Search

In this investigation, novel cellulose fibers were acquired from the Bassia Indica plant to serve as a reinforcement source in composite materials. The morphological characteristics were studied using Scanning Electron Microscopy (SEM). The surface chemistry, crystallinity, and functional groups of Bassia Indica fibers were analyzed using X-ray Diffraction (XRD), Energy Dispersive X-ray (EDX) spectroscopy, and Attenuated Total Reflectance-Fourier Transform Infrared spectroscopy (ATR-FTIR), which assess the crystal structure, elemental composition, and surface functional groups, respectively. The thermal behavior of Bassia Indica fibers were assessed through Thermogravimetric Analysis (TGA). Anatomical techniques demonstrated the abundant presence of fibroblasts in the fibers. The presence of lignocellulosic fiber (lignin, cellulose and hemicellulose) was confirmed through ATR-FTIR analysis. The analysis of physical properties unveiled a fiber density of 1.065 ± 0.025 g/cm³ and a diameter of 145.58 ± 7.89 μm. The crystalline size of Bassia Indica fibers reached 2.23 nm, with a crystallinity index of 40.12 %, and an activation energy of 93.78 kJ/mol, TGA research revealed that Bassia Indica fibers are thermally stable up to 260.24 °C. Additionally, the fibers experienced maximum degradation at 321.23 °C. Weibull statistical analysis was performed using parameters 2 and 3 to calculate the observed dispersion in the experimental tensile results after analyzing the mechanical properties of the fibers possessing a tensile strength of 417.50 ± 7.08 MPa, Young's modulus of 17.46 ± 1.55 GPa, stress at failure of 1.17 ± 0.02 % and interfacial shear strength of 6.99 ± 1.10 MPa. The results were additionally compared to how they were stated in the relevant sources. Bassia Indica fibers can be considered a viable choice for reinforcing lightweight bio-composites.

Solar ovens are eco-friendly ovens that use solar energy, a clean, sustainable and above all free source of energy. In the context of the economic and environmental crises facing the world today, solar cookers are considered a good alternative to electric cookers or those based on wood combustion. Several types of solar cooker have been developed in recent years. However, the box type remains the most efficient and simplest. To this end, an experimental study of three types of box-type solar cookers (triangle, trapezoid and rectangle) was carried out in this work. For each type of solar cooker, the effect of the number of reflectors added to the Cookers system was examined. The experimental tests were carried out in August 2023 under the climatic conditions of Morocco's eastern region. The evaluation of the systems studied is based on the hourly evolution of air, absorber and load temperatures for each type of solar furnace in different cases. Thermal photos were also taken using a Dia-Cam thermal imaging camera to visualize temperature distribution and analyze the thermal behavior of the systems. The obtained results show that the thermal behavior of three solar furnaces and the evolution of the absorber temperature depend on the load used. In addition, a significant improvement in absorber temperature and water boiling time was observed with the addition of solar reflectors. For example, the absorber temperature was increased by up to 40 °C and the water boiling time was reduced by more than 120 min in the case of triangle-type furnaces.

Summary: Background: Blood-based biomarkers of Alzheimer’s disease (AD) have become increasingly important as scalable tools for diagnosis and determining clinical trial eligibility. P-tau217 is the most promising due to its excellent sensitivity and specificity for AD-related pathological changes. Methods: We compared the performance of two commercially available plasma p-tau217 assays (ALZpath p-tau217 and Janssen p-tau217+) in 294 individuals cross-sectionally. Correlations with amyloid PET and tau PET were assessed, and Receiver Operating Characteristic (ROC) analyses evaluated both p-tau217 assays for identifying AD pathology. Findings: Both plasma p-tau217 assays were strongly associated with amyloid and tau PET. Furthermore, both plasma p-tau217 assays identified individuals with AD vs other neurodegenerative diseases (ALZpath AUC = 0.95; Janssen AUC = 0.96). Additionally, plasma p-tau217 concentrations rose with AD severity and their annual changes correlated with tau PET annual change. Interpretation: Both p-tau217 assays had excellent diagnostic performance for AD. Our study supports the future clinical use of commercially-available assays for p-tau217. Funding: This research is supported by the Weston Brain Institute, Canadian Institutes of Health Research (CIHR), Canadian Consortium on Neurodegeneration in Aging, the Alzheimer's Association, Brain Canada Foundation, the Fonds de Recherche du Québec - Santé and the Colin J. Adair Charitable Foundation.

It is essential to study the porosity, thermal conductivity, and P-wave velocity of calcarenites, as well as the anisotropy coefficients of the thermal conductivity and P-wave velocity, for civil engineering, and conservation and restoration of historical monuments. This study focuses on measuring the thermal conductivity using the thermal conductivity scanning (TCS) technique and measuring the P-wave velocity using portable equipment. This was applied for some dry and saturated calcarenite samples in the horizontal and vertical directions (parallel and perpendicular to the bedding plane, respectively). The calcarenites were selected from some historical monuments in Morocco. These physical properties were measured in the laboratory to find a reliable relationship between all of these properties. As a result of the statistical analysis of the obtained data, excellent linear relationships were observed between the porosity and both the thermal conductivity and porosity. These relationships are characterized by relatively high coefficients of determination for the horizontal and vertical samples. Based on the thermal conductivity and P-wave velocity values in these two directions, the anisotropy coefficients of these two properties were calculated. The internal structure and the pore fabric of the calcarenite samples were delineated using scanning electron microscopy (SEM), while their chemical and mineral compositions were studied using the energy dispersive X-ray analysis (EDXA) and X-ray diffraction (XRD) techniques.

Introduction: Cerebral small vessel disease (SVD) is a common co-pathology in elderly and individuals with dementia. Neuroimaging markers of SVD include white matter hyperintensities (WMH) and MRI-visible perivascular spaces (PVS). However, the mechanisms underlying changes in these markers over time, whether ischemic or beta-amyloid (Aβ)-related, remain elusive. Here, we evaluated the effects of microstructural injury in the normal-appearing white matter and Aβ in the cerebral cortex on the progression of WMH and PVS over three years. Methods: Data was obtained from two independent cohorts: (i) TRIAD, comprising cognitively normal, MCI, and AD dementia participants (baseline: N=199, follow-up year 1 and 2: N=102 and 62); and (ii) MITNEC-C6, comprising “real-world” patients with mixed dementia and moderate-to- severe WMH burden (baseline: N=52, 2 years follow-up: N=25). We quantified global WMH and PVS volumes from FLAIR and T1w MRI. At baseline, we examined associations between these volumes and diffusion MRI-derived free water. Longitudinally, we employed linear [mixed-effect] models to investigate the relation of WMH or PVS volume changes over time with baseline free water, using cortical Aβ-PET, age, sex, and APOE-ε4 as covariates. Results: In TRIAD and MITNEC-C6 respectively, mean ages were 72±6 and 77±8 y, 60% and 42% were female, and 41% and 48% were Aβ-positive. At baseline, higher free water in normal- appearing white matter was associated with higher WMH volume (β_TRIAD=+0.34±0.06, P_TRIAD

Gastrointestinal stromal tumors (GISTs) arising from the rectum are rare. We report the case of an aggressive rectal gastrointestinal stromal tumor (GIST) in a 60-year-old female that presented for symptoms of constipation and lower gastrointestinal bleeding. Upon rectal examination, a hard mass was found at 6cm from the anal marge. An MRI was indicated that shows a well-demarcated lesion originates from the distal rectum with exophytic growth and central necrosis. The diagnosis of rectal gist was confirmed by colonoscopy with biopsy and immunohistochemical analyses of bioptic material. Liver metastases were seen on computerized tomography (CT). She was referred for palliative chemotherapy. The patient had suffered from intestinal obstruction three weeks after his initial presentation and passed away shortly thereafter. We aimed to report this case as an aggressive and rare GIST localization.

Objective: The essential role of mitochondria in regulation of metabolic function and other physiological processes has garnered enormous interest in understanding the mechanisms controlling the function of this organelle. We assessed the role of the BBSome, a protein complex composed of eight Bardet-Biedl syndrome (BBS) proteins, in the control of mitochondria dynamic and function. Methods: We used a multidisciplinary approach that include CRISPR/Cas9 technology-mediated generation of a stable Bbs1 gene knockout hypothalamic N39 neuronal cell line. We also analyzed the phenotype of BBSome deficient mice in presence or absence of the gene encoding A-kinase anchoring protein 1 (AKAP1). Results: Our data show that the BBSome play an important role in the regulation of mitochondria dynamics and function. Disruption of the BBSome cause mitochondria hyperfusion in cell lines, fibroblasts derived from patients as well as in hypothalamic neurons and brown adipocytes of mice. The morphological changes in mitochondria translate into functional abnormalities as indicated by the reduced oxygen consumption rate and altered mitochondrial distribution and calcium handling. Mechanistically, we demonstrate that the BBSome modulates the activity of dynamin-like protein 1 (DRP1), a key regulator of mitochondrial fission, by regulating its phosphorylation and translocation to the mitochondria. Notably, rescuing the decrease in DRP1 activity through deletion of one copy of the gene encoding AKAP1 was effective to normalize the defects in mitochondrial morphology and activity induced by BBSome deficiency. Importantly, this was associated with improvement in several of the phenotypes caused by loss of the BBSome such as the neuroanatomical abnormalities, metabolic alterations and obesity highlighting the importance of mitochondria defects in the pathophysiology of BBS. Conclusions: These findings demonstrate a critical role of the BBSome in the modulation of mitochondria function and point to mitochondrial defects as a key disease mechanism in BBS.

Summary: Population-scale datasets of healthy individuals capture genetic and environmental factors influencing gene expression. The expression variance of a gene of interest (GOI) can be exploited to set up a quasi loss- or gain-of-function “in population” experiment. We describe here an approach, huva (human variation), taking advantage of population-scale multi-layered data to infer gene function and relationships between phenotypes and expression. Within a reference dataset, huva derives two experimental groups with LOW or HIGH expression of the GOI, enabling the subsequent comparison of their transcriptional profile and functional parameters. We demonstrate that this approach robustly identifies the phenotypic relevance of a GOI allowing the stratification of genes according to biological functions, and we generalize this concept to almost 16,000 genes in the human transcriptome. Additionally, we describe how huva predicts monocytes to be the major cell type in the pathophysiology of STAT1 mutations, evidence validated in a clinical cohort.

Objective: Fibroblast growth factor 21 (FGF21) is a peripherally-derived endocrine hormone that acts on the central nervous system (CNS) to regulate whole body energy homeostasis. Pharmacological administration of FGF21 promotes weight loss in obese animal models and human subjects with obesity. However, the central targets mediating these effects are incompletely defined. Methods: To explore the mechanism for FGF21's effects to lower body weight, we pharmacologically administer FGF21 to genetic animal models lacking the obligate FGF21 co-receptor, β-klotho (KLB), in either glutamatergic (Vglut2-Cre) or GABAergic (Vgat-Cre) neurons. In addition, we abolish FGF21 signaling to leptin receptor (LepR-Cre) positive cells. Finally, we examine the synergistic effects of FGF21 and leptin to lower body weight and explore the importance of physiological leptin levels in FGF21-mediated regulation of body weight. Results: Here we show that FGF21 signaling to glutamatergic neurons is required for FGF21 to modulate energy expenditure and promote weight loss. In addition, we demonstrate that FGF21 signals to leptin receptor-expressing cells to regulate body weight, and that central leptin signaling is required for FGF21 to fully stimulate body weight loss during obesity. Interestingly, co-administration of FGF21 and leptin synergistically leads to robust weight loss. Conclusions: These data reveal an important endocrine crosstalk between liver- and adipose-derived signals which integrate in the CNS to modulate energy homeostasis and body weight regulation.

A 58-year-old female had undergone previous mechanical mitral replacement with a Starr-Edwards ball and cage valve (Edwards Lifesciences, Irvine, CA) at 11 years of age for rheumatic disease. The valve functioned well until pannus resulted in prosthetic valve stenosis with class IV dyspnea and pulmonary hypertension. She underwent reoperative mitral replacement with an On-X mechanical mitral prosthesis (Cryolife, Kennesaw, GA) 48 years after initial implantation. To our knowledge, this case represents the longest known implant period of a ball and cage mitral valve in the literature. This presentation highlights the durability of this historic prosthesis, along with the role of reoperative surgery decades after initial implantation. Résumé: Une femme de 58 ans avait subi un remplacement mécanique d’une valve mitrale par une valve à bille Starr-Edwards alors (Edwards Lifesciences, Irvine, CA) qu’elle avait 11 ans par suite d’une maladie rhumatismale. La valve avait bien fonctionné jusqu’à ce que la formation de pannus entraîne une sténose de celle-ci s’accompagnant de dyspnée de classe IV et d’hypertension pulmonaire. La femme a subi une intervention chirurgicale visant à remplacer la valve sténosée par une valve mécanique On-X (Cryolife, Kennesaw, GA) 48 ans après l’implantation initiale. À notre connaissance, il s’agit de la plus longue période d’implantation connue d’une valve mécanique mitrale à bille Starr-Edwards rapportée dans la littérature. Le présent article met en évidence la durabilité de cette prothèse historique, ainsi que le rôle de la chirurgie réopératoire des décennies après l’implantation initiale.

Objective: Bone morphogenetic protein 8B (BMP8B) plays a major role in the regulation of energy homeostasis by modulating brown adipose tissue (BAT) thermogenesis and white adipose tissue (WAT) browning. Here, we investigated whether BMP8B's role in metabolism is affected by obesity and the possible molecular mechanisms underlying that action. Methods: Central treatments with BMP8B were performed in rats fed a standard (SD) and high-fat diet (HFD), as well as in genetically modified mice. Energy balance studies, infrared thermographic analysis of BAT and molecular analysis of the hypothalamus, BAT and WAT were carried out. Results: We show for the first time that HFD-induced obesity elicits resistance to the central actions of BMP8B on energy balance. This obesity-induced BMP8B resistance is explained by i) lack of effects on AMP-activated protein kinase (AMPK) signaling, ii) decreased BMP receptors signaling and iii) reduced expression of Bardet-Biedl Syndrome 1 (BBS1) protein, a key component of the protein complex BBSome in the ventromedial nucleus of the hypothalamus (VMH). The possible mechanistic involvement of BBS1 in this process is demonstrated by lack of a central response to BMP8B in mice carrying a single missense disease-causing mutation in the Bbs1 gene. Conclusions: Overall, our data uncover a new mechanism of central resistance to hormonal action that may be of relevance in the pathophysiology of obesity.

Summary: Background: Tau in Alzheimer's disease (AD) is assessed via cerebrospinal fluid (CSF) and Positron emission tomography (PET). Novel methods to detect phosphorylated tau (pTau) in blood have been recently developed. We aim to investigate agreement of tau status as determined by [18F]MK6240 tau-PET, plasma pTau181 and pTau231. Methods: We assessed cognitively unimpaired young, cognitively unimpaired, mild cognitive impairment and AD individuals with [18F]MK6240, plasma pTau181, pTau 231, [18F]AZD4694 amyloid-PET and MRI. A subset underwent CSF assessment.We conducted ROC curves to obtain cut-off values for plasma pTau epitopes. Individuals were categorized as positive or negative in all biomarkers. We then compared the distribution among concordant and discordant groups in relation to diagnosis, Aβ status, APOEε4 status, [18F]AZD4694 global SUVR, hippocampal volume and CSF pTau181. Findings: The threshold for positivity was 15.085 pg/mL for plasma pTau181 and 17.652 pg/mL for plasma pTau231. Most individuals had concordant statuses, however, 18% of plasma181/PET, 26% of plasma231/PET and 25% of the pTau231/pTau181 were discordant. Positivity to at least one biomarker was often accompanied by diagnosis of cognitive impairment, Aβ positivity, APOEε4 carriership, higher levels of [18F]AZD4694 global SUVR, hippocampal atrophy and CSF pTau181. Interpretation: Plasma pTau181, pTau231 and [18F]MK6240 seem to reflect different stages of tau progression. Plasma biomarkers can be useful in the context of diagnostic information and clinical trials, to evaluate the disease stage. Moreover, they seem to confidently evaluate tau-PET positivity. Funding: Moreover, this study was supported by Weston Brain Institute, Canadian Institute of Health Research and Fonds de Recherche du Québec.

3,6-Dimethyl-1-phenyl-1H-pyrazolo[3,4-d]pyrimidin-4(5H)-one 3 was prepared by an intramolecular cyclization of N-(4-cyano-3-methyl-1-phenyl-1H-pyrazol-5-yl) acetamide 2 in ethanol in the presence of piperidine. N-allylation and N-propargyl alkylation of N-substituted pyrazolo[3,4-d] pyrimidin-4(5H)-one 3 yielded the corresponding dipolarophiles 4 and 5 which afford by condensation with arylnitrile oxides in toluene the expected new isoxazolines 6 and isoxazoles 7, respectively. On the other hand, the aminopyrazole 1 in refluxing with ethanol in the presence of sodium hydroxide afforded the corresponding carboxamide 8, which then, was converted to its ethyl 3-methyl-4-oxo-1-phenyl-4,5-dihydro-1H-pyrazolo[3,4-d] pyrimidine-6-carboxylate 9 with neat diethyl oxalate. The dipolarophile 10 on regiospecific 1,3-dipolar cycloaddition with arylnitrile oxides affords isoxazoles 11 and the unexpected deethoxycarbonylated isoxazoles 12. The target compounds were completely characterized by 1H NMR, 13C NMR, IR and HRMS. Keywords: Aminopyrazole-carbonitrile, Pyrazolo[3,4-d]pyrimidinones, 1,3-dipolar cycloaddition, Isoxazolines, Isoxazoles

Objectives: Endothelial cells that line the entire vascular system play a pivotal role in the control of various physiological processes, including metabolism. Additionally, endothelial dysfunction is associated with many pathological conditions, including obesity. Here, we assessed the role of the BBSome, a protein complex composed of eight Bardet-Biedl syndrome (BBS) proteins in endothelial cells. Methods: We studied the effects of BBSome disruption in endothelial cells on vascular function, body weight, glucose homeostasis, and the liver and retina. For this, we generated mice with selective BBSome disruption in endothelial cells through Bbs1 gene deletion. Results: We found that endothelial cell–specific BBSome disruption causes endothelial dysfunction, as indicated by the impaired acetylcholine-induced vasorelaxation in both the aorta and mesenteric artery. This was associated with an increase in the contractile response to thromboxane A2 receptor agonist (U46619) in the mesenteric artery. Mechanistically, we demonstrated that mice lacking the Bbs1 gene in endothelial cells show elevated vascular angiotensinogen gene expression, implicating renin-angiotensin system activation in the vascular changes evoked by endothelial BBSome deficiency. Strikingly, our data indicate that endothelial BBSome deficiency increases body weight and fat mass and causes hepatosteatosis along with alterations in hepatic expression of lipid metabolism–related genes and metabolomics profile. In addition, electroretinogram and optical coherence tomography analyses revealed functional and structural abnormalities in the retina, evoked by absence of the endothelial BBSome. Conclusions: Our findings demonstrate that the BBSome in endothelial cells is required for the regulation of vascular function, adiposity, hepatic lipid metabolism, and retinal function.

Objectives: The hypothalamic ventromedial nucleus (VMH) plays a major role in metabolic control, but the molecular mechanisms involved remain poorly defined. We analyzed the relevance of the BBSome, a protein complex composed of 8 Bardet–Biedl syndrome (BBS) proteins including BBS1, in VMH steroidogenic factor 1 (SF1) neurons for the control of energy homeostasis and related physiological processes. Methods: We generated mice bearing selective BBSome disruption, through Bbs1 gene deletion, in SF1 neurons (SF1Cre/Bbs1fl/fl). We analyzed the consequence on body weight, glucose homeostasis, and cardiovascular autonomic function of BBSome loss in SF1 neurons. Results: SF1Cre/Bbs1fl/fl mice had increased body weight and adiposity under normal chow conditions. Food intake, energy absorption, and digestive efficiency were not altered by Bbs1 gene deletion in SF1 neurons. SF1Cre/Bbs1fl/fl mice exhibited lower energy expenditure, particularly during the dark cycle. Consistent with this finding, SF1Cre/Bbs1fl/fl mice displayed reduced sympathetic nerve traffic and expression of markers of thermogenesis in brown adipose tissue. SF1Cre/Bbs1fl/fl mice also had lower sympathetic nerve activity to subcutaneous white adipose tissue that was associated with a protein expression profile that promotes lipid accumulation. Notably, despite obesity and hyperinsulinemia, SF1Cre/Bbs1fl/fl mice did not exhibit significant changes in glucose metabolism, insulin sensitivity, blood pressure, and baroreflex sensitivity. Conclusions: Our findings demonstrate that the SF1 neuron BBSome is necessary for the regulation of energy homeostasis through modulation of the activity of the sympathetic nervous system and that the SF1 neuron BBSome is required for the development of obesity-related comorbidities.

Experimental measurements and numerous theoretical models have been employed to comprehend the dynamics of charge carriers in manganite system. The present work highlights the electrical transport of La0.5Ca0.4Ag0.1MnO3 compound in the temperature range [80 K–700 K]. It is found that the conductivity spectra of the studied sample present a double Jonscher variation, universal Jonscher evolution and Drude variation respectively for low, intermediate and high temperature ranges. The temperature dependence of the frequency exponent confirms the efficiency of the quantum mechanical tunneling, the non-overlapping small polaron tunneling and the correlated barrier hopping mechanisms at separated dispersive regions. DC conductivity analysis confirms the semiconductor behavior of the studied sample. Then, the transport properties have been explained in term of a thermally activated small polaron hopping and Mott-variable range hopping processes respectively at high and low temperature sides. Also, the disorder energy is predicted to decrease with rising frequency which could be due to variation in the separation path between the hop centers. Moreover, Greaves variable range hopping model is the suitable one that describes the transport properties in the intermediate temperature range. The scaling approach indicates that the time temperature superposition principle is valid in the temperature side [180 K–360 K].

The activity developed in vast areas of northwest africa causes serious invasions of different species of orthoptera insect which poses a great danger to agriculture and thus to nutrition of peoples and animals in general. In (Algeria), FAO considers the regions of naama, tindouf, adrar and bechar in Algeria as the theater of signaling of swarms and intervention. In this article, we want to shed light on the peculiarities of this insect (orthoptera), its statistics, its species and the families it belongs to in the arid region called naama (southwestern Algeria). The study of orthoptera in the arid region of naama (southern west of Algeria) conducted at three stations (Mecheria, Ben ammar) and the wetland of (Ain ben khelil) during the period from august 2015 until august 2017 allowed to identify nineteen (19) species divided into two sub-orders ensifera and caelifera. They are divided into five families (Tettigonidae, Gryllidae Pamphagidae, Acrididae, and Pyrgomorphidae). Acrididae family is the largest with five species. Oedipodinae subfamily is the most numerous genera and species it includes four (4) different types genders and seven species (7). The highest diversity index of the shannon-weaver is obtained at the wetland ain ben khelil is 2.12 bits, followed by the station of ben ammar with 2.06 bits and station of mecheria remains in third with 1.89 bit values of fairness are close to one corresponding to populations in balance entered them. The determination of species, genders and families of this population is based on several morphological criteria such as the shape of the pronotum, and the color of membranous wings and the shape of the hind legs.

In the recent years, the dominant cementitious materials have been industrial by products such as fly ash. This present data describes some of the cementitious products that are attracting attention in the global research community and the properties and characteristics of these materials that affect their performance such durability, mechanically properties and reduction of carbon dioxid (CO2). The present investigation deals with the chemical synthesis of cementitious material using fly ash of eggs shell rich in calcium(Ca) and sand dune(southern west of Algeria) rich in silica(SiO2).The composition of geopolymers synthesized are the most compressive resistant with a maximum stress of 49.71 MPa, the most flexible (E = 2.63 GPa) and the most ductile (εr = 65.42%).The characteristic properties of the chemically synthesized cementitious materials were analyzed by the chemical composition analysis XRF, XRD and SEM analyses.

Orthoptera are capable of threat of agriculture, human health and resists to all pesticides used. This problem is become an objectif of many research's. Pesticide resistance is the adaptation of insects to this materials resulting in decreased susceptibility to that chemical. In other hand, insects develop a resistance through natural selection such chemically transformation, physiological phenomena and genetic. In our study, natural chitin was extracted from cuticle of orthoptera insect (southern of Algeria) using a chemical strategy consists on hydrochloric acid, sodium hydroxide and hydrogen peroxide. The average yield of extracted chitin (96.95% w) indicates that the cuticles of orthoptera are a rich source of chitin. Cuticle exhibit a heterogeneous morphology characterized by a compact structure with well-defined fibrous. For extracted chitin and after demineralization, we can appreciate important changes in the surface of material. We observed round shaped black spots indicated that they are composed almost exclusively by K2O and CaO (cuticle) in the other hand we observed several white taches behind black spots, here we suggest that white taches present chitin extracted. The most resistant orthoptera are the ones to survive and transform their properties by chemical process such as transformation of chitin to chitosan and physiological development such as age. In this study, we have found that the first generation has a great resistance to insecticides. After insecticide application we observed a descendant's resistance decreased a larger because sensitive insects have been selectively killed. After repeated applications resistant insects may comprise the minority. Finally we can said, insecticide resistance can be found in many types and we can conclude that physiological resistance and chemical resistance coexist together and cannot separate. In the physiological resistance, the insect populations may develop the ability to avoid or reduce lethal insecticide exposure. In contrast, chemical resistance refers to modification mechanisms, including reduced cuticle penetration and decreased or increased target site sensitivity. The extracted chitin sample and chitosan were characterized by several characterizations such as X-ray diffraction, scanning electron microscopy SEM, FTIR and 1HRMN spectroscopy.

In this data we report on conductors polymers nanocomposites synthesized by in situ polymerization of aniline (ANI) and/or 4-aminobenzylamine (4-ABA) in presence of chromium montmorillonite (MMT-Cr+3) and ammonium persulfate as oxidizing agent. Homopolymers and copolymers (PANI-co-4-ABA) were prepared at various initial monomer composition and were characterized by Fourier transform Infrared (FT-IR) and UV–vis spectroscopy, X-ray diffraction (XRD) and cyclic voltammeter. The data describes the behavior of the corresponding homopolymers Poly (4-ABA) and (PANI) and showed that the in-situ polymerization produced real nanocomposites containing aniline and 4-aminobenzylamine units and films of products exhibit good electrochemical properties. Keywords: Polyaniline, Nanocomposites, In situ polymerization, Poly (4-aminobenzylamine), Montmorillonite clay

Noncoding RNAs (ncRNAs) comprise a class of versatile transcripts that are highly involved in the regulation of a wide range of biological processes. Functional long ncRNAs (> 200 nts in length) often adopt secondary structures that arise co-transcriptionally. To maintain the secondary structure elements as well as preparation homogeneity of such transcripts, native-like conditions should be maintained throughout the in vitro synthesis, purification and chemical tagging processes. In this optimized protocol, we describe a simple method for obtaining homogenous samples followed by chemically tagging the 3′ termini of natively-purified structured ncRNA domains that are longer than 200 nts. This protocol replaces traditional hazardous radioactive labeling with fluorescence tagging, and eliminates laborious and time consuming RNA purification and concentration steps and replaces them with straightforward recovery of RNA through centrifugal filtration, preserving the homogeneity and mono-dispersion of the preparations. The protocol provides: • An integrative, simple and straightforward approach for synthesis, purification and labeling of structured ncRNAs whilst maintaining their secondary structure intact. • Replacing hazardous, laborious and time-consuming radioactive labeling of RNA with much simpler fluorescence tagging, thereby facilitating potential downstream applications such as electrophoretic mobility shift assay (EMSA). • A versatile protocol that could be applicable to a wide-range of chemical tags and in principle could be used to label DNA or RNA.

Objective: Crosstalk between adipocytes and local neurons may be an important regulatory mechanism to control energy homeostasis. We previously reported that perturbation of adipocyte de novo lipogenesis (DNL) by deletion of fatty acid synthase (FASN) expands sympathetic neurons within white adipose tissue (WAT) and stimulates the appearance of “beige” adipocytes. Here we tested whether WAT DNL activity can also influence neuronal regulation and thermogenesis in brown adipose tissue (BAT). Methods and results: Induced deletion of FASN in all adipocytes in mature mice (iAdFASNKO) enhanced sympathetic innervation and neuronal activity as well as UCP1 expression in both WAT and BAT. This increased sympathetic innervation could be observed at both 22 °C and 30 °C, indicating it is not a response to heat loss but rather adipocyte signaling. In contrast, selective ablation of FASN in brown adipocytes of mice (iUCP1FASNKO) failed to modulate sympathetic innervation and the thermogenic program in BAT. Surprisingly, DNL in brown adipocytes was also dispensable in maintaining euthermia when UCP1FASNKO mice were cold-exposed. Conclusion: These results indicate that DNL in white adipocytes influences long distance signaling to BAT, which can modify BAT sympathetic innervation and expression of genes involved in thermogenesis. Keywords: Adipocytes, Lipogenesis, Brown adipose tissue, Thermogenesis, Sensory nerve, Sympathetic nerve, SNS outflow

Abstract Background To assess the diagnostic and prognosis value of myocardial native T2 measurement in the distinction between Light-chain (AL) and Transthyretin (ATTR) cardiac amyloidosis (CA). Methods Forty-four patients with CA (24 AL; 20 ATTR) and 40 healthy subjects underwent 1.5 T cardiovascular magnetic resonance (CMR). They all underwent T1 and T2 mapping (modified Look-Locker inversion recovery), cine and late gadolinium enhancement (LGE) imaging. The Query Amyloid Late Enhancement (QALE) score, myocardial native T2, T1 and extra cellular volume fraction (ECV) were calculated for all patients. Results Of the 44 patients, 36 (82%) exhibited enhancement on LGE images. Mean QALE score of AL (7.9 ± 6) and ATTR (10.5 ± 5) patients were similar (p = 0.6). Myocardial native T2 was significantly (p

Objectives: The autonomic nervous system is critically involved in mediating the control by leptin of many physiological processes. Here, we examined the role of the leptin receptor (LepR) in proopiomelanocortin (POMC) and agouti-related peptide (AgRP) neurons in mediating the effects of leptin on regional sympathetic and parasympathetic nerve activity. Methods: We analyzed how deletion of the LepR in POMC neurons (POMCCre/LepRfl/fl mice) or AgRP neurons (AgRPCre/LepRfl/fl mice) affects the ability of leptin to increase sympathetic and parasympathetic nerve activity. We also studied mice lacking the catalytic p110α or p110β subunits of phosphatidylinositol-3 kinase (PI3K) in POMC neurons. Results: Leptin-evoked increase in sympathetic nerve activity subserving thermogenic brown adipose tissue was partially blunted in mice lacking the LepR in either POMC or AgRP neurons. On the other hand, loss of the LepR in AgRP, but not POMC, neurons interfered with leptin-induced sympathetic nerve activation to the inguinal fat depot. The increase in hepatic sympathetic traffic induced by leptin was also reduced in mice lacking the LepR in AgRP, but not POMC, neurons whereas LepR deletion in either AgRP or POMC neurons attenuated the hepatic parasympathetic nerve activation evoked by leptin. Interestingly, the renal, lumbar and splanchnic sympathetic nerve activation caused by leptin were significantly blunted in POMCCre/LepRfl/fl mice, but not in AgRPCre/LepRfl/fl mice. However, loss of the LepR in POMC or AgRP neurons did not interfere with the ability of leptin to increase sympathetic traffic to the adrenal gland. Furthermore, ablation of the p110α, but not the p110β, isoform of PI3K from POMC neurons eliminated the leptin-elicited renal sympathetic nerve activation.Finally, we show trans-synaptic retrograde tracing of both POMC and AgRP neurons from the kidneys. Conclusions: POMC and AgRP neurons are differentially involved in mediating the effects of leptin on autonomic nerve activity subserving various tissues and organs. Keywords: Leptin, Autonomic nervous system, Energy homeostasis, Cardiovascular regulation

Objective: Hypothalamic arcuate nucleus-specific pro-opiomelanocortin deficient (ArcPomc−/−) mice exhibit improved glucose tolerance despite massive obesity and insulin resistance. We demonstrated previously that their improved glucose tolerance is due to elevated glycosuria. However, the underlying mechanisms that link glucose reabsorption in the kidney with ArcPomc remain unclear. Given the function of the hypothalamic melanocortin system in controlling sympathetic outflow, we hypothesized that reduced renal sympathetic nerve activity (RSNA) in ArcPomc−/− mice could explain their elevated glycosuria and consequent enhanced glucose tolerance. Methods: We measured RSNA by multifiber recording directly from the nerves innervating the kidneys in ArcPomc−/− mice. To further validate the function of RSNA in glucose reabsorption, we denervated the kidneys of WT and diabetic db/db mice before measuring their glucose tolerance and urine glucose levels. Moreover, we performed western blot and immunohistochemistry to determine kidney GLUT2 and SGLT2 levels in either ArcPomc−/− mice or the renal-denervated mice. Results: Consistent with our hypothesis, we found that basal RSNA was decreased in ArcPomc−/− mice relative to their wild type (WT) littermates. Remarkably, both WT and db/db mice exhibited elevated glycosuria and improved glucose tolerance after renal denervation. The elevated glycosuria in obese ArcPomc−/−, WT and db/db mice was due to reduced renal GLUT2 levels in the proximal tubules. Overall, we show that renal-denervated WT and diabetic mice recapitulate the phenotype of improved glucose tolerance and elevated glycosuria associated with reduced renal GLUT2 levels observed in obese ArcPomc−/− mice. Conclusion: Hence, we conclude that ArcPomc is essential in maintaining basal RSNA and that elevated glycosuria is a possible mechanism to explain improved glucose tolerance after renal denervation in drug resistant hypertensive patients.

Brown adipose tissue (BAT) is a specialized tissue critical for non-shivering thermogenesis producing heat through mitochondrial uncoupling; whereas white adipose tissue (WAT) is responsible of energy storage in the form of triglycerides. Another type of fat has been described, the beige adipose tissue; this tissue emerges in existing WAT depots but with thermogenic ability, a phenomenon known as browning. Several peripheral signals relaying information about energy status act in the brain, particularly the hypothalamus, to regulate thermogenesis in BAT and browning of WAT. Different hypothalamic areas have the capacity to regulate the thermogenic process in brown and beige adipocytes through the sympathetic nervous system (SNS). This review discusses important concepts and discoveries about the central control of thermogenesis as a trip that starts in the hypothalamus, and taking the sympathetic roads to reach brown and beige fat to modulate thermogenic functions.

Objective: We have previously shown that the consumption of a low-carbohydrate ketogenic diet (KD) by mice leads to a distinct physiologic state associated with weight loss, increased metabolic rate, and improved insulin sensitivity [1]. Furthermore, we identified fibroblast growth factor 21 (FGF21) as a necessary mediator of the changes, as mice lacking FGF21 fed KD gain rather than lose weight [2]. FGF21 activates the sympathetic nervous system (SNS) [3], which is a key regulator of metabolic rate. Thus, we considered that the SNS may play a role in mediating the metabolic adaption to ketosis. Methods: To test this hypothesis, we measured the response of mice lacking all three β-adrenergic receptors (β-less mice) to KD feeding. Results: In contrast to wild-type (WT) controls, β-less mice gained weight, increased adipose tissue depots mass, and did not increase energy expenditure when consuming KD. Remarkably, despite weight-gain, β-less mice were insulin sensitive. KD-induced changes in hepatic gene expression of β-less mice were similar to those seen in WT controls eating KD. Expression of FGF21 mRNA rose over 60-fold in both WT and β-less mice fed KD, and corresponding circulating FGF21 levels were 12.5 ng/ml in KD-fed wild type controls and 35.5 ng/ml in KD-fed β-less mice. Conclusions: The response of β-less mice distinguishes at least two distinct categories of physiologic effects in mice consuming KD. In the liver, KD regulates peroxisome proliferator-activated receptor alpha (PPARα)-dependent pathways through an action of FGF21 independent of the SNS and beta-adrenergic receptors. In sharp contrast, induction of interscapular brown adipose tissue (BAT) and increased energy expenditure absolutely require SNS signals involving action on one or more β-adrenergic receptors. In this way, the key metabolic actions of FGF21 in response to KD have diverse effector mechanisms.

The unfolded protein response (UPR), induced by endoplasmic reticulum (ER) stress, regulates the expression of factors that restore protein folding homeostasis. However, in the liver and kidney, ER stress also leads to lipid accumulation, accompanied at least in the liver by transcriptional suppression of metabolic genes. The mechanisms of this accumulation, including which pathways contribute to the phenotype in each organ, are unclear. We combined gene expression profiling, biochemical assays, and untargeted lipidomics to understand the basis of stress-dependent lipid accumulation, taking advantage of enhanced hepatic and renal steatosis in mice lacking the ER stress sensor ATF6α. We found that impaired fatty acid oxidation contributed to the early development of steatosis in the liver but not the kidney, while anorexia-induced lipolysis promoted late triglyceride and free fatty acid accumulation in both organs. These findings provide evidence for both direct and indirect regulation of peripheral metabolism by ER stress.

Natural materials (e.g. rocks and soils) are porous media, whose microstructures present a wide diversity. They generally consist of a heterogeneous solid phase and a porous phase which may be fully or partially saturated with one or more fluids. The prediction of elastic and acoustic properties of porous materials is very important in many fields, such as physics of rocks, reservoir geophysics, civil engineering, construction field and study of the behavior of historical monuments. The aim of this work is to predict the elastic and acoustic behaviors of isotropic porous materials of a solid matrix containing dry, saturated and partially saturated spherical pores. For this, a homogenization technique based on the Mori–Tanaka model is presented to connect the elastic and acoustic properties to porosity and degree of water saturation. Non-destructive ultrasonic technique is used to determine the elastic properties from measurements of P-wave velocities. The results obtained show the influence of porosity and degree of water saturation on the effective properties. The various predictions of Mori–Tanaka model are then compared with experimental results for the elastic and acoustic properties of calcarenite.

Activation of the brain renin-angiotensin system (RAS) stimulates energy expenditure through increasing of the resting metabolic rate (RMR), and this effect requires simultaneous suppression of the circulating and/or adipose RAS. To identify the mechanism by which the peripheral RAS opposes RMR control by the brain RAS, we examined mice with transgenic activation of the brain RAS (sRA mice). sRA mice exhibit increased RMR through increased energy flux in the inguinal adipose tissue, and this effect is attenuated by angiotensin II type 2 receptor (AT2) activation. AT2 activation in inguinal adipocytes opposes norepinephrine-induced uncoupling protein-1 (UCP1) production and aspects of cellular respiration, but not lipolysis. AT2 activation also opposes inguinal adipocyte function and differentiation responses to epidermal growth factor (EGF). These results highlight a major, multifaceted role for AT2 within inguinal adipocytes in the control of RMR. The AT2 receptor may therefore contribute to body fat distribution and adipose depot-specific effects upon cardio-metabolic health.

Objective: Elevations in brain angiotensin-II cause increased energy expenditure and a lean phenotype. Interestingly, the metabolic effects of increased brain angiotensin-II mimic the actions of leptin, suggesting an interaction between the two systems. Here we demonstrate that angiotensin-type 1a receptors (AT1aR) in the subfornical organ (SFO), a forebrain structure emerging as an integrative metabolic center, play a key role in the body weight-reducing effects of leptin via brown adipose tissue (BAT) thermogenesis. Methods: Cre/LoxP technology coupled with targeted viral delivery to the SFO in a mouse line bearing a conditional allele of the Agtr1a gene was utilized to determine the interaction between leptin and SFO AT1aR in metabolic regulation. Results: Selective deletion of AT1aR in the SFO attenuated leptin-induced weight loss independent of changes in food intake or locomotor activity. This was associated with diminished leptin-induced increases in core body temperature, blunted upregulation of BAT thermogenic markers, and abolishment of leptin-mediated sympathetic activation to BAT. Conclusions: These data identify a novel interaction between angiotensin-II and leptin in the control of BAT thermogenesis and body weight, and highlight a previously unrecognized role for the forebrain SFO in metabolic regulation.

A new class of dicationic ionic liquids (ILs) were synthesized for electrochemical applications at high temperatures. The syntheses are based on a dialkylation reaction of N-alkylpiperidine followed by anion exchange. The structures of ILs, based on piperidinium combined with hexafluorophosphate anion, were identified by using 1H, 13C, 19F, 31P NMR and FT-IR spectroscopy. ILs’ thermal properties were investigated in the temperature range from −50 to 350 °C by using differential scanning calorimetry (DSC). In the frequency of 10−2–106 Hz range, dielectric measurements were performed on ILs’ samples at various temperatures from −80 to 20 °C, i.e. around the glass transition temperature. The peak relaxation was observed near to this temperature. Also, the conductivity was investigated and the energy activation determined. The temperature dependence of the relaxation times was shown to be governed by the Arrhenius equation.

Summary: Hypothalamic endoplasmic reticulum (ER) stress is a key mechanism leading to obesity. Here, we demonstrate that ceramides induce lipotoxicity and hypothalamic ER stress, leading to sympathetic inhibition, reduced brown adipose tissue (BAT) thermogenesis, and weight gain. Genetic overexpression of the chaperone GRP78/BiP (glucose-regulated protein 78 kDa/binding immunoglobulin protein) in the ventromedial nucleus of the hypothalamus (VMH) abolishes ceramide action by reducing hypothalamic ER stress and increasing BAT thermogenesis, which leads to weight loss and improved glucose homeostasis. The pathophysiological relevance of this mechanism is demonstrated in obese Zucker rats, which show increased hypothalamic ceramide levels and ER stress. Overexpression of GRP78 in the VMH of these animals reduced body weight by increasing BAT thermogenesis as well as decreasing leptin and insulin resistance and hepatic steatosis. Overall, these data identify a triangulated signaling network involving central ceramides, hypothalamic lipotoxicity/ER stress, and BAT thermogenesis as a pathophysiological mechanism of obesity. : The brain senses lipids, such as fatty acids, and modifies energy metabolism accordingly. However, it is unclear whether other lipid species may be involved. Contreras et al. now demonstrate that ceramides regulate energy balance through the induction of hypothalamic lipotoxicity and modulation of endoplasmic reticulum functionality. This leads to changes in sympathetic tone and brown adipose tissue (BAT)-induced thermogenesis, impacting body weight.