Unbiased multitissue transcriptomic analysis reveals complex neuroendocrine regulatory networks mediated by spinal cord injury-induced immunodeficiency.

BACKGROUND: Spinal cord injury (SCI), which causes loss of sensory and motor function in the body below the level of injury, is a devastating disease of the central nervous system. SCI leads to severe secondary immunosuppression, called SCI-induced immunodeficiency syndrome (SCI-IDS), which is characterized by increased susceptibility to infection and further exacerbates neurological dysfunction. Several studies have suggested that SCI-IDS is an independent risk factor for poor neurological prognosis. SCI-IDS predominantly occurs following injury above the T5 levels and eventually leads to systemic immune failure, possibly via the sympathetic-adrenal medullary axis and the hypothalamic‒pituitary‒adrenal (HPA) axis. However, the mechanism remains unclear. METHODS AND OBJECTIVES: The concentrations of adrenocorticotropic hormone and cortisol in plasma, as well as changes in sympathetic activity (blood pressure and catecholamine levels in plasma), were assessed in rats in the high-level (T3) spinal cord injury (T3-SCI) group and the low-level (T10) spinal cord injury (T10-SCI) group. Second, the differential regulation of the gene network between the sympathetic-adrenal medullary axis and the HPA axis was explored by histology and multitissue transcriptomics, and the neuroendocrine-immune network associated with SCI-IDS was further elucidated. RESULTS: The spleen and thymus gland, which are secondary immune organs, were significantly atrophied in rats in the T3-SCI group, and the white pulp of the spleen was significantly atrophied. The level of cortisol, which is mediated by the adrenal glands, was markedly elevated, but norepinephrine levels were markedly decreased. There was no difference in adrenocorticotropic hormone expression between any of the groups. The transcriptome analysis results showed that the downregulated differentially expressed genes (DEGs) in the T3-SCI group were enriched in the GO term immunoregulation, indicating that splenic immune function was markedly impaired after high-level SCI. The upregulated DEGs in the hypothalamus (hub genes: Nod2, Serpine1, Cebpb, Nfkbil1, Ripk2, Zfp36, Traf6, Akap8, Gfer, Cxcl10, Tnfaip3, Icam1, Fcgr2b, Ager, Dusp10, and Mapkapk2) were significantly enriched in inflammatory pathways, and the downregulated genes (hub genes: Grm4, Nmu, P2ry12, rt1-bb1, Oprm1, Zfhx2, Gpr83, and Chrm2) were enriched in pathways related to inhibitory Gi-mediated G protein-coupled receptor (Gi-GPCR) neurons and neuropeptide changes. The upregulated genes in the adrenal glands (hub genes: Ciart, per2, per3, cry1, and cry2) were enriched in cortisol secretion and circadian rhythm changes, and the downregulated genes (hub genes: IL7r, rt1-bb, rt1-bb1, rt1-da, rt1-ba, cd74, cxcr3, vcam1, ccl5, bin1, and IL8) were significantly enriched in MHC-mediated immune responses. CONCLUSIONS: To explore the possible mechanism underlying SCI-IDS, this study assessed the differential regulation of the gene network associated with neuroendocrine immunity after SCI. Progressive neuroinflammation spreads after injury, and neurotransmission through Gi-mediated G protein-coupled receptors in the HPA axis and neuropeptide production by the hypothalamus are inhibited. Disruption of the connection between the hypothalamus and the adrenal glands causes autonomous regulation of the adrenal glands, disturbance of circadian rhythm and finally hypercortisolemia, leading to general suppression of peripheral adaptive immunity. Neuraxial nerve inflammation caused by SCI persists indefinitely, blocking nerve repair; persistent system-wide immunosuppression in the periphery results in increased susceptibility to infection, leading to poor neurological prognosis.

Diagnostic Accuracy of the Eating Assessment Tool-10 (EAT-10) in Screening Dysphagia: A Systematic Review and Meta-Analysis.

The Eating Assessment Tool-10 (EAT-10) is used worldwide to screen people quickly and easily at high risk for swallowing disorders. However, the best EAT-10 cutoff value is still controversial. In this systematic review and meta-analysis, we estimated and compared the diagnostic accuracy of EAT-10 cutoff values of 2 and 3 for screening dysphagia. We searched the PubMed, Web of Science, EMBASE, Cochrane Library, CNKI, WANFANG, and VIP databases from May 2008 to March 2022. The meta-analysis included 7 studies involving 1064 subjects from 7 different countries. Two studies were classified as high quality and five studies as medium quality. With an EAT-10 cutoff value of 2, using flexible endoscopic evaluation of swallowing or video fluoroscopic swallowing study as the gold standard, the pooled sensitivity, specificity, positive and negative likelihood ratios, and diagnostic odds ratio were 0.89 (95% confidence interval [CI] 0.82-0.93), 0.59 (95% CI 0.39-0.77), 2.17 (95% CI 1.38-3.42), 0.19 (95% CI 0.13-0.29), and 11.49 (95% CI 5.86-22.53), respectively. When a cutoff of 3 was used, these values were 0.85 (95% CI 0.68-0.94), 0.82 (95% CI 0.65-0.92), 4.84 (95% CI 1.72-13.50), 0.18 (95% CI 0.07-0.46), and 26.24 (95% CI 5.06-135.95), respectively. Using EAT-10 cutoff values of 2 and 3, the areas under the curve were 0.873 (95% CI 0.82-0.93) and 0.903 (95% CI 0.88-0.93), respectively, showing good diagnostic performance. EAT-10 can be used as a preliminary screening tool for dysphagia. However, a cutoff of 3 is recommended for EAT-10 due to better diagnostic accuracy.

Nonylphenol induces depressive behavior in rats and affects gut microbiota: A dose-dependent effect.

Nonylphenol (NP), an endocrine disruptor absorbed through food intake, was investigated in this study for its potential dose-response relationship with the manifestation of depression-like behavior in rats. Based on this, the mechanisms of NP-induced depressive behavior, encompassing neurotransmitters, gut barrier function, inflammatory response, gut microbiota composition and metabolites were further explored. At medium and high NP doses, both mRNA and protein levels of zonula occludens protein-1 and claudin-1 were considerably downregulated, concomitant with an elevation in tumor necrosis factor-α and interleukin-1ß expression in a dose-dependent effect, resulting in damage to the gut mucosa. Despite a minimal impact on behavior and gut barriers at low NP doses, alterations in gut microbiota composition were observed. During NP exposure, dose-dependent changes in the gut microbiota revealed a decline in microbial diversity linked to the synthesis of short-chain fatty acids. NP not only adversely affected the gut microbiota structure but also exacerbated central nervous system damage through the gut-brain axis. The accumulation of NP may cause neurotransmitter disturbances and inflammatory responses in the hippocampus, which also exacerbate depressed behavior in rats. Therefore, NP could exacerbate the inflammatory response in the hippocampus and colon by compromising intestinal barrier integrity, facilitating the proliferation of pathogenic bacteria, impairing butyrate metabolism, and perturbing neurotransmitter homeostasis, thus aggravating the depressive behavior of rats. It is noteworthy that the changes in these indicators were related to the NP exposure dose.

The role of mitochondrial energy metabolism in neuroprotection and axonal regeneration after spinal cord injury.

Mitochondrial dysfunction occurs in the early stage of axonal degeneration after spinal cord injury and involves oxidative stress, energy deficiency, imbalance of mitochondrial dynamics, etc., which play a key role in axonal degeneration and regeneration under physiological and pathological conditions. Failure of axonal regeneration can lead to long-term structural and functional damage. Several recent studies have shown that improved mitochondrial energy metabolism provides conditions for axonal regeneration and central nervous system repair. Here, we describe the role of mitochondrial energy metabolism in neuroprotection and axonal regeneration after spinal cord injury and review recent advances in targeted mitochondrial therapy.

3D-Printed Composite Bioceramic Scaffolds for Bone and Cartilage Integrated Regeneration.

Osteoarthritis may result in both cartilage and subchondral bone damage. It is a significant challenge to simultaneously repair cartilage due to the distinct biological properties between cartilage and bone. Here, strontium copper tetrasilicate/ß-tricalcium phosphate (Wesselsite[SrCuSi4O10]/Ca3(PO4)2, WES-TCP) composite scaffolds with different WES contents (1, 2, and 4 wt %) were fabricated via a three-dimensional (3D) printing method for the osteochondral regeneration. The physicochemical properties and biological activities of the scaffolds were systematically investigated. 2WES-TCP (WES-TCP with 2 wt % WES) composite scaffolds not only improved the compressive strength but also enhanced the proliferation of both rabbit bone mesenchymal stem cells (rBMSCs) and chondrocytes, as well as their differentiation. The in vivo study further confirmed that WES-TCP scaffolds significantly promoted the regeneration of both bone and cartilage tissue in rabbit osteochondral defects compared with pure TCP scaffolds owing to the sustained and controlled release of bioactive ions (Si, Cu, and Sr) from bioactive scaffolds. These results show that 3D-printed WES-TCP scaffolds with bilineage bioactivities take full advantage of the bifunctional properties of bioceramics to reconstruct the complex osteochondral interface, which broadens the approach to engineering therapeutic platforms for biomedical applications.

Correlation between dysphagia and serum albumin levels and prognosis: a retrospective study.

Introduction: Introduction: dysphagia is a common complication of stroke, and serum albumin is widely recognized as a strong prognostic marker of health and/or disease status. However, the correlation between dysphagia and serum albumin levels has not been established. Objectives: to observe the correlation between dysphagia and serum albumin levels and prognosis in patients with stroke. Methods: we performed a retrospective study of patients hospitalized between June 1, 2018, and June 1, 2022. A total of 1,370 patients were enrolled. The patients were divided into two groups: dysphagia and non-dysphagia. Binary logistic regression and multiple linear regression models were used to analyze the correlation between dysphagia, albumin, modified Rankin Scale (mRS), activities of daily living (ADL), and length of hospital stay (LOS). Results: after adjusting for confounding factors, the risk of pneumonia in the dysphagia group was 2.417 times higher than that in the non-dysphagia group (OR = 2.417, 95 % CI: 1.902-3.072, p = 0.000). The risk of mRS ≥ 3 and modified Barthel index (MBI) < 60 in patients with dysphagia was 3.272-fold (OR = 3.272, 95 % CI: 2.508-4.269, p < 0.001) and 1.670-fold (OR = 1.670, 95 % CI: 1.230-2.268, p < 0.001), respectively; and the risk of hypoproteinemia was 2.533 times higher (OR = 2.533, 95 % CI: 1.879-3.414, p = 0.000). Stepwise linear regression showed that dysphagia was significantly correlated with lower albumin levels and higher mRS, lower ADL, and longer LOS in patients with stroke (ß = -0.220, ß = 0.265, ß = -0.210, and ß = 0.147, respectively; p < 0.001). Conclusions: dysphagia in patients with stroke is associated with decreased albumin levels and has an impact on its prognosis.

Introducción: Introducción: la disfagia es una complicación común del accidente cerebrovascular, y la albúmina sérica es ampliamente reconocida como un fuerte marcador pronóstico del estado de salud y/o enfermedad. Sin embargo, no se ha establecido la correlación entre la disfagia y los niveles de albúmina sérica. Objetivos: observar la correlación entre la disfagia y los niveles de albúmina sérica y el pronóstico en pacientes con accidente cerebrovascular. Métodos: realizamos un estudio retrospectivo de pacientes hospitalizados entre el 1 de junio de 2018 y el 1 de junio de 2022. Se inscribieron un total de 1.370 pacientes, los cuales fueron divididos en dos grupos: con disfagia y sin disfagia. Se utilizaron modelos de regresión logística binaria y de regresión lineal múltiple para analizar la correlación entre la disfagia, la albúmina, la escala de Rankin modificada (ERm), las actividades de la vida diaria (AVD) y el tiempo de estancia hospitalaria (TEH). Resultados: después de ajustar por factores de confusión, el riesgo de neumonía en el grupo de disfagia fue 2,417 veces mayor que en el grupo sin disfagia (OR = 2,417, IC 95 %: 1,902-3,072, p = 0,000). El riesgo de ERm ≥ 3 y el índice de Barthel modificado (MBI) < 60 en pacientes con disfagia se multiplicó por 3,272 veces (OR = 3,272, IC 95 %: 2,508-4,269, p < 0,001) y 1,670 veces (OR = 1,670, IC 95 %: 1,230-2,268, p < 0,001), respectivamente; el riesgo de hipoproteinemia fue 2,533 veces mayor (OR = 2,533, IC 95 %: 1,879-3,414, p = 0,000). La regresión lineal por pasos mostró que la disfagia se correlacionó significativamente con niveles más bajos de albúmina y ERm más altos, AVD más bajos y TEH más prolongados en pacientes con accidente cerebrovascular (ß = -0,220, ß = 0,265, ß = -0,210 y ß = 0,147, respectivamente; p < 0,001). Conclusiones: la disfagia en pacientes con accidente cerebrovascular se asocia a una disminución de los niveles de albúmina y repercute en su pronóstico.

Regeneration of Humeral Head Using a 3D Bioprinted Anisotropic Scaffold with Dual Modulation of Endochondral Ossification.

Tissue engineering is theoretically thought to be a promising method for the reconstruction of biological joints, and thus, offers a potential treatment alternative for advanced osteoarthritis. However, to date, no significant progress is made in the regeneration of large biological joints. In the current study, a biomimetic scaffold for rabbit humeral head regeneration consisting of heterogeneous porous architecture, various bioinks, and different hard supporting materials in the cartilage and bone regions is designed and fabricated in one step using 3D bioprinting technology. Furthermore, orchestrated dynamic mechanical stimulus combined with different biochemical cues (parathyroid hormone [PTH] and chemical component hydroxyapatite [HA] in the outer and inner region, respectively) are used for dual regulation of endochondral ossification. Specifically, dynamic mechanical stimulus combined with growth factor PTH in the outer region inhibits endochondral ossification and results in cartilage regeneration, whereas dynamic mechanical stimulus combined with HA in the inner region promotes endochondral ossification and results in efficient subchondral bone regeneration. The strategy established in this study with the dual modulation of endochondral ossification for 3D bioprinted anisotropic scaffolds represents a versatile and scalable approach for repairing large joints.

Development and Application of Three-Dimensional Bioprinting Scaffold in the Repair of Spinal Cord Injury.

Spinal cord injury (SCI) is a disabling and destructive central nervous system injury that has not yet been successfully treated at this stage. Three-dimensional (3D) bioprinting has become a promising method to produce more biologically complex microstructures, which fabricate living neural constructs with anatomically accurate complex geometries and spatial distributions of neural stem cells, and this is critical in the treatment of SCI. With the development of 3D printing technology and the deepening of research, neural tissue engineering research using different printing methods, bio-inks, and cells to repair SCI has achieved certain results. Although satisfactory results have not yet been achieved, they have provided novel ideas for the clinical treatment of SCI. Considering the potential impact of 3D bioprinting technology on neural studies, this review focuses on 3D bioprinting methods widely used in SCI neural tissue engineering, and the latest technological applications of bioprinting of nerve tissues for the repair of SCI are discussed. In addition to introducing the recent progress, this work also describes the existing limitations and highlights emerging possibilities and future prospects in this field.

Behavioral disorders caused by nonylphenol and strategies for protection.

Nonylphenol (NP) is widely used in daily production and life due to its good emulsification. In this review, we discuss toxicology studies that examined behavioral disorders caused by NP, the corresponding toxicological mechanisms in the central nervous system (CNS), and strategies for protection. Available in vitro and in vivo evidence suggests that exposure to NP during adulthood or early childhood is associated with cognitive dysfunction, including depression-like behaviors, anxiety-like behaviors, and impaired learning and memory. The main mechanisms underlying NP-related cognitive disorders include inflammation, destruction of synaptic plasticity, and destruction of important signaling pathways that affect the synthesis and secretion of neurotransmitters. The effects and mechanisms of NP exposure on CNS-mediated reproductive function, including interference with the expression of hormones, proteins, and enzymes, are discussed. Other abnormal behaviors such as locomotor activity and swimming behavior are also described. Several measures to prevent NP neurotoxicity are summarized. These measures are based on the toxicological mechanisms underlying NP exposure and include external protection and internal self-regulation of the nervous system. Finally, a new treatment idea is proposed based on the gut-brain axis. Characterizing the behavioral changes and underlying toxicity mechanisms associated with NP exposure and investigating the possible methods of treatment will help to expand the understanding of these mechanisms and could lead to more effective treatments.

Tissue Engineering Strategies for Peripheral Nerve Regeneration.

A peripheral nerve injury (PNI) has severe and profound effects on the life of a patient. The therapeutic approach remains one of the most challenging clinical problems. In recent years, many constructive nerve regeneration schemes are proposed at home and abroad. Nerve tissue engineering plays an important role. It develops an ideal nerve substitute called artificial nerve. Given the complexity of nerve regeneration, this review summarizes the pathophysiology and tissue-engineered repairing strategies of the PNI. Moreover, we discussed the scaffolds and seed cells for neural tissue engineering. Furthermore, we have emphasized the role of 3D printing in tissue engineering.

Development and Application of 3D Bioprinted Scaffolds Supporting Induced Pluripotent Stem Cells.

Three-dimensional (3D) bioprinting is a revolutionary technology that replicates 3D functional living tissue scaffolds in vitro by controlling the layer-by-layer deposition of biomaterials and enables highly precise positioning of cells. With the development of this technology, more advanced research on the mechanisms of tissue morphogenesis, clinical drug screening, and organ regeneration may be pursued. Because of their self-renewal characteristics and multidirectional differentiation potential, induced pluripotent stem cells (iPSCs) have outstanding advantages in stem cell research and applications. In this review, we discuss the advantages of different bioinks containing human iPSCs that are fabricated by using 3D bioprinting. In particular, we focus on the ability of these bioinks to support iPSCs and promote their proliferation and differentiation. In addition, we summarize the applications of 3D bioprinting with iPSC-containing bioinks and put forward new views on the current research status.

RBP and Alb in neonatal hydronephrosis and its association with IL-12 levels in pregnant women before delivery.

Expression levels of retinol-binding protein (RBP) and albumin (Alb) in the kidney of patients with neonatal hydronephrosis were detected to explore whether RBP and Alb can be used as diagnostic indicators for neonatal hydronephrosis. Blood and urine samples from neonates with hydronephrosis in the obstetrics and gynaecology department of Hongqi Hospital Affiliated to Mudanjiang Medical University from January 2016 to January 2018, and healthy newborns were collected. RBP and Alb levels in neonates, and the expression of IL-12 in serum of the mothers were detected by ELISA. To establish the rat model, 30 male Sprague Dawley (SD) rats were randomly divided into two groups: sham operation group (n=15) and unilateral ureteral obstruction (UUO) (n=15). Expression of RBP and Alb protein was detected by western blot analysis. Another 30 female SD rats were randomly divided into the Sham and IL-12 knockdown groups. The Sham group was given NC treatment, while IL-12 knockdown group was given treatment with IL-12 knockdown adenovirus through tail vein injection. Results of ELISA showed that serum RBP and renal urinary Alb levels were higher in neonates with hydronephrosis compared with the control group (P=0.009 or P=0.013). Compared with the control group, levels of IL-12 were significantly lower in mother of neonatal hydronephrosis group (P=0.001). After the IL-12 knockdown treatment in pregnant rats, levels of RBP and Alb hydronephrosis-related indicators were significantly increased. The incidence of hydronephrosis in rats delivered via IL-12 knockdown pregnant rats was significantly higher than that of normal pregnant rats (P=0.001). The combination of RBP and Alb in the diagnosis of neonatal hydronephrosis has important clinical significance, and neonatal hydronephrosis is closely related to the level of IL-12 in mothers before birth. Our findings provide new ideas and theoretical basis for the diagnosis and prediction of neonatal hydronephrosis.

Correlation between dysphagia and serum albumin levels and prognosis: a retrospective study / Correlación entre la disfagia y los niveles de albúmina sérica y el pronóstico: un estudio retrospectivo

Introduction: dysphagia is a common complication of stroke, and serum albumin is widely recognized as a strong prognostic marker of healthand/or disease status. However, the correlation between dysphagia and serum albumin levels has not been established.Objectives: to observe the correlation between dysphagia and serum albumin levels and prognosis in patients with stroke.Methods: we performed a retrospective study of patients hospitalized between June 1, 2018, and June 1, 2022. A total of 1,370 patients wereenrolled. The patients were divided into two groups: dysphagia and non-dysphagia. Binary logistic regression and multiple linear regressionmodels were used to analyze the correlation between dysphagia, albumin, modified Rankin Scale (mRS), activities of daily living (ADL), andlength of hospital stay (LOS).Results: after adjusting for confounding factors, the risk of pneumonia in the dysphagia group was 2.417 times higher than that in the non-dysphagia group (OR = 2.417, 95 % CI: 1.902-3.072, p = 0.000). The risk of mRS ≥ 3 and modified Barthel index (MBI) < 60 in patients with dysphagia was 3.272-fold (OR = 3.272, 95 % CI: 2.508-4.269, p < 0.001) and 1.670-fold (OR = 1.670, 95 % CI: 1.230-2.268, p < 0.001), respectively; and the risk of hypoproteinemia was 2.533 times higher (OR = 2.533, 95 % CI: 1.879-3.414, p = 0.000). Stepwise linear regression showed that dysphagia was significantly correlated with lower albumin levels and higher mRS, lower ADL, and longer LOS in patients with stroke (β = -0.220, β = 0.265, β = -0.210, and β = 0.147, respectively; p < 0.001). Conclusions: dysphagia in patients with stroke is associated with decreased albumin levels and has an impact on its prognosis. (AU)

Introducción: la disfagia es una complicación común del accidente cerebrovascular, y la albúmina sérica es ampliamente reconocida como un fuerte marcador pronóstico del estado de salud y/o enfermedad. Sin embargo, no se ha establecido la correlación entre la disfagia y los niveles de albúmina sérica. Objetivos: observar la correlación entre la disfagia y los niveles de albúmina sérica y el pronóstico en pacientes con accidente cerebrovascular. Métodos: realizamos un estudio retrospectivo de pacientes hospitalizados entre el 1 de junio de 2018 y el 1 de junio de 2022. Se inscribieron untotal de 1.370 pacientes, los cuales fueron divididos en dos grupos: con disfagia y sin disfagia. Se utilizaron modelos de regresión logística binaria y de regresión lineal múltiple para analizar la correlación entre la disfagia, la albúmina, la escala de Rankin modificada (ERm), las actividades de la vida diaria (AVD) y el tiempo de estancia hospitalaria (TEH). Resultados: después de ajustar por factores de confusión, el riesgo de neumonía en el grupo de disfagia fue 2,417 veces mayor que en el gruposin disfagia (OR = 2,417, IC 95 %: 1,902-3,072, p = 0,000). El riesgo de ERm ≥ 3 y el índice de Barthel modificado (MBI) < 60 en pacientes condisfagia se multiplicó por 3,272 veces (OR = 3,272, IC 95 %: 2,508-4,269, p < 0,001) y 1,670 veces (OR = 1,670, IC 95 %: 1,230-2,268, p <0,001), respectivamente; el riesgo de hipoproteinemia fue 2,533 veces mayor (OR = 2,533, IC 95 %: 1,879-3,414, p = 0,000). La regresión linealpor pasos mostró que la disfagia se correlacionó significativamente con niveles más bajos de albúmina y ERm más altos, AVD más bajos y TEHmás prolongados en pacientes con accidente cerebrovascular (β = -0,220, β = 0,265, β = -0,210 y β = 0,147, respectivamente; p < 0,001).Conclusiones: la disfagia en pacientes con accidente cerebrovascular se asocia a una disminución de los niveles de albúmina y repercute ensu pronóstico. (AU)

[Analysis on pneumoconiosis characteristic and its prediction in one coal mine].

OBJECTIVE: We aimed to investigate the characteristic of pneumoconiosis on coal miners and provide scientific evidences for its prevention. METHODS: To analyze the data of pneumoconiosis from one coal mine with the historical study and to predict its development tendency by the grey model of GM (1,1). RESULTS: (1) The year of work experience of pneumoconiosis (stage I) was 19.9 years and the age of its diagnosis (stage I) was 51.4 years. There was an obvious tendency that they became longer with years' back-shift. (2) During near forty years, the progression rates of pneumoconiosis from stage I to II and II to III were 13.6% and 11.2%, and the mean time was 8.3 and 8.1 years, respectively. It was obvious that the progression rate decreased gradually and the span prolonged with years' back-shift. (3) The complication rate of pneumoconiosis with lung tuberculosis was 12.5% and it increased with the progression of pneumoconiosis. The rate in dead cases was significantly higher than that in live cases (P < 0.01). (4) The sequence of death causes was pneumoconiosis (20.0%), lung tuberculosis (18.3%), chronic cor pulmonale (17.9%), and pulmonary carcinoma (9.0%), et al. (5) It was predicted that there would be 28 new cases every year during 2001-2020 years and the accumulated numbers of pneumoconiosis would be 2854 cases in 2020, but with a downward trends in the prevalence of -1.7%. CONCLUSION: It was suggested that the prevalence of pneumoconiosis should decrease obviously. However, it still remains a challenge about the task of effectively preventing and curing it or its complication.