OBJECTIVES: This study evaluated the effect of lactic acid and acetic acid on the microhardness of a silorane-based composite compared to two methacrylate-based composite resins. MATERIALS AND METHODS: Thirty disc-shaped specimens each were fabricated of Filtek P90, Filtek Z250 and Filtek Z350XT. After measuring of Vickers microhardness, they were randomly divided into 3 subgroups (n = 10) and immersed in lactic acid, acetic acid or distilled water. Microhardness was measured after 48 hr and 7 day of immersion. Data were analyzed using repeated measures ANOVA (p < 0.05). The surfaces of two additional specimens were evaluated using a scanning electron microscope (SEM) before and after immersion. RESULTS: All groups showed a reduction in microhardness after 7 day of immersion (p < 0.001). At baseline and 7 day, the microhardness of Z250 was the greatest, followed by Z350 and P90 (p < 0.001). At 48 hr, the microhardness values of Z250 and Z350 were greater than P90 (p < 0.001 for both), but those of Z250 and Z350 were not significantly different (p = 0.095). Also, the effect of storage media on microhardness was not significant at baseline, but significant at 48 hr and after 7 day (p = 0.001 and p < 0.001, respectively). Lactic acid had the greatest effect. CONCLUSIONS: The microhardness of composites decreased after 7 day of immersion. The microhardness of P90 was lower than that of other composites. Lactic acid caused a greater reduction in microhardness compared to other solutions.
Acetic Acid ; Biofilms* ; Composite Resins ; Immersion ; Lactic Acid ; Water

Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy with an unfavorable outcome. The present research aimed to identify novel biological targets for AML diagnosis and treatment. In this study, we per‑ formed an in-silico method to identify antisense RNAs (AS-RNAs) and their related co-expression genes. GSE68172 was selected from the AML database of the Gene Expression Omnibus and compared using the GEO2R tool to find DEGs. Antisense RNAs were selected from all the genes that had significant expression and a survival plot was drawn for them in the GEPIA database, FOXD2-AS1 was chosen for further investigation based on predetermined criteria (logFC ≥|1| and P < 0.05) and its noteworthy association between elevated expression level and a marked reduction in the overall survival (OS) in patients diagnosed with AML. The GEPIA database was utilized to investigate FOXD2-AS1-related co-expression and similar genes. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and gene ontology (GO) function analysis of the mentioned gene lists were performed using the DAVID database. The protein–protein interaction (PPI) network was then constructed using the STRING database.Hub genes were screened using Cytoscape software. Pearson correlation analysis was conducted using the GEPIA database to explore the relationship between FOXD2-AS1 and the hub genes. The transcription of the selected cod‑ ing and non-coding genes, including FOXD2-AS1, CDC45, CDC20, CDK1, and CCNB1, was validated in 150 samples, including 100 primary AML non-M3 blood samples and 50 granulocyte colony stimulating factor (G-CSF)-mobilized healthy donors, using quantitative Real-Time PCR (qRT-PCR). qRT-PCR results displayed significant upregulation of lnc-FOXD2-AS1, CDC45, and CDK1 in primary AML non-M3 blood samples compared to healthy blood samples (P = 0.0032, P = 0.0078, and P = 0.0117, respectively). The expression levels of CDC20 and CCNB1 were not statistically different between the two sets of samples (P = 0.8315 and P = 0.2788, respectively). We identified that AML patients with upregulation of FOXD2-AS1, CDK1, and CDC45 had shorter overall survival (OS) and Relapse-free survival (RFS) compared those with low expression of FOXD2-AS1, CDK1, and CDC45. Furthermore, the receiver operating charac‑ teristic (ROC) curve showed the potential biomarkers of lnc -FOXD2-AS1, CDC45, and CDK1 in primary AML non-M3 blood samples. This research proposed that the dysregulation of lnc-FOXD2-AS1, CDC45, and CDK1 can contribute to both disease state and diagnosis as well as treatment. The present study proposes the future evolution of the func‑ tional role of lnc-FOXD2-AS1, CDC45, and CDK1 in AML development.

Infertility is one of the disorders that worries many couples around the world, although novel and molecular methods can be used to cure this disease in different stages. One of the factors that causes infertility in men and women is the increased oxidative stress within the cells, which can lead to damage in zygote formation. ROMO1 is one of the most important proteins in the production of reactive oxygen species. This protein can enhance oxidative stress in the cells and body through cellular pathways, such as TNF-α and NF-κB routes, which will eventually lead to many diseases, especially infertility. We engage several international databases by using keywords; ROMO1, Infertility, and Reactive Oxygen Species, and gained a great quantity of information about ROMO1, Infertility, and Oxidative Stress. Although not proven, it is hypothesized that ROMO1 might elevate oxidative stress by activating NF-κB pathway in the cells, furthermore, TNF-αcan arouse ROMO1 that can end up with apoptosis and cell death, which consequently can have a lot of disturbing effects on the body, especially the reproductive system. To sum up, revealing the exact cellular and molecular mechanisms of ROMO1-dependent TNF-α and NF-κB pathways in the pathogenesis of infertility might find interesting therapeutic and management strategies for this disorder.

There is no denying that the massive spread of COVID-19 around the world has worried everyone. The virus can cause mild to severe symptoms in various organs, especially the lungs. The virus affects oxidative stress in the cells. Reactive Oxygen Species modulator 1 (ROMO1) is one of the most important mitochondrial proteins that plays a critical regulatory role in the production of Reactive Oxygen Species (ROS). According to the studies, COVID-19 can promote oxidative stress through some important pathways, for instance, TNF-α and NF-κB routes. Furthermore, ROMO1 is closely related to these pathways and its dysfunction may affect these routes, then promote oxidative stress, and ultimately cause tissue damage, especially in the lungs. Another factor to consider is that the TNF-α and NF-κB pathways are associated with ROMO1, COVID-19, and oxidative stress. To summarize, it is hypothesized that COVID-19 may increase oxidative stress by affecting ROMO1. Understanding the exact molecular mechanisms of ROMO1 in the pathogenesis of COVID-19 can pave the way to find better therapeutic strategies.

Objective: Uropathogenic Escherichia coli is known to cause urinary tract infections, and the endotoxin (lipopolysaccharide [LPS]) of this bacterium may cause deficiencies of sperm quality and morphology. In the present study, the effects of LPS on mouse sperm were studied, and the levels of interleukin (IL)-17A and possible changes in testis tissue were evaluated. Methods: LPS of uropathogenic E. coli was extracted using the methanol-chloroform method, followed confirmation using sodium dodecyl sulfate-polyacrylamide electrophoresis. Purified LPS (100 µg/kg) or phosphate-buffered saline was injected intraperitoneally into BALB/c mice for 7 days consecutively in the test and control groups, Mice were sacrificed on days 3, 7, and 42 after the first injection. Blood was tested for levels of IL-17A using the enzyme-linked immunosorbent assay method. Testis tissue and sperm were collected from each mouse and were studied according to standard protocols. Results: The mean sperm count and motility significantly decreased (p=0.03) at 3, 7, and 42 days after the injections. The level of IL-17A in the test groups increased, but not significantly (p=0.8, p=0.11, and p=0.15, respectively). Microscopic studies showed no obvious changes in the morphology of the testis tissue; however, significant changes were observed in the cellular parenchyma on day 42. Conclusion LPS can stimulate the immune system to produce pro-inflammatory cytokines, resulting in an immune response in the testis and ultimately leading to deficiency in sperm parameters and testis tissue damage. In addition, the presence of LPS could significantly impair sperm parameters, as shown by the finding of decreased motility.

Objective: Uropathogenic Escherichia coli is known to cause urinary tract infections, and the endotoxin (lipopolysaccharide [LPS]) of this bacterium may cause deficiencies of sperm quality and morphology. In the present study, the effects of LPS on mouse sperm were studied, and the levels of interleukin (IL)-17A and possible changes in testis tissue were evaluated. Methods: LPS of uropathogenic E. coli was extracted using the methanol-chloroform method, followed confirmation using sodium dodecyl sulfate-polyacrylamide electrophoresis. Purified LPS (100 µg/kg) or phosphate-buffered saline was injected intraperitoneally into BALB/c mice for 7 days consecutively in the test and control groups, Mice were sacrificed on days 3, 7, and 42 after the first injection. Blood was tested for levels of IL-17A using the enzyme-linked immunosorbent assay method. Testis tissue and sperm were collected from each mouse and were studied according to standard protocols. Results: The mean sperm count and motility significantly decreased (p=0.03) at 3, 7, and 42 days after the injections. The level of IL-17A in the test groups increased, but not significantly (p=0.8, p=0.11, and p=0.15, respectively). Microscopic studies showed no obvious changes in the morphology of the testis tissue; however, significant changes were observed in the cellular parenchyma on day 42. Conclusion LPS can stimulate the immune system to produce pro-inflammatory cytokines, resulting in an immune response in the testis and ultimately leading to deficiency in sperm parameters and testis tissue damage. In addition, the presence of LPS could significantly impair sperm parameters, as shown by the finding of decreased motility.

Objective: The present study investigated sperm chromatin quality and testosterone levels in acrylamide-treated mice and the possible protective effects of vitamin E on the fertility potential of spermatozoa. Methods: Thirty-two adult male mice were divided equally into four groups. Group 1 was the control, group 2 received acrylamide (10 mg/kg, water solution), group 3 received vitamin E (100 mg/kg, intraperitoneal), and group 4 received both acrylamide and vitamin E. After 35 days, spermatozoa from the right cauda epididymis were analyzed in terms of count, motility, morphology, and viability. Sperm DNA integrity and chromatin condensation were assessed by acridine orange (AO), aniline blue (AB), toluidine blue (TB), and chromomycin A3 (CMA3) staining. Results: In acrylamide-treated mice, significantly lower sperm concentration, viability, motility, and testosterone levels were found in comparison with the control and acrylamide+vitamin E groups (p<0.05). In the vitamin E group, significantly more favorable sperm parameters and testosterone levels were found than in the other groups (p<0.05). There were also significantly more spermatozoa with less condensed chromatin in the acrylamide-treated mice than in the other groups. Moreover, significantly more spermatozoa with mature nuclei (assessed by AB, CMA3, AO, and TB staining) were present in the vitamin E group than in the control and acrylamide+vitamin E groups. Conclusion This study revealed the deleterious effects of acrylamide on sperm parameters and sperm chromatin quality. Vitamin E can not only compensate for the toxic effects of acrylamide, but also improve sperm chromatin quality in mice.

Today, the incidence of cancer in the world is rising, and it is expected that in the next several decades, the number of people suffering from cancer or (the cancer rate) will double. Cancer is defined as the excessive and uncontrolled growth of cells; of course (in simple terms), cancer is considered to be a set of other diseases that ultimately causes normal cells to be transformed into neoplastic cells. One of the most important causes of the onset and exacerbation of cancer is excessive oxidative stress. One of the most important proteins in the inner membrane of mitochondria is Reactive Oxygen Species (ROS) Modulator 1 (ROMO1) that interferes with the production of ROS, and with increasing the rate of this protein, oxidative stress will increase, which ultimately leads to some diseases, especially cancer. In this overview, we use some global databases to provide information about ROMO1 cellular signaling pathways, their related proteins and molecules, and some of the diseases associated with the mitochondrial protein, especially cancer.
Diagnosis ; Incidence ; Membranes ; Mitochondria ; Mitochondrial Proteins ; Oxidative Stress ; Reactive Oxygen Species

PURPOSE: Febrile seizures are induced by fever and are the most common type of seizures in children. Although numerous studies have been performed on febrile seizures, their pathophysiology remains unclear. Recent studies have shown that cytokines may play a role in the pathogenesis of febrile seizures. The present study was conducted to identify potential links between serum interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and febrile seizures. METHODS: Ninety-two patients with simple or complex febrile seizures (46 patients per seizure type), and 46 controls with comparable age, sex, and severity of temperature were enrolled. RESULTS: The median concentrations of serum IL-1beta in the simple, complex febrile seizure, and control groups were 0.05, 0.1, and 0.67 pg/mL, respectively (P=0.001). Moreover, the median concentrations of TNF-alpha in the simple, complex febrile seizure, and control groups were 2.5, 1, and 61.5 pg/mL, respectively (P=0.001). Furthermore, there were significant differences between the case groups in serum IL-1beta and TNF-alpha levels (P<0.05). CONCLUSION: Unlike previous studies, our study does not support the hypothesis that increased IL-1beta and TNF-alpha production is involved in the pathogenesis of febrile seizures.
Child ; Cytokines ; Fever ; Humans ; Interleukin-1beta* ; Seizures ; Seizures, Febrile* ; Tumor Necrosis Factor-alpha*

PURPOSE: Early diagnosis and treatment of acute pyelonephritis in children is of special importance in order to prevent serious complications. This study was conducted to determine the diagnostic value of serum interleukin (IL)-6 and IL-8 in children with acute pyelonephritis. METHODS: Eighty-seven patients between 1 month to 12 years old with urinary tract infection (UTI) were divided into 2 groups based on the result of 99m-technetium dimercapto-succinic acid renal scan: acute pyelonephritis (n=37) and lower UTI (n=50) groups. White blood cell (WBC) count, neutrophil (Neutl) count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) concentration, platelet count, and serum IL-6 and IL-8 concentrations of both groups were measured and compared. RESULTS: There was a significant difference between two groups regarding WBC count, Neutl count, ESR, and CRP concentration (P<0.05). In addition, the difference between the two groups regarding serum IL-6 and IL-8 concentrations was not significant (IL-6, 60 and 35.4 pg/mL and IL-8, 404 and 617 pg/mL, respectively). The sensitivity and specificity of serum IL-6 and IL-8 for diagnosis of acute pyelonephritis were 73%, 42% and 78%, 32%, respectively. Sensitivity, specificity, negative and positive predictive values of serum IL-6 and IL-8 were less than those of acute phase serum reactants such as CRP. CONCLUSION: This study showed that there was no significant difference between acute pyelonephritis and lower UTI groups regarding serum IL-6 and IL-8 levels. Therefore, despite confirming results of previous studies, it seems that IL-6 and IL-8 are not suitable markers for differentiating between acute pyelonephritis and lower UTI.
C-Reactive Protein ; Child ; Early Diagnosis ; Erythrocyte Count ; Humans ; Interleukin-6 ; Interleukin-8 ; Interleukins ; Leukocytes ; Neutrophils ; Platelet Count ; Pyelonephritis ; Sensitivity and Specificity ; Urinary Tract Infections