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Kinesin Family Member 21B (KIF21B) encoded by KIF21B (MIM*608322), belongs to the Kinesin superfamily proteins, which play a key role in microtubule organisation in neuronal dendrites and axons. Recently, heterozygous variants in KIF21B were implicated as the cause of intellectual disability and brain malformations in four unrelated individuals. We report a 9-year-old male with delayed speech, hyperactivity, poor social interaction, and autistic features. A parent-offspring trio exome sequencing identified a novel de novo rare heterozygous variant, NM_001252102.2: c.1513A>C, p.(Ser505Arg) in exon 11 of KIF21B. In vivo functional analysis using in utero electroporation in mouse embryonic cortex revealed that the expression of Ser505Arg KIF21B protein in the cerebral cortex impaired the radial migration of projection neurons, thus confirming the pathogenicity of the variant. Our report further validates pathogenic variants in KIF21B as a cause of neurodevelopmental disorder.

KIF21B is a kinesin protein that promotes intracellular transport and controls microtubule dynamics. We report three missense variants and one duplication in KIF21B in individuals with neurodevelopmental disorders associated with brain malformations, including corpus callosum agenesis (ACC) and microcephaly. We demonstrate, in vivo, that the expression of KIF21B missense variants specifically recapitulates patients’ neurodevelopmental abnormalities, including microcephaly and reduced intra- and inter-hemispheric connectivity. We establish that missense KIF21B variants impede neuronal migration through attenuation of kinesin autoinhibition leading to aberrant KIF21B motility activity. We also show that the ACC-related KIF21B variant independently perturbs axonal growth and ipsilateral axon branching through two distinct mechanisms, both leading to deregulation of canonical kinesin motor activity. The duplication introduces a premature termination codon leading to nonsense-mediated mRNA decay. Although we demonstrate that Kif21b haploinsufficiency leads to an impaired neuronal positioning, the duplication variant might not be pathogenic. Altogether, our data indicate that impaired KIF21B autoregulation and function play a critical role in the pathogenicity of human neurodevelopmental disorder. Kinesins regulate intracellular transport and microtubule dynamics. Here, the authors show that KIF21B variants in humans associate with corpus callosum agenesis and microcephaly. Using mice and zebrafish, they showed the cellular mechanisms altered by the missense KIF21B variants.

Background Morin is a flavonoid found in many edible fruits. The hippocampus and entorhinal cortex play crucial roles in memory formation and consolidation. This study aimed to characterize the effect of morin on recognition and space memory in healthy C57BL/6 adult mice and explore the underlying molecular mechanism. Methods Morin was administered i.p. at 1, 2.5, and 5 mg/kg/24 h for 10 days. The Morris water maze (MWM), novel object recognition, novel context recognition, and tasks were conducted 1 day after the last administration. The mice's brains underwent histological characterization, and their protein expression was examined using immunohistochemistry and Western blot techniques. Results In the MWM and novel object recognition tests, mice treated with 1 mg/kg of morin exhibited a significant recognition index increase compared to the control group. Besides, they demonstrated faster memory acquisition during MWM training. Additionally, the expression of pro‐brain‐derived neurotrophic factor (BDNF), BDNF, and postsynaptic density protein 95 proteins in the hippocampus of treated mice showed a significant increase. In the entorhinal cortex, only the pro‐BDNF increased. Morin‐treated mice exhibited a significant increase in the hippocampus's number and length of dendrites. Conclusion This study shows that morin improves recognition memory and spatial memory in healthy adult mice. Morin improves recognition and spatial memory in healthy adult mice. We suggest that the molecular mechanism for these effects involves the increased production and BDNF secretion by astrocytes.

The use of refined used lubricating oils (RULO) is an opportunity for use for the industrial sector, improving the environment. The objective of the research was to evaluate different RULO/diesel mixtures from the AT80 and AT40C1 treatments. The experiment consisted of applying different proportions of RULO, forming five different mixtures between ALUR/diesel. The mixes were 85/15, 70/30, 55/45, 40/60 and 30/70. The results showed that the best mixtures were M4 and M5 of the AT80 treatment, with average density of 0.80 g/cm3, viscosity of 5.83 cP, electrical stability of 1694.33 V, flash point of 95°C and 96.67% oil. With these results, a new alternative and use is created, reducing diesel and economic costs for the oil industry that prepares oil-based drilling fluids. El aprovechamiento de los aceites lubricantes usados refinados (ALUR), son una oportunidad de uso para el sector industrial, mejorando el medio ambiente. El objetivo de la investigación fue evaluar diferentes mezclas de ALUR/diesel a partir de los tratamientos AT80 y AT40C1. El experimento consistió en aplicar diferentes proporciones de ALUR, formando cinco mezclas diferentes entre el ALUR/diésel. Las mezclas fueron 85/15, 70/30, 55/45, 40/60 y 30/70. Los resultados mostraron que las mejores mezclas fueron M4 y M5 del tratamiento AT80, con promedios de densidad de 0.80 g/cm3, viscosidad de 5.83 cP, estabilidad eléctrica de 1694.33 V, punto de inflamación de 95°C y 96.67% de aceite. Con estos resultados se crea una nueva alternativa y aprovechamiento, disminuyendo el diésel y los costos económicos a la industria petrolera que prepara fluidos de perforación base aceite.

The purpose of this research was to evaluate the refining of used lubricating oils (ULOs), and their possible use as drilling fluids. 17 treatments were evaluated and sulfuric acid and nonylphenol were used as reagents at concentrations of 0.12, 0.24 and 0.36 g/mL and temperatures of 40, 60, 80 and 100 °C. AT80 and AT100 ULOs treated at 80 and 100 °C without reagents, presented an average density of 0.84 g/cm-3, a viscosity of 76.3 and 75.3 cP, an electrical stability of 1,731.3 and 1,394.6 V and a flash point of 183 and 190 °C as higher. The ST40C1 and ST40C2 treatments, added with reagents, showed similar results to AT80 and AT100 in the evaluated variables, but they are more expensive treatments. According to the results, it is concluded that the refined ULO can be a substitute for the oil used in the formulation of oil-based drilling fluids.

The improper handling of used lubricating oil (ULO) in Tabasco, Mexico, and worldwide is a serious problem posing a high risk of soil and water pollution. Therefore, this study evaluated the handling of ULO in 10 municipalities in the state of Tabasco. Collection sites were chosen by simple random sampling. The ULO collected was assessed for solids, water, oil and density. The results show that small generators have the greatest potential to generate ULO in Tabasco. Huimanguillo, Comalcalco and Cardenas were the municipalities with the highest ULO generation. The ULO with the highest quality for its low water and solids content was collected in Jalpa de Mendez, Comalcalco and Car Dealerships. 1,287 automotive repair shops were tested in the 10 municipalities that were included

Completion of neuronal migration is critical for brain development. Kif21b is a plus-end directed kinesin motor protein that promotes intracellular transport and controls microtubule dynamics in neurons. Here we report a physiological function of Kif21b during radial migration of projection neurons in the mouse developing cortex. In vivo analysis in mouse and live imaging on cultured slices demonstrate that Kif21b regulates the radial glia-guided locomotion of new-born neurons independently of its motility on microtubules. Unexpectedly we show that Kif21b directly binds and regulates the actin cytoskeleton both in vitro and in vivo in migratory neurons. We establish that Kif21b-mediated regulation of actin cytoskeleton dynamics influences branching and nucleokinesis during neuronal locomotion. Altogether, our results reveal atypical roles of Kif21b on the actin cytoskeleton during migration of cortical projection neurons.

The corpus callosum (CC) is the largest interhemispheric connection that is largely formed by the axons of layer 2/3 callosal projection neurons (CPNs) through a series of tightly regulated cellular events, including neuronal specification, migration, axon extension and branching. Defects in any of those steps may prevent the proper development of the corpus callosum resulting in a spectrum of disorders collectively referred to as corpus callosum dysgenesis (CCD). Here, we report four unrelated families carrying bi-allelic variants in WDR47 presenting with CCD together with other neuroanatomical phenotypes such as microcephaly, cerebellar abnormalities and hydrocephalus. Using a combination of in vitro and in vivo mouse models and complementation assays, we show that independently from its previously identified functions in neuronal migration and axonal extension, WDR47 is required for survival of callosal neurons by contributing to the maintenance of mitochondrial and microtubule homeostasis. We further provide evidence that severity of the CCD phenotype is determined by the degree of the loss of function caused by the human variants. Taken together, we identify WDR47 as a causative gene of a new neurodevelopmental syndrome characterized by corpus callosum abnormalities and other neuroanatomical malformations.

Completion of neuronal migration is critical for brain development. Kif21b is a plus-end directed kinesin motor protein that promotes intracellular transport and controls microtubule dynamics in neurons. Here we report a physiological function of Kif21b during radial migration of projection neurons in the mouse developing cortex. In vivo analysis in mouse and live imaging on cultured slices demonstrate that Kif21b regulates the radial glia-guided locomotion of new-born neurons independently of its motility on microtubules. Unexpectedly we show that Kif21b directly binds and regulates the actin cytoskeleton both in vitro and in vivo in migratory neurons. We establish that Kif21b-mediated regulation of actin cytoskeleton dynamics influences branching and nucleokinesis during neuronal locomotion. Altogether, our results reveal atypical roles of Kif21b on the actin cytoskeleton during migration of cortical projection neurons.Competing Interest StatementThe authors have declared no competing interest.

Acinetobacter baumannii (named in honor of the American bacteriologists Paul and Linda Baumann) is a Gram-negative, multidrug-resistant (MDR) pathogen that causes nosocomial infections, especially in intensive care units (ICUs) and immunocompromised patients with central venous catheters. A. baumannii has developed a broad spectrum of antimicrobial resistance, associated with a higher mortality rate among infected patients compared with other non-baumannii species. In terms of clinical impact, resistant strains are associated with increases in both in-hospital length of stay and mortality. A. baumannii can cause a variety of infections; most involve the respiratory tract, especially ventilator-associated pneumonia, but bacteremia and skin wound infections have also been reported, the latter of which has been prominently observed in the context of war-related trauma. Cases of meningitis associated with A. baumannii have been documented. The most common risk factor for the acquisition of MDR A baumannii is previous antibiotic use, following by mechanical ventilation, length of ICU/hospital stay, severity of illness, and use of medical devices. Current efforts focus on addressing all the antimicrobial resistance mechanisms described in A. baumannii, with the objective of identifying the most promising therapeutic scheme. Bacteriophage- and artilysin-based therapeutic approaches have been described as effective, but further research into their clinical use is required