Kejserrytter8321

This systematic review aims to explore the changes in expression of neuropeptides and/or their receptors following experimental trigeminal neuropathic pain in animals.

MEDLINE, Embase, and Scopus were searched for publications up to 31st March 2021. Study selection and data extraction were completed by two independent reviewers based on the eligibility criteria. The quality of articles was judged based on the Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE) risk-of-bias tool.

A total of 19 studies satisfied the eligibility criteria and were included for narrative synthesis. Methods of trigeminal neuropathic pain induction were nerve ligation, nerve compression/crush, nerve transection and dental pulp injury. Animal behaviours used for pain verification were evoked responses to mechanical and thermal stimuli. Non-evoked behaviours, including vertical exploration, grooming and food consumption, were also employed in some studies. Calcitonin gene-related peptide (CGRP) and substance P were the most frequently reported neuropeptides. Overall, unclear to high risk of bias was identified in the included studies.

Limited evidence has suggested the pro-nociceptive role of CGRP in trigeminal neuropathic pain. In order to further translational pain research, animal models of trigeminal neuropathic pain and pain validation methods need to be optimised. Complete reporting of future studies based on available guidelines to improve confidence in research is encouraged.

Limited evidence has suggested the pro-nociceptive role of CGRP in trigeminal neuropathic pain. In order to further translational pain research, animal models of trigeminal neuropathic pain and pain validation methods need to be optimised. Complete reporting of future studies based on available guidelines to improve confidence in research is encouraged.Infection associated with multidrug-resistant (MDR) bacteria has become a serious threat to public health, and there is an urgent demand of developing new antibiotics that offer combinatorial therapy to effectively combat MDR. Herein, a multifunctional two-dimensional nanoantibiotic was facilely designed and established on the basis of the covalent conjugation of CO-releasing molecule (CORM-401) and electrostatic adsorption of hyaluronic acid (HA) onto single-layered graphene quantum dots (SGQDs) to assemble SGQDs-CORM@HA nanosheets, abbreviated as SCH. Upon the enrichment of as-prepared nanoantibiotics in the community of targeted microbe, bacterial-secreted hyaluronidase (HAase) would cleave HA on SCH, and the sharp edges as well as the reactive sites on SGQDs-CORM nanosheets were exposed for cascade activation of synergistic antibacterial effects. Specifically, ultrathin SGQDs-CORM nanosheets can penetrate into bacterial cells deemed as the unique "nanoknife" effect. Under white light irradiation, SGQDs-CORM nanosheets can act as a high-efficient photosensitizer to generate cytotoxic singlet oxygen (1O2), as a well-recognized reactive oxygen species (ROS), to produce high oxidative stress and damage bacteria. As a complementary to photodynamic therapy (PDT), the accumulation of local ROS further triggered the release of CO to hinder the bacterial growth via causing plasma membrane damage and inducing metabolic disorders. Such synergistic treatment regimen arising from cascade-activated "nanoknife" effect and photodynamic/CO gas therapy, was devoted to outstanding on-demand antibacterial performance both in vitro and in vivo. Fascinatingly, the nanoplatform showed good biocompatibility toward both normal somatic cells and non-targeted bacteria. The remarkable antibacterial capability and admirable biocompatibility endow SCH with great potential to fight against MDR pathogens for in-coming clinical translations.Various conventional treatment strategies for volumetric muscle loss (VML) are often hampered by the extreme donor site morbidity, the limited availability of quality muscle flaps, and complicated, as well as invasive surgical procedures. The conventional biomaterial-based scaffolding systems carrying myoblasts have been extensively investigated towards improving the regeneration of the injured muscle tissues, as well as their injectable forms. However, the applicability of such designed systems has been restricted due to the lack of available vascular networks. Considering these facts, here we present the development of a unique set of two minimally invasively injectable modular microtissues, consisting of mouse myoblast (C2C12)-laden poly(lactic-co-glycolic acid) porous microspheres (PLGA PMs), or the micro-muscles, and human umbilical vein endothelial cell (HUVEC)-laden poly(ethylene glycol) hollow microrods (PEG HMs), or the microvessels. Besides systematic in vitro investigations, the myogenic performance of these modular composite microtissues, when co-injected, was explored in vivo using a mouse VML model, which confirmed improved in situ muscle regeneration and remolding. Together, we believe that the construction of these injectable modular microtissues and their combination for minimally invasive therapy provides a promising method for in situ tissue healing.Dendritic cells (DCs) rely on glycolysis for their energy needs to induce pro-inflammatory antigen-specific immune responses. Therefore, inhibiting DC glycolysis, while presenting the self-antigen, may prevent pro-inflammatory antigen-specific immune responses. Previously we demonstrated that microparticles with alpha-ketoglutarate (aKG) in the polymer backbone (paKG MPs) were able to generate anti-inflammatory DCs by sustained delivery of the aKG metabolite, and by modulating energy metabolism of DCs. Herein, we demonstrate that paKG MPs-based delivery of a glycolytic inhibitor, PFK15, using paKG MPs induces anti-inflammatory DCs (CD86LoMHCII+) by down-regulating glycolysis, CD86, tnf and IL-6 genes, while upregulating oxidative phosphorylation (OXPHOS) and mitochondrial genes. Furthermore, paKG MPs delivering PFK15 and a self-antigen, collagen type II (bc2), in vivo, in a collagen-induced autoimmune arthritis (CIA) mouse model, normalized paw inflammation and arthritis score, by generating antigen-specific immune responses. Specifically, these formulations were able to reduce activation of DCs in draining lymph nodes and impressively generated proliferating bc2-specific anti-inflammatory regulatory T cells in joint-associated popliteal lymph nodes. These data strongly suggest that sustained glycolytic inhibition of DCs in the presence of an antigen can induce antigen-specific immunosuppressive responses, therefore, generating a technology that can be applicable for treating autoimmune diseases.Impairments in social and role functioning have been associated with the prodromal phase of psychosis. Additionally, sleep disturbances impacting daily functioning have been detected across the schizophrenia spectrum. Relationships between social functioning, sleep quality, and psychotic-like experiences (PLEs) in undergraduate-level student populations are less understood. The current project aimed to investigate whether self-reported measures of sleep quality would moderate the relationship between social functioning and PLE endorsement in a community sample of 3042 undergraduate student participants between the ages of 18-35. Participants completed the Social Functioning Scale, the Pittsburgh Sleep Quality Index, and the Prodromal Questionnaire, which indexed PLEs. Bivariate correlations revealed significant associations between social functioning, sleep, and PLEs. As expected, poor sleep and poor social functioning were associated with increased endorsement of PLEs. Contrary to expectation, poor sleep quality was associated with better social functioning. In hierarchical multiple regression models, the interaction between social functioning and sleep was not associated with PLE endorsement. Results indicated that both poor sleep and poor social functioning were significantly associated with PLEs when included in the same model. These findings suggest that poor social functioning and disrupted sleep may act additively to influence PLEs, and that they are both important contributors to psychotic symptoms. Due to deleterious effects of poor sleep on physical and emotional health, these findings provide impetus to further investigate relationships between sleep quality, social functioning, and PLEs using such high-resolution methods as actigraphy, mobile sensing, ecological momentary assessment, and neuroimaging.Raffinose, stachyose and verbascose form the three major members of the raffinose family oligosaccharides (RFO) accumulated during seed development. Raffinose synthase (RS; EC 2.4.1.82) and stachyose synthase (STS; EC 2.4.1.67) have been associated with raffinose and stachyose synthesis, but the precise mechanism for verbascose synthesis is not well understood. In this study, full-length RS (2.7 kb) and STS (2.6 kb) clones were isolated by screening a cDNA library prepared from developing lentil seeds (18, 20, 22 and 24 days after flowering [DAF]) to understand the roles of RS and STS in RFO accumulation in developing lentil seeds. The nucleotide sequences of RS and STS genes were similar to those reported for Pisum sativum. Patterns of transcript accumulation, enzyme activities and RFO concentrations were also comparable to P. sativum. However, during lentil seed development raffinose, stachyose and verbascose accumulation corresponded to transcript accumulation for RS and STS, with peak transcript abundance occurring at about 22-24 DAF, generally followed by a sequential increase in raffinose, stachyose and verbascose concentrations followed by a steady level thereafter. Enzyme activities for RS, STS and verbascose synthase (VS) also indicated a sudden increase at around 24-26 DAF, but with an abrupt decline again coinciding with the subsequent steady state increase in the RFO. Galactangalactan galactosyl transferase (GGT), the galactinol-independent pathway enzyme, however, exhibited steady increase in activity from 24 DAF onwards before abruptly decreasing at 34 DAF. Although GGT activity was detected, isolation of a GGT sequence from the cDNA library was not successful.The safety and quality of aquatic foods are a public concern due to their content of pollutants, such as arsenic. A formula is derived for quantifying the benefit-risk ratio (HQ) of the essential polyunsaturated fatty acids vs. arsenic in Chinses mitten crabs. Among these arsenic species, the proportion of inorganic arsenic, which is extremely harmful to the human body, is less then 5%, and its level does not exceed the national standard limit. Meanwhile, comparing with the HQ from the original method, the HQs from groups 0 min, 5 min, 15 min are significantly higher(p  less then  0.05). This suggests the original assessment method could underestimate the risk of eating crabs. Eating steamed crabs is easier to digest essential fatty acids (EFAs) than eating raw crabs, and it also protects consumers against arsenic exposure. To achieve a good balance of dietary benefits and risks, the steaming duration of the crabs should exceed 30 min.The excitatory neurotransmitter glutamate gates post-synaptic N-methyl-d-aspartate (NMDA) receptors (NMDARs) to mediate extracellular Ca2+ entry and stimulate neuronal nitric oxide (NO) synthase to release NO and trigger neurovascular coupling (NVC). Neuronal and glial NMDARs may also operate in a flux-independent manner, although it is unclear whether their non-ionotropic mode of action is involved in NVC. Recently, endothelial NMDARs were found to trigger Ca2+-dependent NO production and induce NVC, but the underlying mode of signaling remains elusive. Herein, we report that GluN1 protein, as well as GluN2C and GluN3B transcripts and proteins, were expressed and that NMDA did not elicit inward currents, but induced a dose-dependent increase in intracellular Ca2+ concentration ([Ca2+]i) in the human brain microvascular endothelial cell line, hCMEC/D3. A multidisciplinary approach, including live cell imaging, whole-cell patch-clamp recordings, pharmacological manipulation and gene targeting, revealed that NMDARs increase the [Ca2+]i in a flux-independent manner in hCMEC/D3 cells.