Bosnian Journal of Basic Medical Sciences (BJBMS)
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Biosurfactant derived from probiotic Lactobacillus acidophilus exhibits broad-spectrum antibiofilm activity and inhibits the quorum sensing-regulated virulence
Antimicrobial resistance by pathogenic bacteria has become a global risk to human health in recent years. The most promising approach to combating antimicrobial resistance is to target virulent traits of bacteria. In the present study, a biosurfactant derived from the probiotic strain Lactobacillus acidophilus was tested against three Gram-negative bacteria to evaluate its inhibitory potential on their biofilms, and whether it affected the virulence factors controlled by quorum sensing (QS). A reduction in the virulence factors of Chromobacterium violaceum (violacein production), Serratia marcescens (prodigiosin production) and Pseudomonas aeruginosa (pyocyanin, total protease, LasB elastase and LasA protease production) was observed at different sub-MIC concentrations in a dose-dependent manner. Biofilm development was reduced by 65.76%, 70.64% and 58.12% at the highest sub-MIC levels for C. violaceum, P. aeruginosa and S. marcescens, respectively. Biofilm formation on glass surfaces exhibited significant reduction, with less bacterial aggregation and reduced formation of extracellular polymeric materials. Additionally, swimming motility and exopolysaccharides (EPS) production were shown to be reduced in the presence of the L. acidophilus-derived biosurfactant. Furthermore, molecular docking analysis performed on compounds identified through gas chromatography–mass spectrometry (GC-MS) analysis of QS and biofilm proteins yielded further insights into the mechanism underlying the anti-QS activity. Therefore, the present study has clearly demonstrated that a biosurfactant derived from L. acidophilus can significantly inhibit virulence factors of Gram-negative pathogenic bacteria. This could provide an effective method to inhibit the formation of biofilms and QS in Gram-negative bacteria
Reducing the risks of nuclear war—The role of health professionals
In January, 2023, the Science and Security Board of the Bulletin of the Atomic Scientists moved the hands of the Doomsday Clock forward to 90s before midnight, reflecting the growing risk of nuclear war. In August, 2022, the UN Secretary-General António Guterres warned that the world is now in “a time of nuclear danger not seen since the height of the Cold War.” The danger has been underlined by growing tensions between many nuclear armed states.
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Expression of CD31, CD34, and smooth muscle actin (SMA) in endothelial cells of dental pulp vessels
The dental pulp is a highly vascularized and innervated loose connective tissue surrounded by hard dental tissues – enamel and dentine. With the primary dentin formation and the closure of the root apex, the conditions in the dental pulp change and pulp tissue compliance are reduced. Endothelial cells of pulpal blood vessels are highly differentiated and are capable of adaptation to changes in the environment. We aimed to evaluate the phenotypic plasticity of endothelial cells of pulpal blood vessels in permanent premolars with open (N = 6) or closed root apex (N = 30). The pulp tissue was stained with hematoxylin-eosin (HE) for the histological analysis, and immunohistochemically for a cluster of differentiation 31 (CD31), a cluster of differentiation 34 (CD34), and for smooth muscle actin (SMA) to detect vessels with CD31, CD34, and SMA positive endothelial cells. We used the student’s t-test and Pearson correlation test for the statistical analysis. We found a significantly higher percentage of the vessels with CD31 (P = 0.005) and CD34 (P = 0.000) positive endothelial cells in the group of teeth with closed root apex compared to the group with open apex. A significant positive correlation between SMA positive and CD31 positive vessels (P = 0.003) and between CD31 positive and CD34 positive vessels (P = 0.031) was also found. We conclude that the endothelial cells of dental pulp vessels express a small amount of CD31, but have a pronounced expression of SMA and CD34, which indicates their progenitor potential and contractile ability
Hypomethylation of the ENPP3 promoter region contributes to the occurrence and development of ovarian endometriosis via the AKT/mTOR/4EBP1 signaling pathway
Growing evidence indicates that aberrant methylation is pivotal in the development and progression of endometriosis (EMs). This study explores the relationship between abnormal methylation of the ENPP3 promoter and the pathogenesis of ovarian EMs, focusing on its regulatory effect on ENPP3 expression. We analyzed the methylation levels of ENPP3 in ectopic endometrial tissues from ovarian EMs patients and in normal endometrial tissues from women without EMs. The expression and distribution of ENPP3 were evaluated using RT-qPCR and immunohistochemistry. Transwell assays were conducted to examine the impact of ENPP3 overexpression on the migratory and invasive capabilities of endometrial stromal cells. Our results demonstrated significantly reduced methylation levels at the CpG sites of the ENPP3 promoter region in ectopic endometrial tissues compared to normal endometrial tissues. RT-qPCR findings revealed a marked increase in ENPP3 expression in ovarian EMs tissues relative to endometrial tissues from patients without EMs, and this upregulation was negatively correlated with the methylation levels of the ENPP3 promoter region. Immunohistochemical analyses confirmed elevated ENPP3 expression in the glandular epithelial cells and stroma of ovarian EMs tissues. Furthermore, in vitro experiments showed that overexpressed ENPP3 notably intensified the invasion and migration of endometrial stromal cells. Transcriptome sequencing and functional analyses indicated that the increased ENPP3 expression activated the AKT/mTOR/4EBP1 signaling pathway. In summary, the study suggests that hypomethylation in the ENPP3 promoter region may contribute to the initiation and advancement of ovarian EMs by activating the AKT/mTOR/4EBP1 pathway, supporting the theory that EMs might be an epigenetically regulated disorder
Effect of vascular endothelial growth factor rs35569394 in esophageal cancer and response to chemotherapy
The objective of this study was to investigate the possible association between the single nucleotide polymorphism (SNP), rs35569394, of the vascular endothelial growth factor gene (VEGF) and the risk of esophageal cancer (EC) in the Han Chinese population. A total of 290 EC subjects and 322 ethnically matched unrelated healthy controls free from the esophageal disease were studied. Genomic DNA was isolated from peripheral blood by salting out. Genotyping of VEGF rs35569394 polymorphism was carried out via polymerase chain reaction followed by agarose gel electrophoresis. The results showed that the distribution of genotypes was significantly different across the gender groups (p=0.032) and clinical stages (p=0.034). VEGF rs35569394 was associated with EC risk (p= 0.012, OR=1.34). A gender analysis break-down showed that rs35569394-D allele frequency was significantly higher in females than in the controls (p=0.0004, OR=1.81). Moreover, significant associations were also found in females under the dominant model (II versus ID+DD: χ2=8.18, p=0.003, OR=2.12) and the recessive model (II+ID versus DD: χ2=8.25, p=0.004, OR=2.39). Additionally, we found that the genotype, rs35569394-DD, was associated with a complete response + partial response to chemotherapy when compared with rs35569394-II (χ2=4.67, p=0.030, OR=0.47). In conclusion, our case-control study showed that the VEGF rs35569394 was significantly associated with the clinical stages and the increased risk of EC in Han Chinese females. In addition, the genotype rs35569394-DD showed a better response to chemotherapy
Impact of subchorionic hematoma on pregnancy outcomes in women with recurrent pregnancy loss
We conducted a retrospective cohort study with the aim of investigating the relationship between subchorionic hematoma (SCH) and pregnancy outcomes in women with recurrent pregnancy loss (RPL). We reviewed all RPL patients who came to the Fourth Hospital of Shijiazhuang from January 2019 to June 2021. Two groups were divided according to the presence or absence of SCH. Live birth rate was considered as the primary outcome. Secondary outcomes included adverse pregnancy outcomes and complications. Univariable and multivariable analyses were conducted. Of 274 RPL women included in the final analysis, 49 (17.9%) had SCH. The occurrence of thrombophilia was significantly higher in SCH group than that in non-SCH group (38.8% vs 24.4%, P=0.041). There were no significant differences between the two groups in live birth rate, adverse pregnancy outcomes and pregnancy complications. Among women with SCH, live birth rate or SCH duration was not associated with continued use of low-dose aspirin (LDA) after the diagnosis of SCH. Our findings suggest that SCH does not reduce live birth rate in RPL women or increase the risk of adverse pregnancy outcomes or pregnancy complications. Continued use of LDA after the detection of a hematoma is unlikely to affect SCH duration or the live birth rate
VHL tumor suppressor as a novel potential candidate biomarker in papillary thyroid carcinoma
Papillary thyroid carcinoma (PTC) is the most common type of endocrine cancer, with an increasing incidence worldwide. The treatment of PTC is currently the subject of clinical controversy, making it critically important to identify molecular markers that would help improve the risk stratification of PTC patients and optimize the therapeutic approach. The VHL tumor suppressor gene has been implicated in tumorigenesis of various types of carcinoma and linked with their aggressive biological behavior. The role of VHL in the origin and development of PTC has only recently begun to be revealed. In this narrative review we attempt to summarize the existing knowledge that implicates VHL in PTC pathogenesis and to outline its potential significance as a candidate molecular biomarker for the grouping of PTC patients into high and low risk groups
Promotive role of USP29-mediated deubiquitination in malignant proliferation of colorectal cancer cells via the KIAA1429/SOX8 axis
Colorectal cancer (CRC) is regarded as one of the most prevalent neoplasms worldwide, and ubiquitination and N6-methyladenosine (m6A) modification regulate the outgrowth of multiple cancers. This study attempted to explore the effect of ubiquitin-specific peptidases 29 (USP29) on the malignant proliferation of CRC cells via stabilizing Vir-like m6A methyltransferase associated (VIRMA/KIAA1429). First, upregulations of USP29, KIAA1429, and SRY-box transcription factor 8 (SOX8) were found in CRC tissues and cells through real-time quantitative polymerase chain reaction and Western blotting. After transfection of si-USP29, the proliferation of CRC cells was evaluated by the cell counting kit-8, colony formation and 5-ethynyl-2’-deoxyuridine assays, and we observed that depletion of USP29 inhibited the proliferation of CRC cells. Co-immunoprecipitation confirmed the binding of USP29 to KIAA1429. Mechanically, USP29 mediated deubiquitination to stabilize the protein levels of KIAA1429, and KIAA1429 promoted the stability of SOX8 mRNA through m6A modification. Moreover, overexpression of KIAA1429 or SOX8 reversed the inhibitory effects of USP29 depletion on CRC cell proliferation. Finally, the xenograft tumor model revealed the promotive role of USP29 in the proliferation of CRC cells in vivo. Altogether, USP29 facilitates the malignant proliferation of CRC cells via upregulating the KIAA1429/SOX8 axis
COP27 Climate Change Conference: Urgent action needed for Africa and the world
The 2022 report of the Intergovernmental Panel on Climate Change (IPCC) paints a dark picture of the future of life on earth, characterised by ecosystem collapse, species extinction, and climate hazards such as heatwaves and floods (1). These are all linked to physical and mental health problems, with direct and indirect consequences of increased morbidity and mortality. To avoid these catastrophic health effects across all regions of the globe, there is broad agreement—as 231 health journals argued together in 2021—that the rise in global temperature must be limited to less than 1.5oC compared with pre-industrial levels.
While the Paris Agreement of 2015 outlines a global action framework that incorporates providing climate finance to developing countries, this support has yet to materialise (2). COP27 is the fifth Conference of the Parties (COP) to be organised in Africa since its inception in 1995. Ahead of this meeting, we—as health journal editors from across the continent—call for urgent action to ensure it is the COP that finally delivers climate justice for Africa and vulnerable countries. This is essential not just for the health of those countries, but for the health of the whole world.Read more in the PDF..
Corrigendum: Evaluation of cerebrospinal fluid neurofilament light chain levels in multiple sclerosis and non-demyelinating diseases of the central nervous system: clinical and biochemical perspective
Corrigendum to: Evaluation of cerebrospinal fluid neurofilament light chain levels in multiple sclerosis and non-demyelinating diseases of the central nervous system: clinical and biochemical perspective.
This corrigendum corrects funding information to: This project was partly supported by Gazi University Scientific Research Projects Coordination Unit (BAP) (project code: 01/2019-38). The authors would like to thank Gazi University for funding this project.
The authors sincerely apologize for the error and confirm that this correction does not change the conclusion of the article