Hartmancraig7306
As such, Salmonella is released in the host cytosol. Collectively, our findings demonstrate that the modulation of the host cell cycle occurring during Salmonella infection is related to a disparity in the permissivity of cells arrested in G1 and G2/M, due to their intrinsic characteristics.When I invite authors to submit a punctum to Autophagy, my e-mail includes the following "Note for international authors I would like to point out that I personally edit all the puncta for accuracy, but also for English grammar and spelling. I make this point to all international authors as I do not want you to worry extensively about the writing. As a native English speaker, it is easy for me to make small changes of this nature." I do not claim to be an expert in English grammar; however, I am indeed a native English speaker, I read a lot, and I am even fond of using the dictionary (both hard copy and online). Also, I do a lot of editing. Thus, I thought I would share some common mistakes to help reduce the required edits for papers that are submitted to Autophagy.Macroautophagy/autophagy is a conserved mechanism responsible for the degradation of unnecessary or dysfunctional components and recycling of the nutrients they contain in order to promote cellular or organismal longevity. In plants photosynthesis is massively impaired under extended darkness stress and the transition to heterotrophic metabolism results in carbon and nitrogen starvation which induces metabolic and autophagic shifts to recycle nutrients for plant survival. The majority of research concerning dark-induced senescence focuses on single genes or pathways, and the global characterization of primary and lipid metabolites and autophagy remains limited. To address these aspects we recently developed a time-resolved genome-wide association-based approach to analyze these shifts following 0 d, 3 d and 6 d of darkness. Six patterns of metabolic shifts and 215 associations with enzymes, transcriptional regulators and autophagy genes (such as AT2G31260/ATG9, AT4G16520/ATG8F, AT5G45900/ATG7 and AT2G05630/ATG8D) were identified. Furthermore detailed characterization of candidate genes further demonstrated that the metabolic and autophagic shifts in response to dark-induced senescence is under tightly coordinated genetic regulation.Osteosarcoma is one of the most common primary malignant tumors of bone in adolescents. Human umbilical vein endothelial cells (HUVECs) derived exosomes are associated with osteosarcoma cell stemness. Little is known about the function of HUVECs-exosomes in osteosarcoma cell stemness. This work aimed to investigate the mechanism of action of HUVECs-exosomes in regulating stem cell-like phenotypes of osteosarcoma cells. HUVECs were treated with GW4869 (exosome inhibitor). Human osteosarcoma cells (U2OS and 143B) were treated with HUVECs supernatant, HUVECs-exosomes with or without RO4929097 (γ secretase inhibitor, used to block Notch signaling pathway). We found that HUVECs supernatant and HUVECs-exosomes enhanced the proportions of STRO-1+CD117+ cells and the expression of stem cell-related proteins Oct4 and Sox2. Both HUVECs supernatant and HUVECs-exosomes promoted the sarcosphere formation efficiency of U2OS and 143B cells. These stem-like phenotypes of U2OS and 143B cells conferred by HUVECs-exosomes were repressed by GW4869. Moreover, HUVECs-exosomes promoted the expression of Notch1, Hes1 and Hey1 in the U2OS and 143B cells. RO4929097 treatment reversed the impact of HUVECs-exosomes on Notch1, Hes1, and Hey1 expression by inhibiting Notch1 signaling pathway. In conclusion, this work demonstrated that HUVECs-exosomes promoted cell stemness in osteosarcoma through activating Notch signaling pathway. Thus, our data reveal the mechanism of HUVECs-exosomes in regulating cell stemness of osteosarcoma, and provide a theoretical basis for osteosarcoma treatment by exosomes.Mitochondria are critical organelles that maintain cellular metabolism and overall function. The catabolic pathway of autophagy plays a central role in recycling damaged mitochondria. Although the autophagy pathway is indispensable for some cancer cell survival, our latest study shows that rare autophagy-dependent cancer cells can adapt to loss of this core pathway. this website In the process, the autophagy-deficient cells acquire unique dependencies on alternate forms of mitochondrial homeostasis. These rare autophagy-deficient clones circumvent the lack of canonical autophagy by increasing mitochondrial dynamics and by recycling damaged mitochondria via mitochondrial-derived vesicles (MDVs). These studies are the first to implicate MDVs in cancer cell metabolism although many unanswered questions remain about this non-canonical pathway.Long non-coding RNA LIFR-AS1 is low-expressed in many cancers, but its functions in papillary thyroid carcinoma (PTC) were not defined and require further study. The relationship between LIFR-AS1 expression and clinicopathological characteristics of patients with PTC was statistically analyzed. The downregulation of LIFR-AS1 in PTC tissues and cell lines was predicted by bioinformatics analysis and verified by qRT-PCR. After overexpressing or silencing LIFR-AS1, the regulatory role of LIFR-AS1 in PTC was examined by performing MTT, colony formation, wound healing, Transwell, ELISA, tube formation and xenograft tumor experiment. MiR-31-5p and SID1 transmembrane family member 2 (SIDT2) expressions in PTC tissues or cell lines were detected by qRT-PCR, Western blot, or in situ hybridization. The relationship between miR-31-5p and LIFR-AS1/SIDT2 was predicted by LncBase, TargetScan or Pearson correlation test and then verified by Dual-Luciferase Reporter assay, RNA pull-down assay and qRT-PCR. The regulatory effect of LIFR-AS1/miR-31-5p/SIDT2 axis on the biological behaviors of PTC cells was confirmed by functional experiments and rescue experiments mentioned above. The tumor size and lymphatic metastasis were correlated with LIFR-AS1 overexpression. Overexpressed LIFR-AS1 suppressed tumorigenesis in vivo. LIFR-AS1 and SIDT2 expressions were suppressed in PTC tissues, while that of miR-31-5p was elevated in PTC tissues. LIFR-AS1 was negatively correlated with miR-31-5p. LIFR-AS1 sponged miR-31-5p to upregulate SIDT2, thereby inhibiting the viability, proliferation, migration, invasion, and the secretion of vascular endothelial growth factor (VEGF) of PTC cells and angiogenesis of human umbilical vein endothelial cells (HUVECs). This paper demonstrates that LIFR-AS1/miR-31-5p/SIDT2 axis modulated the development of PTC.Oral squamous cell carcinoma (OSCC) is the most common oral cancer, with an increasing worldwide incidence and a worsening prognosis. Emerging evidence confirms that circular RNAs (circRNAs) play a critical role in tumor progression via sponging miRNAs. A previous study substantiated the function of circANKS1B in several cancers. However, its role in OSCC remains unclear. This study revealed the high expression of circANKS1B in OSCC tissues and cells. Moreover, the expression level of circANKS1B was highly positively correlated with the expression of transforming growth factor-beta1 (TGF-β1) in OSCC tissues. Additionally, overexpression of circANKS1B enhanced the protein expression of TGF-β1 in OSCC cells, while its inhibition reduced TGF-β1 protein levels. Noticeably, the loss-function of circANKS1B restrained OSCC cell invasion, migration, and epithelial to mesenchymal transition (EMT) by decreasing N-cadherin expression and enhancing E-cadherin expression. Furthermore, the knockdown of circANKS1B sensitized OSCC cells to cisplatin by suppressing cell viability and increasing cell apoptosis and caspase-3 activity. Mechanically, bioinformation software (circinteractome and starBase 3.0) and dual-luciferase reporter assays corroborated that circANKS1B could sponge miR-515-5p. Moreover, miR-515-5p could directly target TGF-β1 to suppress its expression. Importantly, inhibition of miR-515-5p or supplementation with TGF-β1 overturned the effects of circANKS1B knockdown on cell invasion, migration, and cisplatin resistance. Thus, these findings highlight that circANKS1B might act as an oncogenic gene to facilitate the metastatic potential and cisplatin resistance in OSCC by sponging miR-515-5p to regulate TGF-β1. Collectively, circANKS1B may be a promising target for therapy and overcoming chemoresistance in OSCC.Lemierre's syndrome is a triad consisting of oropharyngeal infection, internal jugular vein thrombophlebitis, and systemic embolisation typically involving lung and brain. Orbital involvement in this life-threatening condition is rare but potentially blinding and may be an indicator of intracranial involvement. We describe a case of odontogenic Lemierre's syndrome complicated by extensive orbital and intracranial septic venous thrombosis, with optic and cranial neuropathy resulting in monocular blindness and ophthalmoplegia. A multidisciplinary approach with abscess drainage, antibiotic and antithrombotic therapy, and close radiological monitoring was critical for preserving contralateral vision and neurological function.
Italy experienced SARS-CoV-2 spread during the second wave and the southern regions were severely affected. In this prospective study, we assessed the changes in SARS-CoV-2 seroprevalence rates in non-vaccinated blood donors to evaluate the spread of SARS-CoV-2 among healthy individuals in our geographical area.
8,183 healthy blood donors visiting the Transfusion Centre at the University Hospital "Riuniti" of Foggia (Italy) to donate blood from May 2020 to March 2021 were tested twice for anti-SARS-CoV-2 antibodies by Ortho Clinical Diagnostics VITROS
3600 through anti-SARS-CoV-2 Total and IgG reagent kit. None of the subjects had diagnosed symptomatic COVID-19 infection, and none had received vaccination.
Overall, 516 out of 8,183 had antibodies to SARS-CoV-2 (total and IgG antibodies) (6.3%, 95% CI 0.03-0.15%), 387 were male and 129 female. There was a significant increase of seropositive donors from May 2020 to March 2021 (
< .001). The difference in seroprevalence was significantly associated with age but not sex (2-sided
< .05 for age; 2-sided
≥ .05 for sex) in both groups.
Our study showed a significant increase in SARS-CoV-2 seroprevalence in blood donors and suggests that asymptomatic individuals might contribute to the spread of SARS-CoV-2. These results may contribute to revised containment measures, priorities in vaccine campaigns and monitoring of seroprevalence in public places like Transfusion Centres. Serologic testing of blood donors may be relevant to monitor SARS-CoV-2 circulation in the general population.
Our study showed a significant increase in SARS-CoV-2 seroprevalence in blood donors and suggests that asymptomatic individuals might contribute to the spread of SARS-CoV-2. These results may contribute to revised containment measures, priorities in vaccine campaigns and monitoring of seroprevalence in public places like Transfusion Centres. Serologic testing of blood donors may be relevant to monitor SARS-CoV-2 circulation in the general population.
To describe the socioeconomic profile, awareness level and reasons for the delay in accessing timely eye care for cataract surgery in patients of lens-induced glaucoma (LIG).
This cross-sectional observational study included all patients with LIG who presented to a tertiary eye care centre in central rural India between March 2019 to February 2020. Data were collected through a questionnaire.
Out of the 731 patients included in the study, the majority were females (69.36%). The mean age of the patients at presentation was 62.66±10.37years. Only a few participants, 193 (26.40%) were aware of LIG. Lower socioeconomic profile, older age, female gender and illiteracy were found to be strongly associated with awareness about LIG (
<.001). Patients waiting for the winter season (58.27%) to get operated was the major reason for delayed presentation to the hospital. Other reasons for the delayed presentation were - need not felt (feeling that intervention was not necessary) due to good vision in other eye (14.