With the deep integration of tumor diagnosis and treatment technologies and critical care medicine, oncology critical care has emerged as an innovative interdisciplinary field, whose standardized development is crucial for improving the prognosis of cancer patients. Based on complex system theory and incorporating cutting-edge clinical practices, this paper systematically elaborates on five core principles for promoting the high-quality development of oncology critical care: complex system thinking, value-based healthcare, interdisciplinary integration, spatiotemporal holism, and humanistic experience. These five principles provide a top-level design framework for the discipline in terms of conceptual understanding, comprehensive management, developmental paradigms, clinical treatment, and service models. They aim to establish a patient-centered oncology critical care system that balances medical quality and efficiency, ultimately maximizing patient survival benefits across their entire life cycle.

ObjectiveTo investigate the intervention mechanism of the traditional Chinese medicine Number 2 Feibi recipe （N2FBR） in idiopathic pulmonary fibrosis （IPF）， focusing on its effects on endoplasmic reticulum （ER） stress， apoptosis， stemness maintenance， and regenerative capacity of alveolar type Ⅱ epithelial cells （AT2 cells）， and to validate the modern translational pathway of the theory of "deficiency of Zong Qi leading to pulmonary atelectasis and atrophy". MethodsA mouse model of pulmonary fibrosis was induced by bleomycin （BLM）. Mice were randomly divided into blank control， model， low-， and high-dose N2FBR intervention groups （9.1， 18.2 g·kg^-1）， and prednisolone intervention group （6.5 mg·kg^-1）. Pulmonary histopathological changes and collagen deposition were evaluated using hematoxylin-eosin （HE） and Masson's trichrome staining. Hydroxyproline （HYP） content was measured by the alkaline hydrolysis method. Lung coefficient and pulmonary function parameters were evaluated. The mRNA expression levels of fibrosis-related factors， including collagen type Ⅰ alpha 1 chain （ColIa1）， alpha-smooth muscle actin （α-SMA）， and tissue inhibitor of metalloproteinase 1 （Timp1）， were detected by real-time polymerase chain reaction （Real-time PCR）. Cell apoptosis was assessed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） assay. Apoptosis of AT2 cells was further evaluated by double immunofluorescence staining for surfactant protein C （SPC） and cysteine-aspartic protease-3 （Caspase-3）. Endoplasmic reticulum （ER） stress in AT2 cells was examined by double staining for SPC and protein kinase R-like endoplasmic reticulum kinase （PERK）. Ultrastructural changes of ER and lamellar bodies in AT2 cells were observed by transmission electron microscopy （TEM）. The expression levels of key proteins involved in ER stress and apoptosis pathways， including PERK， activating transcription factor 4 （ATF4）， and Caspase-3， were detected by Western blot. Double immunofluorescence staining of SPC and Ki-67 antigen （Ki-67） was performed to evaluate the proliferative capacity of AT2 cells. Lineage tracing technology （labeling AT2 cells with GFP） combined with Krt8 labeling was used to evaluate intermediate differentiation states， and morphological transformation of AT2 cells into alveolar type Ⅰ epithelial cells （AT1） was observed. ResultsBLM-induced mice exhibited significant structural disruption of lung tissue， increased collagen deposition， elevated lung coefficient， decreased pulmonary function， and upregulation of fibrosis-related factors （P<0.01）. High-dose N2FBR treatment significantly ameliorated lung tissue damage and dysfunction， significantly reduced HYP content （P<0.01）， and significantly downregulated ColIa1， α-SMA， and Timp1 expression （P<0.01）. Apoptosis analysis showed increased TUNEL-positive and Caspase-3-positive AT2 cells in the model group， which was significantly reduced by high-dose N2FBR treatment. TEM revealed swollen ER structures in AT2 cells of the model group， which tended to return to normal following treatment. PERK protein staining analysis showed evident ER stress in AT2 cells of the model group， which were markedly alleviated in the treatment group. The expression levels of ER stress-related proteins PERK and ATF4， as well as the apoptosis-related protein Caspase-3， were elevated in the model group and significantly reduced after treatment. TEM also revealed disrupted lamellar body structures in the model group， which tended to recover in the treatment group. Regarding the proliferative capacity of AT2 cells， the proportion of Ki-67⁺SPC⁺ AT2 cells significantly increased in the treatment group （P<0.01）. Lineage tracing showed that the proportion of keratin 8-positive green fluorescent protein-positive （Krt8⁺GFP⁺） cells increased in the model group， indicating differentiation arrest. This proportion was significantly reduced in the treatment group， and the morphology of GFP⁺ cells exhibited a flattened， extended shape， suggesting restored differentiation toward AT1 cells. ConclusionN2FBR alleviates ER stress in AT2 cells， reduces AT2 cell apoptosis， restores lamellar body structure and function， enhances proliferation activity， and alleviates differentiation arrest to promote differentiation into AT1 cells， thereby repairing the alveolar epithelium and effectively blocking the progression of pulmonary fibrosis. Its traditional Chinese medicine mechanism of "replenishing Zong Qi， harmonizing Qi and blood， and unblocking pulmonary meridians" closely aligns with the modern regulatory pathway of AT2 stem cells， providing a novel theoretical basis and experimental evidence for the intervention of IPF with traditional Chinese medicine.

ObjectiveTo investigate the intervention mechanism of the traditional Chinese medicine Number 2 Feibi recipe （N2FBR） in idiopathic pulmonary fibrosis （IPF）， focusing on its effects on endoplasmic reticulum （ER） stress， apoptosis， stemness maintenance， and regenerative capacity of alveolar type Ⅱ epithelial cells （AT2 cells）， and to validate the modern translational pathway of the theory of "deficiency of Zong Qi leading to pulmonary atelectasis and atrophy". MethodsA mouse model of pulmonary fibrosis was induced by bleomycin （BLM）. Mice were randomly divided into blank control， model， low-， and high-dose N2FBR intervention groups （9.1， 18.2 g·kg^-1）， and prednisolone intervention group （6.5 mg·kg^-1）. Pulmonary histopathological changes and collagen deposition were evaluated using hematoxylin-eosin （HE） and Masson's trichrome staining. Hydroxyproline （HYP） content was measured by the alkaline hydrolysis method. Lung coefficient and pulmonary function parameters were evaluated. The mRNA expression levels of fibrosis-related factors， including collagen type Ⅰ alpha 1 chain （ColIa1）， alpha-smooth muscle actin （α-SMA）， and tissue inhibitor of metalloproteinase 1 （Timp1）， were detected by real-time polymerase chain reaction （Real-time PCR）. Cell apoptosis was assessed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） assay. Apoptosis of AT2 cells was further evaluated by double immunofluorescence staining for surfactant protein C （SPC） and cysteine-aspartic protease-3 （Caspase-3）. Endoplasmic reticulum （ER） stress in AT2 cells was examined by double staining for SPC and protein kinase R-like endoplasmic reticulum kinase （PERK）. Ultrastructural changes of ER and lamellar bodies in AT2 cells were observed by transmission electron microscopy （TEM）. The expression levels of key proteins involved in ER stress and apoptosis pathways， including PERK， activating transcription factor 4 （ATF4）， and Caspase-3， were detected by Western blot. Double immunofluorescence staining of SPC and Ki-67 antigen （Ki-67） was performed to evaluate the proliferative capacity of AT2 cells. Lineage tracing technology （labeling AT2 cells with GFP） combined with Krt8 labeling was used to evaluate intermediate differentiation states， and morphological transformation of AT2 cells into alveolar type Ⅰ epithelial cells （AT1） was observed. ResultsBLM-induced mice exhibited significant structural disruption of lung tissue， increased collagen deposition， elevated lung coefficient， decreased pulmonary function， and upregulation of fibrosis-related factors （P<0.01）. High-dose N2FBR treatment significantly ameliorated lung tissue damage and dysfunction， significantly reduced HYP content （P<0.01）， and significantly downregulated ColIa1， α-SMA， and Timp1 expression （P<0.01）. Apoptosis analysis showed increased TUNEL-positive and Caspase-3-positive AT2 cells in the model group， which was significantly reduced by high-dose N2FBR treatment. TEM revealed swollen ER structures in AT2 cells of the model group， which tended to return to normal following treatment. PERK protein staining analysis showed evident ER stress in AT2 cells of the model group， which were markedly alleviated in the treatment group. The expression levels of ER stress-related proteins PERK and ATF4， as well as the apoptosis-related protein Caspase-3， were elevated in the model group and significantly reduced after treatment. TEM also revealed disrupted lamellar body structures in the model group， which tended to recover in the treatment group. Regarding the proliferative capacity of AT2 cells， the proportion of Ki-67⁺SPC⁺ AT2 cells significantly increased in the treatment group （P<0.01）. Lineage tracing showed that the proportion of keratin 8-positive green fluorescent protein-positive （Krt8⁺GFP⁺） cells increased in the model group， indicating differentiation arrest. This proportion was significantly reduced in the treatment group， and the morphology of GFP⁺ cells exhibited a flattened， extended shape， suggesting restored differentiation toward AT1 cells. ConclusionN2FBR alleviates ER stress in AT2 cells， reduces AT2 cell apoptosis， restores lamellar body structure and function， enhances proliferation activity， and alleviates differentiation arrest to promote differentiation into AT1 cells， thereby repairing the alveolar epithelium and effectively blocking the progression of pulmonary fibrosis. Its traditional Chinese medicine mechanism of "replenishing Zong Qi， harmonizing Qi and blood， and unblocking pulmonary meridians" closely aligns with the modern regulatory pathway of AT2 stem cells， providing a novel theoretical basis and experimental evidence for the intervention of IPF with traditional Chinese medicine.

With the continuous development of society, a large number of new chemicals are continuously emerging, which presents a challenge to current risk assessment and safety management of chemicals. Traditional toxicology research methods have certain limitations in quickly, efficiently, and accurately assessing the toxicity of many chemicals, and cannot meet the actual needs. In response to this challenge, computational toxicology that use mathematical and computer models to achieve the prediction of chemical toxicity has emerged. In the meantime, as researchers increasingly pay attention to understanding the interaction mechanisms between exogenous chemical substances and the body from the system level, and multiomics technologies develop rapidly such as genomics, transcriptomics, proteomics, and metabolomics, huge amounts of data have been generated, providing rich information resources for studying the interactions between chemical substances and biological molecules. System toxicology and network toxicology have also developed accordingly. Of these, network toxicology can integrate these multiomics data to construct biomolecular networks, and then quickly predict the key toxicological targets and pathways of chemicals at the molecular level. This paper outlined the concept and development of network toxicology, summarized the main methods and supporting tools of network toxicology research, expounded the application status of network toxicology in studying potential toxicity of exogenous chemicals such as agricultural chemicals, environmental pollutants, industrial chemicals, and foodborne chemicals, and analyzed the development prospects and limitations of network toxicology research. This paper aimed to provide a reference for the application of network toxicology in other fields.

[Objective] To study the molecular biological mechanism for a case of ABO blood group B subtype, and perform three-dimensional modeling of the mutant enzyme. [Methods] The ABO phenotype was identified by the tube method and microcolumn gel method; the ABO gene of the proband was detected by sequence-specific primer polymerase chain reaction (PCR-SSP), and the exon 6 and 7 of the ABO gene were sequenced and analyzed. Homologous modeling of Bw.03 glycosyltransferase (GT) was carried out by Modeller and analyzed by PyMOL2.5.0 software. [Results] The weakening B antigen was detected in the proband sample by forward typing, and anti-B antibody was detected by reverse typing. PCR-SSP detection showed B, O gene, and the sequencing results showed c.721 C>T mutation in exon 7 of the B gene, resulting in p. Arg 241 Trp. Compared with the wild type, the structure of Bw.03GT was partially changed, and the intermolecular force analysis showed that the original three hydrogen bonds at 241 position disappeared. [Conclusion] Blood group molecular biology examination is helpful for the accurate identification of ambiguous blood group. Homologous modeling more intuitively shows the key site for the weakening of Bw.03 GT activity. The intermolecular force analysis can explain the root cause of enzyme activity weakening.

This article presents a case study of a patient who visited the Geriatric Department of Peking Union Medical College Hospital due to "palpitations, shortness of breath for more than 2 years, limb weakness for 6 months, edema, and nocturnal dyspnea for 2 months". The patient exhibited decreased muscle strength in the limbs and involvement of swallowing and respiratory muscles, alongside complications of heart failure and various arrhythmias which were predominantly atrial. Laboratory tests revealed the presence of multiple autoantibodies and notably anti-mitochondrial antibodies. Following a comprehensive multidisciplinary evaluation, the patient was diagnosed with anti-mitochondrial antibody-associated inflammatory myopathy. Treatment involved a combination of glucocorticoids and immunosuppressants, along with resistance exercises for muscle strength and rehabilitation training for lung function, resulting in significant improvement of clinical symptoms. The case underscores the importance of collaborative multidisciplinary approaches in diagnosing and treating rare diseases in elderly patients, where careful consideration of clinical manifestations and subtle abnormal clinical data can lead to effective interventions.

BACKGROUND/OBJECTIVES: Stroke represents the primary cause of death and persistent disability globally, leading to around 5.5 million annual patient fatalities. The objective was to explore the relationship of dietary fiber with all-cause and cardiovascular disease (CVD) mortality risk in patients with stroke. SUBJECTS/METHODS: We extracted stroke patients’ data from the National Health and Nutrition Examination Survey (NHANES) database. All-cause and CVD mortality were outcomes. Dietary fiber consists of non-digestible forms of carbohydrates, usually polysaccharides that originate from plant-based foods. Covariates including demographic data, vital signs, comorbidities, laboratory parameters, and medication use were screened using the weighted multivariate Cox regression models with backward elimination. Weighted univariate and multivariate Cox regression models were performed to explore the relationship between dietary fiber intake and all-cause/CVD mortality, with hazard ratios (HRs) and 95% confidence intervals (CIs). The association was further investigated in different subgroups. RESULTS: A total of 1,578 patients with stroke were included, of whom 688 (43.6%) died.Total fiber and vegetable fiber intake were analyzed as categorical variables, and the lowest intake was considered reference groups. High intake of total fiber (HR, 0.73; 95% CI, 0.57–0.94) and high intake of vegetable fiber (HR, 0.63; 95% CI, 0.48–0.82) were related to lower all-cause mortality risk in individuals with stroke. Similar findings were also observed between higher total fiber (HR, 0.56; 95% CI, 0.37–0.85) and vegetable fiber intake (HR, 0.57; 95% CI, 0.36–0.89) with decreased CVD mortality risk. The relationship between higher total fiber intake and lower all-cause mortality risk was discovered in individuals aged ≥ 60 yrs, smoking, non-CVD, and chronic kidney disease (CKD). High total fiber, or vegetable fiber consumption was linked to lower CVD mortality risk in stroke individuals aged ≥ 60 yrs, females, body mass index ≥ 30 kg/m 2 , non-smoking, and CKD. CONCLUSION Dietary fiber intake and vegetable fiber intake may benefit the prognosis of patients with stroke. Increasing dietary fiber consumption, especially vegetable fiber intake, potentially benefits the prognosis of stroke patients.

BACKGROUND/OBJECTIVES: Stroke represents the primary cause of death and persistent disability globally, leading to around 5.5 million annual patient fatalities. The objective was to explore the relationship of dietary fiber with all-cause and cardiovascular disease (CVD) mortality risk in patients with stroke. SUBJECTS/METHODS: We extracted stroke patients’ data from the National Health and Nutrition Examination Survey (NHANES) database. All-cause and CVD mortality were outcomes. Dietary fiber consists of non-digestible forms of carbohydrates, usually polysaccharides that originate from plant-based foods. Covariates including demographic data, vital signs, comorbidities, laboratory parameters, and medication use were screened using the weighted multivariate Cox regression models with backward elimination. Weighted univariate and multivariate Cox regression models were performed to explore the relationship between dietary fiber intake and all-cause/CVD mortality, with hazard ratios (HRs) and 95% confidence intervals (CIs). The association was further investigated in different subgroups. RESULTS: A total of 1,578 patients with stroke were included, of whom 688 (43.6%) died.Total fiber and vegetable fiber intake were analyzed as categorical variables, and the lowest intake was considered reference groups. High intake of total fiber (HR, 0.73; 95% CI, 0.57–0.94) and high intake of vegetable fiber (HR, 0.63; 95% CI, 0.48–0.82) were related to lower all-cause mortality risk in individuals with stroke. Similar findings were also observed between higher total fiber (HR, 0.56; 95% CI, 0.37–0.85) and vegetable fiber intake (HR, 0.57; 95% CI, 0.36–0.89) with decreased CVD mortality risk. The relationship between higher total fiber intake and lower all-cause mortality risk was discovered in individuals aged ≥ 60 yrs, smoking, non-CVD, and chronic kidney disease (CKD). High total fiber, or vegetable fiber consumption was linked to lower CVD mortality risk in stroke individuals aged ≥ 60 yrs, females, body mass index ≥ 30 kg/m 2 , non-smoking, and CKD. CONCLUSION Dietary fiber intake and vegetable fiber intake may benefit the prognosis of patients with stroke. Increasing dietary fiber consumption, especially vegetable fiber intake, potentially benefits the prognosis of stroke patients.

BACKGROUND/OBJECTIVES: Stroke represents the primary cause of death and persistent disability globally, leading to around 5.5 million annual patient fatalities. The objective was to explore the relationship of dietary fiber with all-cause and cardiovascular disease (CVD) mortality risk in patients with stroke. SUBJECTS/METHODS: We extracted stroke patients’ data from the National Health and Nutrition Examination Survey (NHANES) database. All-cause and CVD mortality were outcomes. Dietary fiber consists of non-digestible forms of carbohydrates, usually polysaccharides that originate from plant-based foods. Covariates including demographic data, vital signs, comorbidities, laboratory parameters, and medication use were screened using the weighted multivariate Cox regression models with backward elimination. Weighted univariate and multivariate Cox regression models were performed to explore the relationship between dietary fiber intake and all-cause/CVD mortality, with hazard ratios (HRs) and 95% confidence intervals (CIs). The association was further investigated in different subgroups. RESULTS: A total of 1,578 patients with stroke were included, of whom 688 (43.6%) died.Total fiber and vegetable fiber intake were analyzed as categorical variables, and the lowest intake was considered reference groups. High intake of total fiber (HR, 0.73; 95% CI, 0.57–0.94) and high intake of vegetable fiber (HR, 0.63; 95% CI, 0.48–0.82) were related to lower all-cause mortality risk in individuals with stroke. Similar findings were also observed between higher total fiber (HR, 0.56; 95% CI, 0.37–0.85) and vegetable fiber intake (HR, 0.57; 95% CI, 0.36–0.89) with decreased CVD mortality risk. The relationship between higher total fiber intake and lower all-cause mortality risk was discovered in individuals aged ≥ 60 yrs, smoking, non-CVD, and chronic kidney disease (CKD). High total fiber, or vegetable fiber consumption was linked to lower CVD mortality risk in stroke individuals aged ≥ 60 yrs, females, body mass index ≥ 30 kg/m 2 , non-smoking, and CKD. CONCLUSION Dietary fiber intake and vegetable fiber intake may benefit the prognosis of patients with stroke. Increasing dietary fiber consumption, especially vegetable fiber intake, potentially benefits the prognosis of stroke patients.

BACKGROUND/OBJECTIVES: Stroke represents the primary cause of death and persistent disability globally, leading to around 5.5 million annual patient fatalities. The objective was to explore the relationship of dietary fiber with all-cause and cardiovascular disease (CVD) mortality risk in patients with stroke. SUBJECTS/METHODS: We extracted stroke patients’ data from the National Health and Nutrition Examination Survey (NHANES) database. All-cause and CVD mortality were outcomes. Dietary fiber consists of non-digestible forms of carbohydrates, usually polysaccharides that originate from plant-based foods. Covariates including demographic data, vital signs, comorbidities, laboratory parameters, and medication use were screened using the weighted multivariate Cox regression models with backward elimination. Weighted univariate and multivariate Cox regression models were performed to explore the relationship between dietary fiber intake and all-cause/CVD mortality, with hazard ratios (HRs) and 95% confidence intervals (CIs). The association was further investigated in different subgroups. RESULTS: A total of 1,578 patients with stroke were included, of whom 688 (43.6%) died.Total fiber and vegetable fiber intake were analyzed as categorical variables, and the lowest intake was considered reference groups. High intake of total fiber (HR, 0.73; 95% CI, 0.57–0.94) and high intake of vegetable fiber (HR, 0.63; 95% CI, 0.48–0.82) were related to lower all-cause mortality risk in individuals with stroke. Similar findings were also observed between higher total fiber (HR, 0.56; 95% CI, 0.37–0.85) and vegetable fiber intake (HR, 0.57; 95% CI, 0.36–0.89) with decreased CVD mortality risk. The relationship between higher total fiber intake and lower all-cause mortality risk was discovered in individuals aged ≥ 60 yrs, smoking, non-CVD, and chronic kidney disease (CKD). High total fiber, or vegetable fiber consumption was linked to lower CVD mortality risk in stroke individuals aged ≥ 60 yrs, females, body mass index ≥ 30 kg/m 2 , non-smoking, and CKD. CONCLUSION Dietary fiber intake and vegetable fiber intake may benefit the prognosis of patients with stroke. Increasing dietary fiber consumption, especially vegetable fiber intake, potentially benefits the prognosis of stroke patients.