Factors influencing the therapeutic failure of high-flow nasal cannula oxygen humidification in patients with interstitial pneumonia complicated by respiratory failure.

OBJECTIVE: The aim of this study was to explore the factors influencing the treatment failure of high-flow nasal cannula (HFNC) therapy in patients with interstitial pneumonia (IP) complicated by respiratory failure. PATIENTS AND METHODS: A total of 158 patients with IP and respiratory failure treated with HFNC in our hospital from January 2020 to August 2023 were selected as the study population. Based on treatment efficacy, they were categorized into the HFNC treatment failure group and the HFNC treatment success group. Clinical data were compared between the two groups. Multiple logistic regression analysis was employed to identify independent factors influencing treatment failure, and the predictive value of these factors for HFNC treatment failure was assessed using receiver operating characteristic (ROC) curve analysis. RESULTS: After 7 days of HFNC treatment, among the 158 patients with IP and respiratory failure, 25 (15.8%) declared treatment failure, while the remaining 133 (84.2%) showed treatment success. Patients in the HFNC treatment failure group had significantly higher age, duration of IP, pre-treatment respiratory rate, C-reactive protein (CRP), and controlling nutritional status (CONUT) scores compared to the HFNC treatment success group. The PaO2/FiO2 ratio, left ventricular ejection fraction, and Glasgow Coma Scale (GCS) were significantly lower in the HFNC treatment failure group (p<0.05). Multiple logistic regression analysis revealed that pre-treatment PaO2/FiO2 ratio, CRP, CONUT, and GCS scores were independent factors influencing HFNC treatment failure in patients with IP and respiratory failure (p<0.05). Lower PaO2/FiO2 ratio and GCS scores, and higher CRP and CONUT scores were associated with an increased risk of HFNC treatment failure. ROC curve analysis indicated that pre-treatment PaO2/FiO2 ratio, CRP, CONUT, and GCS scores in patients with IP and respiratory failure had a high predictive value for HFNC treatment failure (p<0.05). CONCLUSIONS: The HFNC failure rate in patients with IP and respiratory failure is 15.8%. Pre-treatment PaO2/FiO2 ratio, CRP, CONUT, and GCS scores are independent factors associated with HFNC treatment failure and warrant clinical attention.

MEG3 promotes liver cancer by activating PI3K/AKT pathway through regulating AP1G1.

OBJECTIVE: This study aims to explore the biological function of maternally expressed gene 3 (MEG3) in liver cancer and the potential mechanism of phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) pathway in regulating proliferation and invasion of hepatoma cells. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (qRT-PCR) was applied to examine the level of MEG3 in 72 pairs of liver cancer tissues and corresponding adjacent tissues. Expression levels of MEG3 and AP1G1 in hepatocellular carcinoma cell lines including SMMC-7721 and BEL-7402 were detected. After transfection of MEG3-siRNA or AP1G1 overexpression plasmid, the proliferative and invasive abilities of hepatoma cells were detected through cell counting kit-8 (CCK-8) and cell invasion assay. The effects of MEG3 and AP1G1 on the cell cycle of hepatoma cell lines were examined using flow cytometry. Western blot was conducted to estimate the changes in the protein levels of AP1G1, p-PI3K, p-AKT and VEGF before and after transfection. RESULTS: The level of MEG3 in hepatoma cancer tissues and cell lines was significantly reduced, especially in patients with advanced liver cancer. Knockdown of MEG3 significantly promoted proliferation and invasion of hepatoma cells, but accelerated cell cycle. Western blot analysis revealed that knockdown of MEG3 reduced the level of AP1G1 and activated the PI3K/AKT pathway. In addition, rescue experiments demonstrated that overexpression of AP1G1 partially reversed the promotive effect of lowly-expressed MEG3 on cell proliferation and invasion, suggesting that low expression of MEG3 may activate PI3K/AKT pathway by inhibiting AP1G1 expression. CONCLUSIONS: Low expression of MEG3 could promote the proliferative and invasive abilities of hepatoma cells and accelerate cell cycle. The mechanism may be related to the inhibition of AP1G1 expression and activation of PI3K/AKT pathway.

[Clinical significance and mechanism of upregulation of PI3Kp110α in non-small cell lung carcinoma].

Objective: To investigate the clinical significance and mechanism of upregulation of phosphoinositide 3-kinase p110α(PI3Kp110α)in non-small cell lung carcinoma (NSCLC). Methods: Expressions of PI3Kp110α and other components in PI3K signaling pathway (including phospho-Akt (p-Akt, Ser 473), MET, ROS1, HER-2, ALK, total EGFR and mutant EGFR) and p53 (the transcription factor of PIK3CA) mutation in NSCLC were detected by immunohistochemistry. The relationships between PI3Kp110α expression and clinicopathological characteristics, expressions of other proteins in PI3K pathway and p53 mutation were analyzed. Results: In 170 NSCLC patients, 72 cases (42.4%) showed lower expression and 98 cases (57.6%) showed higher expression of PI3Kp110α. Upregulation of PI3Kp110α was not significantly associated with gender, age, T stage and pathologic grade (P>0.05). While upregulation of PI3Kp110α was significantly associated with smoking status of patients, pathologic classification, N stage, TNM stage and Ki-67 index (P<0.05). Expression of PI3Kp110α was positively correlated with expressions of MET (P<0.05) and mutant EGFR (P=0.018), while not significantly related with expressions of p-Akt(Ser473), HER-2, ALK, ROS1, total EGFR or p53 mutation (P>0.05). Conclusions: Upregulation of PI3Kp110α is closely related with tumorigenesis of non-smoking lung adenocarcinoma. MET overexpression and EGFR mutation may be crucial to upregulate expression of PI3Kp110α in NSCLC. Overexpression of PI3Kp110α may inhibit tumor cell proliferation in NSCLC through a different pathway other than classical PI3K pathway. Upregulation of PI3Kp110α may predict favorable prognosis of NSCLC patients.

[Minor salivary duct carcinoma of the larynx: a case report].

Salivary duct carcinoma SDC is a rare disease, especially in the larynx. From the pathology point of view, SDC histomorphology is very similar to breast ductal carcinoma. From the immunohistochemistry, epithelial antibodies are positive, but the SMA is negative. From the review of papers, total resection is the first choice for the treatment, but the local recurrence and distant metastasis are the main influence factors for survival rate. Now we still lack the clinical experience for such disease.

[Clinical significance of expression of PI3Kp110α in breast cancer].

Objective: To study the clinical significance of PI3Kp110α expression in breast cancer. Methods: The expressions of PI3Kp110α, HER2, PTEN, p-Akt and Ki-67 in invasive ductal carcinoma (IDC), adjacent ductal carcinoma in situ (DCIS) and normal breast tissue were detected by immunohistochemistry in 102 cases of breast cancer. The expression of PI3Kp110α in IDC was compared with those in DCIS and normal breast tissues. Correlations between expression of PI3Kp110α and expression of HER2, PTEN, p-Akt and Ki-67 index in IDC were analyzed. Correlation between expression of PI3Kp110α and stage of IDC was studied as well. Results: In the normal breast tissues, there were 97 cases (95.1%) with low level and 5 cases (4.9%) with high level expression of PI3Kp110α. In the DCIS tissues, there were 67 cases (65.7%) with low level and 35 cases (34.3%) with high level expression of PI3Kp110α. In the IDC tissues, there were 14 cases (13.7%) with low level and 88 cases (86.3%) with high level expression of PI3Kp110α. The difference between expression of PI3Kp110α in normal breast tissue, DCIS and IDC was significant (P<0.001). In the IDC tissues, expression of PI3Kp110α was negatively correlated with expression of HER2 (rs=-0.213, P=0.032) and PTEN (rs=-0.197, P=0.047), while was not significantly correlated with expression of p-Akt (P=0.119) and Ki-67 index (P=0.636). In contrast, expressions of HER-2 and p-Akt were positively correlated with Ki-67 index (P=0.001, P=0.035), while expression of HER2 was not correlated with p-Akt (P=0.177). Expression of PI3Kp110α was negatively correlated with T stage and TNM stage (P=0.003, P=0.016), while not correlated with N stage and M stage(both P>0.05). Expression of HER-2 was positively correlated with T stage (P=0.037), while not correlated with N stage, M stage and TNM stage (P>0.05 for all). Neither Ki-67 index nor expression of PTEN and p-Akt (P=0.194) were correlated with T stage, N stage, M stage and TNM stage. Conclusions: Expression of PI3Kp110α plays an important role in oncogenesis and development of breast cancer. Based on the fact that expression of PI3Kp110α is negatively correlated with expression of HER2 and PTEN and with T stage and TNM stage, we may conclude that increased expression of PI3Kp110α is another independent pathway in breast cancer development, and breast cancer patients with high expression of PI3Kp110α may have a better prognosis.

CS based confocal microwave imaging algorithm for breast cancer detection.

Based on compressive sensing (CS) technology, a high resolution confocal microwave imaging algorithm is proposed for breast cancer detection. With the exploitation of the spatial sparsity of the target space, the proposed image reconstruction problem is cast within the framework of CS and solved by the sparse constraint optimization. The effectiveness and validity of the proposed CS imaging method is verified by the full wave synthetic data from numerical breast phantom using finite-difference time-domain (FDTD) method. The imaging results have shown that the proposed imaging scheme can improve the imaging quality while significantly reducing the amount of data measurements and collection time when compared to the traditional delay-and-sum imaging algorithm.

Downregulation of miR-518a-3p activates the NIK-dependent NF-κB pathway in colorectal cancer.

The aim of the present study was to investigate the biological role and underlying mechanisms of action of miR-518a-3p in the progression and invasion of colorectal cancer (CRC). Reverse transcription-quantitative PCR (RT-qPCR) was used to examine the mRNA expression levels of miR-518a-3p in 5 CRC cell lines (SW480, SW620, HCT116, HT29 and LoVo) in a normal colonic cell line, NCM460, as well as in tumor tissues with or without metastases. The biological effects of miR-518a-3p were assessed in the CRC cell lines by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometric analysis, and RT­qPCR and western blot analyses were employed to evaluate the expression of miR-518a-3p targets. The regulation of NF-κB-inducing kinase (NIK) by miR-518a-3p was confirmed using luciferase activity assays. Our results revealed that miR-518a-3p was significantly downregulated in the CRC cell lines compared with the normal colonic cell line (P<0.05), as well as in the CRC tissues with distant metastases compared with the tissues without metastases. The downregulation of miR-518a-3p was associated with tumor size, distant metastasis and TNM stage in the patients with CRC. Moreover, the ectopic expression of miR-518a-3p and the inhibition of NIK by RNA interference markedly reduced cell proliferation and enhanced the apoptosis of CRC cells. Further experiments revealed that NIK, a regulator of NF-κB, was a downstream target of miR-518a-3p. The presents findings indicate that miR-518a-3p plays an important role in the progression of CRC by targeting NIK.

Astragalus membranaceus injection delayed allograft survival related with CD4+ CD25+ regulatory T cells.

INTRODUCTION: Recently it has been reported that Astragalus membranaceus injection (AMI) inhibits immune responses, but whether it affects alloimmunity is not clear. It has been shown that the CD4(+) CD25(+) regulatory T cells (Treg) down-regulate immune responses. The aim of our study was to investigate the effects of AMI on allograft survival and its relation to Treg. MATERIALS AND METHODS: Allografted mice were administered AMI for 14 consecutive days with observations of graft survival. The specific recall response, the ratio of Treg, the expression of Foxp3 mRNA, and interleukin (IL)-10 secretion were measured by mixed lymphocyte reactions (MLR), FCM, reverse transcriptase-polymerase chain reaction, and radioimmunoassay, respectively. RESULTS: AMI significantly prolonged allograft survival by up-regulating the Treg ratio and promoting Foxp3 expression (P < .05). The ratio of Tregs, the expression of Foxp3 mRNA, and the IL-10 level in the AMI administration group increased from day 7, to reach a maximum at day 14, recovering to the initial level on day 21. No obvious difference was detected between the AMI and a cyclosporine group. CONCLUSION: AMI administered in vivo prolonged allograft survival associated with promotion of Treg activities.