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Frequency of occurrence of dry mouth in women with high risk of cardiovascular diseases during the menopause
Get PDFAmong the risk factors for dry mouth, or xerostomia, are both estrogen deficiency in women during menopause and the use of medications with xerogenic properties. Until now, it has not been clearly determined, whether dryness in the oral cavity in women during menopause is only associated with subjective sensations or is accompanied by qualitative and quantitative changes in mixed saliva. To determine the frequency and nature of xerostomia syndrome in women during menopause with high and extremely high risk of cardiovascular diseases. The study involved 35 patients (with subjective sensations of dryness in the oral cavity) and 20 apparently healthy women. All study participants were questioned for any dental complaints, and the quantitative indicators of the oral fluid were assessed. An individualized oral hygiene complex and a moisturizing gel were prescribed as correction of the subjective signs of xerostomia. The follow-up visit was carried out after 1 month. The patients in natural menopause felt slight subjective manifestations of dry mouth confirmed by objective decrease in salivary secretion; whereas in most cases subjective dryness in the oral cavity is accompanied by normal secretion. The prescribed complex for correction of dental complaints ensures decrease in the subjective signs of dryness, decrease in taste distortion and halitosis
Study of the possibilities of determining mobile sulfur by physical-chemical and chemical methods in various substrates in the presence of orthanilic K
Get PDFThe article presents the results of testing the developed method for determining mobile sulfur in wood ash and various soil substrates. Determination of sulfur in sulfate form in presence of orthanilic K is possible due to the indicator’s ability to form coloured complexes with Ba2+ ion. We examined the ranges of volumetric and photometric determination. The accuracy of the analysis was determined by comparison with a certified method. We present optimal conditions for the successful determination of the mobile sulfur with the titration and with spectrophotometric method. The results of experiments confirming the capabilities of the method under study are presented
Towards a potential paradigm shift in health data collection and analysis: Contemporary challenges of Human-Machine interaction
Get PDFIndustrial Revolution 4.0 transforms healthcare systems. The first three technological revolutions changed the relationship between human and machine interaction due to the exponential growth of the number of machines. The fourth revolution has placed humans in a scenario where heterogeneous data is generated in unprecedented quantity and quality, not only through traditional methods enhanced by digitization, but also through ubiquitous computing, machine-to-machine interactions, and smart environment. The modern cyber-physical space underlines the role of humans in the expanding context of computerization and big data processing. In healthcare, where data collection and analysis particularly depend on human efforts, the disruptive nature of these developments is evident. Adaptation to this process requires deep scrutiny of the trends and recognition of future medical data technologies` evolution. Significant difficulties arise from discrepancies in requirements by healthcare, administrative and technology stakeholders. Black box and grey box decisions made in medical imaging and diagnostic Decision Support Software are often not transparent enough for the professional, social and medico-legal requirements. While Explainable AI proposes a partial solution for AI applications in medicine, the approach has to be wider and multiplex. LLM potential and limitations are also discussed. This paper lists the most significant issues in these topics and describes possible solutions
Evaluation of Cytotoxic Activity and Apoptosis-Inducing Potential of 5,6,7-Trihydroxyflavone against Breast Cancer and Cervical Cancer Cell Lines
No full textBackground: Breast cancer and cervical cancer are the leading causes of mortality in women worldwide, necessitating ongoing efforts to develop effective treatments. Anticancer drug development is an important aspect of cancer research, with the goal of discovering and designing compounds that target specific aspects of cancer biology while causing minimal harm to normal cells. Compounds that interact with DNA are an intriguing class of chemotherapeutic drugs used to treat cancer. This study investigated the anticancer effect of 5,6,7-Trihydroxyflavone (THF) on breast cancer and cervical cancer cells. Methods: The anticancer potential of 5,6,7-Trihydroxyflavone (THF) against two human breast cancer cell lines (the MDA-MB231 cell line (HTB-26™) and the MCF-7 cell line (HTB-22™)) and one human cervical cancer cell line (the HeLa cell line and the CRM-CCL-2™) was explored using in-vitro cell based assays including 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay, Lactate dehydrogenase release and Caspase-3 activity followed by the Herring sperm DNA (HS-DNA) binding UV-visible spectrophotometric assay. For in-silico investigations, Molecular docking studies (using P53, Caspase, and nuclear factor-kappa B (NF-κB)) and molecular dynamic simulation studies were performed followed by the density functional theorys (DFTs) calculations. Results: Significant growth inhibition (GI50) values of 11.1 ± 1.06, 3.23 ± 0.81, and 6.14 ± 0.96 μM were found against HeLa, MDA-MB231, and MCF-7 cells, respectively. From the LDH-release assay and Caspase-3 assay, THF was found more potential towards MDA-MB231 cells. The results showed that, compared with control, the percentage LDH release and Caspase-3 activities of THF were found statistically significant (increased) when compared between the two different concentrations (p < 0.05) and were found highly significant as p < 0.001, compared to control. THF was also discovered to bind to DNA via groove binding, with both electrostatic and non-electrostatic interactions contributing to the free energy of the binding. At the end, THFs remarkable cytotoxic potential was demonstrated by molecular docking and molecular dynamics simulations. Conclusion: These findings suggest the potential application of THF that this could be the hypothetical compound, which would need extensive preclinical and clinical testing before being considered a viable treatment option
Hibiscetin Mitigates Cisplatin-evoked Renal Toxicity through the Modulation of Activated Caspase-3/COX-2/iNOS/p53
No full textBackground: Renal toxicity is a significant concern in various clinical settings, yet its examination with a focus on particular parameters remains limited. A variety of factors including medications, chemicals, environmental toxins, and medical conditions can contribute to renal toxicity. Cisplatin (CP) is a widely used chemotherapeutic agent for the treatment of various cancers. However, one of its significant side effects is nephrotoxicity, which can lead to acute kidney injury. The purpose of this research was to investigate the potential protective effects of hibiscetin against CP-induced nephrotoxicity in rats. Methods: The study employed a simple randomization method, involving four groups of six rats each. The groups were designated as follows: the normal control group, the CP injected group, the CP + hibiscetin group (10 mg/kg), and the hibiscetin-treated group (10 mg/kg) for 25 days. Various biochemical parameters were measured, including kidney function markers [blood urea nitrogen (BUN), serum albumin, creatinine, creatinine clearance], tubular damage biomarkers [N-Acetyl-b-D-glucosaminidase (NAG)], antioxidant levels [superoxide dismutase (SOD), glutathione transferase (GST), catalase (CAT), and malondialdehyde (MDA)], anti-inflammatory markers [interleukins-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukins-33 (IL-33), interleukins-6 (IL-6), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2)], and apoptotic markers (Caspase-3 and p53). The assessment was performed using serum and urine samples. Antioxidants, inflammatory markers, and apoptotic markers were measured using kidney tissue homogenate. Results: The findings of the study show that the administration of hibiscetin significantly reduced the biochemical, enzymatic, and inflammatory alterations induced by CP in rats. This protective effect was evident in the modulation of various biomarkers, including IL-1β, IL-6, IL-33, TNF-α, iNOS, COX-2, p53, and Caspase-3 (Casp-3). Notably, hibiscetin exhibited statistically significant effects in counteracting CP-induced nephrotoxicity (p < 0.05). Conclusions: The current study suggests that hibiscetin may be effective in nephroprotection in rats induced with CP
Knockdown of METTL4 Reduces Mitochondrial DNA 6mA Modification and Alleviates Myocardial Ischemia-Reperfusion Injury
No full textBackground: Myocardial ischemia-reperfusion injury (MIRI) is damage caused by restoring coronary blood supply after myocardial ischemia. Recombinant mouse methyltransferase-like protein 4 (METTL4), a N6-methyladenin (6mA) methylase-related protein, is associated with cardiovascular disease. However, the role and mechanism of METTL4 in MIRI have yet to be clarified. This study aims to explore whether METTL4 regulates MIRI by mitochondrial DNA 6mA modification. Methods: We first constructed a MIRI rats model and an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model from mouse cardiomyocytes (HL-1). The 6mA level of mitochondrial DNA, METTL4 expression, and mitochondrial DNA (mtDNA) copy number were confirmed using Dot blot, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) in the rat and cell models, respectively. Functionally, cell proliferation and apoptosis were assessed by cell counting kit-8 (CCK-8) and flow cytometry, respectively. In addition, the levels of adenosine triphosphate (ATP) and mitochondria-related genes were monitored by enzyme-linked immunosorbent assay (ELISA) and qRT-PCR. Results: Our results showed that mitochondrial DNA 6mA and METTL4 levels were higher in MIRI model rats and OGD/R HL-1 model cells (p < 0.001). Then, we showed that knockdown of METTL4 induces proliferation and attenuates apoptosis of OGD/R HL-1 cells (p < 0.01, p < 0.001). We also found that METTL4 silencing reduces mitochondrial DNA 6mA modification and increases mitochondrial DNA (mtDNA) copy in OGD/R HL-1 cells (p < 0.001). The results indicated that silencing METTL4 reduces ATP and increases the levels of mitochondria-related genes in OGD/R HL-1 cells (p < 0.01, p < 0.001). Conclusions: METTL4 silencing reduces mitochondrial DNA 6mA modification, increases mitochondrial DNA copy number, improves mitochondrial dysfunction, and inhibits apoptosis. Therefore, inhibition of METTL4 might be a therapeutic strategy for MIRI
Deciphering Tetraspanins: Dual Roles in Cancer Progression and Therapeutic Implications
No full textTetraspanins, characterized by their four transmembrane domains, function as versatile platforms for interactions with a wide range of molecules. Recent research has increasingly focused on the utility of tetraspanins as potential prognostic markers and indicators of metastatic likelihood, varying according to the type of cancer. This review comprehensively examines the multifaceted functions of tetraspanins, highlighting their dual roles as enhancers and inhibitors in cancer development. Furthermore, it provides a detailed exploration of the signaling pathways and interactions associated with tetraspanins that could significantly impact the course and treatment of cancer
Decreased Resolvin D1 and Increased Fatty Acid Oxidation Contribute to Severity Score of Krabbe Disease in Twitcher Mice
No full textBackground: Krabbe disease is due to a deficiency of lysosomal enzyme galactosylceramidase, which leads to destruction of the myelin sheath around nerves in the brain and spinal cord. In addition, Krabbe disease is associated with neuroinflammation in which harmful amounts of lipids are produced. To assess the importance of the regulation of lipid metabolism in the pathogenesis and intervention options in Krabbe disease, the aim of this study was to identify a set of specific biomarkers in a mouse model of the disease and to analyze the correlation between each biomarker. Methods: In this study, fatty acid mediators were investigated in twitcher mice, a natural model of Krabbe disease, and the genotype was determined. Mass spectrometry was used to quantify F₂-isoprostanes and immune techniques were used to investigate F₂-isoprostanes, resolvin D1 (RvD1), peroxisome proliferator-activated receptor gamma, apelin, and the apelin receptor in the brains of heterozygous and affected homozygous mice and in wild-type control mice. Results: The results of molecular analysis showed that there was a reduction in peroxisome proliferator-activated receptor gamma in the brains of both heterozygous and affected homozygous mice (p < 0.001). In addition, in the brains of mice with Krabbe disease RvD1 levels were decreased (p < 0.001), oxidation of arachidonic acid was increased (p < 0.001) and low levels of apelin (p < 0.001) were associated with an increase in apelin receptor (p < 0.05). RvD1 and apelin levels were associated with disease severity (r = –0.638, p < 0.001 and r = –0.725, p < 0.001, respectively). Conclusion: Our results indicate that mutation of the galactosylceramidase gene is associated with altered homeostasis of fatty acid oxidative metabolism. These homeostatic alterations reflect the disease phenotype. Our findings highlight a relevant aspect of fatty acid metabolism in the Krabbe disease brain and support the view that fatty acid metabolism is an active player in the pathogenesis of this still incurable disease
Attenuation of Transfusion-Related Acute Lung Injury by FAK Inhibitor PF-562271
No full textBackground: Transfusion-related acute lung injury (TRALI) is a form of acute lung injury (ALI) that can cause complications such as respiratory distress, hypoxia, fever, and tachycardia in patients. A study using mice found that the focal adhesion kinase (FAK) inhibitor PF-562271 improved ALI. This study aimed to investigate whether PF-562271 could inhibit the progression of inflammation in a mouse model of TRALI. Methods: Platelets were collected from experimental mice and stored for 5 days. The mice were injected intraperitoneally with lipopolysaccharide (LPS), and then the stored platelets were injected into the mice through the tail vein to establish the TRALI model. Lung tissue samples were collected from the mice after the experiment. Pathological changes in the lung tissue, lung wet/dry weight ratio, myeloperoxidase (MPO) activity, and the expression of Tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), Interleukin-8 (IL-8), and FAK protein were analyzed to determine the effects of PF-562271 on TRALI in mice. Results: Histological analysis revealed that the alveolar interstitium was filled with inflammatory cells and the alveolar septum was significantly widened in the TRALI model group. The lung wet/dry weight ratio confirmed that the pulmonary edema induced in the TRALI group was more severe than that in the LPS group (p < 0.001). MPO activity was higher in the TRALI group than in the LPS group (p < 0.001). The mRNA expression of TNF-α, IL-6, and IL-8, and protein expression of FAK in the lung tissue were up-regulated (p < 0.05, p < 0.01, p < 0.001). After 24 h of FAK inhibitor intervention, the pulmonary edema in TRALI mice was significantly reduced, the infiltration of inflammatory cells in the lung tissue was improved, the lung function was better, and the expression of inflammatory factors was downregulated (p < 0.05, p < 0.01, p < 0.001). Conclusions: We successfully constructed a mouse TRALI model infused with aged platelets and found that the FAK inhibitor PF-562271 could alleviate the lung injury caused by TRALI and increase the survival rate of TRALI mice. Therefore, FAK inhibitors may have potential applications in the treatment of TRALI
Effect of Squalene Synthase on Malignant Phenotypes and Anti-Cancer Effect of Celastrol on Prostate Cancer Cells
No full textBackground: Prostate cancer (PC) is one of the most common malignant tumors, and the effect of celastrol on squalene synthase (SQS) in PC is unknown. This study aimed to investigate the effect of celastrol on SQS in PC. Methods: The protein expression was detected by Western blot. Cell proliferation capacity was detected by cell counting kit-8 (CCK-8) kit (450 nm optical density values). Cell scratch (wounding healing rate) and transwell assays (migration cells number) detected the cells migration abilities. Messenger RNA (mRNA) expression was detected using a real-time polymerase chain reaction test. Results: Celastrol decreased the expression of SQS in PC cells, and the knockdown of the SQS-encoding gene farnesyl-diphosphate farnesyltransferase 1 (fdft1) with and without celastrol treatment decreased PC cell proliferation and migration abilities. Furthermore, overexpression of the fdft1 gene attenuated the proliferation and migration abilities of PC-3 cells. Treatment with celastrol with fdft1 gene overexpression can still decrease the proliferation and migration abilities of PC-3 cells. Conclusion: This study verified that celastrol decreases the proliferation and migration abilities of PC-3 and Lymph Node Carcinoma of the prostate (LNCaP) cells and revealed that celastrol reduces SQS expression. The results indicate that the inhibitory effect of celastrol on the malignant phenotypes of PC cells is partly dependent on SQS, and SQS is involved in the malignant behaviour of PC cells. Furthermore, there may be a dual effect dependent on the SQS protein expression level on the malignant phenotypes of PC cells