OBJECTIVE To survey the distribution and diversity of bacteria among COPD patients in our hospital′s comprehensive intensive care unit(ICU).METHODS All 166 strains of bacteria were divided into three groups:from noninvasive positive pressure ventilation,from mechanical ventilation and from standard medical treatment and compared their difference.RESULTS The most common pathogens were Candida albicans(38.8%),Klebsiella pneumoniae(10.2%) and Escherichia coli(8.2%) in the standard medical treatment group;C.albicans(45.5%),Pseudomonas aeruginosa(9.1%) and K.pneumoniae(9.1%) in the noninvasive positive pressure ventilation group;however,P.aeruginosa(23.2%),C.albicans(17.9%)and Acinetobacter baumannii(12.6%) in the mechanical ventilation group,respectively.Accompanying with the mechanical ventilation,the resistant-drug rates were observably increased.CONCLUSIONS The percentage of Gram-negative bacilli and fungal infection in the COPD patients of comprehensive ICU is very high.So we should supervise and control the results of antibiotics susceptibility.

Objective: To determine the efficacy and safety of the Yinmei Kuijie decoction combined with 5-aminosalicylic acid (5-ASA) in treating mildly to moderately active ulcerative colitis (UC) under real-world conditions. Methods: This multicenter, prospective, non-randomized, observational study will be conducted in real-world settings. A total of 204 eligible patients will be consecutively enrolled in the study. Patients in the combination treatment group will receive Yinmei Kuijie decoction in combination with 5-ASA, whereas those in the control group will be treated with 5-ASA alone. The primary endpoint will be a clinical response at week 12, defined as a ≥3 point and ≥30% reduction from baseline in the Mayo total score with ≥1 reduction in rectal bleeding or rectal bleeding score = 0 or 1. Secondary efficacy endpoints at week 12 will include health-related quality of life, mucosal healing, and inflammation indicators. Conclusion The results of this study may provide evidence of the efficacy and safety of Yinmei Kuijie decoction combined with 5-ASA in treating patients with mildly to moderately active UC under real-world principles. The results will provide a basis for further confirmatory studies on the efficacy of Yinmei Kuijie decoction.

The risk of colorectal cancer is substantially higher in patients with long-term colorectal inflammation than in the general population.Prolonged inflammation is an essential factor that triggers colorectal cancer.The dynamic pathological evolution process of the classic"inflammation-mediated carcinogenesis"in the colorectum is proctocolitis→dysplasia→cancer.Traditional Chinese medicine lacks a systematic consensus on the pathogenesis of colorectal"inflammation-mediated carcinogenesis".This article proposes the theory of"pathogenic factors lurk intestinal collaterals"to explain the development law of pathogenesis in the dynamic evolution of colorectal"inflammation-mediated carcinogenesis".Internal and external factors can trigger the movement of the latent pathogenic factors,thereby damaging the intestinal tissues,when latent pathogenic factors are hidden in the intestinal collaterals,and the healthy qi is unable to expel them.The prolonged course of the disease further weakens the healthy qi,allowing the latent pathogenic factors to accumulate in the intestinal collaterals,intertwine with phlegm-dampness and blood stasis,accelerate accumulation,and lead to cancer."Latent pathogens trapped in the intestinal collaterals"is the core pathogenesis during inflammation-mediated carcinogenesis.Thus,to prevent colorectal inflammation-mediated carcinogenesis,consideration should be given to the principle of driving away pathogenic factors and dredging the collaterals in clinical practice.The theory regarding"latent pathogens trapped in the intestinal collaterals"can provide a theoretical reference for syndrome differentiation and treating colorectal inflammation-mediated carcinogenesis and offer novel ideas for clinical treatment.

Objective:To investigate the repair effect of electrospun gelatin polycaprolactone (GT/PCL) nanofiber aerogels (NFA) combined with cartilage extracellular matrix (ECM) for treatment of cartilage injuries in rabbits.Methods:Firstly, the GT/PCL electrospun membrane was prepared by electrospinning and was ground into the short fiber at high speed. ECM was extracted and separated from fresh bovine articular cartilage, which mixed with the short fiber solution (10 ∶1). Subsequently, it was used to prepared GT/PCL/ECM (NFA) three-dimensional scaffold. Finally, the physical characteristics of the three different scaffolds (GT/PCL, ECM and GT/PCL/ECM) were detected by scanning electron microscope and Fourier-transform infrared (FTIR) spectrometer, including the composition, microstructure, swelling rate, porosity, compressive strength and degradation rates. And the biocompatibility research was getting on by co-culturing the scaffold with chondrocytes. Fifteen male New Zealand white rabbits were divided into blank control group (Group A, n=5), ECM group (group B, n=5) and composite scaffold(GT/PCL/ECM)group (Group C, n=5) according to the random number table. An injury model was established and three types of bio-scaffold materials were implanted into different groups. At 3 weeks, the cartilage repair was evaluated among groups by semi quantitative global MRI scoring system (WORMS). After the animals were killed, the knee joints of each group were scored by the international society for cartilage repair histological score (ICRs); the ICRs histological score was performedby HE staining and safranine green staining. Results:Three scaffolds showed a porous three-dimensional structure under the scanning electron microscope. FIRT showed that GT and PCL were introduced into the scaffolds successfully. The GT/PCL NAF was loose and unable to be characterized by materials science. The swelling rate of GT/PCL/ECM scaffold [(1, 092.0±32.2)%] was higher than that of ECM scaffold [(933.6±16.3)%] ( P<0.01). The porosity of GT/PCL/ECM scaffold [(92.3±2.3)%] was higher than that of ECM scaffold [(85.9±2.2)%] ( P<0.05). The compressive strength of ECM scaffold [(2.7±0.1)kPa] and of GT/PCL/ECM scaffold [(2.4±0.1)kPa] showed no statistical difference ( P>0.05). The degradation rate of ECM scaffold was higher than that of GT/PCL/ECM scaffold, but the difference was not statistically significant ( P>0.05). The cytotoxicity rating of GT/PCL/ECM scaffold was grade I, indicating that its biocompatibility was better. At 3 weeks, the MRI WORMS score in Group C [(49.0±11.4)points] was significantly higher than that in Group B [(40.0±6.7)points] and that in Group A [(24.0±6.5) points] ( P<0.05 or 0.01); the general ICRS score of group C was [(7.4±1.1) points], which was significantly higher than that of group B [(4.6±1.1)points] and group A [(3.0±1.2)points] ( P<0.01); The ICRS histological scores of group C and group B were [(6.8±0.8)points] and [(4.2±0.8)points] respectively compared with group A [(2.8±0.8)points] were significantly higher ( P<0.05 or 0.01). Conclusion:GT/PCL/ECM (NFA) scaffold has similar tissue structure to natural cartilage and is superior to traditional ECM scaffold in physical properties and biocompatibility, which provides a stable environment for chondrocyte adhesion and growth, promotes collagen regeneration, and thus accelerates the repair of cartilage injury.

Objective To evaluate the performance of a clinical-radiomics model for differentiating focal organizing pneumonia(FOP)and lung adenocarcinoma(LUAD).Methods We retrospectively analyzed the data of 60 patients with FOP confirmed by postoperative pathology at the First Medical Center of the Chinese PLA General Hospital from January,2019 to December,2022,who were matched with 120 LUAD patients using propensity score matching in a 1∶2 ratio.The independent risk factors for FOP were identified by logistic regression analysis of the patients'clinical data.The cohort was divided into a training set(144 patients)and a test set(36 patients)by random sampling.Python 3.7 was used for extracting 1835 features from CT image data of the patients.The radiographic features and clinical data were used to construct the model,whose performance was validated using ROC curves in both the training and test sets.The diagnostic efficacy of the model for FOP and LUAD was evaluated and a diagnostic nomogram was constructed.Results Statistical analysis revealed that an history of was an independent risk factor for FOP(P=0.016),which was correlated with none of the hematological findings(P>0.05).Feature extraction and dimensionality reduction in radiomics yielded 30 significant labels for distinguishing the two diseases.The top 3 most discriminative radiomics labels were GraylevelNonUniformity,SizeZoneNonUniformity and shape-Sphericity.The clinical-radiomics model achieved an AUC of 0.909(95%CI:0.855-0.963)in the training set and 0.901(95%CI:0.803-0.999)in the test set.The model showed a sensitivity of 85.4%,a specificity of 83.5%,and an accuracy of 84.0%in the training set,as compared with 94.7%,70.6%,and 83.3%in the test set,respectively.Conclusion The clinical-radiomics nomogram model shows a good performance for differential diagnosis of FOP and LUAD and may help to minimize misdiagnosis-related overtreatment and improve the patients'outcomes.

Objective To evaluate the performance of a clinical-radiomics model for differentiating focal organizing pneumonia(FOP)and lung adenocarcinoma(LUAD).Methods We retrospectively analyzed the data of 60 patients with FOP confirmed by postoperative pathology at the First Medical Center of the Chinese PLA General Hospital from January,2019 to December,2022,who were matched with 120 LUAD patients using propensity score matching in a 1∶2 ratio.The independent risk factors for FOP were identified by logistic regression analysis of the patients'clinical data.The cohort was divided into a training set(144 patients)and a test set(36 patients)by random sampling.Python 3.7 was used for extracting 1835 features from CT image data of the patients.The radiographic features and clinical data were used to construct the model,whose performance was validated using ROC curves in both the training and test sets.The diagnostic efficacy of the model for FOP and LUAD was evaluated and a diagnostic nomogram was constructed.Results Statistical analysis revealed that an history of was an independent risk factor for FOP(P=0.016),which was correlated with none of the hematological findings(P>0.05).Feature extraction and dimensionality reduction in radiomics yielded 30 significant labels for distinguishing the two diseases.The top 3 most discriminative radiomics labels were GraylevelNonUniformity,SizeZoneNonUniformity and shape-Sphericity.The clinical-radiomics model achieved an AUC of 0.909(95%CI:0.855-0.963)in the training set and 0.901(95%CI:0.803-0.999)in the test set.The model showed a sensitivity of 85.4%,a specificity of 83.5%,and an accuracy of 84.0%in the training set,as compared with 94.7%,70.6%,and 83.3%in the test set,respectively.Conclusion The clinical-radiomics nomogram model shows a good performance for differential diagnosis of FOP and LUAD and may help to minimize misdiagnosis-related overtreatment and improve the patients'outcomes.

It is believed that "deficiency qi retention and stagnation" is the fundamental pathogenesis of coronary microvascular dysfunction （CMD） after percutaneous coronary intervention （PCI）. Patients often have severe coronary vessel congestion before PCI， leading to emptiness in the heart's collaterals， which results in deficiency of healthy qi， poor movement of blood and body fluids， so the heart collaterals are susceptible to stagnation and stasis，then phlegm and stasis generate； after PCI， it is easy to damage the healthy qi then lead to qi deficiency， causing qi， blood， and body fluids fail to transport， thereby leading to blood stasis and phlegm turbidity retention， generating heat and wind to damage the heart and body. It is proposed that the prevention before PCI should replenish qi and collaterals， expel blood stasis and resolve phlegm， to support "deficient qi" in heart collaterals and prevent "stagnation" after PCI. Postoperative management should focus on replenishing qi and protecting the collaterals， eliminating pathogen and controlling development， so as to avoid exacerbating deficiency and stagnation by damaging healthy qi， and eliminate pathogen and unblock the collaterals to interrupt the pathogenesis， which prevent "retention and stagnation" from changes.

Objective:To investigate the clinical features and therapeutic efficacy of patients with hereditary leiomyomatosis and renal cell carcinoma(RCC) syndrome-associated RCC (HLRCC-RCC) in China.Methods:The clinical data of 119 HLRCC-RCC patients with fumarate hydratase (FH) germline mutation confirmed by genetic diagnosis from 15 medical centers nationwide from January 2008 to December 2021 were retrospectively analyzed. Among them, 73 were male and 46 were female. The median age was 38(13, 74) years. The median tumor diameter was 6.5 (1.0, 20.5) cm. There were 38 cases (31.9%) in stage Ⅰ-Ⅱand 81 cases (68.1%) in stage Ⅲ-Ⅳ. In this group, only 11 of 119 HLRCC-RCC patients presented with skin smooth muscle tumors, and 44 of 46 female HLRCC-RCC patients had a history of uterine fibroids. The pathological characteristics, treatment methods, prognosis and survival of the patients were summarized.Results:A total of 86 patients underwent surgical treatment, including 70 cases of radical nephrectomy, 5 cases of partial nephrectomy, and 11 cases of reductive nephrectomy. The other 33 patients with newly diagnosed metastasis underwent renal puncture biopsy. The results of genetic testing showed that 94 patients had FH gene point mutation, 18 had FH gene insertion/deletion mutation, 4 had FH gene splicing mutation, 2 had FH gene large fragment deletion and 1 had FH gene copy number mutation. Immunohistochemical staining showed strong 2-succinocysteine (2-SC) positive and FH negative in 113 patients. A total of 102 patients received systematic treatment, including 44 newly diagnosed patients with metastasis and 58 patients with postoperative metastasis. Among them, 33 patients were treated with tyrosine kinase inhibitor (TKI) combined with immune checkpoint inhibitor (ICI), 8 patients were treated with bevacizumab combined with erlotinib, and 61 patients were treated with TKI monotherapy. Survival analysis showed that the median progression-free survival (PFS) of TKI combined with ICI was 18 (5, 38) months, and the median overall survival (OS) was not reached. The median PFS and OS were 12 (5, 14) months and 30 (10, 32) months in the bevacizumab combined with erlotinib treatment group, respectively. The median PFS and OS were 10 (3, 64) months and 44 (10, 74) months in the TKI monotherapy group, respectively. PFS ( P=0.009) and OS ( P=0.006) in TKI combined with ICI group were better than those in bevacizumab combined with erlotinib group. The median PFS ( P=0.003) and median OS ( P=0.028) in TKI combined with ICI group were better than those in TKI monotherapy group. Conclusions:HLRCC-RCC is rare but has a high degree of malignancy, poor prognosis and familial genetic characteristics. Immunohistochemical staining with strong positive 2-SC and negative FH can provide an important basis for clinical diagnosis. Genetic detection of FH gene germ line mutation can confirm the diagnosis. The preliminary study results confirmed that TKI combined with ICI had a good clinical effect, but it needs to be confirmed by the results of a large sample multi-center randomized controlled clinical study.

Cryoablation therapy with explicit anti-tumor mechanisms and histopathological manifestations has a long history.A large number of clinical practice has shown that cryoablation therapy is safe and effective,making it an ideal tumor treatment method in theory.Previously,its efficacy and clinical application were constrained by the limitations of refrigerants and refrigeration equipment.With the development of the new generation of cryoablation equipment represented by argon helium knives,significant progress has been made in refrigeration efficien-cy,ablation range,and precise temperature measurement,greatly promoting the progression of tumor cryoablation technology.This consensus systematically summarizes the mechanism of cryoablation technology,indications for oral mucosal melanoma(OMM)cryotherapy,clinical treatment process,adverse reactions and management,cryotherapy combination therapy,etc.,aiming to provide reference for carrying out the standardized cryoablation therapy of OMM.

ObjectiveTo investigate the therapeutic effect of Dayuanyin on acute lung injury induced by H1N1 infection and decipher the potential mechanism. MethodThe constituents in Dayuanyin were analyzed by ultra-high performance liquid chromatography-quadrupole-exactive orbitrap mass spectrometry （UHPLC-Q-Exactive Orbitrap MS）. Forty-eight female BALB/c mice were randomized into normal， model， oseltamivir （19.5 mg·kg^-1）， and low-， medium-， and high-dose （2.73， 5.46， 10.92 g·kg^-1） Dayuanyin groups. The normal and model groups were administrated with deionized water by gavage， and the other groups were administrated with the corresponding drugs by gavage. On day 3 of drug administration， the normal group received nasal inhalation of normal saline， and the other groups were inoculated intranasally with A/RP/8/34 （H1N1） for the modeling of influenza virus infection. Mice were administrated with drugs continuously for 7 days and weighed daily. Sampling was performed 12 h after the last administration， and the lung tissue was weighed to calculate the lung index. Hematoxylin-eosin staining was performed to observe the pathological and morphological changes of the lung tissue and bronchi. The cytometric bead array （CBA） was used to measure the serum levels of interferon-gamma （IFN-γ）， C-X-C motif ligand 1 （CXCL1）， tumor necrosis factor-alpha （TNF-α）， chemokine ligand 2 （CCL2）， interleukin-12p70 （IL-12p70）， chemokine ligand 5 （CCL5）， interleukin-1β （IL-1β）， chemokine （C-X-C motif） ligand 10 （CXCL10）， granulocyte-macrophage colony-stimulating factor （GM-CSF）， interleukin-10 （IL-10）， interferon-beta （IFN-β）， interferon-alpha （IFN-α）， and interleukin-6 （IL-6）. According to the results of mass spectrometry and network pharmacology， we analyzed the mechanism of Dayuanyin in treating acute lung injury caused by H1N1. The protein levels of extracellular signal-regulated kinase 1/2 （ERK1/2）， p38 mitogen-activated protein kinase （p38 MAPK）， nuclear factor-kappa B （NF-κB）， and their phosphorylated forms were determined by Western blot. The mRNA levels of myeloid differentiation factor 88 （MyD88）， Toll-like receptor 3 （TLR3）， Toll-like receptor 7 （TLR7）， and Toll-like receptor 8 （TLR8） in the lung tissue were measured by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultA total of 57 compounds， including paeoniflorin and baicalein， were detected in Dayuanyin. Compared with the normal group， the model group showed decreased body weight （P<0.01）， lung edema and hemorrhage， increased lung index （P<0.01）， and elevated levels of IFN-γ， IL-12p70， CCL5， IL-1β， CXCL10， GM-CSF， IFN-β， and IL-6 （P<0.01）. Compared with the model group， Dayuanyin attenuated alveolar wall thickening， capillary congestion， and immune cell infiltration， reduced the alterations in body weight and lung index （P<0.01）， and down-regulated the protein levels of IFN-γ， IL-12p70， CCL5， IL-1β， CXCL10， GM-CSF， IFN-β， and IL-6 （P<0.01）. A total of 57 key genes were predicted by network pharmacological analysis， of which the MAPK signaling pathway was the main target signaling pathway. Compared with the normal group， the model group showed up-regulation in the protein levels of phosphorylation （p）-ERK1/2， p-p38 MAPK， and p-NF-κB （P<0.01） and the mRNA levels of TLR7， TLR8， MyD88， and TLR3 （P<0.05， P<0.01）. Compared with the model group， Dayuanyin lowered the phosphorylation levels of ERK1/2， p38 MAPK， and NF-κB p65 in a dose-dependent manner （P<0.01） and down-regulated the mRNA levels of TLR3， TLR7， TLR8， and MyD88 （P<0.01）. ConclusionDayuanyin can prevent and control H1N1 infection-induced acute lung injury by inhibiting the TLR/MAPK/NF-κB signaling pathway.