temperature (0.58–1.06 °C; P <.001), thermal sensation (0.07–0.50 units; P =.017), and sweat rate (0.06–0.46 L·h−1; P =.017). Skin temperature, heart rate, and blood lactate concentration were not significantly different between conditions (P ≥.598). There was no overall change preheating to postheating (P ≥.114) or an effect of condition (P ≥.251) on repeated sprint times. Conclusions: ICE is effective at lowering objective and subjective thermal strain when consumed between sets of repeated wheelchair sprints in the heat. However, ICE has no effect on on-court repeated 20-m sprint performance. [ABSTRACT FROM AUTHOR]

Heterozygous RTN2 variants have been previously identified in a limited cohort of families affected by autosomal dominant spastic paraplegia (SPG12-OMIM:604805) with a variable age of onset. Nevertheless, the definitive validity of SPG12 remains to be confidently confirmed due to the scarcity of supporting evidence. In this study, we identified and validated seven novel or ultra-rare homozygous loss-of-function RTN2 variants in 14 individuals from seven consanguineous families with distal hereditary motor neuropathy (dHMN) using exome, genome and Sanger sequencing coupled with deep-phenotyping. All affected individuals (seven males and seven females, aged 9–50 years) exhibited weakness in the distal upper and lower limbs, lower limb spasticity and hyperreflexia, with onset in the first decade of life. Nerve conduction studies revealed axonal motor neuropathy with neurogenic changes in the electromyography. Despite a slowly progressive disease course, all patients remained ambulatory over a mean disease duration of 19.71 ± 13.70 years. Characterization of Caenorhabditis elegans RTN2 homologous loss-of-function variants demonstrated morphological and behavioural differences compared with the parental strain. Treatment of the mutant with an endoplasmic/sarcoplasmic reticulum Ca2+ reuptake inhibitor (2,5-di-tert-butylhydroquinone) rescued key phenotypic differences, suggesting a potential therapeutic benefit for RTN2-disorder. Despite RTN2 being an endoplasmic reticulum (ER)-resident membrane shaping protein, our analysis of patient fibroblast cells did not find significant alterations in ER structure or the response to ER stress. Our findings delineate a distinct form of autosomal recessive dHMN with pyramidal features associated with RTN2 deficiency. This phenotype shares similarities with SIGMAR1-related dHMN and Silver-like syndromes, providing valuable insights into the clinical spectrum and potential therapeutic strategies for RTN2-related dHMN. [ABSTRACT FROM AUTHOR]

Purpose: To compare the effects of typical competition versus high-intensity intermittent warm-up (WU) on thermoregulatory responses and repeated sprint performance during wheelchair rugby game play. Methods: An intermittent sprint protocol (ISP) simulating the demands of wheelchair rugby was performed by male wheelchair rugby players (7 with cervical spinal cord injury [SCI] and 8 without SCI) following 2 WU protocols. These included a typical competition WU (control) and a WU consisting of high-intensity efforts (INT). Core temperature (Tcore), thermal sensation, and thermal comfort were recorded. Wheelchair performance variables associated to power, speed, and fatigue were also calculated. Results: During the WU, Tcore was similar between conditions for both groups. During the ISP, a higher Tcore was found for SCI compared to NON-SCI (38.1 [0.3] vs 37.7 [0.3] °C: P =.036, d = 0.75), and the SCI group experienced a higher peak Tcore for INT compared with control (39.0 [0.4] vs 38.6 [0.6] °C; P =.004). Peak Tcore occurred later in the ISP for players with SCI (96 [5.8] vs 48 [2.7] min; P <.001). All players reported a higher thermal sensation and thermal comfort following INT (P <.001), with no differences between conditions throughout the ISP. No significant differences were found in wheelchair performance variables during the ISP between conditions (P ≥.143). Conclusions: The high-INT WU increased thermal strain in the SCI group during the ISP, potentially due to increased metabolic heat production and impaired thermoregulation, while not impacting on repeated sprint performance. It may be advisable to limit high-INT bouts during a WU in players with SCI to mitigate issues related to hyperthermia in subsequent performance. [ABSTRACT FROM AUTHOR]

Wilson disease (WD) is caused by mutations in the ATP7B gene that encodes a copper (Cu) transporting ATPase whose trafficking from the Golgi to endo‐lysosomal compartments drives sequestration of excess Cu and its further excretion from hepatocytes into the bile. Loss of ATP7B function leads to toxic Cu overload in the liver and subsequently in the brain, causing fatal hepatic and neurological abnormalities. The limitations of existing WD therapies call for the development of new therapeutic approaches, which require an amenable animal model system for screening and validation of drugs and molecular targets. To achieve this objective, we generated a mutant Caenorhabditis elegans strain with a substitution of a conserved histidine (H828Q) in the ATP7B ortholog cua‐1 corresponding to the most common ATP7B variant (H1069Q) that causes WD. cua‐1 mutant animals exhibited very poor resistance to Cu compared to the wild‐type strain. This manifested in a strong delay in larval development, a shorter lifespan, impaired motility, oxidative stress pathway activation, and mitochondrial damage. In addition, morphological analysis revealed several neuronal abnormalities in cua‐1 mutant animals exposed to Cu. Further investigation suggested that mutant CUA‐1 is retained and degraded in the endoplasmic reticulum, similarly to human ATP7B‐H1069Q. As a consequence, the mutant protein does not allow animals to counteract Cu toxicity. Notably, pharmacological correctors of ATP7B‐H1069Q reduced Cu toxicity in cua‐1 mutants indicating that similar pathogenic molecular pathways might be activated by the H/Q substitution and, therefore, targeted for rescue of ATP7B/CUA‐1 function. Taken together, our findings suggest that the newly generated cua‐1 mutant strain represents an excellent model for Cu toxicity studies in WD. [ABSTRACT FROM AUTHOR]

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