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This paper aims to study the distribution and drug sensitivity of pathogenic bacteria in patients with chronic obstructive pulmonary disease (COPD) complicated with pulmonary infection, so as to provide the basis for the correct use of clinical antibiotics. 1 500 strains of pathogenic bacteria were randomly selected from sputum culture samples of patients with COPD complicated with pulmonary infection in a hospital in Changsha from March 2017 to February 2022 for culture identification and drug sensitivity test. The distribution of pathogenic bacteria and the drug resistance characteristics and trends of the main Gram-negative bacteria (Klebsiella pneumoniae, Pseudomonas aeruginosa, Acinetobacter baumannii) were counted and analyzed. A total of 1 251 strains (83.40%) of Gram-negative bacteria were detected from 1 500 pathogenic bacteria, of which 384 strains (25.60%) were Klebsiella pneumoniae, 333 strains (22.20%) were Pseudomonas aeruginosa, and 303 strains (20.20%) were Acinetobacter baumannii were the top. 126 strains of Gram-positive bacteria (8.40%) were detected from 1 500 pathogenic bacteria, of which 69 strains of Staphylococcus aureus (4.60%) and 27 strains of Streptococcus pneumoniae (1.80%) were the top. 123 strains of fungi (8.20%) were detected from 1 500 pathogenic bacteria, mainly 96 strains of Candida albicans (6.40%). The results of drug sensitivity analysis showed that the change of drug resistance rate of Klebsiella pneumoniae to Gentamicin, Levofloxacin, Ceftazidime and Aztreonam was statistically significant (P<0.05). The drug resistance trend of Pseudomonas aeruginosa to Aztreonam was statistically significant (P<0.05). Acinetobacter baumannii showed a high resistance rate to most antibiotics, and the resistance trend to Levofloxacin, Cotrimoxazole and Meropenem is statistically significant (P<0.05). Anti-infection is an important measure in the treatment of COPD, and timely and correct selection of sensitive antibiotics is the key link. This study provides help for the clinically accurate selection of appropriate antibiotics for the treatment of COPD, and also helps to understand the development trend of bacterial resistance in this region, which has important clinical value and significance. [ABSTRACT FROM AUTHOR]

Lung adenocarcinoma (LUAD) is one of the common cancers. Studies show that MMP-1 is involved in tumor progression, yet relevant regulatory mechanism in LUAD remains to be further elucidated. Here, we demonstrated from bioinformatics analysis for GEO data that MMP-1 was differentially up-regulated in LUAD. miR-202-3p, identified as the upstream regulator of MMP-1 by both bioinformatics and dual-luciferase assays, was differentially down-regulated in LUAD and presented a negative correlation with MMP-1. Following cell biological experiments proved that knocking down the expression of MMP-1 inhibited the proliferation, migration and invasion of LUAD cells, while overexpressed miR-202-3p posed a similar suppressive effect on cancer progression. Additionally, rescue assay further identified that overexpression of MMP-1 attenuated the suppressive effect of up-regulated miR-202-3p on malignant progression of LUAD cells. In all, this research suggests a mechanism by which MMP-1 under the regulation of miR-202-3p modulates the proliferation, migration and invasion of LUAD cells, which may contribute to the development of new therapeutic strategies. [ABSTRACT FROM AUTHOR]

The Netrins is one of a small phylogenetically conserved family members which are lamininrelated secreted proteins. The Netrins play a critical role in cell migration and axon guidance. Its homologues have been widely described in various animals. Netrins can be subdivided into two subfamilies, classical Netrins and Netrin-Gs. Since the members of Netrin-G subfamily exhibit a high degree of similarity and there is only one member, Netrin-G1, identified in human, it is presumed that there must be new members in human too. In this paper the total RNA in brains was extracted from 20 weeks human embryos, and the cDNA Library was constructed by using a cDNA PCR Library Kit. A full-length human netrin-G cDNA, named netrin-G2, was generated by using special primers and PCRs. Finally, a primary study about the expression of human netrin-G2 was carried out by northern blot analysis and a research about the relationship between human Netrin-G2 and other Netrins family members was determined by phylogenetic tree analysis. Human netrin-G2 was indeed a new member of netrin-G subfamily, which mapped to chromosome 9q34. The final assembled cDNA sequence of human netrin-G2 was 2428 bps in length, which could encoding a 530-amino acid protein. Northern blot analysis revealed that netrin-G2 expressed specifically in brain and seldom in other tissues. These results suggested that netrin-G2 might play an important role in the development of central nervous system and might contribute to excitatory neurotransmission and neural modulation. [ABSTRACT FROM AUTHOR]

The Netrins is one of a small phylogenetically conserved family members which are lamininrelated secreted proteins. The Netrins play a critical role in cell migration and axon guidance. Its homologues have been widely described in various animals. Netrins can be subdivided into two subfamilies, classical Netrins and Netrin-Gs. Since the members of Netrin-G subfamily exhibit a high degree of similarity and there is only one member, Netrin-G1, identified in human, it is presumed that there must be new members in human too. In this paper the total RNA in brains was extracted from 20 weeks human embryos, and the cDNA Library was constructed by using a cDNA PCR Library Kit. A full-length human netrin-G cDNA, named netrin-G2, was generated by using special primers and PCRs. Finally, a primary study about the expression of human netrin-G2 was carried out by northern blot analysis and a research about the relationship between human Netrin-G2 and other Netrins family members was determined by phylogenetic tree analysis. Human netrin-G2 was indeed a new member of netrin-G subfamily, which mapped to chromosome 9q34. The final assembled cDNA sequence of human netrin-G2 was 2428 bps in length, which could encoding a 530-amino acid protein. Northern blot analysis revealed that netrin-G2 expressed specifically in brain and seldom in other tissues. These results suggested that netrin-G2 might play an important role in the development of central nervous system and might contribute to excitatory neurotransmission and neural modulation. [ABSTRACT FROM AUTHOR]

Immune checkpoint inhibitor pneumonitis (ICIP) is thought to be a self-limiting disease; however, an effective treatment option does not currently exist. This study aimed to determine the clinical efficacy of combination therapy with glucocorticoids and pirfenidone for ICIP related to programmed cell death protein-1 (PD-1) inhibitors. We conducted a retrospective analysis of 45 patients with advanced non-small cell lung cancer who developed ICIP following PD-1 inhibitor and albumin-bound paclitaxel or carboplatin treatment at our hospital. The PD-1 inhibitor was discontinued, and glucocorticoids were used alone or in combination with pirfenidone to treat ICIP. The relevant clinical data of these patients were collected and analyzed. Compared with the glucocorticoid alone group, the glucocorticoid-pirfenidone group showed significant improvement in forced vital capacity (FVC), carbon monoxide diffusing capacity [%], peripheral capillary oxygen saturation, and 6-minute walk distance (P < .05). There were benefits with respect to the St. George's Respiratory Questionnaire score and the recurrence rate of ICIP, but there was no significant difference between the 2 groups (P > .05). Adding pirfenidone to glucocorticoid treatment was shown to be safe and may be more beneficial than glucocorticoids alone for improving pulmonary interstitial lesions, reversing ICIP, and preventing its recurrence., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

Background: Long non-coding RNAs (lncRNAs) are increasingly observed as regulatory factors for the initiation and progression of varying kinds of cancers. However, studies on lncRNAs in non-small cell lung cancer (NSCLC) progression are currently lacking., Objectives: We intended to determine the role of lncRNA LINC00472 and its downstream regulatory mechanism in NSCLC, thus providing novel ideas for targeted therapies for NSCLC., Material and Methods: The target signaling axis comprising the lncRNA/microRNA/mRNA was identified through bioinformatics analysis. Subcellular localization of LINC00472 was assessed with fluorescence in situ hybridization (FISH). Cellular function experiments were conducted to examine the proliferation, migration, invasion, and apoptosis of NSCLC cells, and dual-luciferase and RNA binding protein immunoprecipitation assays were performed to validate the binding relationship. Quantitative real-time polymerase chain reaction (qPCR) and western blot were utilized to assess the expression levels of the investigated gene and protein, respectively., Results: The LINC00472 expression was markedly decreased in NSCLC tissues and cells. The FISH, combined with nuclear-cytoplasm separation assay, demonstrated that LINC00472 was mainly located in the cytoplasm. The overexpression of LINC00472 restrained proliferation and metastasis of NSCLC in vitro. The LINC00472 could target and repress miR-1275 level, and overexpression of LINC00472 reduced the miR-1275-dependent malignant cell phenotype in NSCLC. Further study revealed that HOXA2 was a downstream target of miR-1275 and was negatively modulated by miR-1275. Rescue assays exhibited that the overexpression of miR-1275 or inhibition of HOXA2 reversed the impact of LINC00472 overexpression on the malignant progression of NSCLC cells. The LINC00472 repressed the epithelial-mesenchymal transition (EMT) of NSCLC cells through miR-1275/HOXA2., Conclusions: The LINC00472 functioned as a competing endogenous RNA to modulate HOXA2 level by sponging miR-1275 in NSCLC. Simultaneously, the LINC00472/miR-1275/HOXA2 axis may be a possible therapeutic target and biomarker for NSCLC.

Wnt/β-catenin signaling plays a key role in pathological cardiac remodeling in adults. The identification of a tissue-specific Wnt/β-catenin interaction factor may provide a tissue-specific clinical targeting strategy. Drosophila Pygo encodes the core interaction factor of Wnt/β-catenin. Two Pygo homologs ( Pygo1 and Pygo2 ) have been identified in mammals. Different from the ubiquitous expression profile of Pygo2 , Pygo1 is enriched in cardiac tissue. However, the role of Pygo1 in mammalian cardiac disease is yet to be elucidated. In this study, we found that Pygo1 was upregulated in human cardiac tissues with pathological hypertrophy. Cardiac-specific overexpression of Pygo1 in mice spontaneously led to cardiac hypertrophy accompanied by declined cardiac function, increased heart weight/body weight and heart weight/tibial length ratios, and increased cell size. The canonical β-catenin/T-cell transcription factor 4 (TCF4) complex was abundant in Pygo1 -overexpressing transgenic ( Pygo1 -TG) cardiac tissue, and the downstream genes of Wnt signaling, that is, Axin2 , Ephb3 , and c-Myc, were upregulated. A tail vein injection of β-catenin inhibitor effectively rescued the phenotype of cardiac failure and pathological myocardial remodeling in Pygo1 -TG mice. Furthermore, in vivo downregulated pygo1 during cardiac hypertrophic condition antagonized agonist-induced cardiac hypertrophy. Therefore, our study is the first to present in vivo evidence demonstrating that Pygo1 regulates pathological cardiac hypertrophy in a canonical Wnt/β-catenin-dependent manner, which may provide new clues for tissue-specific clinical treatment via targeting this pathway. NEW & NOTEWORTHY In this study, we found that Pygo1 is associated with human pathological hypertrophy. Cardiac-specific overexpression of Pygo1 in mice spontaneously led to cardiac hypertrophy. Meanwhile, cardiac function was improved when expression of Pygo1 was interfered in hypertrophy-model mice. Our study is the first to present in vivo evidence demonstrating that Pygo1 regulates pathological cardiac hypertrophy in a canonical Wnt/β-catenin-dependent manner, which may provide new clues for a tissue-specific clinical treatment targeting this pathway.