Background:Chronic obstructive pulmonary disease (COPD) often coexists with pulmonary hypertension (PH), leading to exacerbated morbidity and mortality. Conventional treatments focus on bronchodilation, anti-inflammatory agents, and vasodilators, emphasizing the need for novel interventions. Atorvastatin and azithromycin have pleiotropic properties that may benefit COPD with concomitant PH. However, the combined impact of these medications on lung and right heart function in this patient population remains underexplored. Methods:A retrospective cohort study involving 229 stable COPD patients with concomitant PH assessed the effects of atorvastatin combined with azithromycin. Patients were divided into atorvastatin monotherapy and atorvastatin plus azithromycin combination therapy groups and underwent a 6-month treatment period. Blood testing, pulmonary function testing, and echocardiographic assessment of right heart function were conducted before and after treatment. Results:The combination therapy group exhibited significant improvements in blood gas indicators (mean PaO2 increase: 1.22 kPa, 95% CI: 0.82-1.62 kPa, p < 0.001), lung function (mean FEV1 increase: 0.18 L, 95% CI: 0.08-0.28 L, p < 0.001), right heart function (mean PAPs reduction: 8.0 mmHg, 95% CI: 7.0-9.0 mmHg, p < 0.001), respiratory distress, and daily living ability compared to the monotherapy group. Positive correlations were observed between improvements in pulmonary function and daily living ability. The combination therapy resulted in a significantly higher total effective rate (84.48% vs. 72.73%, p = 0.042) compared to the monotherapy group. Conclusion:This retrospective study suggests potential associations between combination therapy with atorvastatin and azithromycin and improvements in functional outcomes in COPD patients with concomitant PH. These findings warrant prospective validation in randomized controlled trials.

Airway smooth muscle cell (ASMC) dysfunction, including altered cell viability, proliferation-apoptosis imbalance, and proinflammatory activation, contributes to the pathogenesis of chronic obstructive pulmonary disease (COPD) associated inflammatory processes. We investigated the role of the miR-155-5p/SOCS1/NF-κB axis in these processes. We performed integrative analyses of GEO dataset mining (GSE5058), clinical samples from COPD patients, a mouse model of LPS/cigarette smoke–induced pulmonary inflammation, and mechanistic in vitro studies in ASMCs. The expression levels of miR-155-5p and SOCS1 were assessed by RT-qPCR and Western blotting. ASMC viability, apoptosis, invasion, cell cycling, and cytokine production were tested. Target interaction was validated by dual-luciferase reporter assay, and pathway involvement was assessed by analysis of the NF-κB signaling. miR-155-5p expression increased, and SOCS1 decreased in COPD lung tissues and serum (both p < 0.001), with an inverse correlation (r = − 0.48, p < 0.005). In mice, elevated miR-155-5p was associated with greater lung injury, higher TNF-α/IL-6 production, increased Cyclin D1 and phosphorylated NF-κB p65, and reduced p21, SOCS1, and cleaved caspase-3 (all p < 0.05). In ASMCs, miR-155-5p promoted cell viability, invasion, S-phase entry, apoptosis resistance, and cytokine production (all p < 0.05). miR-155-5p directly bound the SOCS1 3′UTR. miR-155-5p inhibition or SOCS1 overexpression attenuated NF-κB activation and rescued these phenotypes; SOCS1 overexpression reduced 70

The stress hyperglycemia ratio (SHR), a novel marker reflecting relative hyperglycemia, has been increasingly recognized for its prognostic value in cardiovascular and metabolic diseases. However, its association with early renal damage in hypertensive patients remains underexplored. This study aims to investigate the independent relationship between SHR and albuminuria in a nationally representative cohort of adults with hypertension. This cross-sectional analysis included 8732 adults with hypertension from the National Health and Nutrition Examination Survey 2005-2018. Multivariable logistic regression models were used to evaluate the independent association between SHR and albuminuria, with adjustment for demographic, lifestyle, and clinical covariates. Restricted cubic splines (RCS) were employed to model nonlinear relationships. Stratified analyses were conducted across various subgroups. The prevalence of albuminuria was 15%. After full adjustment for confounders, compared to the reference quartile (Q2), the highest SHR quartile was significantly associated with an increased odds of albuminuria (OR: 2.34; 95% CI: 1.62-3.36; p < 0.001). RCS analysis revealed a nonlinear, J-shaped association between continuous SHR and albuminuria (p for nonlinearity < 0.001), with risk markedly increasing beyond an SHR of approximately 0.91. Subgroup analyses confirmed the robustness of this association across most strata, including age, gender, BMI, eGFR, diabetes status, and cancer history, with no significant interactions observed (all p-interaction > 0.05). In this large, population-based study, an elevated SHR is significantly and independently associated with a higher prevalence of albuminuria among US adults with hypertension.

We investigated serum miR-155 in chronic obstructive pulmonary disease (COPD) and its clinical utility. miR-155 in peripheral blood mononuclear cells (PBMCs) and serum cytokines (IL-1β, IL-6, IL-8, TNF-α) were quantified, and associations with disease occurrence, inflammation, severity, and prognosis were assessed over one year. A total of 117 participants were enrolled: 59 COPD patients (29 acute exacerbation [AECOPD], 30 stable), 31 heavy smokers, and 27 healthy controls. miR-155 was measured by RT-PCR and cytokines by ELISA. COPD patients were prospectively followed and categorized as frequent exacerbators (FE) or non-frequent exacerbators (NFE) to evaluate miR-155's predictive value. miR-155 was significantly elevated in COPD and heavy-smoking groups versus controls (P < 0.01) and higher in AECOPD than stable COPD (P < 0.01). ROC analysis identified optimal cutoff 0.578 (sensitivity 68.97%, specificity 96.67%, AUC = 0.8724). In AECOPD, miR-155 was lower in invasive pulmonary aspergillosis (IPA) than non-IPA patients (P < 0.01). All inflammatory cytokines were significantly elevated in AECOPD versus other groups (P < 0.01). miR-155 showed positive correlations with IL-1β (R = 0.22, 95% CI 0.03-0.39, P < 0.05), IL-6 (R = 0.20, 95% CI 0.01-0.37, P < 0.05), IL-8 (R = 0.20, 95% CI 0.02-0.37, P < 0.05), TNF-α (R = 0.22, 95% CI 0.04-0.39, P < 0.05), GOLD stage (R = 0.35, 95% CI 0.10-0.55, P < 0.01), and ABE grouping (R = 0.66, 95% CI 0.49-0.79, P < 0.01). FE patients had higher miR-155 than NFE (P < 0.001), with moderate correlation to exacerbation frequency (R = 0.63, 95% CI 0.45-0.76, P < 0.01). miR-155 is involved in smoking-related COPD pathogenesis and shows promise as a biomarker for identifying AECOPD and differentiating IPA from non-IPA infections. Its correlations with inflammatory cytokines and disease severity support its utility in assessing inflammatory burden and clinical severity. Elevated miR-155 predicts frequent exacerbations, highlighting its potential as a prognostic biomarker.

Tumour cell immune infiltration is linked to spindle pole component 25 (SPC25). The purpose of this work was to examine the function and molecular mechanism of SPC25 in immune escape in lung adenocarcinoma (LUAD). SPC25 expression in LUAD was examined using The Cancer Genome Atlas (TCGA) database, and RT-qPCR was used to confirm the results. The study involved the use of CD8+ T lymphocytes for immunoinfiltration analysis of SPC25, Gene Set Enrichment Analysis (GSEA) analysis of signalling pathways enriched by SPC25, identification of putative regulatory molecules of SPC25, and confirmation through the use of dual-luciferase and ChIP tests. To evaluate LUAD cell capacity for immune escape, a co-culture technique was employed. Measurements of glutamine uptake, glutamate and α-ketoglutarate levels, NADPH/NADP and GSH/GSSG ratios, and SLC1A5 expression were used to assess the levels of glutamine metabolism. LUAD had increased SPC25 expression. In LUAD cells, immune escape was facilitated by SPC25 knockdown, whereas overexpression had the reverse effect. SPC25 enrichment in the glutamine metabolism pathway was shown by GSEA analysis. Through increased glutamine metabolism brought on by SPC25 overexpression, immune escape was improved in LUAD and could be mitigated by GPNA therapy. E2F8 was also shown to be the transcription factor associated with SPC25, and they showed a binding interaction. By inhibiting glutamine metabolism through SPC25, knocking down E2F8 prevented immune escape in LUAD cells. On the other hand, the suppression of immune escape in LUAD cells caused by E2F8 knockdown was overcome by overexpression of SPC25. In LUAD, E2F8 stimulates SPC25 expression to facilitate glutamine metabolism and encourage immune escape. Our research validates a novel immune escape pathway driven by SPC25 in LUAD cells, providing LUAD patients with potentially effective immunotherapeutic approaches.

Elevated urinary albumin excretion, quantified as the urinary albumin-to-creatinine ratio (UACR), is a marker of endothelial injury and chronic kidney disease. This study investigates the prevalence and prognostic significance of elevated UACR in asthma patients. Using data from the National Health and Nutrition Examination Survey (NHANES 2001–2018), 6,930 adults with asthma were analyzed. Participants were stratified by UACR categories: < 30 mg/g (Group 1), 30–300 mg/g (Group 2), and ≥ 300 mg/g (Group 3). Furthermore, for Group1, we further divided it into tertiles. Kaplan–Meier curves, Cox proportional hazards models, restricted cubic splines, and subgroup analyses were employed to assess associations between UACR and mortality. Among 6,930 adults with asthma, 809 all-cause and 195 cardiovascular deaths occurred. Elevated UACR was prevalent in 12.6

Background:Chlamydia abortus is a zoonotic pathogen that commonly causes abortion, pelvic inflammatory disease, or septicemia during pregnancy in humans. It can occasionally lead to pneumonia. Case Presentation:We report a 35-year-old male with pneumonia complicated by psychiatric symptoms and pneumomediastinum. Initial treatment with cefotaxime and piperacillin-tazobactam failed. On admission, chest CT revealed bilateral pulmonary inflammation, pneumomediastinum, and cervical subcutaneous emphysema. Bronchoalveolar lavage fluid underwent Targeted Next-Generation Sequencing, identifying Chlamydia abortus. Treatment with doxycycline and moxifloxacin led to resolution of fever, psychiatric symptoms, and pulmonary lesions. The patient continued oral doxycycline post-discharge, and follow-up CT showed near-complete recovery. Conclusion:Chlamydia abortus infection can cause pneumonia with psychiatric symptoms, pneumomediastinum, and cervical emphysema-complications not previously reported. Targeted Next-Generation Sequencing (Targeted NGS) plays a crucial role in the early and precise detection of Chlamydia abortus, improving diagnostic accuracy and treatment timeliness. Doxycycline is effective in the treatment of Chlamydia abortus infection and contributed to the patient's recovery.

Objective:The goal of this study was to investigate the effect of antico-agulant intervention on inflammatory factors in rats with chronic obstructive pulmonary disease(COPD)and its correlation with thrombus factors.Methods:Sixty Wistar rats were randomly assigned to one of three groups:model group(n=20),anticoagulation in-tervention group(n=20),and healthy control group.The rats in the healthy control group were fed normally,with no special treatment.The rats in the model group and the anti-coagulation intervention groups had COPD models created by cigarette smoking com-bined with intratracheal injection of lipopolysaccharide.Following successful modeling,rats in the model group received a subcutaneous injection of normal saline,while the rats in the anticoagulation intervention group received a subcutaneous injection of low molecular weight heparin sodium.The three groups were compared in terms of lung his-tomorphology,pulmonary function measures,serum levels of inflammatory and throm-botic markers.The link between inflammatory variables and thrombus components in COPD model rats was determined using Pearson correlation analysis.Results:The mean lining interval(MLI)and the ratio of alveolar area to total lung area(PAA)in the model group and the anticoagulation groups were larger than those in the healthy control group,whereas the mean alveolar number(MAN)was lower.MLI and PAA were lower in the anticoagulation intervention group than in the model group,whereas MAN was higher in the model group(P<0.05).Tidal volume,minute ventilation,and FEV1/FVC were lower in the model and anticoagulation intervention groups than in the healthy control group,but lung compliance was higher in the model and anticoagulation intervention groups.Tidal volume,minute ventilation volume,and FEV1/FVC were higher in the anticoagu-lation intervention group than in the model group,whereas lung compliance was worse in the model group(P<0.05).The serum levels of tumor necrosis factor-α(TNF-α),inter-leukin-8(IL-8)and interleukin-6(IL-6)in the model and anti-coagulation intervention groups were higher than those in the healthy control group,but lower in the anti-coagu-lation intervention group than in the model group(P<0.05).The serum levels of tissue factor(TF)and tissue factor pathway inhibitor-1(TFPI-1)were higher in the model group and anticoagulation intervention groups than those in the healthy control group,while the levels of the above thrombotic factors were lower in the anticoagulation intervention group than those in the model group(P<0.05).Pearson correlation analysis revealed that TNF-α,IL-8 and IL-6 levels were favorably linked with TF and TFPI-1 levels in COPD model rats(P<0.05).Conclusion:Anticoagulant therapy can successfully en-hance pulmonary function in COPD rats,while also negatively regulating inflammatory and thrombus factors,and there is a strong link between inflammatory factors and throm-bus factors.

Background The risk factors for osteoporosis and its prognostic value in patients with bronchiectasis is not well characterized. We explored the risk factors for osteoporosis and its prognostic impact in hospitalized non-cystic fibrosis bronchiectasis (NCFB) patients in Southeast China. Methods This observational cohort study consecutively enrolled 179 hospitalized patients with NCFB bronchiectasis between 2017 and 2021. The risk factors and the impact of osteoporosis on all-cause mortality were assessed. Results 21.2% (38/179) of hospitalized NCFB patients were diagnosed with osteoporosis. Patients with osteoporosis had more severe symptoms (assessed by chronic airway assessment test, CAT, median 22 vs. 17, P = 0.017), poorer quality of life (assessed by St. George Respiratory Questionnaires, SQRC, median 42 vs. 27, P = 0.007), more severe disease stage (assessed by bronchiectasis severity index, BSI, median 14 vs. 11, P = 0.02), more comorbidities (assessed by Bronchiectasis Aetiology Comorbidity Index, BACI, median 5 vs. 4, P = 0.021) than patients without. Age, female sex, anemia, post-infection, and history of regular inhaled corticosteroid treatment were independent risk factors for osteoporosis in those patients. 21 patients (11.7%) died over a median follow-up period of 32 months. The all-cause mortality in NCFB patients with osteoporosis [28.94% (11/38)] was significantly higher than those without osteoporosis [7.09% (10/141)] [hazard ratio (HR) 5.34, 95% confidence interval (CI) 2.26–12.67, P < 0.001]. After adjusting for BSI and other confounding factors, osteoporosis was still independently associated with all-cause mortality in hospitalized NCFB patients (HR 4.29, 95% CI 1.75–10.49, P < 0.001). Conclusions Osteoporosis had an independent effect on all-cause mortality in hospitalized NCFB patients. Management of comorbidities, including bone health, is a critical aspect of treating NCFB patients.

Background. High-flow nasal cannula (HFNC) can be used in stable chronic obstructive pulmonary disease (COPD) patients, but the effect of HFNC on clinical outcomes in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is still uncertain. Methods. We searched electronic literature databases for randomized controlled trials (RCTs) comparing HFNC with noninvasive ventilation (NIV) in hypercapnic patients with AECOPD. The primary endpoint of this meta-analysis was PaCO2, PaO2, and SpO2. The secondary outcomes were the respiratory rate, mortality, complications, and intubation rate. Results. We included 7 RCTs with a total of 481 patients. There were no significant differences on measures of PaCO2 (MD = −0.42, 95%CI −3.60 to 2.75, Z = 0.26, and P = 0.79), PaO2 (MD = −1.36, 95%CI −4.69 to 1.97, Z = 0.80, and P = 0.42), and SpO2 (MD = −0.78, 95%CI −1.67 to 0.11, Z = 1.72, P = 0.08) between the HFNC group and the NIV group. There was no significant difference in measures of the mortality and intubation rate between the HFNC group (OR = 0.72, 95%CI 0.30 to 1.69, Z = 0.76, and P = 0.44) and the NIV group (OR = 2.38, 95%CI 0.49 to 11.50, Z = 1.08, and P = 0.28), respectively. But the respiratory rate in the HFNC group was lower than that in the NIV group (MD = −1.13, 95%CI −2.13 to −0.14, Z = 2.23, and P = 0.03), and fewer complications were found in the HFNC group (OR = 0.26, 95%CI 0.14 to 0.47, Z = 4.46, and P < 0.00001). Conclusion. NIV was noninferior to HFNC in decreasing PaCO2 and increasing PaO2 and SpO2. Similarly, the mortality and intubation rate was similar among the two groups. The respiratory rate and complications were inferior in the AECOPD group treated with HFNC.

BACKGROUND:As reported, long non-coding RNAs are a pivotal player in lung squamous cell carcinoma (LSCC) progression. We noticed the remarkably upregulated transmembrane-4-l-six-family-19 antisense RNA 1 (TM4SF19-AS1) in LSCC and further demonstrated the function it played in LSCC and the possible molecular mechanism.METHODS:Via bioinformatics approach, we evaluated TM4SF19-AS1 and TM4SF19 levels in LSCC tissue, and real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot revealed their mRNA and protein levels in LSCC cells. Cell Counting Kit-8 and colony formation assays analyzed the proliferation ability of LSCC cells, and cell adhesion ability was detected via cell adhesion assay. RNA immunoprecipitation and chromatin immunoprecipitation analyzed the underlying mechanism of TM4SF19-AS1 regulating its target, while methylation-specific PCR indicated the methylation level of TM4SF19-AS1.RESULTS:TM4SF19-AS1 was markedly upregulated in LSCC. Functional assays revealed that TM4SF19-AS1 could facilitate the proliferation and adhesion of LSCC. Besides, we revealed the mechanism of TM4SF19-AS1 regulation that it directly bound to WD repeat-containing protein 5 (WDR5), and was then recruited to TM4SF19 promoter region, which activated DNA demethylation, thereby suppressing malignant LSCC progression.CONCLUSION:Our research demonstrated that TM4SF19-AS1 affected LSCC cell proliferation by recruiting WDR5 to manipulate transmembrane-4-lsix-family-member-19 (TM4SF19), which offers a new observation on LSCC pathogenesis, indicating that TM4SF19-AS1 is able to be a promising target for LSCC treatment.

The occurrence of paclitaxel (PTX) resistance in nonsmall cell lung cancer (NSCLC) is a major challenge for NSCLC treatment. Circular RNAs (circRNAs) have been reported to associate with cancer resistance, but the role of circ_0010235 in PTX resistance of NSCLC is unclear. The expression of circ_0010235 and microRNA-512-5p (miR-512-5p) were determined by quantitative real-time PCR. Cell counting kit-8 assay, transwell assay and flow cytometry were performed to measure the PTX resistance, proliferation, migration, invasion and apoptosis of cells. All proteins were assessed via western blot analysis. The combination between miR-512-5p and circ_0010235 or FAM83F was predicted by the online database and confirmed by a dual-luciferase reporter assay. Angiogenesis assay was used to detect the ability of cells to form blood vessels. Animal experiments were employed to confirm the effect of circ_0010235 on NSCLC tumor growth in vivo. Circ_0010235 and FAM83F were upregulated in PTX-resistant NSCLC tissues and cells. Circ_0010235 knockdown suppressed the resistance to PTX, proliferation, angiogenesis and migration/invasion in A549/PTX and H1299/PTX cells but promoted apoptosis rate. MiR-512-5p could be sponged by circ_0010235, and its overexpression had an inhibition effect on the PTX resistance of NSCLC cells. FAM83F was a target of miR-512-5p and circ_0010235 could modulate FAM83F expression by sponging miR-512-5p. In vivo experiments revealed that silenced circ_0010235 could improve the sensitivity of the tumor to PTX. Therefore, these findings advocated targeting the circ_0010235/miR-512-5p/FAM83F axis as a potential therapeutic option for patients with NSCLC who are resistant to PTX.

This study aims to investigate the risk factors associated with impaired pulmonary diffusing capacity among patients with noncystic fibrosis bronchiectasis (NCFB) and compare the predictive value of several scoring systems for the impairment in these patients. Between July 2019 and June 2021, patients who were admitted to the hospital and diagnosed with NCFB were included in this study. Clinical data were collected and analyzed retrospectively. A total of 175 NCFB patients were included in the analysis. Multivariate logistic regression analysis revealed that impaired pulmonary diffusing capacity diagnosed by carbon monoxide diffusing capacity (DLCO) <80% prediction was associated with age, Reiff score, body mass index (BMI), comorbid chronic obstructive pulmonary disease (COPD), and interstitial lung disease (ILD). Disease duration, frequency of exacerbation, hemoglobin level, and COPD were independent risk factors for impaired pulmonary diffusing capacity diagnosed by DLCO/alveolar volume (VA) <80% prediction. Age, Reiff score, and smoking status were independent risk factors for decreased VA diagnosed by VA <80% prediction. The areas under the curve (AUC) for discrimination of DLCO <80% prediction were 0.822 (0.760–0.885) for Bronchiectasis Severity Index (BSI), 0.787 (0.718–0.856) for FACED, 0.795 (0.729–0.863) for E-FACED, and 0.767 (0.694–0.839) for modified Medical Research Council (mMRC) scores; the AUC for discrimination of DLCO/VA <80% prediction was 0.803 (0.727–0.880) for BSI, 0.752 (0.669–0.835) for FACED, 0.757 (0.676–0.839) for E-FACED, and 0.762 (0.679–0.845) for mMRC, respectively. The BSI had the largest AUC, but the differences between those scoring systems had no statistical significance ( P = 0.181 for DLCO <80% prediction and P = 0.105 for DLCO/VA <80% prediction). The mMRC score (up to 2 grades) showed a high specificity for discriminating diffusing dysfunction (88.3% for DLCO <80% prediction and 76.1% for DLCO/VA <80% prediction). In NCFB patients, several factors such as age, Reiff score, BMI, exacerbation frequency, disease duration, and comorbid COPD and ILD were associated with impaired pulmonary diffusing capacity, which requires more attention in managing those patients. In addition, several scoring methods, including a simple index of mMRC, showed a comparable and moderate performance for predicting pulmonary diffusing impairment and would facilitate the systematic evaluation of the diffusing capacity of NCFB patients.

Pulmonary rehabilitation (PR) is an essential method for Acute exacerbation in chronic obstructive pulmonary disease (AECOPD) recovery. We perform a meta-analysis to compare early PR with usual care. A literature search was performed through these databases: PubMed, MEDLINE database, Google Scholar, Cochrane, Embase from inception to July 2021. Eligible trials were clinical randomized controlled trials comparing the effects of early PR and usual care in AECOPD patients. The primary endpoint of this meta-analysis was FEV1% predicted, 6-min walk test (6MWD), modified Medical Research Council (mMRC) and George Respiratory Questionnaire-total (SGRQ-total). The secondary outcomes were borg dyspnea score, short-form 36 health survey questionnaire physical (SF-36 physical) and SF-36 mental. We included 13 RCTs with a total of 866 patients. There were no significant effects of the PR group on measures of FEV1% predicted (MD = 0.50, 95%CI -1.43 to 2.44, Z = 0.51, p = 0.61), borg dyspnea score (MD = -0.88, 95%CI -1.89 to 0.13, Z = 1.71, p = 0.09) and SF-36 mental (MD = 4.34, 95%CI -1.64 to 10.32, Z = 1.42, p = 0.16) compared with usual care. PR group achieved better 6MWD (MD = 97.58, 95%CI 17.21 to 177.96, Z = 2.38, p = 0.02), mMRC (MD = -0.36, 95%CI -0.52 to -0.21, Z = 4.56, p < 0.00001), SGRQ-total (MD= -9.67, 95%CI -16.23 to -3.11, Z = 2.89, p = 0.004) and SF-36 physical (MD = 4.98, 95%CI 0.60 to 9.35, Z = 2.23, p = 0.03) compared with usual care group. Early PR in AECOPD patients would lead to better 6MWD, mMRC, SGRQ-total and SF-36 physical. But there were no significant effects of the PR group on measures of FEV1% predicted, borg dyspnea score and SF-36 mental.

Pandoraea sputorum (P. sputorum) infection is of great concern as these gram-negative bacillus species are multidrug-resistant and usually isolated from the patients' respiratory tract suffering from cystic fibrosis (CF). A few cases of infection have also been reported in non-CF patients due to its rare pathogenic nature with unclear and overlapping clinical, biochemical, and microbiological characteristics with other species. Here, we report an unusual case of a 46-year-old non-CF female, who presented with multiple pelvic fractures, acute traumatic brain injury, multiple rib fractures, and multiple burns (18% of the total body surface area, II°) by the collapse of a brick kiln, suffered from P. sputorum sepsis due to wound infection. Pandoraea species were isolated both from her blood and wound secretion. Antibiotic susceptibility testing indicated susceptibility to imipenem, tetracyclines, sulfamethoxazole, and ampicillin/sulbactam but resistance to meropenem, quinolones, aminoglycosides, and other beta-lactams. 16S ribosomal RNA (rRNA) PCR assays and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) were used to confirm the bacteria as P. sputorum. After effective anti-infection of intravenous antibiotics (imipenem 1.0 Q8H with tigecycline 50 mg Q12H for 14 days), wound care, and other comprehensive treatment for two months, the patient improved and was discharged from the hospital eventually. After reviewing the literature, we observed that the susceptibility results of Pandoraea species were often multidrug-resistant and had a unique pattern of being resistant to meropenem but sensitive to imipenem. Biofilm formation, carbapenemase production, and unique gene procession differed from the environmental isolates could help explain its resistance. This case report highlights the potential virulence of Pandoraea species as a pathogen in patients with no underlying disease. Although they are often multi-resistant, imipenem can be a preferred treatment for Pandoraea species in the earliest identification steps.

This report describes a case of disseminated nocardiosis, caused by Nocardia vulneris, in a 61-year-old man with macroglobulinemia and presenting with repeated fever, cough, shortness of breath, and muscle pain. The isolated Nocardia strain was resistant to ciprofloxacin, but susceptible to amikacin, gentamicin, tobramycin, linezolid, trimethoprim-sulfamethoxazole, amoxicillin/clavulanic, moxifloxacin, ceftriaxone, cefotaxim, and imipenem. The patient was started on combined meropenem and doxycycline treatment, followed by trimethoprim-sulfamethoxazole, which was subsequently switched to a combination treatment of linezolid, amikacin, and trimethoprim-sulfamethoxazole. The patient recovered, and his condition remained stable. Although infection by Nocardia vulneris is rare, and it is easy to miss detection in clinical practice, clinicians should be aware of the possibility of this infection. In addition, the MIC value of the drug sensitivity test should be ascertained when there is a wide choice of medicines. The current case was treated successfully with linezolid, amikacin, and trimethoprim-sulfamethoxazole. In cases of disseminated nocardiosis, the patient should be treated with antimicrobial therapy for at least 12 months. Furthermore, bacteriological examination and antimicrobial susceptibility testing should be performed regularly.

Headings Background : This is a case of a human disseminated nocardiosis caused by Nocardia vulneris which made the patient presenting with fever, cough, shortness of breath, muscle pain and multiple tubercle. Methods : Bacterial culture the blood, sputum, lung rinses and scalp pus samples of the patient, Nocardia vulneris was isolated and identified using the 16s ribosomal RNA gene sequence sequence data. and determine the sensitivity of the isolated bacteria to antibiotics and analysis of the strain's antibiotic treatment. Results : The isolated was identified as Nocardia brasiliensis , which was resistant to ciprofloxacin, but susceptible to amikacin, gentamicin, tobramycin, linezolid, trimethoprim-sulfamethoxazole, amoxicillin/clavulanic, moxifloxacin, ceftriaxone, cefotaxim, imipenem. The patient recovered and his condition remained stable by combinations with linezolid, amikacin and trimethoprim-sulfamethoxazole. Conclusions : This is the first case report of disseminated nocardiosis caused by Nocardia vulneris , and the current case was treated successfully with linezolid, amikacin and trimethoprim-sulfamethoxazole. Clinicians should be aware of its diagnostic, and the MIC value of the drug sensitivity test should be concerned when there is a wide choice of medicines, for the disseminated cases which are diagnosed definitely should be treated with at least 12 months of antimicrobial therapy, bacteriological examination and antimicrobial susceptibility testing should be performed repeatedly.

INTRODUCTION:Low-concentration oxygen is an established way for the treatment of chronic obstructive pulmonary disease (COPD) with Type II respiratory failure. Hypercapnia can complicate both COPD exacerbations and stable COPD. Treating with noninvasive ventilation (NIV) can reduce carbon dioxide tension in arterial (PaCO2 ) in hypercapnic COPD. As an open system, high-flow nasal cannula oxygen (HFNC) is easy to tolerate and use. More researches are needed to focus on how HFNC is used to treat COPD patients with hypercapnic respiratory failure.METHODS:The Cochrane Library, Medline, EMBASE, and CINAHL database were retrieved from inception to October 2019. Eligible trials were clinical randomized controlled trials comparing the effects of HFNC and conventional oxygen on hypercapnic COPD patients. Two researchers assessed the quality of each study and extracted the data into RevMan 5.3 independently. The primary outcome was PaCO2 and the secondary outcome was PaO2 .RESULTS:Four RCTs with 329 patients were included. The research results indicated that PaCO2 in the HFNC group was similar to the conventional oxygen group. No significant difference were observed in PaCO2 (MD -0.98, CI: -2.67 to 0.71, Z = 1.14, p = 0.25) and PaO2 (MD -0.72, CI: -6.99 to 5.55, Z = 0.23, p = 0.82) between the HFNC group and conventional oxygen group.CONCLUSIONS:Our meta-analysis showed no difference in PO2 and PCO2 between the HFNC and conventional oxygen. But we should treat this conclusion with caution because the number of studies and participants is small and, there is heterogeneity in the PaO2 and PCO2 measurements between stable and AECOPD.

Purpose Lung cancer causes significant mortality across the globe. This study aimed at the exploration of the regulatory role of microRNA (miR)-466 in lung cancer. Methods qRT-PCR analysis was used to infer the expression levels of miR-466 and Runt-related transcription factor 2 (RUNX2). CCK8 kit was used for assessment of cell proliferation. Colony forming assay was employed for examining the viability of cancer cells. The wound healing and Matrigel assays were used for investigating the rates of migration and invasion of cancer cells, respectively. Dual luciferase assay was performed to assess the interaction between miR-466 and RUNX2. Western blotting was performed to determine the protein expression. Results The results indicated that miR-466 is downregulated in lung cancer cells. Its overexpression led to significant decline of proliferation of cancer cells. The migration and invasion of lung cancer cells transfected with mir-466 mimics also got repressed. At molecular level, the regulatory role of miR-466 was exerted through the RUNX2 transcription factor whose silencing mimicked the effects of miR-466 overexpression. Conclusion Taken all together, miR-466 suppression is associated with the growth and progression of lung cancer. The miR-466 overexpression declined the proliferation and metastasis of cancer cells and these effects were modulated through miR-466/RUNX2 molecular axis.

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