Howezacho5735
9%) and 87min (127.3%) in the underestimated and overestimated perception groups, respectively. In the adjusted model, the underestimated group was more likely to have an ISI score > 14 (OR = 1.812, P = .006). The overestimated group was more likely to be older (OR = 1.025, P = .025) and has severe OSA (OR = 1.729, P = .035).
There are two patterns of sleep state misperception in patients withOSA underestimation associated with comorbid insomnia symptoms and overestimation associated with severe OSA. These findings enhance understanding of the pathophysiology of sleep state misperception in patients withOSA.
There are two patterns of sleep state misperception in patients with OSA underestimation associated with comorbid insomnia symptoms and overestimation associated with severe OSA. These findings enhance understanding of the pathophysiology of sleep state misperception in patients with OSA.
Breast cancer (BC) is the most common malignancy in females and is the second leading cause of cancer-related death among women worldwide. Midkine (MDK) is a heparin-binding growth factor that is abnormally expressed at high levels in various human malignancies. We aimed to uncover the biological function and molecular mechanism of MDK in BC cells.
MDA-MB-231-shMDK and T47D-shMDK BC cells were established. The in vitro biological functions of MDK were demonstrated by CCK-8 assays, Transwell assays and Western blotting, whereas qPCR pathway arrays were implemented to explore the mechanism of MDK in BC cells. Functionally, we verified that silencing MDK significantly suppressed BC cell proliferation and migration by inhibiting the activation of the nuclear factor kappa B (NF-κB) pathway and the nuclear distribution of NF-κB. Rolipram Meanwhile, Ingenuity Pathway Analysis (IPA) and a qPCR pathway array revealed that silencing MDK decreased the expression of NR3C1, a potential downstream target of the NF-κB pathway. We also confirmed that treatment with an NF-κB inhibitor suppressed NR3C1 expression in BC cells. Finally, we demonstrated that silencing NR3C1 repressed BC cell proliferation and migration.
Our findings highlight a novel mechanism by which MDK influences BC progression via regulation of the NF-κB-NR3C1 pathway.
Our findings highlight a novel mechanism by which MDK influences BC progression via regulation of the NF-κB-NR3C1 pathway.
The Indian endemic cichlid Etroplus canarensis (Canara pearl spot) is an endangered fish and is one among the three Indian cichlids (Etroplinae) that had a restricted distribution in the South Canara region of Karnataka, India. Despite considerable investigations, the phylogeny of Indian Cichlids and its biogeographical origin is still ambiguous and remains a question under discussion which is scrutinized based on whole mitogenomes in the present study.
We report the 16,339bp complete mitochondrial genome of E. canarensis for the first time using the next-generation sequencing methods. Comparison of gene arrangement and genome characterization was found to commensurate with the previous reports on two Indian cichlid fishes, E. suratensis and E. maculatus. ND6 has been identified as a gene with the highest evolutionary rate and COI and COII is the most conserved gene based on p-genetic distance calculation. Substitution rate (ka/ks) was found to be very low indicating a reduced rate of evolution among subfamily Etroplinae accounting for its subsided species divergence of Indian cichlids. Phylogenetic analysis of Indian cichlids based on a combined dataset of 12 protein-coding genes representing cichlids generated high posterior probability values pillaring paraphyletic nature of Indian Malagasy lineage and monophyletic Indian genus Etroplus.
The mitogenome sequence of E. canarensis may provide fundamental molecular data useful for further researches on genetic diversity, endemicity and the conservation of this endangered freshwater fish.
The mitogenome sequence of E. canarensis may provide fundamental molecular data useful for further researches on genetic diversity, endemicity and the conservation of this endangered freshwater fish.
Small cell lung cancer (SCLC) is the most malignant type of lung cancer. We previously reported that arsenic trioxide (As
O
) inhibited tumor initiating cells (TICs) of SCLC in vitro. In the present study, we aimed to identify the above effect in vivo and shed light on its underlying mechanism.
TICs were enriched by culturing human SCLC cell line as sphere cells in specified serum-free medium. The expression of stem cell markers, CD133 and CD44, and the in vivo tumorigenicity of both TICs and their parental cells were examined. To demonstrate the inhibitory effect of As
O
on TICs, cell proliferation, clone formation and sphere formation assays were performed. CD133 and Notch pathway-related factors were also measured after As
O
treatment. Xenograft models were established by injecting TICs into nude mice. Mice were treated with As
O
for 14days. Afterwards, the tumor volume and the expression of CD133 and Notch1 were evaluated. TICs obtained by the above-mentioned method showed elevated levels of stem cell markers and increased tumorigenicity compared with their parental cells. As
O
treatment largely inhibited TICs proliferation, sphere formation and clonogenic capacity. As
O
also reduced the expression of CD133 and down-regulated Notch pathway in TICs. Furthermore, As
O
potently inhibited tumor growth, decreased the expression of CD133 and down-regulated Notch1 in tumors originating from TICs.
Our data demonstrate that As
O
has a remarkable inhibitory effect on TICs of SCLC both in vitro and in vivo, and the mechanism might involve the down-regulation of Notch pathway.
Our data demonstrate that As2O3 has a remarkable inhibitory effect on TICs of SCLC both in vitro and in vivo, and the mechanism might involve the down-regulation of Notch pathway.
Lung adenocarcinoma (LUAD) is one of the most prevalent human cancers worldwide. The homeobox-B (HOXB) gene cluster has been reported to contribute to cancer development. Nevertheless, the expression status, clinical significance and biological role of HOXB genes in LUAD remain largely unclear.
This study comprehensively investigated the transcriptional levels and prognostic values of the HOXB genes in LUAD based on The Cancer Genome Atlas (TCGA) database. Flow cytometry, CCK-8, and Transwell assays were used for detecting apoptosis, proliferation, and migration, respectively. We discovered that eight members of the HOXB cluster genes (HOXB2, HOXB3, HOXB4, HOXB6, HOXB7, HOXB8, HOXB9, and HOXB13) were dysregulated in LUAD tumor tissues. Increased expression of HOXB3, HOXB6, HOXB7, HOXB8, or HOXB9 was independently associated with unsatisfactory overall survival (OS) in LUAD patients. In addition, a high level of HOXB3 also predicted poor patient relapse-free survival (RFS), suggesting that HOXB3 may play a vital role in the progression of LUAD compared to other members of the HOXB cluster. Additionally, further analysis by TIMER and TISIDB algorithms revealed that HOXB3 was positively correlated with a panel of immune checkpoint molecules (ICMs), tumor-infiltrating lymphocytes (TILs), and tumor immune regulators (TIRs). Gene enrichment analysis based on KEGG showed that HOXB3 was closely associated with multiple tumor-related biological processes and signaling pathways. Functionally, the in vitro experiments revealed that depletion of HOXB3 significantly alleviated the resistance of LUAD cells to apoptosis, and suppressed cell proliferation and migration.
Our study suggests that HOXB3 may play an oncogenic role in LUAD and correlate with tumor immunity.
Our study suggests that HOXB3 may play an oncogenic role in LUAD and correlate with tumor immunity.
Fatty acid elongases (FAEs), which catalyse elongation reactions of a carbon chain of very-long-chain fatty acids, play an important role in shoot development in rice. The elongation reactions consist of four sequential reactions catalysed by distinct enzymes, which are assumed to form an elongation complex. However, no interacting proteins of ONION1 (ONI1) and ONI2, which are ketoacyl CoA synthase catalyzing the first step and are required for shoot development in rice, are reported.
In this study ketoacyl CoA reductase (KCR) that interacts with ONI1 and ONI2 was searched. A database search identified 10 KCR genes in the rice genome. Among the genes, the expression pattern of KCR1 was similar to that of ONI2. Yeast two-hybrid analysis showed interaction of ONI2 with KCR1, which was confirmed by GST pull-down assay. No interacting partner of ONI1 was identified.
Our results suggest that ONI2 and KCR1 form an FAE complex that may play a role in biosynthesizing VLCFAs during shoot development.
Our results suggest that ONI2 and KCR1 form an FAE complex that may play a role in biosynthesizing VLCFAs during shoot development.Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in more than 4.4 million deaths worldwide as of August 24, 2021. Viral infections such as SARS-CoV2 are associated with endoplasmic reticulum (ER) stress and also increased the level of reactive oxygen species. Activating transcription factor 4 (ATF4) is preferentially translated under integrated stress conditions and controls the genes involved in protein homeostasis, amino acid transport and metabolism, and also protection from oxidative stress. The GRP78, regulated either directly or indirectly by ATF4, is an essential chaperone in the ER and overexpressed and appears on the surface of almost all cells during stress and function as a SARS-CoV2 receptor. In this mini-review article, we briefly discuss the effects of SARS-CoV2 infection on the ER stress, and then the stress modulator functions of ATF4 and GRP78 as novel therapeutic targets were highlighted. Finally, the effects of GRP78 inhibitory components as potential factors for targeted therapies for COVID-19 critical cases were discussed.The gut-brain axis is believed to constitute a bidirectional communication mechanism that affects both mental and digestive processes. Recently, the role of the gut microbiota in cognitive performance has been the focus of much research. In this paper, we discuss the effects of gut microbiota and nutrition on spatial memory and learning. Studies have shown the influence of diet on cognitive capabilities such as spatial learning and memory. It has been reported that a high-fat diet can alter gut microbiota which subsequently leads to changes in spatial learning and memory. Some microorganisms in the gut that can significantly affect spatial learning and memory are Akkermansia muciniphila, Bifidobacterium, Lactobacillus, Firmicutes, Bacteroidetes, and Helicobacter pylori. For example, a reduction in the amount of A. muciniphila in the gut leads to increased intestinal permeability and induces immune response in the brain which then negatively affects cognitive performances. We suggest that more studies should be carried out regarding the indirect effects of nutrition on cognitive activities via alteration in gut microbiota.
