YokoCo

Endometriosis, a benign gynecologic and chronic inflammatory disease, is defined by the presence of endometrial tissue outside the uterus characterized mainly by pelvic pain and infertility. Because endometriosis affects approximately 10% of females, it represents a significant socioeconomic burden worldwide having tremendous impact on daily quality of life. Accurate and prompt diagnosis is crucial for the management of this debilitating disorder. Unfortunately, diagnosis is typically delayed to lack of specific symptoms and readily accessible biomarkers. Although histopathologic examination remains the current gold standard, this approach is highly invasive and not applicable for early screening. Recent work has focused on the identification of reliable biomarkers including immunologic, ie, immune cells, antibodies and cytokines, as well as genetic and biochemical markers, ie, microRNAs, lncRNAs, circulating and mitochondrial nucleic acids, along with some hormones, glycoproteins and signaling molecules. Confirmatory research studies are, however, needed to more fully establish these markers in the diagnosis, progression and staging of these endometrial lesions.

The mechanism of neuropathic pain after spinal cord injury is complex, and the communication between neurons, glia, and blood vessels in neurovascular units significantly affects the occurrence and development of neuropathic pain. After spinal cord injury, a domino chain reaction occurs in the neuron-glia-vessel, which affects the permeability of the blood-spinal cord barrier and jointly promotes the development of neuroinflammation. This article discusses the signal transduction between neuro-glial-endothelial networks from a multidimensional point of view and reviews its role in neuropathic pain after spinal cord injury.

to assess evidence available in the literature about the use of sedation and analgesia for intratracheal intubation of newborns.

Endometriosis is the leading cause of chronic pelvic pain. Alterations in brain functional connectivity have been reported in adult women with endometriosis-associated pain (EAP), however, it is still unknown if similar patterns of changes exist in adolescents.

Scientific data regarding the prevalence of COVID-19 neurological manifestations and prognosis in Latin America countries is still lacking. Therefore, the study aims to understand neurological manifestations of SARS-CoV 2 infection and outcomes in the Brazilian population.

There are conflicting reports in the literature regarding the effectiveness of motor imagery (MI) and action observation (AO) in individuals with chronic non-specific neck pain (CNSNP). This study sought to systematically investigate whether mental practice has any impact on pain, functionality and quality-of-life in individuals with CNSNP.

Neuropathic pain is still a serious and unsolved health problem. Activation of α7 nicotinic acetylcholine receptor (α7nAChR) is known to modulate neuropathic pain by inhibiting microglial activation and BDNF/TrkB/KCC2 signaling. We previously identified that trifluoro-icaritin (ICTF) has an attenuated effect on spared nerve injury (SNI)-induced neuropathic pain, but its potential mechanisms remain unknown. Here, the pain-related behaviors were determined by paw withdrawal threshold (PWT), CatWalk gait analysis, rotarod test, open field test and elevated plus maze test. The expression of pain-related signal molecules was evaluated by Western blot and immunofluorescence staining. The results showed that ICTF (5.0 mg/kg, i.p.) successfully relieved SNI-induced mechanical allodynia and anxiety-like behavior, we subsequently found there existed either positive or negative correlation between mechanical allodynia and gait parameters or rotating speed following ICTF treatment. Moreover, ICTF not only enhanced the expression of spinal α7nAChR, KCC2, CD206 and IL-10, but also decreased the levels of spinal BDNF, TrkB, CD11b, Iba-1, CD40 and IL-1β in SNI rats. Conversely, α7nAChR antagonist α-Bgtx (I.T.) effectively reversed the inhibitory effects of ICTF on SNI rats, resulting in a remarkable improvement of mechanical allodynia, activation of microglia. and suppression of α7nAChR-mediated BDNF/TrkB/KCC2 signaling. Additionally, exogenous BDNF (I.T.) dramatically abrogated both blockade of BDNF/TrkB/KCC2 cascade and alleviation of mechanical allodynia by ICTF treatment. Altogether, the study highlighted that ICTF could relieve SNI-induced neuropathic pain by suppressing microglial activation via α7nAChR-mediated inhibition of BDNF/TrkB/KCC2 signaling in the spinal cord, suggesting that ICTF may be served as a possible painkiller against neuropathic pain.

As the ability to capture single-cell expression profiles has grown in recent years, neuroscientists studying a wide gamut of brain regions have discovered remarkable heterogeneity within seemingly related populations (Saunders et al., 2018a; Zeisel et al., 2015). These "molecular subtypes" have been demonstrated even within brain nuclei expressing the same neurotransmitter (Saunders et al., 2018a; Poulin et al., 2020; Ren et al., 2019; Okaty et al., 2020). Recently, dopamine (DA) neurons of the substantia nigra pars compacta (SNc) and adjacent ventral tegmental area (VTA) have been revealed to be diverse not only when comparing between these two dopaminergic nuclei, but within them, and with the distribution of identified subtypes often agnostic to traditional neuroanatomical boundaries (Saunders et al., 2018a; Hook et al., 2018; Kramer et al., 2018; La Manno et al., 2016; Poulin et al., 2014; Tiklova et al., 2019; Poulin et al., 2018). Such molecularly defined subpopulations have been the subject of several recent studies. Investigations of these subtypes have ultimately unveiled many distinctive properties across several domains, such as their axonal projections and functional properties (Poulin et al., 2018; Wu et al., 2019; Pereira Luppi et al., 2021; Evans et al., 2017; Evans et al., 2020). These key differences between subtypes have begun to corroborate the biological relevance of DA neuron taxonomic schemes. We hypothesize that these putative molecular subtypes, with their distinctive circuits, could shed light on the wide variety of dopamine-related symptoms observed across several diseases including depression, chronic pain, addiction, and Parkinson's Disease. While it is difficult to reconcile how a single neurotransmitter can be involved in so many seemingly unrelated phenotypes, one solution could be the existence of several individual dopaminergic pathways serving different functions, with molecular subtypes serving as distinct nodes for these pathways. Indeed, this conceptual framework is already the dogma for anatomically distinct DA pathways, including the mesocortical, mesolimbic and mesostriatal pathways (Bjorklund & Dunnett, 2007). Here, we discuss our existing knowledge of DA neuron subtypes and attempt to provide a roadmap for how their distinctive properties can provide novel insights into the motor symptoms of Parkinson's disease (PD) (Fig. 1A). By exploring the differences between molecular subtypes and correlating this to their relative degeneration within the SNc, we may gain a deeper understanding of the cell-intrinsic mechanisms underlying why some DA neurons degenerate more than others in PD. Similarly, by mapping the inputs, projections, and functions of individual subtypes, we may better understand their individual roles in the circuit-level dysfunction of dopaminergic diseases.

The present study investigated the involvement of mediodorsal thalamic (MD) GABA-A receptors in cetirizine/morphine-induced anti-allodynia using a rat model of neuropathic pain. To assess the importance of the prefrontal cortex (PFC) for chronic pain processing, its expression level changes of glial fibrillary acidic protein (GFAP) were measured following drug treatments. Each animal was subjected to chronic constriction of the sciatic nerve surgery simultaneously with the MD cannulation under stereotaxic surgery. The results showed that the administration of morphine (3-5mg/kg) or cetirizine (1-3mg/kg) produced significant analgesia in neuropathic rats. Systemic administration of cetirizine (2.5mg/kg) potentiated the analgesic response to a low and intolerance dose of morphine (3mg/kg). Intra-MD microinjection of muscimol, a selective GABA-A receptor agonist (0.005-0.01μg/rat), increased the cetirizine/morphine-induced anti-allodynia, while muscimol by itself did not affect neuropathic pain. The neuropathic pain was associated with the increased PFC expression level of GFAP, suggesting the impact of chronic pain on PFC glial management. Interestingly, the anti-allodynia was associated with a decrease in the PFC expression level of GFAP under the drugs' co-administration. Thus, cetirizine has a significant potentiating effect on morphine response in neuropathic pain via interacting with the MD GABA-A receptors. It seems that neuropathic pain affects the prefrontal cortex GFAP signaling pathway. In clinical studies, these findings can be considered to create a combination therapy with low doses of GABA-A receptor agonist plus cetirizine and morphine to manage neuropathic pain.