BACKGROUND:Macrophages play a key role in the occurrence and progression of lung diseases,and autophagy plays an important role in maintaining environmental homeostasis and functional stability in macrophages.It has been suggested that macrophage autophagic activity has two sides in lung inflammatory diseases.OBJECTIVE:To summarize the relationship between macrophage autophagy and lung diseases,thereby providing reference for exploring the prevention and treatment strategies of lung inflammatory diseases by targeting macrophage autophagy.METHODS:Literature retrieval was performed in CNKI and PubMed for relevant literature published from database inception to September 2024.The search terms were"macrophage autophagy,efferocytosis,macrophage polarization,acute lung injury,pneumonia,chronic obstructive pulmonary disease,pulmonary fibrosis,asthma"in Chinese and English,respectively.The search results were included or excluded based on the selection criteria,and 100 papers that met the criteria were finally included in the review.RESULTS AND CONCLUSION:(1)The obstruction of autophagy flow will induce the polarization imbalance of macrophages and impair their efferocytosis,resulting in the increase of M1 macrophages and aggravating inflammation.(2)The judgment of autophagic activity should be based on whether the autophagy flow is smooth or not,and it is essential to evaluate the degradation ability of autophagy.Some studies failed to comprehensively detect the degradation ability of autophagy lysosomes to assess whether the autophagy flow is unobtrusive.As a result,the so-called two-sided view of pulmonary macrophage autophagy in pulmonary inflammatory diseases in such studies is actually related to the one-sided judgment of autophagy activity.(3)The pathological manifestations vary across different pulmonary diseases and even at different stages of the same disease.Activation of macrophage autophagy plays a positive role in regulating pulmonary inflammatory homeostasis in conditions such as acute lung injury,infectious pneumonia,mild chronic obstructive pulmonary disease,early-stage pulmonary fibrosis,and secondary asthma.However,in the severe fibrotic stage of chronic obstructive pulmonary disease and the progressive stage of pulmonary fibrosis,the activation of pulmonary macrophage autophagy aggravates pulmonary fibrosis,reflecting the dual nature of macrophage autophagy.In allergic asthma,autophagy is activated in lung-resident macrophages but suppressed in infiltrating monocyte-derived macrophages from circulation.The former is closely related to airway stenosis,and the latter aggravates pneumonia disorders.Therefore,identifying the types and progression stages of lung diseases,along with accurately assessing autophagic activity,is crucial for future investigations into the relationship between macrophage autophagy and disease pathogenesis,thereby facilitating the development of therapeutic strategies in the future.

BACKGROUND:Macrophages play a key role in the occurrence and progression of lung diseases,and autophagy plays an important role in maintaining environmental homeostasis and functional stability in macrophages.It has been suggested that macrophage autophagic activity has two sides in lung inflammatory diseases.OBJECTIVE:To summarize the relationship between macrophage autophagy and lung diseases,thereby providing reference for exploring the prevention and treatment strategies of lung inflammatory diseases by targeting macrophage autophagy.METHODS:Literature retrieval was performed in CNKI and PubMed for relevant literature published from database inception to September 2024.The search terms were"macrophage autophagy,efferocytosis,macrophage polarization,acute lung injury,pneumonia,chronic obstructive pulmonary disease,pulmonary fibrosis,asthma"in Chinese and English,respectively.The search results were included or excluded based on the selection criteria,and 100 papers that met the criteria were finally included in the review.RESULTS AND CONCLUSION:(1)The obstruction of autophagy flow will induce the polarization imbalance of macrophages and impair their efferocytosis,resulting in the increase of M1 macrophages and aggravating inflammation.(2)The judgment of autophagic activity should be based on whether the autophagy flow is smooth or not,and it is essential to evaluate the degradation ability of autophagy.Some studies failed to comprehensively detect the degradation ability of autophagy lysosomes to assess whether the autophagy flow is unobtrusive.As a result,the so-called two-sided view of pulmonary macrophage autophagy in pulmonary inflammatory diseases in such studies is actually related to the one-sided judgment of autophagy activity.(3)The pathological manifestations vary across different pulmonary diseases and even at different stages of the same disease.Activation of macrophage autophagy plays a positive role in regulating pulmonary inflammatory homeostasis in conditions such as acute lung injury,infectious pneumonia,mild chronic obstructive pulmonary disease,early-stage pulmonary fibrosis,and secondary asthma.However,in the severe fibrotic stage of chronic obstructive pulmonary disease and the progressive stage of pulmonary fibrosis,the activation of pulmonary macrophage autophagy aggravates pulmonary fibrosis,reflecting the dual nature of macrophage autophagy.In allergic asthma,autophagy is activated in lung-resident macrophages but suppressed in infiltrating monocyte-derived macrophages from circulation.The former is closely related to airway stenosis,and the latter aggravates pneumonia disorders.Therefore,identifying the types and progression stages of lung diseases,along with accurately assessing autophagic activity,is crucial for future investigations into the relationship between macrophage autophagy and disease pathogenesis,thereby facilitating the development of therapeutic strategies in the future.

Objective To investigate the relationship between the expression of discoidin,CUB and LCCL domain containing protein 1(DCBLD1)and cytoskeleton associated protein 2(CKAP2)in cervical cancer(CC)tissues and epithelial mesenchymal transition(EMT)and clinical prognosis.Methods 94 CC patients diagnosed and treated in Shiyan Hospital of Traditional Chinese Medicine from February 2017 to February 2019 were selected.The expression of DCBLD1 messenger ribonucleic acid(mRNA),CKAP2 mRNA,N-cadherin(N-cad)mRNA,vimentin(Vim)mRNA and TWIST mRNA in tissues was detected by real-time fluorescence quantitative PCR(qRT-PCR).The expressions of DCBLD1 and CKAP2 were detected by immunohistochemistry(IHC).Pearson correlation analysis was used to analyze the relationship between DCBLD1 mRNA,CKAP2 mRNA and EMT-related indicators.Kaplan-Meier survival curve was drawn to compare the prognosis of CC patients with different DCBLD1 mRNA and CKAP2 mRNA expression.COX regression analysis was used to analyze the prognostic factors of CC patients.Results The expression of DCBLD1 mRNA,CKAP2 mRNA,N-cad mRNA,Vim mRNA and TWIST mRNA in CC cancer tissues was higher than that in adjacent tissues,and the differences were statistically significant(t=32.763～52.824,all P<0.05).The positive rates of DCBLD1 protein(89.36%)and CKAP2 protein(87.23%)in CC cancer tissues were higher than those in adjacent normal tissues(7.45%,6.38%),and the differences were statistically significant(χ2=126.278,123.396,all P<0.001).The expression of DCBLD1 mRNA and CKAP2 mRNA in CC cancer tissues were positively correlated with the expression of N-cad mRNA,Vim mRNA and TWIST mRNA(r=0.655～0.744,all P<0.001).The expression of DCBLD1 mRNA and CKAP2 mRNA in patients with FIGO stage IB2～IIB and lymph node metastasis were higher than those in patients with stage IA～IB1 and without lymph node metastasis(t=25.644～35.674,all P<0.05).The 5-year progression free survival rates of the high expression groups of DCBLD1 mRNA and CKAP2 mRNA were 63.04%and 62.22%,respectively,which were lower than those of the low expression groups of DCBLD1 mRNA and CKAP2 mRNA(91.67%and 91.84%),respectively,and the differences were statistically significant(Log-Rank χ2=7.181,6.527,all P<0.05).FIGO stage IB2～IIB,high DCBLD1 mRNA and high CKAP2 mRNA were risk factors affecting the prognosis of CC patients(Wald χ2=8.277,15.877,10.927,all P<0.05).Conclusion The expression of DCBLD1 and CKAP2 in CC cancer tissues is significantly increased,which is related to EMT related indicators and plays a promoting role in the progression of CC tumors.They are new prognostic markers for CC.

Objective To investigate the relationship between the expression of discoidin,CUB and LCCL domain containing protein 1(DCBLD1)and cytoskeleton associated protein 2(CKAP2)in cervical cancer(CC)tissues and epithelial mesenchymal transition(EMT)and clinical prognosis.Methods 94 CC patients diagnosed and treated in Shiyan Hospital of Traditional Chinese Medicine from February 2017 to February 2019 were selected.The expression of DCBLD1 messenger ribonucleic acid(mRNA),CKAP2 mRNA,N-cadherin(N-cad)mRNA,vimentin(Vim)mRNA and TWIST mRNA in tissues was detected by real-time fluorescence quantitative PCR(qRT-PCR).The expressions of DCBLD1 and CKAP2 were detected by immunohistochemistry(IHC).Pearson correlation analysis was used to analyze the relationship between DCBLD1 mRNA,CKAP2 mRNA and EMT-related indicators.Kaplan-Meier survival curve was drawn to compare the prognosis of CC patients with different DCBLD1 mRNA and CKAP2 mRNA expression.COX regression analysis was used to analyze the prognostic factors of CC patients.Results The expression of DCBLD1 mRNA,CKAP2 mRNA,N-cad mRNA,Vim mRNA and TWIST mRNA in CC cancer tissues was higher than that in adjacent tissues,and the differences were statistically significant(t=32.763～52.824,all P<0.05).The positive rates of DCBLD1 protein(89.36%)and CKAP2 protein(87.23%)in CC cancer tissues were higher than those in adjacent normal tissues(7.45%,6.38%),and the differences were statistically significant(χ2=126.278,123.396,all P<0.001).The expression of DCBLD1 mRNA and CKAP2 mRNA in CC cancer tissues were positively correlated with the expression of N-cad mRNA,Vim mRNA and TWIST mRNA(r=0.655～0.744,all P<0.001).The expression of DCBLD1 mRNA and CKAP2 mRNA in patients with FIGO stage IB2～IIB and lymph node metastasis were higher than those in patients with stage IA～IB1 and without lymph node metastasis(t=25.644～35.674,all P<0.05).The 5-year progression free survival rates of the high expression groups of DCBLD1 mRNA and CKAP2 mRNA were 63.04%and 62.22%,respectively,which were lower than those of the low expression groups of DCBLD1 mRNA and CKAP2 mRNA(91.67%and 91.84%),respectively,and the differences were statistically significant(Log-Rank χ2=7.181,6.527,all P<0.05).FIGO stage IB2～IIB,high DCBLD1 mRNA and high CKAP2 mRNA were risk factors affecting the prognosis of CC patients(Wald χ2=8.277,15.877,10.927,all P<0.05).Conclusion The expression of DCBLD1 and CKAP2 in CC cancer tissues is significantly increased,which is related to EMT related indicators and plays a promoting role in the progression of CC tumors.They are new prognostic markers for CC.

Neurofibromatosis Type 1 （NF1） is an autosomal dominant hereditary neurological disorder. One of the typical manifestations of NF1 is neurofibroma, which can develop gradually over time. When the volume exceeds 100 cm², it is referred to as giant neurofibroma, representing a tumor-like proliferation of Schwann cells within the nerve fiber sheath. The Department of Otolaryngology at the Affiliated Hospital of Guangdong Medical University received a rare case involving a patient with giant neurofibromatosis affecting the maxillofacial region, neck, and chest. The patient underwent successful surgical treatment with the collaboration of various medical disciplines.
Humans ; Head and Neck Neoplasms/surgery* ; Neck ; Neurofibromatoses ; Neurofibromatosis 1/surgery* ; Thoracic Neoplasms/surgery*

The tumor microenvironment (TME) is the cellular milieu in which tumor cells thrive, comprising interacting cells and associated factors that form a complex network of interactions, directly or indirectly influencing the initiation, progression, and metastasis of lung cancer. Through TCM pattern identification, it has been observed thatphlegm-pathogen is closely associated with disorder in the inflammatory-metabolic-immune microenvironments of lung cancer. This involves three key pathological mechanisms: "phlegm-stasis complicated by toxin, qi deficiency with exuberant phlegm, and phlegm-pathogen impairing healthy qi". Molecular mechanism studies have revealed that phlegm-resolving agents can extensively modulate multiple targets or pathways, thereby remodeling the inflammatory-metabolic-immune microenvironments of lung cancer. Consequently, a comprehensive therapeutic strategy integrating "resolving phlegm, dispelling stasis, and detoxifying; supplementing qi, warming yang, and resolving phlegm; and reinforcing healthy qi, tonifying the lung, and eliminating phlegm" is essential to reshape the lung cancer TME and enhance antitumor efficacy.

Hepatitis B virus(HBV)is the most common cause of hepatocellular carcinoma(HCC),which is the predominant liver cancer type in Southeast Asia.Approximately 350 million individuals suffer from persistent hepatitis B infection worldwide.HBV promotes HCC development through direct and indirect mechanisms.HBV DNA integrates into the host genome during the initial stages of tumorigenesis,causing insertional mutagenesis of cancer-related genes and genomic instability.Extrachromosomal circular DNA(ecDNA)is formed,which is efficiently amplified in large quantities to express viral genes and host oncogenes.Moreover,virus-associated proteins,such as the regulatory HBV X(HBx)protein and/or the modified preS/S envelope protein,alter the expression of genes associated with multiple functions in host cells.In this review,we summarize the role of the HBx and preS/S proteins in pro-moting tumorigenesis.In addition to summarizing the specific mechanism of HBV-related tumorigen-esis,the concerns and perspectives for future study are discussed.

Objective : To investigate the effects of cinnamaldehyde(CA) on the growth, metastasis and apoptosis of human endometriosis(EMs) cells and to explore whether the mechanism is related to ribosomal protein S7(RPS7) expression. Methods : Endometriosis cells were divided into control group, CA group, sh-NC group, CA+sh-RPS7 group. Effects of CA on cell growth in human endometriotic cells were determined using Cell Counting Kit-8(CCK-8) and colony formation assay. Effects of CA on cell metastasis were performed by motility assay and Transwell assay. Effects of CA on cell apoptosis were evaluated by Hoechst 33258 staining and flow cytometry. Meanwhile, the levels of PCNA, E-cadherin, Vimentin, Bax and Bcl-2 were evaluated using Western blot in human endometriotic cells with treatment CA. The expression of RPS7 was detected by qRT-PCR and Western blot assay. The RPS7 overexpression of human endometriotic cells was established by cell transfection. CA-mediated effects on cell proliferation and apoptosis were determined by CCK-8 assay and flow cytometry in human endometriotic cells with RPS7 overexpression. Results : CA repressed cell growth as well as down-regulated PCNA. The half inhibitory concentration(IC50) value was 53.60 μmol/L after 24 h treatment, and colony formation rate was 25.32%. Additionally, CA inhibited metastasis which was associated with downregulated Vimentin and upregulated E-cadherin. The relative migration rates were 35% and 29% as well as invasion rate was 40%. Further, CA induced apoptosis by cell cycle G2/M phase arrest and cell apoptosis rate was 25.1%, which related to the up-regulation of of Bax and the down-regulation of Bcl-2. CA inhibited the expression of RPS7 and overexpression of RPS7 promoted cell proliferation and suppressed apoptosis in CA-mediated cells. Conclusion CA inhibits cell growth, metastasis, and induces cell apoptosis by downregulating the expression of RPS7.

Objective To investigate the effect of angiotensinogen (AGT), angiotensin-converting enzyme (ACE) and AngII receptor (ATR) gene polymorphisms combined with climatic factors on the incidence of essential hypertension (EH) in Tibetan population in Gannan area. Methods A follow-up study was conducted to select 671 Tibetan people in Gannan area who were physically examined in April 2019 at the Health Management Center of the Second Hospital of Lanzhou University and agreed to be enrolled as a fixed cohort, and the blood pressure values of the enrolled subjects were measured after 3.5 years of follow-up, and a total of 501 cases were obtained. At the same time, the peripheral blood of all subjects was collected and the polymorphisms of AGT, ACE and ATR genes were detected by gene chip technology, and the possible interactions were analyzed by logistic regression model, fork generation method and multifactor-dimensionality reduction (MDR). Results Sunshine time was a protective factor for the incidence of hypertension in the Tibetan population of Gannan (OR=0.781), while relative humidity (OR=1.182), air pressure (OR=1.338) and temperature (OR=1.449) were the risk factors for the incidence of hypertension. According to the results of partial correlation analysis, temperature had no effect on the incidence of hypertension after controlling air pressure. There was an additive interaction between high air pressure and the polymorphisms of rs699 (OR=1.650, 95%CI: 1.293-2.399, P<0.001) and rs5049 (OR=1.711, 95%CI: 1.337-4.920, P<0.001) genes of AGT gene; there was a multiplicative interaction between relative humidity and rs699 (OR=0.472, 95%CI: 0.120-0.783, P<0.05);there was a multiplicative interactions between the altitude ≥ 3000m and rs699 (OR=1.503, 95%CI: 1.220-3.174, P<0.01), rs5049 (OR=1.673, 95%CI: 1.380-3.961, P<0.001) or rs2148582 (OR=0.519, 95%CI: 0.284-0.716, P<0.05).However, there was no interaction between climatic factors and ACE or ATR gene polymorphisms on the incidence of hypertension. Conclusion Climatic factors and altitude ≥3 000 m are closely related to the incidence of hypertension in the Tibetan population of Gannan area, and the interaction between AGT gene polymorphisms and climatic factors affects the incidence of hypertension in the population of this area.

Nano-boron nitride (nano-BN) is a kind of nanomaterials with exceptional mechanical properties, thermal stability and electrical conductivity, and has broad application prospects in industry, energy, electronics and biomedicine. However, with the continuous expansion of its applications, the health effects and potential toxicity of nano-BN on organisms have gradually emerged, and become one of the current research hotspots of nano-BN. The toxicity studies of nano-BN will not only contribute to understanding its potential hazards but also provide crucial theoretical foundations for its safety assessment and health risk evaluation. Therefore, it is of great significance to comprehensively analyze and review the available in vivo and in vitro toxicity studies of nano-BN. This paper discussed the reported influencing factors of nano-BN toxicity, including its morphological characteristics, surface modifications, cell types, exposure dose and time, and further analyzed the oxidative stress, mitochondrial damage, DNA damage, and other related toxic mechanisms induced by nano-BN. Currently, the toxicity research of nano-BN remains limited, particularly due to insufficient human exposure data, unclear chronic toxicity in vivo, and restricted use of cell types for in vitro experiments. Future research should focus on these gaps.