Design, Characterization, and Incorporation of the Alkaline Aluminosilicate Binder in Temperature-Insulating Composites.

This paper covers the design of binder formulations and technology for low-energy building materials based on alkaline aluminosilicate binders developed for special uses. The microstructure of the binders was investigated using scanning electron and atomic force microscopy examination techniques. The identification of phase compositions was performed by means of X-ray diffraction.

[Clinical case report of acute dinitrophenol poisoning with a fatal outcome of Udmurt Republic].

Was to conduct the analysis of patient's clinical observation with acute dinitrophenol poisoning, admitted to a toxicological department of CCH №6 of Izhevsk, Udmurt Republic in 2021 yr. In this clinical case report, a 19 years old girl, who took 20 tablets of dinitrophenol, illegally obtained in online-shop, died. The fatal outcome was realized by the uncoupling of oxidative phosphorylation mechanism and cellular respiration, which in its turn led to serious dystrophic changes in all organs and tissues.

Comment on "Pushing the frontiers of density functionals by solving the fractional electron problem".

Kirkpatrick . (Reports, 9 December 2021, p. 1385) trained a neural network-based DFT functional, DM21, on fractional-charge (FC) and fractional-spin (FS) systems, and they claim that it has outstanding accuracy for chemical systems exhibiting strong correlation.

Liquid biopsy as a tool for predicts of severe COVID-19 and hospitalised community-acquired pneumonia.

Unlabelled: Cell-free DNA (cfDNA) is released into the circulation after apoptosis, necrosis, and active secretion from cells. In a healthy individual, cfDNA is present in small amounts, has a short half-life, and is predominantly derived from circulating hematopoietic cells. The composition and quantity of cfDNA dramatically changes during pathological conditions.

Mitigation of Corrosion Initiated by Cl and SO-ions in Blast Furnace Cement Concrete Mixed with Sea Water.

The use of blast furnace cement is an effective way to meet the requirements of sustainable development. However, CEM III/C is characterized by slow strength gain. The problem can be worse for plasticized reinforced blast furnace cement concretes mixed with sea water in view of shorter durability.

Neuronal Lipoprotein Lipase Deficiency Alters Neuronal Function and Hepatic Metabolism.

The autonomic regulation of hepatic metabolism offers a novel target for the treatment of non-alcoholic fatty liver disease (NAFLD). However, the molecular characteristics of neurons that regulate the brain-liver axis remain unclear. Since mice lacking neuronal lipoprotein lipase (LPL) develop perturbations in neuronal lipid-sensing and systemic energy balance, we reasoned that LPL might be a component of pre-autonomic neurons involved in the regulation of hepatic metabolism.

Inefficient Secretion of Anti-sigma Factor FlgM Inhibits Bacterial Motility at High Temperature.

Temperature is one of the key cues that enable microorganisms to adjust their physiology in response to environmental changes. Here we show that motility is the major cellular function of Escherichia coli that is differentially regulated between growth at normal host temperature of 37°C and the febrile temperature of 42°C. Expression of both class II and class III flagellar genes is reduced at 42°C because of lowered level of the upstream activator FlhD.

Differences in Stability, Activity and Mutation Effects Between Human and Mouse Leucine-Rich Repeat Kinase 2.

Mutations in the Leucine-rich repeat kinase 2 (LRRK2) gene have been implicated in the pathogenesis of Parkinson's disease (PD). Identification of PD-associated LRRK2 mutations has led to the development of novel animal models, primarily in mice. However, the characteristics of human LRRK2 and mouse Lrrk2 protein have not previously been directly compared.

Proteomic analysis reveals co-ordinated alterations in protein synthesis and degradation pathways in LRRK2 knockout mice.

Mutations in leucine-rich repeat kinase 2 (LRRK2) segregate with familial Parkinson's disease (PD) and genetic variation around LRRK2 contributes to risk of sporadic disease. Although knockout (KO) of Lrrk2 or knock-in of pathogenic mutations into the mouse germline does not result in a PD phenotype, several defects have been reported in the kidneys of Lrrk2 KO mice. To understand LRRK2 function in vivo, we used an unbiased approach to determine which protein pathways are affected in LRRK2 KO kidneys.

Acute Lesioning and Rapid Repair of Hypothalamic Neurons outside the Blood-Brain Barrier.

Neurons expressing agouti-related protein (AgRP) are essential for feeding. The majority of these neurons are located outside the blood-brain barrier (BBB), allowing them to directly sense circulating metabolic factors. Here, we show that, in adult mice, AgRP neurons outside the BBB (AgRP) were rapidly ablated by peripheral administration of monosodium glutamate (MSG), whereas AgRP neurons inside the BBB and most proopiomelanocortin (POMC) neurons were spared.

The G2385R risk factor for Parkinson's disease enhances CHIP-dependent intracellular degradation of LRRK2.

Autosomal dominant mutations in () are associated with Parkinson's disease (PD). Most pathogenic mutations result in amino acid substitutions in the central ROC (Ras of complex proteins)-C-terminus of ROC-kinase triple domain and affect enzymatic functions of the protein. However, there are several variants in , including the risk factor G2385R, that affect PD pathogenesis by unknown mechanisms.

[The current problems of investigations into thanatogenesis and the causes of death considered in the articles published in the journal "Sudebno-meditsinskaya ekspertiza (Forensic Medical Expertise)" during the period from 2000 to 2014].

The objective of the present work was the analysis of the scientometrical characteristics of the publication activity of the authors of the articles concerning the problems of investigations into thanatogenesis and the causes of death that were submitted for the publication in the journal "Sudebno-meditsinskaya ekspertiza" during the period from 2000 to 2014. The analysis was aimed at detecting the priority fields of research of interest not only for domestic but especially for foreign specialists. The study has revealed the most popular Russian-language and foreign journals that were most frequently cited by the authors of "Sudebno-meditsinskaya ekspertiza".

The function of orthologues of the human Parkinson's disease gene LRRK2 across species: implications for disease modelling in preclinical research.

In the period since LRRK2 (leucine-rich repeat kinase 2) was identified as a causal gene for late-onset autosomal dominant parkinsonism, a great deal of work has been aimed at understanding whether the LRRK2 protein might be a druggable target for Parkinson's disease (PD). As part of this effort, animal models have been developed to explore both the normal and the pathophysiological roles of LRRK2. However, LRRK2 is part of a wider family of proteins whose functions in different organisms remain poorly understood.

[THE RISK OF CHOLANGITIS OCCURRENCE AFTER ENDOSCOPIC INTERVENTIONS ON PAPILLA MAGNA OF DUODENUM].

Results of treatment of 72 patients, suffering choledocholithiasis, using transpapillary endoscopic interventions, were analyzed. In patients of the first group a complete endoscopic papillosphincterotomy was performed, and in the second group — a partial endoscopic papillosphincterotomy in combination with balloon dilatation of duodenal papilla magna. The rate of occurrence of late and immediate complications in the groups was compared.

[A case of the fatal injury by technical electricity from a mobile device (cell phone) connected to the circuit].

The authors report a case of the fatal injury by technical electricity from a mobile device (cell phone) attached to the circuit in a moist environment as a result of the unsafe handling of the gadget (when taking the bath).

Leptin potentiates astrogenesis in the developing hypothalamus.

Background: The proper establishment of hypothalamic feeding circuits during early development has a profound influence on energy homeostasis, and perturbing this process could predispose individuals to obesity and its associated consequences later in life. The maturation of hypothalamic neuronal circuitry in rodents takes place during the initial postnatal weeks, and this coincides with a dramatic surge in the circulating level of leptin, which is known to regulate the outgrowth of key neuronal projections in the maturing hypothalamus. Coincidently, this early postnatal period also marks the rapid proliferation and expansion of astrocytes in the brain.

Phosphorylation of LRRK2 by casein kinase 1α regulates trans-Golgi clustering via differential interaction with ARHGEF7.

LRRK2, a gene relevant to Parkinson's disease, encodes a scaffolding protein with both GTPase and kinase activities. LRRK2 protein is itself phosphorylated and therefore is subject to regulation by cell signalling; however, the kinase(s) responsible for this event have not been definitively identified. Here using an unbiased siRNA kinome screen, we identify and validate casein kinase 1α (CK1α) as being responsible for LRRK2 phosphorylation, including in the adult mouse striatum.

Heterogeneity of leucine-rich repeat kinase 2 mutations: genetics, mechanisms and therapeutic implications.

Variation within and around the leucine-rich repeat kinase 2 (LRRK2) gene is associated with familial and sporadic Parkinson's disease (PD). Here, we discuss the prevalence of LRRK2 substitutions in different populations and their association with PD, as well as molecular and cellular mechanisms of pathologically relevant LRRK2 mutations. Kinase activation was proposed as a universal molecular mechanism for all pathogenic LRRK2 mutations, but later reports revealed heterogeneity in the effect of mutations on different activities of LRRK2.

Aldehyde dehydrogenase 1 defines and protects a nigrostriatal dopaminergic neuron subpopulation.

Subpopulations of dopaminergic (DA) neurons within the substantia nigra pars compacta (SNpc) display a differential vulnerability to loss in Parkinson's disease (PD); however, it is not clear why these subsets are preferentially selected in PD-associated neurodegeneration. In rodent SNpc, DA neurons can be divided into two subpopulations based on the expression of aldehyde dehydrogenase 1 (ALDH1A1). Here, we have shown that, in α-synuclein transgenic mice, a murine model of PD-related disease, DA neurodegeneration occurs mainly in a dorsomedial ALDH1A1-negative subpopulation that is also prone to cytotoxic aggregation of α-synuclein.

Unbiased screen for interactors of leucine-rich repeat kinase 2 supports a common pathway for sporadic and familial Parkinson disease.

Mutations in leucine-rich repeat kinase 2 (LRRK2) cause inherited Parkinson disease (PD), and common variants around LRRK2 are a risk factor for sporadic PD. Using protein-protein interaction arrays, we identified BCL2-associated athanogene 5, Rab7L1 (RAB7, member RAS oncogene family-like 1), and Cyclin-G-associated kinase as binding partners of LRRK2. The latter two genes are candidate genes for risk for sporadic PD identified by genome-wide association studies.

Hexokinase activity is required for recruitment of parkin to depolarized mitochondria.

Autosomal recessive parkinsonism genes contribute to maintenance of mitochondrial function. Two of these, PINK1 and parkin, act in a pathway promoting autophagic removal of depolarized mitochondria. Although recruitment of parkin to mitochondria is PINK1-dependent, additional components necessary for signaling are unclear.

Identification of protein phosphatase 1 as a regulator of the LRRK2 phosphorylation cycle.

A cluster of phosphorylation sites in LRRK2 (leucine-rich repeat kinase 2), including Ser910, Ser935, Ser955 and Ser973, is important for PD (Parkinson's disease) pathogenesis as several PD-linked LRRK2 mutants are dephosphorylated at these sites. LRRK2 is also dephosphorylated in cells after pharmacological inhibition of its kinase activity, which is currently proposed as a strategy for disease-modifying PD therapy. Despite this importance of LRRK2 dephosphorylation in mutant LRRK2 pathological mechanism(s) and in LRRK2's response to inhibition, the mechanism by which this occurs is unknown.