Older age and comorbidities are risk factors for increased coronavirus disease 2019 (COVID-19) severity, but few studies have explored their interaction. This study aimed to assess the actual impacts of these factors on disease severity in COVID-19. The enrolled COVID-19 patients were divided into 4 age subgroups (≤44, 45-59, 60-74, and ≥75 years). Logistic regression analysis was conducted to determine the association between comorbidities and disease severity; Kappa consistency test was implemented to verify the study results. Of the 1663 patients with COVID-19, 287 had severe disease. The disease severity was correlated with the age-adjusted Charlson Comorbidity Index in each age group. In the 4 subgroups, the odds ratio of age-adjusted Charlson Comorbidity Index declined with age. After removing age interference, diabetes and cardio-cerebrovascular diseases were the main risk factors for severe disease in patients aged <75 years, whereas only chronic lung disease was associated with disease severity in patients aged ≥75 years. When comorbidities alone were used to predict disease severity, only the predictions were consistent with real outcomes in patients aged ≥75 years, compared with the predictions of high-risk comorbidities mentioned in World Health Organization and Chinese guidelines (Kappa 0.106, P < .05). Although older age and comorbidities were risk factors for severe COVID-19, their effects on disease severity varied across age groups. Additionally, comorbidities had a greater impact on COVID-19 severity in younger patients.
Asthma is characterized by airway inflammation, mucus overproduction, and airway hyperreactivity. Cytokines, especially T helper 2-derived cytokines interleukin (IL)-4, IL-5, and IL-13, are involved in the pathogenesis of asthma. IL-21 has a variety of effects on the immune system. However, the contribution of IL-21 to the development of allergic diseases is currently controversial. The aim of this study was to investigate the effect of IL-21 on asthma airway inflammation in vivo. A murine ovalbumin (OVA)-induced allergic asthma model was used. The concentration of IL-21 in the bronchoalveolar lavage fluid (BALF) of mice was evaluated by enzyme-linked immunosorbent assay. BALF cellularity, lung histopathology, and sera IgE levels were compared between the normal control group, OVA sensitization/challenge group, and OVA sensitization/challenge plus IL-21-administered group. An OVA-induced allergic rhinitis model with IL-21 was used as a positive control and the infiltration of eosinophils in the nasal mucosa was evaluated. The concentration of IL-21 in the BALF was lower in the asthmatic group compared with the normal control group. However, no significant differences in airway eosinophilia, lung histopathology, and sera IgE levels were observed between the OVA sensitization/challenge group and OVA sensitization/challenge plus IL-21-administered group. Decreased eosinophilic infiltration of nasal mucosa was observed in the positive control allergic rhinitis model administered IL-21 during the challenge period. Exogenous administration of IL-21 alone may not alleviate allergic lung inflammation. The role of IL-21 in allergic lung inflammation needs further research.
The mammary gland is a unique organ involved in lactation in dairy livestock, and its development and lactation ability are affected by both genetic and environmental factors. To explore the molecular regulatory mechanisms of these factors, this study used high-throughput sequencing technology and bioinformatics methods to systematically analyze the transcriptome of Laoshan dairy goat mammary gland tissues from different lactation stages. From three libraries, 36,336,892, 36,469,596, and 35,759,380, pure sequences were obtained, with 25,292, 23,665 and 27,220 expressed genes, respectively, resulting in a total of 14,892 nonredundant differentially expressed genes. The Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that these genes were annotated to biological regulation, cellular processes, metabolic processes, cells, organelles, binding, catalytic activity and transcriptional activity, and so on. The genes were mainly involved in cellular processes, environmental information processes, genetic information processes, human diseases, metabolism, and organ systems. Finally, 20 genes related to mammary gland development and lactation were screened to construct a gene regulatory network. These findings support the involvement of the constructed network in the regulation of mammary gland development and lactation, and they not only lay the foundation to further investigate and screen the main genes or molecular genetic markers controlling the development of the mammary gland and lactation ability of dairy goats but also increase the in-depth understanding of the lactation physiology of dairy goats.
Lysophosphatidylcholine (LPC) is generated through the hydrolysis of phospha-tidylcholine (PC) by phospholipase A2 and is converted back to PC by lysophosphatidylcholine acyltransferase 1 (LPCAT1). Elevated levels of (LPC) are known to play a pathogenic role in the inflammatory injury of asthma. However, the role of LPCAT1 in asthma has not yet been reported.To determine whether the exogenous expression of LPCAT1, delivered by using a recombinant lentiviral vector, could attenuate airway inflammation in asthmatic mice.Recombinant lentivirus carrying cDNA encoding LPCAT1 (Lenti-LPCAT1), or EGFP (Lenti-EGFP) as a control, was constructed. BALB/c mice were sensitised with ovalbumin (OVA), and intratracheally pre-treated with an endobronchial administration of the recombinant lentivirus intratracheally 72 hours before the first challenge. After the last OVA challenges, the mice were assessed for airway inflammation, airway hyper-responsiveness and lipid levels.Lenti-LPCAT1-infected HEK293T cells expressed exogenous recombinant LPCAT1 protein that showed high activity of the LPC acyltransferase. OVA sensitisation and challenge significantly increased the levels of saturated species LPC 16:0 and LPC 18:0 levels in the bronchoalveolar lavage fluid (BALF) compared with wild-type mice respectively. The intratracheal Lenti-LPCAT1 instillation obviously down-regulated the OVA-induced release of LPC 16:0 and LPC 18:0. Treatment with Lenti-LPCAT1 ameliorated OVA-induced airway hyper-responsiveness and reduced airway eosinophilia infiltration in lung tissue. Furthermore, the secretion of eotaxin and Th2-associated cytokines IL-5 and IL-13 were inhibited in BALF. The level of OVA-specific IgE in serum was suppressed.These results suggested that the exogenous expression of LPCAT1 may attenuate eosinophil inflammation in the airway by down-regulating the LPC 16:0 and LPC 18:0 BALF levels in asthmatic mice.
Development of specific serum biomarkers is essential to improve diagnosis and prognosis of non-small cell lung cancer (NSCLC).Here, we show that serum and tissue levels of miR-519d are significantly decreased in NSCLC patients.The low expression of miR-519d is associated with lymph node metastases, clinical stage, and a poor prognosis in NSCLC patients.In addition, ROC analysis demonstrated that the serum miR-519d levels can distinguish NSCLC patients from healthy controls.MiR-519d inhibits proliferation, migration, and invasion by lung cancer cells, indicating that it may function as a tumor suppressor in lung cancer.Furthermore, our data demonstrate that HER3 is a target gene of miR-519d in lung cancer cells, and show that by targeting HER3, miR-519d inhibits the PI3K/Akt pathway.These findings demonstrate that the miR-519d levels are decreased in serum and tumor tissues of NSCLC patients, and indicate that miR-519d regulates NSCLC progression by targeting HER3.MiR-519d could potentially serve as a novel serum biomarker for NSCLC.
Submerged plant growth is limited by the reduction of underwater photosynthesis attributed to low CO2 availability, as well as light limitation associated with underwater conditions. Heterotrophic bacteria and fungi play an important role in local aqueous dissolved inorganic carbon (DIC) content surrounding submerged plants. In order to investigate the effects of carbon conversion in plant–microbe interactions on plant growth, in the present study we inoculated the plant medium of Vallisneria natans with Pseudomonas putida KT2440 and measured carbon conversion in the system, as well as several indices of plant growth. The quantity of P. putida KT2440 increased twofold because of the availability of organic matter produced by V. natans. Similarly, P. putida KT2440 supplied DIC for V. natans, improving its photosynthetic rate. Moreover, the significantly higher leaf area, specific leaf area and fresh biomass of V. natans attributed to the presence of P. putida KT2440 demonstrated that the interaction between V. natans and P. putida enhanced the efficiency of nutrient and CO2 uptake by V. natans, promoting V. natans growth. Therefore, we suggest that the carbon and oxygen microcycle based on the protocooperation of V. natans and P. putida KT2440 may accelerate the transformation of carbon to increase carbon availability to promote the growth of both plant and microbe.
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