ObjectiveTo analyze the current research status, hotspots and future trends of the application of digital health technology (DHT) in the rehabilitation of upper limb motor function after stroke. MethodsRelevant literature on the application of DHT in upper limb motor rehabilitation for stroke patients published between January, 2015 and December, 2025 was retrieved from Web of Science Core Collection, CNKI and Wanfang database. CiteSpace 6.4.R1 was used for visualized bibliometric analysis. ResultsA total of 1 295 publications were included, comprising 454 in Chinese and 841 in English. The annual number of publications generally showed an upward trend. China ranked first in publication output in English literature. The institutions with the highest numbers of publications were Huashan Hospital Affiliated to Fudan University and Swiss Federal Institute of Technology in Zurich. Both Chinese and English keywords formed ten clustering groups. Chinese clusters mainly involved occupational therapy, neural mechanisms and home-based rehabilitation, whereas English clusters focused on virtual reality, brain-computer interfaces and machine learning. High-frequency keywords included virtual reality, brain-computer interface, machine learning and deep learning. Chinese keywords with a strong burst included rehabilitation training, while deep learning showed a strong burst in English keywords. Stroke was the most frequently cited journal. Highly cited journals covered multiple disciplines, including rehabilitation medicine, neuroscience and computer science, reflecting the interdisciplinary characteristics of this field. ConclusionResearches on DHT for upper limb motor function rehabilitation in stroke are increasing annually, focusing on core interaction technologies, neural mechanism and artificial intelligence. Future research trends may include inter-disciplinary integration of artificial intelligence with core rehabilitation technologies, neuroimaging-guided targeted interventions, optimisation of home-based rehabilitation systems, and development of multidimensional quantitative assessment models.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveTranscranial magneto-acoustic stimulation (TMAS) is an emerging non-invasive neuromodulation technique that may provide a novel non-pharmacological intervention strategy for Parkinson's disease (PD). PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc), leading to motor impairments such as bradykinesia, tremor, and rigidity. Increasing evidence indicates that mitochondrial dysfunction and impaired mitochondrial quality control are central mechanisms underlying dopaminergic neuronal loss. In particular, abnormalities in mitophagy and mitochondrial fission-fusion balance contribute substantially to oxidative stress, energy metabolic failure, and neuronal injury. At present, most clinical treatments for PD mainly alleviate symptoms but do not effectively halt disease progression. Therefore, exploring new interventions targeting the core pathological mechanisms is of considerable significance. This study aims to investigate whether TMAS can improve neural damage and motor dysfunction in PD mice by regulating mitophagy and the fission/fusion dynamic balance, thereby providing theoretical and experimental support for its application in PD treatment. MethodsMale C57BL/6 mice were used in this study. A PD model was established by intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 7 consecutive days. After model induction, mice in the intervention group received TMAS once daily for 14 consecutive days, whereas the corresponding control group received sham stimulation. The stimulation target was positioned over the primary motor cortex (M1). Motor performance was evaluated using the pole test and the open-field test. To verify the activation effect of TMAS on the target cortical region, c-Fos immunohistochemistry was performed in the M1. To assess nigral dopaminergic neuronal injury, tyrosine hydroxylase (TH) immunohistochemistry was used to quantify TH-positive neurons in the SNc. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels and adenosine triphosphate (ATP) content in the SNc. Western blot was further performed to determine the expression of mitophagy-related proteins, including PINK1, Parkin, LC3-II, and p62, as well as mitochondrial dynamics-related proteins, including Drp1 and Opa1. ResultsTMAS significantly increased the number of c-Fos-positive cells in M1 (P<0.000 1), indicating effective activation of neurons in the targeted cortical region. Compared with the control group, MPTP-treated mice exhibited marked motor dysfunction, including a significant reduction in total distance traveled in the open-field test (P<0.000 1) and mean speed (P=0.000 1), as well as significant prolongation of turn time and total climbing time in the pole test (P<0.000 1). These behavioral impairments were accompanied by a substantial loss of TH-positive dopaminergic neurons in the SNc, whereas TMAS significantly increased TH-positive neuron survival (P<0.000 1). In parallel, MPTP induced a pronounced increase in ROS levels and a significant reduction in ATP content, indicating severe mitochondrial dysfunction and energy metabolism impairment (P<0.01). TMAS treatment significantly improved motor performance, as reflected by the reversal of MPTP-induced impairment in the open-field and pole tests, and significantly reduced ROS accumulation (P<0.01) while restoring ATP production (P<0.001). At the molecular level, MPTP markedly downregulated PINK1 and Parkin, decreased p62 expression, increased LC3-II accumulation, elevated Drp1 expression, and reduced Opa1 expression, whereas TMAS significantly reversed these abnormalities, suggesting restoration of mitophagy-related mitochondrial quality control and re-establishment of mitochondrial fission-fusion balance. Collectively, these findings indicate that TMAS ameliorates MPTP-induced neurotoxicity and restores mitochondrial homeostasis and energy metabolism. ConclusionTMAS effectively attenuates neural damage and improves motor dysfunction in MPTP-induced PD mice. Its neuroprotective effects are closely associated with multidimensional regulation of the mitochondrial quality control system, including restoration of PINK1/Parkin-mediated mitophagy and rebalancing of Drp1/Opa1-related mitochondrial dynamics. Rather than acting only as a symptomatic neuromodulatory intervention, TMAS may influence a key pathological axis of PD by improving mitochondrial homeostasis in SNc and protecting nigral dopaminergic neurons. These findings provide experimental evidence supporting TMAS as a promising non-invasive physical intervention for PD.

ObjectiveHepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. The main risk factors associated with HCC include viral hepatitis (B and/or C), alcohol abuse, and metabolic dysfunction-associated steatotic liver disease (MASLD), which progressively advance to liver fibrosis, cirrhosis, and ultimately evolve into HCC. Surgical resection represents the most effective treatment for HCC, while recent advances in immunotherapy, including immune checkpoint inhibitors and adoptive cell therapies, have provided improved treatment prospects for patients with unresectable HCC. However, the complex metabolic heterogeneity of HCC limits the therapeutic efficacy. Metabolic intermediates acyl-CoA not only provide energy and substrates for numerous biochemical reactions but also serve as donors for protein lysine acylation, a major class of post-translational modification (PTM). Therefore, a deeper understanding of the molecular mechanisms underlying protein lysine acylation and hepatocarcinogenesis is urgently needed. MethodsThe levels of protein lysine acylation and silence information regulator 5 (SIRT5) expression levels in clinical HCC samples were analyzed by Western blot. Quantitative malonylome and succinylome of HCC samples were analyzed by antibody-based affinity enrichment coupled with tandem mass spectrometry. The proliferation of HCC cells was analyzed with Cell Counting Kit-8 (CCK-8) assays, the apoptosis was quantified by Annexin V-FITC/propidium iodide (PI) staining coupled with flow cytometry, and the ability of cells to migrate was assayed by Transwell assays. The enzymatic activity of glutathione S-transferase Mu 1 (GSTM1) was quantified. Transgenic mice with hepatic overexpression of SIRT5 were constructed using CRISPR-Cas9, and primary hepatocarcinogenesis was induced by administration of diethylnitrosamine. ResultsWestern blot analysis indicated that the expression level of SIRT5 was elevated in clinical samples from HCC patients, and the levels of lysine malonylation, glutarylation, and succinylation were significantly reduced in HCC tissues. Knockout of SIRT5 in MHCC-97H and MHCC-97L hepatoma cells suppressed cell proliferation, and increased the percentage of apoptotic cells significantly. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the differentially malonylome and succinylome of HCC samples revealed significant enrichment in two major classes of biological processes: core energy metabolism (e.g., glycolysis/gluconeogenesis, tricarboxylic acid metabolic process, fatty acid beta oxidation) and detoxification and oxidative stress response (e.g., response to toxic substance, chemical carcinogenesis, reactive oxygen species (ROS)). SIRT5 removes malonylation from lysine residues in GSTM1 and restores its detoxification activity, which is crucial for the survival of hepatocytes under stressed conditions. More importantly, in vivo experiment indicated that hepatic-specific overexpression of SIRT5 in mice accelerated diethylnitrosamine-induced liver fibrosis and hepatocarcinogenesis, indicating the critical role of SIRT5 in HCC progression. ConclusionThis study highlights the previously unrecognized SIRT5-GSTM1 axis as a key regulator in hepatocarcinogenesis, and suggests a potential target for the treatment of patients with HCC.

The child, male,11 years old, Han nationality, student of Qiandongnan Miao Autonomous Prefecture, Guizhou Province, visited the General Hospital of Hunan Medical University on October 1,2024 due to“cough, chest tightness for 10 days and pericardial effusion was found for 8 days.”The child has a history of eating raw crabs. Admission examination: shortness of breath, slightly cyanotic lips, mild trifoveal symptoms, low heart sound, and routine blood showed significant eosinophil elevation. Serological examination showed that pulmonary fluke antibody IgG was positive, chest and abdomen CT and cardiac ultrasound showed a large amount of pericardial effusion, medium pleural effusion on the right side with lower right lung insufficiency, small pleural effusion on the left side, small effusion on the abdominal cavity, three-point Slight reflux of the valve. Considering that it is a clinical diagnosis case of complication flukesomyces disease, the child was given a praziquantel tablet,25 mg/kg,3 times a day, for 3 consecutive days. The treatment was treated at the above dose for 1 week interval for 1 course of treatment, and 3 courses were given. After three months, the child recovered well after the follow-up visit. The child did not complain of special discomfort, and the CT showed a small amount of effusion.

ObjectiveTo develop and validate a diagnostic prediction model for differentiating pulmonary tuberculosis from community-acquired pneumonia based on routine blood parameters. MethodsA total of 642 patients with pulmonary tuberculosis and 503 patients with community-acquired pneumonia were retrospectively enrolled from the Seventh Hospital of Tangshan. They were randomly divided into a training set and an internal validation set at a 7∶3 ratio. Additionally， 218 patients from the 981st Hospital were independently included as an external validation set. The Boruta algorithm and recursive feature elimination were employed to select predictors from 82 blood parameters， sex， and age. A multivariate Logistic regression model was established and evaluated using receiver operating characteristic （ROC） curves， calibration curves， and decision curve analysis. ResultsThe final model incorporated eight predictors， namely uric acid， urea nitrogen， alkaline phosphatase， monoamine oxidase， alanine aminotransferase， glutathione， neutrophil percentage， and age. The model achieved areas under the curve （AUCs） of 0.800 （95%CI： 0.769-0.830）， 0.787 （95%CI： 0.738-0.836）， and 0.736 （95%CI： 0.667-0.835） in the training， internal validation， and external validation sets， respectively. The model demonstrated good calibration， and decision curve analysis showed clinical net benefit within the threshold probability range of 10%-80%. ConclusionThe developed model exhibits good discriminative ability and clinical utility， serving as an effective early screening tool for primary healthcare institutions.

Objective To investigate the malignant phenotypic characteristics of NIH/3T3 cells induced by hexavalent chromium compound under three-dimensional (3D) culture conditions. Methods NIH/3T3 cells in the logarithmic growth phase were divided into four groups: two-dimensional (2D) control group, 2D transformation group, 3D control group, and 3D transformation group. The 2D control group underwent conventional culture, while the 3D control group was cultured with Matrigel. The 2D and 3D transformation groups were exposed to hexavalent chromium compound at a concentration of 0.25 mg/L based on their respective control conditions. Malignant transformation of NIH/3T3 cells was assessed using a soft agar colony formation assay. Malignant phenotypes were evaluated through assays of cell proliferation, apoptosis, cell cycle, wound healing, Transwell migration, and Transwell invasion. Results Cells in both the 2D and 3D transformation groups exhibited anchorage-independent growth, indicating successful malignant transformation. The colony formation rate of cells in the 3D transformation group was higher than that in the 2D transformation group [(6.17±1.31)% vs (1.00±0.41)%, P<0.01]. Compared with the 3D control group, cell proliferation, apoptosis rate, and migration cell count decreased [(100.00±0.00)% vs (95.01±3.49)%, (9.32±0.43)% vs (7.12±0.40)%, (62.50±11.27) vs (48.33±7.31), all P<0.05], while invasion cell count increased [(57.17±9.68) vs (122.83±15.41), P<0.05], and the relative migration area at 12, 24, and 48 hours also increased in 3D transformation group [(4.32±2.09)% vs (10.75±0.45)%, (5.87±1.32)% vs (11.47±0.99)%, (8.74±1.34)% vs (11.79±0.93)%, all P<0.05]. The proportions of cells in G0/G1, S, and G2/M phases between the 3D transformation and 3D control groups had no significant differences (all P>0.05). Conclusion Hexavalent chromium compounds induce key malignant phenotypes in NIH/3T3 cells, including anchorage-independent growth, reduced apoptosis, and enhanced migratory and invasive capacities.

Renal fibrosis is the common pathological endpoint of many forms of chronic kidney disease (CKD), yet the mechanisms determining effective repair versus persistent fibrotic remodeling remain incompletely understood. Peritubular capillaries (PTCs) are not merely passive targets of fibrotic injury, but form a dynamic vascular microenvironment linking regional perfusion, oxygen delivery, tubular metabolism, endothelial barrier integrity, pericyte support, immune-cell trafficking, and extracellular matrix (ECM) remodeling. We propose that PTC abnormalities should not be interpreted simply as reduced capillary density, but as a multidimensional disturbance of microvascular structure and function. Structural vascular preservation does not necessarily indicate effective microcirculation: anatomically detectable capillaries may still exhibit impaired perfusion, barrier dysfunction, abnormal endothelial-pericyte interactions, disturbed oxygen metabolism, or reduced network connectivity. Conversely, increased angiogenesis does not necessarily signify successful vascular repair if vessels remain immature, poorly perfused, or inadequately integrated into the existing network. To organize these abnormalities, we conceptualize PTC remodeling into four predominant but nonexclusive states: endothelial barrier disruption with inflammatory adhesion; endothelial-pericyte uncoupling with no-reflow; dysregulated angiogenesis with network simplification; and capillary rarefaction with fibrotic matrix locking. These states are not sequential stages of CKD. They may coexist within the same kidney, overlap within the same anatomical region, and vary with disease etiology, injury phase, vascular compartment, and treatment exposure. We further propose six dimensions for evaluating PTC status—structural presence, functional perfusion, barrier integrity, pericyte coupling, oxygen metabolism, and network connectivity—so that vascular quantity, function, and reparative capacity are assessed separately rather than inferred from a single endothelial marker or capillary-density measurement. Mechanistically, these states converge on a bidirectional microvascular-fibrotic feedback loop. Barrier disruption facilitates leukocyte recruitment and alters vascular paracrine signaling. Endothelial-pericyte uncoupling compromises capillary stability, whereas abnormal pericyte contraction may increase local vascular resistance and contribute to no-reflow before overt capillary loss. Dysregulated angiogenesis may generate vessels that fail to mature or connect to an effective perfusion network. Progressive capillary rarefaction compromises oxygen delivery, while sustained tubular transport demand and mitochondrial dysfunction may aggravate regional oxygen supply-demand mismatch. Injured tubules, immune cells, endothelial cells, pericytes, and fibroblasts communicate through soluble mediators, extracellular vesicles, direct cell contact, and cell-matrix signaling. Importantly, fibrosis is not merely a downstream consequence of microvascular injury. Altered ECM may increase diffusion distance, modify mechanotransduction, impair endothelial survival and migration, and restrict capillary reopening and regeneration. We use the term matrix locking to describe this sustained constraint on vascular repair, while emphasizing that current evidence does not establish irreversible disease in humans. This framework also has therapeutic implications. PTC-directed treatment should not be reduced to increasing vessel number or uniformly promoting angiogenesis. Instead, intervention should be matched to the dominant and potentially reversible abnormality: preserving endothelial barrier function; restoring endothelial-pericyte stability and reducing pathological microvascular resistance; normalizing angiogenesis so that vascular growth is accompanied by maturation, barrier competence, network integration, and effective perfusion; and, in advanced rarefaction, relieving matrix-related constraints while supporting vascular regeneration. The context- and time-dependent effects of signaling through VEGF, Tie2, PDGF-B/PDGFRβ, eNOS/NO, and related pathways indicate that the same molecular signal may exert different effects depending on disease context and timing. Therapeutic efficacy should therefore be evaluated by restoration of effective microcirculation and tissue function rather than by isolated molecular changes or capillary counts alone. Despite increasing mechanistic evidence, the translational basis for this framework remains limited. Most causal and interventional data derive from animal or cell models, whereas human evidence is largely limited to pathological observations, patient-sample associations, and prognostic studies. Currently available circulating and urinary candidate biomarkers generally lack sufficient specificity for PTC injury or state assignment, and no standardized quantitative thresholds have been externally validated. The four-state model should therefore be regarded as a hypothesis-generating analytical framework rather than a clinicopathological classification system. Future studies should integrate spatially resolved tissue phenotyping, blood and urine biomarkers, and dynamic microcirculatory assessment in longitudinal cohorts. They should test reproducibility, assess prognostic value beyond conventional pathology, estimated glomerular filtration rate, and proteinuria, and determine whether changes in PTC status precede or mediate therapeutic benefit. Linking reproducible microvascular phenotypes to defined mechanisms, treatment response, and long-term renal outcomes will be essential to determine whether state-directed assessment and restoration of the PTC microenvironment can ultimately inform patient stratification and therapeutic decision-making.

Post-stroke cognitive impairment （PSCI） is a highly prevalent severe complication after stroke. In traditional Chinese medicines （TCM）， its core pathogenesis is characterized by deficiency in origin and excess in superficiality： wind， phlegm and blood stasis accumulate， cloud the clear orifices and lead to loss of mental activity， and Xingnao kaiqiao is the targeted principal treatment. This review summarizes the research progress on the pharmacological mechanisms of representative Xingnao kaiqiao-type TCM including Acorus tatarinowii ， Curcumae Radix ， Polygala tenuifolia ， borneol and musk， as well as clinical applications of their related compound formulas and Chinese patent medicines in the treatment of PSCI. The results show that these TCM can improve cognitive function through multiple pathways： targeted regulation of blood-brain barrier permeability， inhibition of neuroinflammation mediated by Toll like receptor 4/nuclear factor-κB， high mobility group protein B1 in ischemic brain tissue and other pathways， and activation of brain-derived neurotrophic factor/tyrosine kinase receptor B， cyclic adenosine monophosphate （cAMP）/protein kinase A/cAMP response element-binding protein and other pathways to promote synaptic plasticity. In terms of clinical application， the evidence chains of formulas based on Acorus tatarinowii and Polygala tenuifolia are relatively complete， which are the core medications to improve cognitive function and activities of daily living； Curcumae Radix has protective potential in the prodromal stage with vascular risk factors； borneol enhances the curative effect of compound prescriptions by improving blood-brain barrier function； musk is mainly used in the acute severe stage. At present， most of the mechanism evidence comes from animal experiments， high-quality large-sample clinical studies directly targeting PSCI populations are still scarce. Subsequent large-sample multicenter studies are needed in the future， combined with multi-omics and multimodal imaging techniques to further clarify its deep-seated mechanism of action.

AIM To investigate the clinical effects of Jinhua Qinggan Granules combined with azithromycin on patients with Mycoplasma pneumoniae pneumonia.METHODS One hundred and three patients were randomly assigned into control group(51 cases)for 1-week intervention of both azithromycin and conventional treatment,and observation group(52 cases)for 1-wee intervention of Jinhua Qinggan Granules,azithromycin and conventional treatment.The changes in clinical effects,remission time for local symptoms(cough,wheezing,fever,pulmonary wet rales),pulmonary function indices(PEF,FEV1,FEV1/FVC),immune function indices(CD4+,CD8+,CD4+/CD8+),NLRP3 inflammatory pathway factors(Caspase-1,IL-1β,IL-18)and incidence of adverse reactions were detected.RESULTS The observation group demonstrated higher total effective rate than the control group(P＜0.05),along with shorter remission time for local symptoms(P＜0.05).After the treatment,the two groups displayed increased pulmonary function indices,CD4+,CD4+/CD8+(P＜0.05),and decreased CD8+,NLRP3 inflammatory pathway factors(P＜0.05),especially for the observation group(P＜0.05).No significant difference in incidence of adverse reactions was found between the two groups(P＞0.05).CONCLUSION For the patients with Mycoplasma pneumoniae pneumonia,Jinhua Qinggan Granules combined with azithromycin can safely and effectively improve clinical symptoms,pulmonary functions and immune functions,whose mechanism may contribute to the regulation of NLRP3 inflammasome pathway expressions.