Browse Articles
Discover research articles across all indexed journals
Therapeutic evaluation of Martynia annua derived carbon dots in epileptic Drosophila model
Abstract This study investigates the synthesis and characterization of Carbon dots (MA-CDs) derived from the aqueous extract of Martynia annua and examining their potential effects in an epilepsy model Drosophila melanogaster. Phytochemical analysis confirmed the presence of saponin, terpeniods, and flavanoids in the leaf extract, which facilitated the green synthesis of MA-CDs. Physicochemical characterization revealed an absorbance peak at 326 nm, the mean size of the particle was 3.17 ± 0.16 nm, and moderate stability (−1.6 mV). To assess the therapeutic potential of MA-CDs alongside the antiepileptic drug Carbamazepine (CBZ), we conducted behavioral and cognitive assays in para bang senseless (parabss1) mutants of Drosophila, a model organism for epilepsy. Seizures induced by vortex and heat shock were significantly mitigated in a dose-dependent manner in flies treated with both MA-CDs and CBZ. However, higher doses of CBZ and MA-CDs increased the climbing ability of the flies. In cognitive assays, CBZ at higher doses improved memory and learning in mutant flies, while MA-CDs also showed significant impact. MA-CDs were consumed at a higher rate than CBZ when incorporated into food. The green synthesized MA-CDs at its higher concentration has garnered its positive effect on the mutants along with the CBZ antiepileptic drug which also has shown its positive effects when different concentration of them were treated to the mutants.
Simplistic synthesis of L-Serine-ZnS composites with distinct morphological nature, enhanced thermal stability and superior photocatalytic enactment for ciprofloxacin removal
Postdocs file for union recognition at University of Michigan
Synergistic deficits in parvalbumin interneurons and dopamine signaling drive ACC dysfunction in chronic pain
Chronic pain arises from maladaptive changes in both peripheral and central nervous systems, including the anterior cingulate cortex (ACC), a key region implicated in descending pain modulation. Chronic pain increases the excitability of pyramidal neurons in the ACC. Although a reduction in inhibitory inputs onto pyramidal neurons has been observed in neuropathic conditions, the identity of the specific interneurons responsible remains unclear. We show that chronic pain selectively impairs parvalbumin (PV), but not somatostatin, interneurons in the rostral ACC. This is characterized by a decrease in the density of PV interneuron processes, a reduction in their surrounding perineuronal net, and a lower expression of PV. Functionally, PV interneurons display diminished inhibitory efficacy in vitro and reduced phasic activation in response to aversive stimuli in vivo. Dopamine (DA) fibers preferentially contact PV interneurons and excite them via D1 dopamine receptor activation, increasing their excitability and enhancing the frequency of inhibitory postsynaptic currents on pyramidal neurons in healthy, but not neuropathic, conditions. Furthermore, we show that this pathway is involved in hunger-induced analgesia: Food deprivation increases DA release in the ACC and consequently decreases pain thresholds in neuropathic mice. Conversely, when mice are not food deprived, neuropathic pain significantly reduces DA release in the ACC. We conclude that the loss of PV interneuron inhibitory efficacy, alongside convergent hypodopaminergic signaling, synergistically contributes to pathological ACC dysfunction and associated symptoms of chronic pain.
Risks of relying on uncertain carbon dioxide removal in climate policy
Mapping the regulatory genetic landscape of complex traits using a chicken advanced intercross line
Phage-mediated peripheral kill-the-winner facilitates the maintenance of costly antibiotic resistance
Abstract The persistence of antibiotic resistant (AR) bacteria in the absence of antibiotic pressure raises a paradox regarding the fitness costs associated with antibiotic resistance. These fitness costs should slow the growth of AR bacteria and cause them to be displaced by faster-growing antibiotic sensitive (AS) counterparts. Yet, even in the absence of antibiotic pressure, slower-growing AR bacteria can persist for prolonged periods of time. Here, we demonstrate a mechanism that can explain this apparent paradox. We hypothesize that lytic phage can modulate bacterial spatial organization to facilitate the persistence of slower-growing AR bacteria. Using surface-associated growth experiments with the bacterium Escherichia coli in conjunction with individual-based computational simulations, we show that phage disproportionately lyse the faster-growing AS counterpart cells located at the biomass periphery via a peripheral kill-the-winner dynamic. This enables the slower-growing AR cells to persist even when they are susceptible to the same phage. This phage-mediated selection is accompanied by enhanced bacterial diversity, further emphasizing the role of phage in shaping the assembly and evolution of bacterial systems. The mechanism is potentially relevant for any antibiotic resistance genetic determinant and has tangible implications for the management of bacterial populations via phage therapy.
Bridging the Interlayer Binding to Ordered π‐Conjugated Units for Constructing High‐Performing Light Polarization Crystals
Abstract The light polarization modulation involves the capacity to respond selectively to light‐mater interaction and is dependent on the optical anisotropy of crystalline materials. The π‐conjugated component is almost typically utilized to produce such materials in the short‐wave ultraviolet region; however, the conflicting link between high optical anisotropy and strong layered habit is difficult to reconcile. As a result, many anisotropic crystals are limited to tiny crystals rather than processing optical devices. This study designs crystals with beneficial but easy‐to‐grow layered structure and strong optical anisotropy by bridging the interlayer binding to ordered π‐conjugated units. To this end, two new hybrid crystals Na 2 [C(NH 2 ) 3 ][HCOO] 3 (1Na) and K 2 [C(NH 2 ) 3 ][HCOO] 3 (2K) are reported by combining cationic regulation and π‐conjugated units. The strong interlayer interaction and stable crystal structure of 1Na have been found to be caused by the orbital hybridization and Lewis acidity of Na + and [HCOO] groups. This allows for the easy growth of centimeter‐large, high optical quality 1Na single crystals, providing crystal assurance for all‐around testing for a practical crystal. Using the most accurate minimal deviation angle method, the birefringence is measured to be 0.174–0.258 @253‐1013 nm, surpassing all reported crystals with the same components of [HCOO] or [C(NH 2 ) 3 ] in the applied short‐wave ultraviolet region as well as the corresponding commercial crystals. More importantly, preliminary Glan–Taylor prism is designed to test its light polarization ability. This work will serve as a guide for future research on innovative short‐wave ultraviolet birefringent crystals.
Bentonite nanoclay and spray techniques as a nano pico technology (NPT) for enhancing mortar in heritage and historical buildings
Windows of susceptibility to neonatal acute kidney injury and nephron loss in a rabbit model
Association of lipid accumulation product with mortality in patients with diabetes mellitus
Age-related decline in retinal function in marmosets
Overview of genetic variants in a cohort of Iranian patients with leukodystrophy
Mitochondrial haplogroup A2 is associated with increased COVID-19 mortality in an admixed Brazilian population
Birds combined calls more than 11 million years ago
Abstract Multiple members of the tit and chickadee (= Parid) family combine two classes of calls, F and D, in a rigid order FD. In Japanese tits, FD has been argued on the basis of multiple experiments to involve syntax and non-trivial compositionality. How ancient are these call combinations? We show that FD combinations (as well as individual F and D calls) are present in nearly all Parid species, and almost absent in their closest relatives, the Remizidae and Stenostiridae. Using phylogenetic tools and ancestral reconstruction methods, we infer that FD combinations very likely emerged between 11 and 26 million years ago in the eastern Himalayas. This result contributes to evolutionary animal linguistics using a comparative phylogenetic approach to reconstruct the evolution of call combinations.
Predicting car accident severity in Northwest Ethiopia: a machine learning approach leveraging driver, environmental, and road conditions
A large language model for multimodal identification of crop diseases and pests
PLAA/UFD-3 regulates P-bodies through its intrinsic disordered domain
Regulation of proteome homeostasis is crucial for the survival and adaptation to changing environments for all species. In eukaryotes, this process is finely tuned through regulation at the level of transcription, translation, protein modification, and protein degradation. The phospholipase A2 activating protein (PLAA) is present in all eukaryotes and believed to be a key player in ubiquitin-dependent protein sorting and degradation via its interactions with ubiquitin and/or the AAA+ ATPase, valosin-containing protein (VCP/p97). PLAA’s molecular targets and interaction network remain unclear. We used Caenorhabditis elegans and unbiased proteome-scale approaches to investigate neuronal specific interactors of the C. elegans PLAA ortholog UFD-3 (ubiquitin fusion degradation 3), its effect on ubiquitinated proteins, and global protein expression changes in an ufd-3 mutant. We found that PLAA may play a unique role in cytoplasmic messenger ribonucleic acid (mRNA) processing bodies (P-bodies). Using biochemical analysis in vitro and fluorescence imaging in C. elegans , we show that UFD-3 directly interacts with the mRNA decapping complex regulatory subunit DCAP-1. UFD-3's intrinsic disordered region (IDR), which contains conserved amino acid motifs, is important for the recruitment of DCAP-1 to P-bodies. Finally, we show that loss of the IDR does not affect UFD-3's role in sorting ubiquitinated proteins through the multivesicular body pathway. Collectively, our results suggest that UFD-3's role in P-bodies is distinct from its role in the ubiquitin-dependent protein degradation pathway and the IDR is only critical for UFD-3-regulated P-bodies pathways. Thus, PLAA/UFD-3 might regulate the proteome via two distinct pathways: ubiquitinated protein turnover, as well as mRNA regulation through P-bodies.