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Schizophrenia (SCZ) imposes a significant burden on patients and their families because of its high prevalence rate and disabling nature. Given the lack of definitive conclusions regarding its pathogenesis, physicians heavily rely on patients' subjective symptom descriptions for diagnosis because reliable diagnostic biomarkers are currently unavailable. The role of the inflammatory response in the pathogenesis of SCZ has been supported by some studies. The findings of these studies showed abnormal changes in the levels of inflammatory factors, such as cytokines (CKs), in both peripheral blood and cerebrospinal fluid (CSF) among individuals affected by SCZ. The findings imply that inflammatory factors could potentially function as risk indicators for the onset of SCZ. Consequently, researchers have directed their attention towards investigating the potential utility of CKs as viable biomarkers for diagnosing SCZ. Extracellular vesicles (EVs) containing disease-specific components exhibit remarkable stability and abundance, making them promising candidates for biomarker discovery across various diseases. CKs encapsulated within EVs secreted by immune cells offer valuable insights into disease progression. This review presents a comprehensive analysis summarizing the relationship between CKs and SCZ and emphasizes the vital role of CKs encapsulated within EVs in the pathogenesis and development of SCZ. [ABSTRACT FROM AUTHOR]

Schizophrenia is a serious mental disease that is regulated by multiple genes and influenced by multiple factors. Due to the complexity of its etiology, the pathogenesis is still unclear. MicroRNAs belong to a class of small non-coding RNAs that are highly conserved in endogenous evolution and play critical roles in multiple biological pathways. In recent years, aberrant miRNA expression has been implicated in schizophrenia, with certain miRNAs emerging as potential diagnostic and prognostic biomarkers for this disorder. In this review, our objective is to investigate the differential expression of miRNAs in schizophrenia, elucidate their potential mechanisms of action, and assess their feasibility as biomarkers. The PubMed electronic database and Google Scholar were searched for the years 2003 to 2024. The study focused on schizophrenia and miRNA as the research topic, encompassing articles related to biomarkers, etiology, action mechanisms, and differentially expressed genes associated with schizophrenia and miRNA. A total of 1488 articles were retrieved, out of which 49 were included in this scope review. This study reviewed 49 articles and identified abnormal expression of miRNA in different tissues of both schizophrenia patients and healthy controls, suggesting its potential role in the pathogenesis and progression of schizophrenia. Notably, several specific miRNAs, including miR-34a, miR-130b, miR-193-3p, miR-675-3p, miR-1262, and miR-218-5p, may serve as promising biological markers for diagnosing schizophrenia. Furthermore, this study summarized potential mechanisms through which miRNAs may contribute to the development of schizophrenia. The studies within the field of miRNA's role in schizophrenia encompass a broad spectrum of focus. Several selected studies have identified dysregulated miRNAs associated with schizophrenia across various tissues, thereby highlighting the potential utility of specific miRNAs as diagnostic biomarkers for this disorder. Various mechanisms underlying dysregulated miRNAs in schizophrenia have been explored; however, further investigations are needed to determine the exact mechanisms by which these dysregulated miRNAs contribute to the pathogenesis of this condition. The exploration of miRNA's involvement in the etiology and identification of biomarkers for schizophrenia holds significant promise in informing future clinical trials and advancing our understanding in this area. [ABSTRACT FROM AUTHOR]

BACKGROUND The content of minerals in kyanite can be analyzed by chemical phase method, but the analytical process is very tedious. Moreover, the existence of heteromorphism and refractory minerals can affect the accuracy of analysis results. An internal standard method by X-ray diffraction (XRD) for direct determination of kyanite requires the use of pure mineral to draw a standard curve, but it is extremely challenging to purify minerals due to the inclusion. The differences between the mineral components of kyanite in different mining areas makes the above two methods applicable only to the quantitative analysis of minerals in the same mining area. OBJECTIVES To simplify analysis the process of mineral composition of kyanite and improve efficiency. METHODS The content of minerals in kyanite was studied by X-ray diffraction. The X-ray diffraction Rietveld refinement method was used to analyze the secondary standard materials and field samples of kyanite, and the results were compared with the diffraction quantitative method and chemical analysis results including RIR method, adiabatic method and K-value method. RESULTS Rietveld refinement method was simple and effective in correcting the diffraction intensity error caused by the preferred orientation. Accurate results can be obtained by Rietveld refinement method more than other methods of X-ray quantitative phase analysis, such as RIR method, adiabatic method, K-value method. The analytic absolute error of minerals with content greater than 5% was less 1%, and significantly lower than the allowable error. The results obtained by Highscore agree well with results measured by Jade, and the double difference of results was less than 0.8%. The relative standard deviation was less than 2.5%. The spiked recoveries of kyanite were 95.3%-101.0%. CONCLUSIONS X-ray diffraction with Rietveld refinement method is simple, and can be used to determine the content of all minerals in kyanite from different mining areas.

Abstract Background Prostatodynia is the main symptom of chronic prostatitis and the main reason that patients go to the hospital for treatment. Although a variety of factors, including inflammatory immune response, nervous system sensitization, and psychological factors, have been shown to play important roles in the induction and development of chronic pain in prostatitis, the underlying cause of chronic prostatodynia maintenance in prostatitis patients remains unclear. Methods A mouse model of chronic prostatitis induced by carrageenan injection was used. The von Frey test was used to measure pain behavior. The microglial and astrocyte activations were immunohistochemically demonstrated with antibodies against Iba1 and GFAP. The expression of cytokine or signaling pathway was detected by enzyme-linked immunosorbent assay (ELISA) and Western blotting. Results In this study, we provide several lines of evidence to demonstrate that activated spinal astrocytes contribute to the later phase (5 weeks after carrageenan injection) of carrageenan-induced prostatitis pain. First, activation of spinal astrocytes but not microglia was found in the spinal cord dorsal horn at 5 weeks. Second, intrathecal injection of the astroglial toxin L-2-Aminoadipate acid (L-AA) but not microglial inhibitor minocycline reduced mechanical allodynia at 5 weeks. Third, chronic prostatitis induced a profound and persistent upregulation of connexin-43 hemichannels in spinal astrocytes, and spinal injection of the connexin-43 inhibitor carbenoxolone (CBX) effectively reduced pain symptoms. Fourth, increased expression and release of chemokine C-X-C motif ligand 1 (CXCL1) in the spinal dorsal horn and intrathecal injection of a CXCL1 neutralizing antibody or the CXCR2 (a major receptor of CXCL1) antagonist SB225002 significantly reduced mechanical allodynia at 5 weeks. Conclusions In this study, we found that a novel mechanism of activated spinal astrocytes plays a crucial role in maintaining chronic prostatitis-induced persistent pain via connexin-43-regulated CXCL1 production and secretion.

Background and Purpose: Overexpression of astrocytic lactoferrin (Lf) was observed in the brain of Alzheimer's disease (AD) patients, whereas the role of astrocytic Lf in AD progression remains unexplored. In this study, we aimed to evaluate the effects of astrocytic Lf on AD progression. Experimental Approach: Male APP/PS1 mice with astrocytes overexpressing human Lf were developed to evaluate the effects of astrocytic Lf on AD progression. N2a‐sw cells also were employed to further uncover the mechanism of astrocytic Lf on β‐amyloid (Aβ) production. Key Results: Astrocytic Lf overexpression increased protein phosphatase 2A (PP2A) activity and reduced amyloid precursor protein (APP) phosphorylation, Aβ burden and tau hyperphosphorylation in APP/PS1 mice. Mechanistically, astrocytic Lf overexpression promoted the uptake of astrocytic Lf into neurons in APP/PS1 mice, and conditional medium from astrocytes overexpressing Lf inhibited p‐APP (Thr668) expression in N2a‐sw cells. Furthermore, recombinant human Lf (hLf) significantly enhanced PP2A activity and inhibited p‐APP expression, whereas inhibition of p38 or PP2A activities abrogated the hLf‐induced p‐APP down‐regulation in N2a‐sw cells. Additionally, hLf promoted the interaction of p38 and PP2A via p38 activation, thereby enhancing PP2A activity, and low‐density lipoprotein receptor‐related protein 1 (LRP1) knockdown significantly reversed the hLf‐induced p38 activation and p‐APP down‐regulation. Conclusions and Implications: Our data suggested that astrocytic Lf promoted neuronal p38 activation, via targeting to LRP1, subsequently promoting p38 binding to PP2A to enhance PP2A enzyme activity, which finally inhibited Aβ production via APP dephosphorylation. In conclusion, promoting astrocytic Lf expression may be a potential strategy against AD. LINKED ARTICLES: This article is part of a themed issue From Alzheimer's Disease to Vascular Dementia: Different Roads Leading to Cognitive Decline. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.6/issuetoc [ABSTRACT FROM AUTHOR]

In this study, a simple and portable electrochemical sensor based on laser-induced graphene (LIG) has been developed to systematically investigate the feasibility of LIG as an electrode to detect organophosphorus pesticides (OPs). It proves that the LIG-based electrode has a relatively high electrochemically active surface area (ECSA) and heterogeneous electron transfer (HET) of 0.100 cm2 and 0.000825 cm s−1, respectively. In addition, zirconium dioxide nanoparticles (ZrO2 NPs) have been modified on the electrode with three different binders, β-cyclodextrin (β-CD), chitosan (CS) and Nafion, to improve the adsorption capacity of the electrode toward OPs, and the effect of the binders on the performance of the as-fabricated sensor has been investigated in detail. The results show that β-CD increases not only the electrochemically active surface area of the electrode but also the redox peak current of methyl parathion (MP). To evaluate the sensitivity of the sensor, differential pulse voltammetry (DPV) curves have been tested in solutions containing different concentrations of MP using ZrO2-β-CD/LIG as an electrode, which shows a detection range of 5–200 ng ml−1 and a detection limit of 0.89 ng ml−1. In summary, the LIG-based sensor has a low detection limit, high sensitivity and good interference resistance, and thus has tremendous potential for the detection of pesticides in the environment. [ABSTRACT FROM AUTHOR]