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In this work, sampling collection strategies were compared for the determination of some heavy metals (Pb, Cr, Ni) and investigate their effects on the marine pollution. The sampling area is a natural bay using as a shipbuilding industries for three decades especially. To determine the permanent heavy metal pollution in this area, the sediment samples were taken different strategies; i) the bay were divided square pieces which is 200 m length, and the samples were taken this distance (total 71 point), ii) the samples were taken along the shore, then 200 m away the shore and 400 m away the shore (total 58 point). After the sample collection using ISO 5667-12 and EPA sampling procedure, the samples were prepared for the metal analysis. Acid treated samples were analyze by graphite furnace atomic absorption spectrometry. As a results both strategies were (are) compared for investigation of some heavy metals pollution in marine sediment. The preliminary results were found between below LOD and 401.0 mg/kg for lead, and between 0.10 and 1005.0 mg/kg for chromium. Finally, the permanent heavy metal pollution is investigated in this bay.

The article presents the clinical and laboratory characteristics of 144 patients with Mediterranean spotted fever (MSF). MSF is a rickettsiosis of the spotted fever group that is caused by Rickettsia conorii and is endemic in the Mediterranean region. The usual vector is the brown dog tick, Rhipicephalus sanguineus. The typical symptoms are fever and rash, with the presence of a black eschar (tache noire) in 30-86% of cases. Although MSF is usually a benign disease, serious complications and rare cases with a fatal outcome have also been reported, typically among elderly patients or those with underlying diseases. Serological confirmation of infection is obtained using indirect immunofluorescence against Rickettsia conorii.

T-cell acute lymphoblastic leukemia (T-ALL) is a type of acute lymphoblastic leukemia from early T-cell progenitors. Interest grows in creating less toxic agents and therapies for chemo-resistant T-ALL cancer. Recently, elemental boron has special properties useful in the creation of new drugs. Studies have revealed the cytotoxic properties of boric acid (BA) on cancer, but not fully understood. We aimed to investigate the effect of BA on cell proliferation, apoptosis, and oxidative stress in the Jurkat cells. The effects of BA on cell viability were determined by 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) assay for 24-48-72 h. The impact of BA on apoptosis was analyzed by acridine orange/ethidium bromide. Expression of apoptosis regulatory genes (Bcl-2, Bax, Caspase-3-8-9) and apoptotic miRNA (miR-21) was used by real-time quantitative polymerase chain reaction (RT-qPCR). The total oxidant status (TOS), total antioxidant status (TAS), and the oxidative stress index (OSI) value were calculated for oxidative stress. We determined the cytotoxic activity of BA on Jurkat cells by using XTT and defined the IC 50 concentration (802.7 μg/mL) of BA. The findings clearly show that BA inhibited Jurkat cell proliferation dose-dependently. BA induced apoptosis through downregulated anti-apoptotic genes, and upregulated pro-apoptotic genes. Additionally, we found that BA significantly reduced the expression of miR-21 (p<0.001). Our findings demonstrated that different doses of BA increased TAS levels while decreasing TOS levels in Jurkat cells. Our study suggests that BA might be potential anti-cancer agent candidate in ALL via inhibition of cell proliferation, induced apoptosis, and reducing the amounts of anti-oxidants in cells., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Krüppel-like factor 4 (KLF4), a zinc finger transcription factor, is found in different human tissues and shows diverse regulatory activities in a cell-dependent manner. In the brain, KLF4 controls various neurophysiological and neuropathological processes, and its contribution to various neurological diseases has been widely reported. Parkinson's disease (PD) is an age-related neurodegenerative disease that might have a connection with KLF4. In this review, we discussed the potential implication of KLF4 in fundamental molecular mechanisms of PD, including aberrant proteostasis, neuroinflammation, apoptosis, oxidative stress, and iron overload. The evidence collected herein sheds new light on KLF4-mediated pathways, which manipulation appears to be a promising therapeutic target for PD management. However, there is a gap in the knowledge on this topic, and extended research is required to understand the translational value of the KLF4-oriented therapeutical approach in PD., (© 2023. The Author(s).)

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, leading to various motor and non-motor symptoms. Several cellular and molecular mechanisms such as alpha-synuclein (α-syn) accumulation, mitochondrial dysfunction, oxidative stress and neuroinflammation are involved in the pathogenesis of this disease. MicroRNAs (miRNAs) play important roles in post-transcriptional gene regulation. They are typically about 21-25 nucleotides in length and are involved in the regulation of gene expression by binding to the messenger RNA (mRNA) molecules. miRNAs like miR-221 play important roles in various biological processes, including development, cell proliferation, differentiation and apoptosis. miR-221 promotes neuronal survival against oxidative stress and neurite outgrowth and neuronal differentiation. Additionally, the role of miR-221 in PD has been investigated in several studies. According to the results of these studies, (1) miR-221 protects PC12 cells against oxidative stress induced by 6-hydroxydopamine; (2) miR-221 prevents Bax/caspase-3 signalling activation by stopping Bim; (3) miR-221 has moderate predictive power for PD; (4) miR-221 directly targets PTEN, and PTEN over-expression eliminates the protective action of miR-221 on p-AKT expression in PC12 cells; and (5) miRNA-221 controls cell viability and apoptosis by manipulating the Akt signalling pathway in PD. This review study suggested that miR-221 has the potential to be used as a clinical biomarker for PD diagnosis and stage assignment., (© 2023 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)

Genome haploidization at meiosis depends on two consecutive nuclear divisions, which are controlled by an oscillatory system consisting of Cdk1-cyclin B and the APC/C bound to the Cdc20 activator. How the oscillator generates exactly two divisions has been unclear. We have studied this question in yeast where exit from meiosis involves accumulation of the APC/C activator Ama1 at meiosis II. We show that inactivation of the meiosis I-specific protein Spo13/MEIKIN results in a single-division meiosis due to premature activation of APC/C Ama1 . In the wild type, Spo13 bound to the polo-like kinase Cdc5 prevents Ama1 synthesis at meiosis I by stabilizing the translational repressor Rim4. In addition, Cdc5-Spo13 inhibits the activity of Ama1 by converting the B-type cyclin Clb1 from a substrate to an inhibitor of Ama1. Cdc20-dependent degradation of Spo13 at anaphase I unleashes a feedback loop that increases Ama1's synthesis and activity, leading to irreversible exit from meiosis at the second division. Thus, by repressing the exit machinery at meiosis I, Cdc5-Spo13 ensures that cells undergo two divisions to produce haploid gametes., (© 2023 The Authors. Published under the terms of the CC BY 4.0 license.)

Parkinson's disease (PD), characterized by loss of nigrostriatal dopaminergic neurons, is one of the most predominant neurodegenerative diseases affecting the elderly population worldwide. The concept of stem cell therapy in managing neurodegenerative diseases has evolved over the years and has recently rapidly progressed. Neural stem cells (NSCs) have a few key features, including self-renewal, proliferation, and multipotency, which make them a promising agent targeting neurodegeneration. It is generally agreed that challenges for NSC-based therapy are present at every stage of the transplantation process, including preoperative cell preparation and quality control, perioperative procedures, and postoperative graft preservation, adherence, and overall therapy success. In this review, we provided a comprehensive, careful, and critical discussion of experimental and clinical data alongside the pros and cons of NSC-based therapy in PD. Given the state-of-the-art accomplishments of stem cell therapy, gene therapy, and nanotechnology, we shed light on the perspective of complementing the advantages of each process by developing nano-stem cell therapy, which is currently a research hotspot. Although various obstacles and challenges remain, nano-stem cell therapy holds promise to cure PD, however, continuous improvement and development from the stage of laboratory experiments to the clinical application are necessary., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)

Here, we revise Pietraszewski's model of groups by assigning participant pairs with two triplets, denoting: (1) the type of game that models the interaction, (2) its critical switching point between alternatives (i.e., the game's similarity threshold), and (3) the perception of strategic similarity with the opponent. These triplets provide a set of primitives that accounts for individuals' strategic motivations and observed behaviors.

Sexual reproduction requires genome haploidization by the two divisions of meiosis and a differentiation program to generate gametes. Here, we have investigated how sporulation, the yeast equivalent of gamete differentiation, is coordinated with progression through meiosis. Spore differentiation is initiated at metaphase II when a membrane-nucleating structure, called the meiotic plaque, is assembled at the centrosome. While all components of this structure accumulate already at entry into meiosis I, they cannot assemble because centrosomes are occupied by Spc72, the receptor of the γ-tubulin complex. Spc72 is removed from centrosomes by a pathway that depends on the polo-like kinase Cdc5 and the meiosis-specific kinase Ime2, which is unleashed by the degradation of Spo13/Meikin upon activation of the anaphase-promoting complex at anaphase I. Meiotic plaques are finally assembled upon reactivation of Cdk1 at entry into metaphase II. This unblocking-activation mechanism ensures that only single-copy genomes are packaged into spores and might serve as a paradigm for the regulation of other meiosis II-specific processes., (© 2022 The Authors. Published under the terms of the CC BY 4.0 license.)

A 60-year-old woman was referred to our clinic for evaluation of her rapidly progressive dyspnea, and she had no previous history of heart disease. A murmur was noted on her examination, and transthoracic echocardiography was so difficult to be performed due to poor acoustic windows so she was referred to do a transesophageal echocardiography that showed an ostium primum atrial septal defect (ASD) with left-to-right shunt and a quadrileaflet mitral valve with severe regurgitation. Later on, she underwent surgery with ostium primum ASD closure by a patch and double cleft repair by suture after right heart catheterization., (© 2021 Wiley Periodicals LLC.)

Objective: Apelin is a novel adipocytokine with a significant role in ischemia/reperfusion injury that is synthesized and secreted in myocardial cells and coronary endothelium. There is debate on its value for the diagnosis and prognosis of myocardial infarction. We aimed to investigate plasma apelin level in patients with acute ST segment elevation (STEMI) and non-ST segment elevation (NSTEMI) myocardial infarction and its relationship with left ventricular function and prognostic parameters., Methods: Forty-one patients with STEMI, 21 patients with NSTEMI and 10 patients as control group with normal coronary angiograms were included. Plasma apelin level at presentation was investigated regarding its relationship with other diagnostic and prognostic parameters., Results: Apelin level was significantly higher in acute myocardial infarction (0.31 ± 0.56 ng/mL) compared to control group (0.08 ± 0.05 ng/mL) (p < 0.01). Likewise, it was found to be significantly higher in STEMI group (0.45 ± 0.73 ng/mL) compared to control group (0.08 ± 0.05 ng/mL) (p < 0.01). Although apelin was higher in NSTEMI group (0.13 ± 0.10 ng/mL) compared to control group (0.08 ± 0.05 ng/mL), this difference was not statistically significant (p > 0.05). No correlation was found between apelin and NT-proBNP, hsCRP, troponin, ejection fraction (EF) and Killip score (p > 0.05). A positive correlation was found between apelin and TIMI, GRACE and Gensini scores (p < 0.05). Only GRACE score was found to be correlated with apelin in MI groups., Conclusion: Apelin level was found to be high in acute myocardial infarction. With its inotropic and vasodilator effects, apelin was thought to have a protective role against severe ischemia., Competing Interests: Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2021.)

Following the outbreak of COVID-19 pandemic, governments around the globe coerced their citizens to adhere to preventive health behaviours, aiming to reduce the effective reproduction numbers of the virus. Driven by game theoretic considerations and inspired by the work of US National Research Council's Committee on Food Habits (1943) during WWII, and the post-WWII Yale Communication Research Program, the present research shows how to achieve enhanced adherence to health regulations without coercion. To this aim, we combine three elements: (i) indirect measurements, (ii) personalized interventions, and (iii) attitude changing treatments (IMPACT). We find that a cluster of short interventions, such as elaboration on possible consequences, induction of cognitive dissonance, addressing next of kin and similar others and receiving advice following severity judgements, improves individuals' health-preserving attitudes. We propose extending the use of IMPACT under closure periods and during the resumption of social and economic activities under COVID-19 pandemic, since efficient and lasting adherence should rely on personal attitudes rather than on coercion alone. Finally, we point to the opportunity of international cooperation generated by the pandemic., Competing Interests: All authors declare having no competing interests., (© 2020 The Authors.)

Background: Recent advances had allowed measurement of myocardial deformation parameters using 3D speckle-tracking echocardiography (STE). Agreement between these two modalities and interchangeability of findings remain as an issue since 2DSTE is more widely available than 3DSTE. The aim of this study was to investigate the correlation and agreement between 2DSTE and 3DSTE in healthy volunteers and in patients with mild mitral stenosis (MS)., Methods: Data from 31 patients with mild MS and 27 healthy volunteers were included in this study. Data were analyzed for the correlation and agreement between 2DSTE and 3DSTE for volumetric, strain, and rotational parameters., Results: There were no significant differences between 2DSTE and 3DSTE in both control and MS groups for left ventricular volumetric and rotational parameters. 3D global longitudinal strain (GLS) and global circumferential strain (GCS) were significantly higher in healthy volunteers (P < 0.001 for both), while only 3DGCS was significantly higher than 2DGCS in MS group (P < 0.001). The correlation between 3DSTE and 2DSTE was weak-to-moderate in both groups for strain and rotational parameters, and overall, correlation coefficients were higher in MS group. An exception was GLS in MS group, where coefficient of correlation was excellent (r = 0.907). Agreement between two modalities was poor for strain and rotational parameters, and the average bias was high., Conclusions: Overall, the agreement between 2DSTE and 3DSTE for strain and rotational measures was poor with a high average bias. The agreement between 2DSTE and 3DSTE is affected by the presence of underlying MS and the direction of strain., (© 2019 Wiley Periodicals, Inc.)

Cells undergoing meiosis produce haploid gametes through one round of DNA replication followed by 2 rounds of chromosome segregation. This requires that cohesin complexes, which establish sister chromatid cohesion during S phase, are removed in a stepwise manner. At meiosis I, the separase protease triggers the segregation of homologous chromosomes by cleaving cohesin's Rec8 subunit on chromosome arms. Cohesin persists at centromeres because the PP2A phosphatase, recruited by the shugoshin protein, dephosphorylates Rec8 and thereby protects it from cleavage. While chromatids disjoin upon cleavage of centromeric Rec8 at meiosis II, it was unclear how and when centromeric Rec8 is liberated from its protector PP2A. One proposal is that bipolar spindle forces separate PP2A from Rec8 as cells enter metaphase II. We show here that sister centromere biorientation is not sufficient to "deprotect" Rec8 at meiosis II in yeast. Instead, our data suggest that the ubiquitin-ligase APC/C Cdc20 removes PP2A from centromeres by targeting for degradation the shugoshin Sgo1 and the kinase Mps1. This implies that Rec8 remains protected until entry into anaphase II when it is phosphorylated concurrently with the activation of separase. Here, we provide further support for this model and speculate on its relevance to mammalian oocytes.

Meiosis consists of DNA replication followed by two consecutive nuclear divisions and gametogenesis or spore formation. While meiosis I has been studied extensively, less is known about the regulation of meiosis II. Here we show that Hrr25, the conserved casein kinase 1δ of budding yeast, links three mutually independent key processes of meiosis II. First, Hrr25 induces nuclear division by priming centromeric cohesin for cleavage by separase. Hrr25 simultaneously phosphorylates Rec8, the cleavable subunit of cohesin, and removes from centromeres the cohesin protector composed of shugoshin and the phosphatase PP2A. Second, Hrr25 initiates the sporulation program by inducing the synthesis of membranes that engulf the emerging nuclei at anaphase II. Third, Hrr25 mediates exit from meiosis II by activating pathways that trigger the destruction of M-phase-promoting kinases. Thus, Hrr25 synchronizes formation of the single-copy genome with gamete differentiation and termination of meiosis., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: The biochemical analysis of pericardial fluid for differentiating transudate from exudate is often ordered and interpreted according to the criteria extrapolated from pleural effusions. However, the validity of this discrimination when applied to pericardial effusion is under question., Methods: Patients who underwent pericardiocentesis between January 2004 and February 2014 were identified. Among them, 216 had essential medical records available and constituted the study population. The parameters specifically analyzed were the following: lactate dehydrogenase, total protein and glucose concentrations in both pericardial fluid and serum; pericardial fluid/serum ratios of lactate dehydrogenase and total protein content; and pH and specific gravity of pericardial fluid., Results: Eighty-one percent of pericardial effusions were classified as exudate according to Light's criteria. Both exudate and transudate fluid characteristics were possible for all etiological causes except for tuberculosis in which all were exudates. Although multiple cutoff points for all parameters were tested, significant overlap between different causes persisted (all having an area under the receiver operating characteristic curve of < 0.7). Thus, a reasonable accuracy to differentiate one cause from another could not be achieved., Conclusions: Although often ordered, the biochemical analysis of pericardial fluid has almost no diagnostic value to distinguish among causes of pericardial effusion in contemporary medicine.

Revealing the genetic changes responsible for antibiotic resistance can be critical for developing novel antibiotic therapies. However, systematic studies correlating genotype to phenotype in the context of antibiotic resistance have been missing. In order to fill in this gap, we evolved 88 isogenic Escherichia coli populations against 22 antibiotics for 3 weeks. For every drug, two populations were evolved under strong selection and two populations were evolved under mild selection. By quantifying evolved populations' resistances against all 22 drugs, we constructed two separate cross-resistance networks for strongly and mildly selected populations. Subsequently, we sequenced representative colonies isolated from evolved populations for revealing the genetic basis for novel phenotypes. Bacterial populations that evolved resistance against antibiotics under strong selection acquired high levels of cross-resistance against several antibiotics, whereas other bacterial populations evolved under milder selection acquired relatively weaker cross-resistance. In addition, we found that strongly selected strains against aminoglycosides became more susceptible to five other drug classes compared with their wild-type ancestor as a result of a point mutation on TrkH, an ion transporter protein. Our findings suggest that selection strength is an important parameter contributing to the complexity of antibiotic resistance problem and use of high doses of antibiotics to clear infections has the potential to promote increase of cross-resistance in clinics., (© The Author 2014. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution.)

Background: There are several reports suggesting that admission hyperglycaemia increases the risk of contrast-induced acute kidney injury (CI-AKI). However, it is not clear whether there has been an association between long-standing poor glycaemic control and the incidence of CI-AKI. The purpose of this study was to examine the impact of poor glycaemic control or elevated glycosylated haemoglobin (HbA1c) on the incidence of CI-AKI in patients with type 2 diabetes mellitus (T2DM)., Methods: The present study prospectively enrolled 133 patients with T2DM undergoing elective coronary angiography (CAG) and/or intervention. All patients had an estimated glomerular filtration rate (eGFR) of ≥60 ml/min/1.73 m(2). Patients were divided into two groups: those with an optimal HbA1c (<7%) and those with an elevated HbA1c (≥7%). All had similar baseline characteristics and were hydrated appropriately. The outcome was assessed by the incidence of CI-AKI., Results: CI-AKI occurred in 2 of 41 patients (4.9%) with optimal HbA1c levels and 5 of 92 patients (5.4%) with elevated HbA1c levels (p = 0.89). The cutoff point of HbA1c was set at 6.5%, but no statistically significant difference between the two groups was observed [1 of 24 patients (4.1%) vs. 6 of 109 patients (5.5%), p = 0.79]. However, despite a high variability in the incidence of CI-AKI, there was no statistically significant difference between the two groups when varying CI-AKI definitions were considered., Conclusion: An elevated HbA1c level is not associated with a higher incidence of CI-AKI compared to optimal HbA1c levels in patients with T2DM (patients with an eGFR of ≥60 ml/min/1.73 m(2)) undergoing CAG and/or intervention.

Background: Efficacy of intravenous (IV) volume expansion in preventing contrast-induced acute kidney injury (CI-AKI) is well known. However, the role of oral hydration has not been well established. The aim of this work was to evaluate the efficacy of oral hydration in preventing CI-AKI., Methods: We prospectively randomized 225 patients undergoing coronary angiography and/or percutaneous coronary intervention in either oral hydration or IV hydration groups. Patients who have at least one of the high-risk factors for developing CI-AKI (advanced age, type 2 diabetes mellitus, anemia, hyperuricemia, a history of cardiac failure or systolic dysfunction) were included in the study. All patients had normal renal function or stage 1-2 chronic kidney disease. Patients in the oral hydration group were encouraged to drink unrestricted amounts of fluids freely whereas isotonic saline infusion was performed by the standard protocol in the IV hydration group., Results: CI-AKI occurred in 8/116 patients (6.9%) in the oral hydration group and 8/109 patients (7.3%) in the IV hydration group (p = 0.89). There was also no statistically significant difference between the two groups when different CI-AKI definitions were taken into account., Conclusion: Oral hydration is as effective as IV hydration in preventing CI-AKI in patients with normal kidney function or stage 1-2 chronic kidney disease, and who also have at least one of the other high-risk factors for developing CI-AKI., (© 2014 S. Karger AG, Basel.)

Aorta to pulmonary artery fistula is an uncommon and potentially fatal condition. This case is of a 48-year-old Caucasian male with congestive heart failure and multiple aortic valve replacement surgeries who presented with an acquired ascending aortic aneurysm to pulmonary artery fistula diagnosed using two-dimensional transthoracic echocardiography via nonstandard imaging windows. Three-dimensional transthoracic echocardiography using live/real time three-dimensional color Doppler was used to assess the size of the opening of the fistula, providing additional value. This patient was surgically managed and is doing well 8 months postoperation., (© 2013, Wiley Periodicals, Inc.)

Objectives: Prolonged lamivudine treatment in adults has been shown to improve hepatitis B e (HBe) seroconversion rates in patients with chronic hepatitis B. This prospective open study reports the results of prolonged lamivudine treatment in a group of children with chronic hepatitis B., Patients and Methods: Twenty-two children and adolescents age 13.2 years (range, 9.5-18 years), who have been treated with lamivudine for 1 year, continued treatment with lamivudine (3 mg/kg/day, up to 100 mg/d) as long as there was evidence of continued biochemical and virological benefit compared with baseline. We evaluated virological and biochemical responses, the occurrence of YMDD mutants and adverse effects during 4 years of follow-up., Results: After 4 years on lamivudine, only 4 patients (18%) underwent HBe seroconversion. In addition, in 3 patients (13%), the treatment was stopped when lamivudine's lack of efficacy became evident. During the 4-year study period, we recorded a continuing decline in the participants' number, mostly because of lack of compliance with treatment (9/22, 41%). Only 5 children were still receiving lamivudine and showing benefit after 4 years. In 2 children, treatment termination and YMDD mutant emergence were associated with hepatitis flare. Besides subclinical elevation of creatine phosphokinase, no other adverse events were recorded during the study period., Conclusions: Four years after starting lamivudine treatment, most children from this study were off lamivudine, mainly because of lack of compliance and poor HBe seroconversion. These findings suggest that continuing treatment with lamivudine for undefined periods is hard to implement and does not improve HBe seroconversion.