Objective To explore the application of artificial intelligence quantitative analysis in the prognostic assessment of patients with connective tissue disease-associated interstitial lung disease(CTD-ILD).Methods A total of 67 patients with CTD-ILD were retrospectively selected.All subjects underwent high-resolution computed tomography(HRCT)scanning and were categorized into three groups,namely mild,moderate and severe groups,based on the results of pulmonary function tests.The survival rates of patients in each group were compared using Kaplan-Meier curves and analysis of variance.The univariate analysis was employed to assess the rela-tionships between artificial intelligence parameters and patient prognosis.Significant results were then incorporated into a multifacto-rial Cox regression model to construct the most accurate predictive model.Results A significant difference in survival rate was observed among the three groups(P<0.05).Univariate analysis revealed that the volume and percentage of lung infection in deceased patients were significantly greater than those in surviving patients,while the lung volume in deceased patients was significantly smaller than that in surviving patients.The analysis showed left lung volume and the percentage of lesion components CT value≤-750 HU as risk factors for prognosis,and the combination of these two factors as the most effective predictive model.Conclusion The artificial intelligence analysis system for lung lesions provides a new systematic and quantitative method for the prognostic assessment of CTD-ILD patients,which can be used for the prognostic assessment and follow-up of CTD-ILD patients.

Alzheimer's disease(AD)is the most common cause of cognitive impairment in the elderly,and the formation of intracellular neurofibrillary tangles(NFT)due to the hyperphos-phorylation of Tau is one of its important pathological features.Compared to β-amyloid,the hyperphosphorylation of Tau and the resulting NFT are more closely related to the decline in cognitive ability.This review focuses on anti-AD drugs targeting Tau,em-phasizing the latest progress in inhibiting the hyperphosphoryla-tion of Tau protein,alleviating the aggregation of Tau protein,re-ducing the cytoskeletal damage caused by the hyperphosphoryla-tion of Tau protein by stabilizing microtubules,and immunothera-py,in the hope of providing new insights into drug research for AD and related cognitive disorders associated with Tau protein.

Central nervous system(CNS)degenerative disorders refer to a spectrum of pathological alterations triggered by struc-tural damage to cerebral neural tissues,clinically manifested as diverse neurological dysfunction syndromes,including multiple sclerosis(MS),neurodegenerative diseases(NDs),and ische-mic stroke.The hallmark pathological features of these disorders involve irreversible neuronal damage and decompensation of functional neural networks,ultimately leading to progressive neurological deficits.Notably,with the accelerating global popu-lation aging,the incidence of these diseases has surged signifi-cantly.According to WHO statistics,they now rank among the top three global causes of disability and mortality.Current re-search has confirmed that the pathogenesis of CNS degenerative disorders exhibits high heterogeneity,encompassing multifaceted pathophysiological processes such as genetic predisposition,oxi-dative stress,protein misfolding,and metabolic dysregulation.This intricate pathogenic network not only complicates clinical differential diagnosis but also poses substantial challenges to the development of precision therapeutic strategies.Importantly,re-cent studies have revealed that mitochondrial homeostasis disrup-tion-induced inflammatory cascades(termed mitochondrial in-flammation)play a pivotal regulatory role in neurodegenerative progression.Key molecular mechanisms include impaired mito-phagy,aberrant mitochondrial DNA(mtDNA)release and NL-RP3 inflammasome activation.This review systematically deci-phers the molecular regulatory network of mitochondrial inflam-mation,with a focus on its biological effects in critical pathologi-cal events such as blood-brain barrier disruption,microglial hy-peractivation and neuronal apoptosis.The overarching aim is to provide a theoretical foundation for developing innovative thera-peutic strategies targeting mitochondrial homeostasis restoration.

Aim To establish a simple and practical method for visualizing neurovascular coupling in the mouse barrel cortex in vivo.Methods Male C57BL/6J mice received stereotaxic in-jections of pAAV-hSyn-jGCaMP7s-WPRE into the barrel cortex to monitor neuronal activity.Three weeks post-injection,a crani-al window was implanted,and TRITC-Dextran 155 ku was ad-ministered intravenously to visualize the vasculature and blood flow dynamics.A custom-built whisker stimulator was used to e-voke controlled neuronal excitation.Two-photon microscopy was employed to monitor neuronal and vascular responses to whisker stimulation in real-time.Results Neuronal calcium signals and plasma signals were clearly observed using two-photon microsco-py.Whisker stimulation led to a significant increase in neuronal calcium signals in the barrel cortex,indicating effective neuronal activation.This neuronal excitation was accompanied by a syn-chronous increase in blood vessel diameter,blood flow velocity and overall blood flow.Conclusions This study successfully establishes a three-dimensional visualization framework(spatial,temporal,and functional)for in vivo visualization of neurovascu-lar coupling in the mouse barrel cortex,which provides a useful tool for investigating the pathophysiological mechanisms of neuro-vascular dysfunction and evaluating the efficacy of potential ther-apies.

Aim To generate a dual-reporter mouse model for tracing microglia and neurons to analyze their dynamic changes in real-time and to investigate the functional role of microglia-neuron interactions through microglial depletion.Methods Mi-croglia reporter mice were crossed with neuron reporter mice to generate Tmem119-e(2A-tdTomato-2A-DTR);Thy1-GFP dual-reporter mice.Genotyping was performed using tail DNA.Con-focal and two-photon microscopy were used to examine neuronal morphology.In vivo two-photon imaging was employed to observe the distribution of microglia and neurons in the brain.Diphtheria toxin(DT)was intraperitoneally injected to deplete microglia.Results The dual-reporter mice were successfully generated with the correct genotype.Both microglia and neurons were visu-alized,and microglia were specifically depleted by DT.Conclu-sions The successful establishment of a dual-reporter mouse model for tracing neurons and microglia will facilitate real-time in vivo observation of microglial and neuronal changes under physiological or pathological conditions,elucidating their specific roles in brain homeostasis.

Objective To explore the application of artificial intelligence quantitative analysis in the prognostic assessment of patients with connective tissue disease-associated interstitial lung disease(CTD-ILD).Methods A total of 67 patients with CTD-ILD were retrospectively selected.All subjects underwent high-resolution computed tomography(HRCT)scanning and were categorized into three groups,namely mild,moderate and severe groups,based on the results of pulmonary function tests.The survival rates of patients in each group were compared using Kaplan-Meier curves and analysis of variance.The univariate analysis was employed to assess the rela-tionships between artificial intelligence parameters and patient prognosis.Significant results were then incorporated into a multifacto-rial Cox regression model to construct the most accurate predictive model.Results A significant difference in survival rate was observed among the three groups(P<0.05).Univariate analysis revealed that the volume and percentage of lung infection in deceased patients were significantly greater than those in surviving patients,while the lung volume in deceased patients was significantly smaller than that in surviving patients.The analysis showed left lung volume and the percentage of lesion components CT value≤-750 HU as risk factors for prognosis,and the combination of these two factors as the most effective predictive model.Conclusion The artificial intelligence analysis system for lung lesions provides a new systematic and quantitative method for the prognostic assessment of CTD-ILD patients,which can be used for the prognostic assessment and follow-up of CTD-ILD patients.

Aim To generate a dual-reporter mouse model for tracing microglia and neurons to analyze their dynamic changes in real-time and to investigate the functional role of microglia-neuron interactions through microglial depletion.Methods Mi-croglia reporter mice were crossed with neuron reporter mice to generate Tmem119-e(2A-tdTomato-2A-DTR);Thy1-GFP dual-reporter mice.Genotyping was performed using tail DNA.Con-focal and two-photon microscopy were used to examine neuronal morphology.In vivo two-photon imaging was employed to observe the distribution of microglia and neurons in the brain.Diphtheria toxin(DT)was intraperitoneally injected to deplete microglia.Results The dual-reporter mice were successfully generated with the correct genotype.Both microglia and neurons were visu-alized,and microglia were specifically depleted by DT.Conclu-sions The successful establishment of a dual-reporter mouse model for tracing neurons and microglia will facilitate real-time in vivo observation of microglial and neuronal changes under physiological or pathological conditions,elucidating their specific roles in brain homeostasis.

Alzheimer's disease(AD)is the most common cause of cognitive impairment in the elderly,and the formation of intracellular neurofibrillary tangles(NFT)due to the hyperphos-phorylation of Tau is one of its important pathological features.Compared to β-amyloid,the hyperphosphorylation of Tau and the resulting NFT are more closely related to the decline in cognitive ability.This review focuses on anti-AD drugs targeting Tau,em-phasizing the latest progress in inhibiting the hyperphosphoryla-tion of Tau protein,alleviating the aggregation of Tau protein,re-ducing the cytoskeletal damage caused by the hyperphosphoryla-tion of Tau protein by stabilizing microtubules,and immunothera-py,in the hope of providing new insights into drug research for AD and related cognitive disorders associated with Tau protein.

Central nervous system(CNS)degenerative disorders refer to a spectrum of pathological alterations triggered by struc-tural damage to cerebral neural tissues,clinically manifested as diverse neurological dysfunction syndromes,including multiple sclerosis(MS),neurodegenerative diseases(NDs),and ische-mic stroke.The hallmark pathological features of these disorders involve irreversible neuronal damage and decompensation of functional neural networks,ultimately leading to progressive neurological deficits.Notably,with the accelerating global popu-lation aging,the incidence of these diseases has surged signifi-cantly.According to WHO statistics,they now rank among the top three global causes of disability and mortality.Current re-search has confirmed that the pathogenesis of CNS degenerative disorders exhibits high heterogeneity,encompassing multifaceted pathophysiological processes such as genetic predisposition,oxi-dative stress,protein misfolding,and metabolic dysregulation.This intricate pathogenic network not only complicates clinical differential diagnosis but also poses substantial challenges to the development of precision therapeutic strategies.Importantly,re-cent studies have revealed that mitochondrial homeostasis disrup-tion-induced inflammatory cascades(termed mitochondrial in-flammation)play a pivotal regulatory role in neurodegenerative progression.Key molecular mechanisms include impaired mito-phagy,aberrant mitochondrial DNA(mtDNA)release and NL-RP3 inflammasome activation.This review systematically deci-phers the molecular regulatory network of mitochondrial inflam-mation,with a focus on its biological effects in critical pathologi-cal events such as blood-brain barrier disruption,microglial hy-peractivation and neuronal apoptosis.The overarching aim is to provide a theoretical foundation for developing innovative thera-peutic strategies targeting mitochondrial homeostasis restoration.