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Trigeminal neuralgia (TN) is one of the most common neuropathic pain disorders and is often combined with other comorbidities if managed inadequately. However, the present understanding of its pathogenesis at the molecular level remains lacking. Long noncoding RNAs (lncRNAs) play crucial roles in neuropathic pain, and many studies have reported that specific lncRNAs are related to TN. This review summarizes the current understanding of lncRNAs in the pathogenesis, diagnosis, and treatment of TN. Recent studies have shown that the lncRNAs uc.48+, Gm14461, MRAK009713 and NONRATT021972 are potential candidate loci for the diagnosis and treatment of TN. The current diagnostic system could be enhanced and improved by a workflow for selecting transcriptomic biomarkers and the development of lncRNA-based molecular diagnostic systems for TN. The discovery of lncRNAs potentially impacts drug selection for TN; however, the current supporting evidence is limited to preclinical studies. Additional studies are needed to further test the diagnostic and therapeutic value of lncRNAs in TN.
Assuntos
Neuralgia , RNA Longo não Codificante , Neuralgia do Trigêmeo , Biomarcadores , Humanos , Neuralgia/terapia , RNA Longo não Codificante/genética , Neuralgia do Trigêmeo/diagnóstico , Neuralgia do Trigêmeo/genética , Neuralgia do Trigêmeo/terapiaRESUMO
With an incidence of 3-4.5 cases per million, adenoid cystic carcinoma (ACC) of the head and neck is one of the most common tumors of the parotid and sublingual salivary glands. In the clinical course, ACC is shown to have an aggressive long-term behavior, which leads to the fact that radical surgical resection of the tumor with tumor-free margins remains the "gold standard" in treating ACC. Particle radiation therapy and systemic molecular biological approaches offer new treatment options. However, risk factors for the formation and prognosis of ACC have not yet been clearly identified. The aim of the present review was to investigate long-term experience of diagnosis and treatment as well as risk and prognostic factors for occurrence and outcome of ACC.
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Multiple biological processes in mammalian cells are implicated in psoriasis (Ps) development and progression, as well as in the pathogenic mechanisms associated with this chronic immune-mediated inflammatory disease (IMID). These refer to molecular cascades contributing to the pathological topical and systemic reactions in Ps, where local skin-resident cells derived from peripheral blood and skin-infiltrating cells originating from the circulatory system, in particular T lymphocytes (T cells), are key actors. The interplay between molecular components of T cell signalling transduction and their involvement in cellular cascades (i.e. throughout Ca2+/CaN/NFAT, MAPK/JNK, PI3K/Akt/mTOR, JAK/STAT pathways) has been of concern in the last few years; this is still less characterised than expected, even though some evidence has accumulated to date identifying them as potential objects in the management of Ps. Innovative therapeutic strategies for the use of compounds such as synthetic Small Molecule Drugs (SMDs) and their various combinations proved to be promising tools for the treatment of Ps via incomplete blocking, also known as modulation of disease-associated molecular tracks. Despite recent drug development having mainly centred on biological therapies for Ps, yet displaying serious limitations, SMDs acting on specific pathway factor isoforms or single effectors within T cell, could represent a valid innovation in real-world treatment patterns in patients with Ps. Of note, due to the intricate crosstalk between intracellular pathways, the use of selective agents targeting proper tracks is, in our opinion, a challenge for modern science regarding the prevention of disease at its onset and also in the prediction of patient response to Ps treatment.
Assuntos
Psoríase , Linfócitos T , Animais , Humanos , Linfócitos T/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Psoríase/tratamento farmacológico , Psoríase/metabolismo , Pele/patologia , Mamíferos/metabolismoRESUMO
The term neurogenic heterotopic ossification (NHO) is used to describe the pathological bone formation in soft tissues, due to spinal cord or brain injury. Commonly is presented with pain and stiffness of the affected joint. NHO affects the quality of life of these patients, delays their rehabilitation and therefore increases morbidity. The aim of this article is to emphasize pathophysiology mechanism and review new molecular treatments of heterotopic ossification (HO). It was demonstrated that potent treatment strategies are based on understanding the molecular mechanisms and aiming to inhibit the pathological process of the HO in various stages. New treatments are targeting several factors such as bone morphogenetic proteins (BMPs), retinoic acid receptors (RARs), hypoxic inhibitors (Hif1-inhibitors, rapamycin), free radical scavengers and immunological agents (imatinib). The endogenous pathways that lead to HO at molecular and cellular levels have been the aim of many studies in recent years. New treatment options for HO should be recommended due to the ineffectiveness of traditional older options, such as anti-inflammatory drugs and radiation, especially in the case of NHO.
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Due to the direct band gap nature, extensive studies have been conducted to improve the optical behavior in monolayer transition metal dichalcogenides (TMDCs) with a formula of MX2 (M = Mo, W; X = S, Se, Te). One of the strongest modulating agents of optical behavior is a molecular superacid treatment; however, the chemical event has not been unveiled. Also, the engineering protocol for keeping the treatment is immature. In this work, we systematically study the superacid treatment procedures on monolayer molybdenum disulfide (MoS2) and propose that the interaction, a hydrophilic interaction, between the superacid molecule and MoS2 surface would be critical. As a result of the interaction, the superacid molecules spontaneously form an acidic layer with the thickness of several nanometers on the surface. The power-dependent photoluminescence (PL) measurement indicates the edge of MoS2 flake is more effective and electronically modulated by the treatment. By understanding the superacid nanolayer formation by the treatment, we succeeded in maintaining the ultrastrong PL in the superacid-treated MoS2 for more than 30 days in the ambient air by encapsulation with transparent organic polymers. This study advances the understanding and designing applications of strong luminescent properties in the superacid-treated TMDCs and paves the way toward engineering exciton dynamics and an experimental platform for treating multibody states.
RESUMO
To advance the development of atomically thin optoelectronics using two-dimensional (2D) materials, engineering strong luminescence with a physicochemical basis is crucial. Semiconducting monolayer transition-metal dichalcogenides (TMDCs) are candidates for this, but their quantum yield (QY) is known to be poor. Recently, a molecular superacid treatment of bis(trifluoromethane)sulfonimide (TFSI) generated unambiguously bright monolayer TMDCs and a high QY. However, this method is highly dependent on the processing conditions and therefore has not been generalized. Here, we shed light on environmental factors to activate the photoluminescence (PL) intensity of the TFSI-treated monolayer MoS2, with a factor of more than 2 orders of magnitude greater than the original by photoactivation. The method is useful for both mechanically exfoliated and chemically deposited samples. The existence of photoirradiation larger than the band gap demonstrates enhancement of the PL of MoS2; on the other hand, activation by thermal annealing, as demonstrated in the previous report, is less effective for enhancing the PL intensity. The photoactivated monolayer MoS2 shows a long lifetime of â¼1.35 ns, more than a 30-fold improvement over the original as exfoliated. The consistent realization of the bright monolayer MoS2 reveals that air exposure is an essential factor in the process. TFSI treatment in a N2 environment was not effective for achieving a strong PL, even after the photoactivation. These findings can serve as a basis for engineering the bright atomically thin materials for 2D optoelectronics.
RESUMO
The interface engineering of two-dimensional (2D) transition-metal dichalcogenides (TMDs) has been regarded as a promising strategy to modulate their outstanding electrical and optoelectronic properties because of their inherent 2D nature and large surface-to-volume ratio. In particular, introducing organic molecules and polymers directly onto the surface of TMDs has been explored to passivate the surface defects or achieve better interfacial properties with neighboring surfaces efficiently, thus leading to great opportunities for the realization of high-performance TMD-based applications. This review provides recent progress in the interface engineering of TMDs with organic molecules and polymers corresponding to the modulation of their electrical and optoelectronic characteristics. Depending on the interfaces between the surface of TMDs and dielectric, conductive contacts or the ambient environment, we present various strategies to introduce an organic interlayer from materials to processing. In addition, the role of native defects on the surface of TMDs, such as adatoms or vacancies, in determining their electrical characteristics is also discussed in detail. Finally, the future challenges and opportunities associated with the interface engineering are highlighted.