[Goods syndrome in chronic active SARS-CoV-2 infection: a case report].

A 54-year-old female patient presented with recurrent cough and sputum production over the past year and was hospitalized several times. CT examination revealed exudative lesions in both lungs, which were partially absorbed after treatment. However, they recurred shortly after discharge, and the patient had to be readmitted. In the past year, the patient had been hospitalized six times, and her throat swabs were positive for SARS-CoV-2 at four different points in time. After receiving anti-infective and antiviral treatment in other hospitals, the above symptoms were relieved. The patient tested negative for SARS-CoV-2, but symptoms recurred soon after. Eventually, the diagnosis of Goods syndrome was made based on the presence of B-cell loss, decreased immunoglobulin levels, an inverted CD4+/CD8+ ratio on admission, and a previous history of thymoma.

[A case report of chronic granulomatous disease with CYBB gene mutation in an adult].

We reported a 28-year-old male patient who had been admitted to a local hospital for several times in the past four years because of recurrent fever and cough. Each chest CT scan during hospitalization showed consolidation accompanied by exudation and mild pleural effusion. After treatment, the consolidation apparently absorbed, but similar symptoms recurred within half a year, and the new consolidation appeared. For this reason, he was diagnosed with tuberculosis or bacterial pneumonia several times in other hospitals, and was hospitalized two to three times a year. Finally, he was diagnosed with chronic granulomatous disease (CGD) with CYBB gene mutation through whole-exome sequencing.

Extending the spectral database of laser-induced breakdown spectroscopy with generative adversarial nets.

As a famous spectroscopy method for substance detection and classification, laser-induced breakdown spectroscopy (LIBS) is not a nondestructive detection method. Considering the precious samples and the experimental environment, sometimes it is difficult to get enough spectra to build the classification model, which is important for qualitative analysis. In this paper, a spectral generation method for extending the spectral database of LIBS is proposed based on generative adversarial nets (GAN). After enough interactive training, the generated spectra looked very similar to the experimental spectra. Evaluated with unsupervised clustering methods PCA and K-means, the generated spectra could not be distinguished from the real spectra. For each type of sample, most of the simulated spectra and experimental spectra were clustered into the same class, which meant the proposed method was effective to extend the spectral database. Using the spectral database extended by this method as training set data to build the SVM model, the results showed that when there were only a few experimental spectra, the combination of the generated spectra and the experimental spectra for building the classification model could achieve better identification results.

LncRNA LINC00342 regulated cell growth and metastasis in non-small cell lung cancer via targeting miR-203a-3p.

OBJECTIVE: Non-small cell lung cancer (NSCLC) is the main form of lung cancer, leading to major causes of cancer mortality. It is well known that lncRNAs may be involved in the pathogenesis of cancer, including NSCLC. The aim of this study was to provide a novel therapeutic target of LINC00342 for the therapy of NSCLC. PATIENTS AND METHODS: The expression of LINC00342 and miR-203a-3p was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation was measured using the MTT assay. Colony formation analysis was performed to count the number of colonies. Cell migration and invasion were measured by transwell. Online software DIANA tools were used to predict binding sites of LINC00342 and miR-203a-3p. Luciferase reporter assay was conducted to confirm the interaction between LINC00342 and miR-203a-3p. RESULTS: The expression of LINC00342 was increased in NSCLC tissues and cells compared with normal tissues and cells. Knockdown of LINC00342 suppressed cell proliferation, colony formation, migration, and invasion. LINC00342 regulated the expression of miR-203a-3p by targeting it directly. MiR-203a-3p was down-regulated in NSCLC tissues and cells compared with normal tissues and cells. Furthermore, LINC00342 promoted NSCLC cells proliferation, colony formation, migration, and invasion by depleting the expression of miR-203a-3p. CONCLUSIONS: This work implied that LINC00342 functions in NSCLC acting as an oncogene. Briefly, LINC00342 contributes to NSCLC cells growth and metastasis via targeting miR-203a-3p competitively.

[Effects of components isolated from Astragalus membranaceus Bunge on cardiac function injured by myocardial ischemia reperfusion in rats].

OBJECTIVE: To investigate the effects of components isolated from Astragalus membranaceus on myocardial ischemia reperfusion injury. METHODS: The myocardial ischemia reperfusion injury model was created by the left anterior descending coronary artery occlusion from the oracotouated rats, and the total saponins, total flavonids and astragaloside i.v. isolated from A. membranaceus on hemodynamics during acute myocardial ischemia, Na(+)-K(+)-ATPase activity, cAMP and malondialdehyede (MDA) contents in the ischemic myocardium were observed. RESULTS: The total saponins, total flavonids and astragaloside i.v. attenuated the declines of the amplitudes of LVSP and +/- LVdp/dtmax in rat heart injured by ischemia reperfusion in vivo, and decreased Na(+)-K(+)-ATPase activity in the ischemic myocardium. Otherwise, the total saponins increased the cAMP content and the total flavonids decreased the level of MDA production in the ischemic myocardium. CONCLUSION: The effects of different components isolated from A. membranaceus on protecting the cardiac function in the process of ischemia reperfusion may be related to the mechanism of improving energy metabolism, scavenging the oxygen free radicals and inhibiting the production of free radicals in the ischemic myocardium.