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1.
Respir Res ; 22(1): 53, 2021 Feb 12.
Article in English | MEDLINE | ID: mdl-33579274

ABSTRACT

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease. Several risk factors such as smoking, air pollution, inhaled toxins, high body mass index and infectious agents are involved in the pathogenesis of IPF. In the present study, this meta-analysis study investigates the prevalence of viral and bacterial infections in the IPF patients and any possible association between these infections with pathogenesis of IPF. METHODS: The authors carried out this systematic literature review from different reliable databases such as PubMed, ISI Web of Science, Scopus and Google Scholar to December 2020.Keywords used were the following "Idiopathic pulmonary fibrosis", "Infection", "Bacterial Infection" and "Viral Infection", alone or combined together with the Boolean operators "OR", "AND" and "NOT" in the Title/Abstract/Keywords field. Pooled proportion and its 95% CI were used to assess the prevalence of viral and bacterial infections in the IPF patients. RESULTS: In this systematic review and meta-analyses, 32 studies were selected based on the exclusion/inclusion criteria. Geographical distribution of included studies was: eight studies in American people, 8; in European people, 15 in Asians, and one in Africans. The pooled prevalence for viral and bacterial infections w ere 53.72% (95% CI 38.1-69.1%) and 31.21% (95% CI 19.9-43.7%), respectively. The highest and lowest prevalence of viral infections was HSV (77.7% 95% CI 38.48-99.32%), EBV (72.02%, 95% CI 44.65-90.79%) and Influenza A (7.3%, 95% CI 2.66-42.45%), respectively. Whereas the highest and lowest prevalence in bacterial infections were related to Streptococcus sp. (99.49%, 95% CI 96.44-99.9%) and Raoultella (1.2%, 95% CI 0.2-3.08%), respectively. CONCLUSIONS: The results of this review were confirmed that the presence of viral and bacterial infections are the risk factors in the pathogenesis of IPF. In further analyses, which have never been shown in the previous studies, we revealed the geographic variations in the association strengths and emphasized other methodological parameters (e.g., detection method). Also, our study supports the hypothesis that respiratory infection could play a key role in the pathogenesis of IP.


Subject(s)
Bacterial Infections/diagnosis , Bacterial Infections/epidemiology , Idiopathic Pulmonary Fibrosis/diagnosis , Idiopathic Pulmonary Fibrosis/epidemiology , Virus Diseases/diagnosis , Virus Diseases/epidemiology , Bacterial Infections/metabolism , Humans , Idiopathic Pulmonary Fibrosis/metabolism , Respiratory Tract Infections/diagnosis , Respiratory Tract Infections/epidemiology , Respiratory Tract Infections/metabolism , Risk Factors , Virus Diseases/metabolism
2.
Cancer Gene Ther ; 28(12): 1229-1255, 2021 12.
Article in English | MEDLINE | ID: mdl-33432087

ABSTRACT

Gastrointestinal (GI) cancers comprise a heterogeneous group of complex disorders that affect different organs, including esophagus, stomach, gallbladder, liver, biliary tract, pancreas, small intestine, colon, rectum, and anus. Recently, an explosion in nucleic acid-based technologies has led to the discovery of long non-coding RNAs (lncRNAs) that have been found to possess unique regulatory functions. This class of RNAs is >200 nucleotides in length, and is characterized by their lack of protein coding. LncRNAs exert regulatory effects in GI cancer development by affecting different functions such as the proliferation and metastasis of cancer cells, apoptosis, glycolysis and angiogenesis. Over the past few decades, considerable evidence has revealed the important role of autophagy in both GI cancer progression and suppression. In addition, recent studies have confirmed a significant correlation between lncRNAs and the regulation of autophagy. In this review, we summarize how lncRNAs play a behind the scenes role in the pathogenesis of GI cancers through regulation of autophagy.


Subject(s)
Autophagy/genetics , Drug Resistance, Neoplasm/genetics , Gastrointestinal Neoplasms/genetics , RNA, Long Noncoding/metabolism , Disease Progression , Humans
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