The safety of titanium dioxide nano-particles (TiO2NPs) is currently being questioned. TiO2NPs have multiple uses in disinfectants, plastics, cosmetics, and food coloring. Our goal was to determine if administering Baicalin (50 mg/kg body weight) could help lessen the harmful effects caused by TiO2NPs (100 mg/kg body weight) in rats. By reducing kidney damage from TiO2NPs, treatment with Bai led to lower levels of creatinine (Cr), urea (Ur), and uric acid (UA). The harmful effects of TiO2NPs can be counteracted by Baicalin, which has demonstrated its ability to protect the kidneys. Additionally, it can restore balance between oxidation and antioxidants by increasing CAT, SOD, GSH, and reducing malondialdehyde levels. Not only does it exhibit anti-inflammatory effects by downregulating IL-6 and TNF- and increasing IL-10, but it also contributes to maintaining equilibrium in the body.
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Investigation of Some Biomarkers Associated with Malignant and Benign Prostate Tumors in Iraqi Males
Prostate cancer (PCa), a challenging ailment, impacts a substantial number of men globally, primarily in prestigious regions. The study aimed to explore the functions of PD-1, PDL-1, PSA, and testosterone markers in detecting the pathogenesis of PCa. Medical City-Baghdad hosted the research from July to October 2021. After examination and diagnosis by the Medical City consultant expert, 40 blood samples (20 benign and 20 malignant) were collected from prostate cancer (PCa) patients. Eight healthy individuals were used as a control group and their blood samples were taken. Patients and controls ranged in age from 20-49. The ELISA technique was employed to assess the levels of program death-1 (PD-1), program death ligand-1 (PDL-1), and prostate specific antigen (PSA), and testosterone parameters. The study found substantial differences (P < 0.05) across age groups and study groups, with malignant patients scoring highest (70.0%) at 40-49 years and benign patients scoring highest (45.0%) at 30-39 years. Elevated levels of PD-1, PDL-1, and PSA are observed in both benign and malignant PCa compared to healthy. Neither benign nor malignant PCa had significantly lower testosterone levels than healthy PCa (P > 0.05). Both PD-1, PDL-1, and PSA show a remarkably high sensitivity (100%) when used to screen patients for prostate cancer. Finally, there is a negative correlation between PSA and PD-1, PDL-1 parameters. The PD-1, PDL-1, and PSA have been found to play significant roles in the development of prostate cancer and have shown high sensitivity in screening for PCa.
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The link between infections and hypersensitivity reactions was revealed by many pioneers. Many researchers found that detectable IgE is specific to bacteria and viruses in sera of infected patients. Some patients undergo a post-COVID-19 bronchospasm due to a reaction to the viral antigens. This study aimed to reveal the association between COVID-19 infection and respiratory allergy in post-COVID-19 convalescent patients. The blood specimens were taken from each of the patients and control individuals. Complete cell blood count (CBC), anti-COVID-19 virus IgM, IgG, as well as IL-5, total IgE and IgE specific for COVID-19 antigen were done for each of patients and control individuals. The results: no significant difference was found in the mean number of the total WBCs, neutrophil and monocyte cells between patients and control individuals. Patients who were suffering from bronchoconstriction and showed high total and specific IgE revealed normal percentage of eosinophil and high basophil. The basophil ratio undergoes an increase in COVID-19 patients who were suffering from bronchoconstriction during and after post-COVID-19 infection. Furthermore, a positive correlation was found between IL-5, total IgE, COVID-19 antigen specific IgE and basophils in patients while a normal relation was found between parameters and control individuals. We can conclude that bronchospasm is one of the post-COVID-19 complications, due to a hypersensitivity reaction to the viral antigens. The production of COVID-19 virus antigen specific IgE has an important role in post-infection allergy as well as its relation to other factors like IL-5 in patients’ sera.
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Social isolation and quarantine have been implemented globally during outbreaks of a highly transmissible microbe. For instance, they were employed during the plague outbreak in 1894 and the COVID-19 pandemic in 2019. While these methods have proven effective against highly transmissible infections, they have also had significant negative consequences. In specific regions like Anbar, Diyala, Salahaddin, and Kirkuk, social isolation occurred during the period of ISIS occupation. After their liberation, these regions experienced a COVID-19 outbreak, and quarantine measures were put in place. This study aimed to investigate the effect of social isolation and quarantine on tuberculosis. Patients from Anbar, Diyala, Salahaddin, and Kirkuk districts were diagnosed with pulmonary or extrapulmonary tuberculosis according to the World Health Organization (WHO) guidelines, using methods like chest X-rays, acid-fast positive sputum slide method, culture, and Mycobacterium tuberculosis gene pert testing. All cases were documented at the Iraqi Ministry of Health. All four districts had the same population, socioeconomic status, and medical guidelines. Anbar showed a significant difference compared to the other districts, while the remaining three districts had no significant differences among themselves. The percentage of extrapulmonary tuberculosis was higher than the global average, indicating misdiagnosis. The age group of less than four years old had the lowest percentage of cases compared to other age groups, indicating the effective management of the BCG program. It can be concluded that social isolation and quarantine implemented during the COVID-19 pandemic might have led to an increase in cases of extrapulmonary tuberculosis in the studied regions.
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During the COVID-19 pandemic, the number of cases of community-acquired pneumonia (CAP) increased dramatically, which significantly changed the dynamics of its incidence time series (TS). Such changes overestimate the predicted values of the incidence of CAP and increase the forecast error. The purpose of this work was to evaluate methods for predicting the dynamics of CAP incidence during the COVID-19 pandemic. The CAP incidence data, registered within the time period from 2011 to 2022 was used. Two TS data were compiled, which did not include and included cases of CAP caused by COVID-19 in 2021-2022. TS data transformation was performed using outliers’ deletion, seasonal decomposition, or X-13-ARIMA-SEATS techniques. Typical monthly dynamics calculation method and several adaptive regression models (ETS, SARIMA, decSARIMA) were used for CAP incidence modeling and forecasting. For CAP incidence TS data that excluded cases of COVID-19 pneumonia, all analyzed transformation techniques effectively smoothed out the outlier period making the TS data suitable for modeling using adaptive regression models. For CAP incidence TS data that included cases of COVID-19 pneumonia, the methods of TS decomposition turned out to be ineffective. An acceptable forecast error was obtained when using typical monthly dynamics model based on the TS data with deleted outliers.
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Purpose: type III interferons (IFNλ) are an early line of defense in upper respiratory tract infections, such as severe acute respiratory syndrome coronavirus 2 (SARS-COV-2). They have a crucial role in the control of the innate immune system and the modulation of immunological responses during the course of acute viral infection and tissue inflammation. The present study was aimed at evaluating the expression of IFNλ genes in Iraqi coronavirus disease (COVID-19)-infected patients. Materials and methods: ninety patients presented with COVID-19 and 50 healthy controls were recruited. Blood samples were obtained from the participants. Haematological and biochemical analyses were performed on the blood samples. IFNλ gene expression was assessed in peripheral blood mononuclear cells (PBMCs) of all the participants by real-time polymerase chain reaction (RT-PCR). Results: all COVID-19 patients had elevated relative expression of IFNλ-I, IFNλ-II, and IFNλ-III genes compared to controls, by 1.85 ± 0.25-, 39.9 ± 15.07-, and 4.001 ± 1.23-fold, respectively. According to the severity of the disease (moderate, severe, and critical), the relative expression of each IFN type was likewise elevated. However, the rise did not reach a significant level. On the other hand, there was a significant difference (p < 0.05) in the mean of relative expression between IFN-I, IFN-II, and IFN-III in total and each category of severity. Conclusion: the findings show that IFNλ gene expression was up-regulated in COVID-19 disease and neither age, sex, nor underlying diseases impacted the variations in expressions.
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Using immunocytochemistry and fluorescence microscopy, it was shown that the expression of the calcium-binding proteins parvalbumin, calbindin and calretinin in GABAergic neurons limited the increase in the level of cytosolic calcium ([Ca2+]i) during the excitotoxic effect of glutamate (GluTox). Under conditions of repeated episodes of hypoxia, Ca2+ oscillations were generated in GABAergic neurons, and the expression of calcium-binding proteins determined the amplitude of hypoxia-induced Ca2+ impulses. Expression of parvalbumin during hypoxia was most effective in suppressing the amplitude of Ca2+ signals. With GluTox, irreversible depolarization of the mitochondria of GABAergic neurons occurred, which lacked calcium-binding proteins, while the expression of parvalbumin, calbindin or calretinin contributed to the preservation of mitochondrial polarization and maintenance of their functioning under the influence of glutamate. At the same time, parvalbumin also turned out to be the most effective calcium-binding protein. As a result, restrictions on the level of [Ca2+]i during GluTox by calcium-binding proteins in GABAergic neurons led to suppression of the production of reactive oxygen species by mitochondria on the one hand, and on the other hand, calcium-binding proteins were able to protect GABAergic neurons from hyperproduction of nitric oxide. Thus, calcium-binding proteins were not only a marker of subtypes of GABAergic neurons, but also determined their physiological parameters under stressor conditions, which can be used to identify the subtype of GABAergic neurons by fluorescent signals of ROS production, nitric oxide, or the kinetics of Ca2+ signals.
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Ulcerative colitis is a persistent and recurrent medical condition for which current treatments have shown limited efficacy, necessitating the exploration of alternative drugs with minimal side effects. This study aimed to examine the anti-oxidative and antiadhesive effects of ezetimibe compared to sulfasalazine in experimentally induced colitis in male rats. A total of 40 adult male Wistar rats were divided into 4 groups: a control group (negative control), an acetic acid group (positive control), an acetic acid + sulfasalazine (100 mg/kg/day) group, and an acetic acid + ezetimibe (10 mg/kg/day) group. Colitis was induced in rats by the inter-rectal administration of 2 ml of 4% (v/v) acetic acid. Sulfasalazine and ezetimibe were administered orally for seven days 1 hour after induction. Malondialdehyde (MDA), myeloperoxidase (MPO), e-selectin, and intracellular adhesive molecule 1 (ICAM-1) were measured in tissue homogenate upon euthanizing the animals. The results showed that the treatment with ezetimibe significantly reduced disease activity index (DAI) and macroscopic colonic scores (MAC) compared to the positive control group. Moreover, ezetimibe notably decreased MDA, MPO, e-selectin, and ICAM-1 in tissue homogenates of treated animals compared to the positive control group. In most comparisons, there were no significant differences between ezetimibe and sulfasalazine effects. These findings suggest that ezetimibe may have a therapeutic effect in the management of ulcerative colitis by reducing oxidative stress and adhesive molecules.
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Retroelements occupy 37% of the human genome and are involved in the regulation of gene expression in cis and in trans. A number of studies have shown that activation of retroelements in neuronal stem cells of the brain contributes to the genomic mosaicism required for the phenotypic diversity of differentiating neurons. These processes occur in the hippocampus, where memory is also formed, so I have proposed a hypothesis according to which retroelements are drivers of memory formation mechanisms. This is due to the sensitivity of retroelements to environmental influences and their ability to transpose into specific loci of the genome with the activation of brain-specific genes. In addition, proteins and non-coding RNAs involved in memory formation evolved from retroelements. The results of experimental articles are presented that prove this hypothesis, as well as refuting the key role of synaptic plasticity in memory consolidation. The cause of aging and neurodegenerative diseases with memory impairment is the pathological activation of retroelements, which can be influenced by specific microRNAs complementary to these retroelements. Therefore, I analyzed scientific articles in Scopus, Wos, PubMed and the MDTE DB database, which made it possible to identify 33 RE-derived microRNAs involved in Alzheimer's disease, of which 14 are associated with aging, and mechanisms of influence on the brain are described for 18 microRNAs. These microRNAs can be used as tools to target pathologically activated retroelements in aging and Alzheimer's disease to improve memory.
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Background: HHV-7 infection has been documented to cause CNS complications. The susceptibility to many diseases, including immune dysfunction and cancers, has been linked to SNP in the promoter region of the interleukin-18 (IL-18) gene. Objectives: to explore the rates of both HHV-7 infection and the polymorphisms in the IL-18 -607C/A (rs1946518) promoter region in a group of Iraqi patients with different brain tumors. Patients and methods: one hundred fifteen (115) freshly obtained brain tissue biopsies were enrolled in this study; 85 were from brain cancer cases whereas 30 autopsies were obtained from cases with apparently normal brain tissues as a control group. Conventional PCR was chosen both for the detection of HHV-7 and IL-18 rs1946518 SNP detection as well as sequencing. Results: according to conventional PCR analysis, 34% showed positive results for the HHV-7 genome, while 66% revealed negative results. In various types of brain cancers, HHV-7-PCR detection results were 11.8%, 5.9%, 29.4%, 11.8%, 5.9%, and 11.8% in tissues from patients with Transitional Meningioma, Meningotheliomatous Meningioma, Glioblastoma Multiforme, Diffuse Fibrillary Astrocytoma, Anaplastic Oligodendroglioma, Atypical Meningioma, and Pilocytic Astrocytoma, respectively. The polymorphism distributions according to GG; AA and GA genotypes of IL-18 607C/A (rs1946518) polymorphism were 37.1%; 57.1%, and 5.7%, respectively, in the patients’ group and 66.7% and 33.3%, respectively, in the control group. Conclusion: the detected rates of HHV-7 as well as IL-18 607C/A (rs1946518) polymorphism have shed light on the possibility that they might have played or contributed a role in the brain tumors’ development.
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