Therapeutic effect of subcutaneous injection of low dose recombinant human granulocyte-macrophage colony-stimulating factor on pulmonary alveolar proteinosis

Zhang, Fen; Wu, Dong; Su, Yucai; Yin, Chengsheng; Shen, Li; Zhang, Yuan; Zhou, Ying; Li, Qiuhong; Hu, Yang; Li, Huiping

doi:10.1186/s12931-019-1261-1

Cited by 166 publications

(129 citation statements)

References 29 publications

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“… 31 In analogy with SARS and MERS, fibrotic changes have indeed been recognised in autopsy studies and may be associated with increased expression of tumour growth factor beta (TGF-β) and connective tissue growth factor. 32 At this stage, it is still unclear who will recover, and who will proceed to uncontrolled cellular proliferation and persistent fibrotic remodelling.…”

Section: Pathophysiology Of Covid-19mentioning

confidence: 99%

Rationale for azithromycin in COVID-19: an overview of existing evidence

et al. 2021

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Azithromycin has rapidly been adopted as a repurposed drug for the treatment of COVID-19, despite the lack of high-quality evidence. In this review, we critically appraise the current pharmacological, preclinical and clinical data of azithromycin for treating COVID-19. Interest in azithromycin has been fuelled by favourable treatment outcomes in other viral pneumonias, a documented antiviral effect on SARS-CoV-2 in vitro and uncontrolled case series early in the pandemic. Its antiviral effects presumably result from interfering with receptor mediated binding, viral lysosomal escape, intracellular cell-signalling pathways and enhancing type I and III interferon expression. Its immunomodulatory effects may mitigate excessive inflammation and benefit tissue repair. Currently, in vivo reports on azithromycin in COVID-19 are conflicting and do not endorse its widespread use outside of clinical trials. They are, however, mostly retrospective and therefore inherently biased. The effect size of azithromycin may depend on when it is started. Also, extended follow-up is needed to assess benefits in the recovery phase. Safety data warrant monitoring of drug–drug interactions and subsequent cardiac adverse events, especially with hydroxychloroquine. More prospective data of large randomised controlled studies are expected and much-needed. Uniform reporting of results should be strongly encouraged to facilitate data pooling with the many ongoing initiatives.

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Section: Pathophysiology Of Covid-19mentioning

confidence: 99%

Rationale for azithromycin in COVID-19: an overview of existing evidence

et al. 2021

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“…An increasing body of literature reveals that these coronaviruses are originally zoonotic, targeting the lower respiratory tract, and causing potentially lethal inflammation in extra-pulmonary organs ( 10 ). Within two decades, there have emerged three highly pathogenic and deadly human coronaviruses: SARS-CoV, MERS-CoV, and SARS-CoV-2 ( 11 ). What started as a novel outbreak of atypical viral pneumonia in December 2019 in Wuhan, China is now officially recognized as COVID-19, with the causative virus classified as SARS-CoV-2, which expresses a genomic homology of about 80% to SARS-CoV, and lesser homology (50%) with MERS-CoV.…”

Section: Introductionmentioning

confidence: 99%

HLA, Immune Response, and Susceptibility to COVID-19

et al. 2021

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The severe acute respiratory syndrome caused by Coronavirus 2 (SARS-CoV-2) that appeared in December 2019 has precipitated the global pandemic Coronavirus Disease 2019 (COVID-19). However, in many parts of Africa fewer than expected cases of COVID-19, with lower rates of mortality, have been reported. Individual human leukocyte antigen (HLA) alleles can affect both the susceptibility and the severity of viral infections. In the case of COVID-19 such an analysis may contribute to identifying individuals at higher risk of the disease and the epidemiological level to understanding the differences between countries in the epidemic patterns. It is also recognized that first antigen exposure influences the consequence of subsequent exposure. We thus propose a theory incorporating HLA antigens, the “original antigenic sin (OAS)” effect, and presentation of viral peptides which could explain with differential susceptibility or resistance to SARS-CoV-2 infections.

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“…The growth of chronic respiratory diseases (CRDs) in recent decades has changed morbidity and mortality trends and has become a problem worldwide [ 1 ]. CRDs represent a group of diseases characterised by abnormal conditions of the respiratory system, including chronic obstructive pulmonary disease (COPD) and asthma, the most common, as well as pneumoconiosis, interstitial lung disease, and pulmonary sarcoidosis, which affect people of all ages.…”

Section: Introductionmentioning

confidence: 99%

Chronic respiratory disease mortality and its associated factors in selected Asian countries: evidence from panel error correction model

2021

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Background Chronic Respiratory Diseases (CRDs) in Asian countries are a growing concern in terms of morbidity and mortality. However, a systematic understanding of the increasing age-adjusted mortality rate of chronic respiratory disease (CRD) and its associated factors is not readily available for many Asian countries. We aimed to determine country-level factors affecting CRD mortality using a panel error correction model. Methods Based on data from the Global Burden of Disease Study 2017, we estimated the trends and distribution of CRD mortality for selected Asian countries from 2010 to 2017. Furthermore, we evaluated the relationship between CRD mortality and Gross Domestic Product (GDP) per capita, average years of schooling, urbanization, and pollutant emission (PM2.5 concentration) using a fixed-effect model. We corrected the estimates for heteroscedasticity and autocorrelation through Prais-Winsten adjustment along with robust standard error. Results Between 2010 and 2017, approximately 21.4 million people died from chronic respiratory diseases in the countries studied. Age-standardized crude mortality rate from CRDs in the period had minimum and maximum values of 8.19 (Singapore in 2016) and 155.42 (North Korea in 2010) per 100,000 population, respectively. The coefficients corrected for autocorrelation and heteroskedasticity based on the final model of our study (Prais-Winsten), showed that all explanatory variables were statistically significant (p < 0.001). The model shows that the 1% increase in GDP per capita results in a 20% increase (0.203) in the CRD mortality rate and that a higher concentration of air pollution is also positively associated with the CRD deaths (0.00869). However, an extra year of schooling reduces the mortality rate by 4.79% (− 0.0479). Further, rate of urbanization is negatively associated with the CRD death rate (− 0.0252). Conclusions Our results indicate that both socioeconomic and environmental factors impact CRD mortality rates. Mortality due to CRD increases with rising GDP per capita and decreases with the percentage of the total population residing in urban areas. Further, mortality increases with greater exposure to PM2.5. Also, higher years of schooling mitigate rising CRD mortality rates, showing that education can act as a safety net against CRD mortality. These results are an outcome of sequential adjustments in the final model specification to correct for heteroscedasticity and autocorrelation.

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Therapeutic effect of subcutaneous injection of low dose recombinant human granulocyte-macrophage colony-stimulating factor on pulmonary alveolar proteinosis

Cited by 166 publications

References 29 publications

Rationale for azithromycin in COVID-19: an overview of existing evidence

Rationale for azithromycin in COVID-19: an overview of existing evidence

HLA, Immune Response, and Susceptibility to COVID-19

Chronic respiratory disease mortality and its associated factors in selected Asian countries: evidence from panel error correction model

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