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In this article, a patient with intracranial mass which occurred during immunsupressive therapy because of renal transplantation was reported. The patient had concomitant central nervous system tuberculosis and primary central nervous system lymphoma. The patient, who had had renal transplantation performed, had increased complications of infectious disease, malignancies and atypic manifestations because of immunsupressive drugs. [ABSTRACT FROM AUTHOR]

Breast lymphomas are quite rare extranodal lymphomas. While they represent approximately 0.04-0.5% of the primary cancers of the breast, their prevalence is 0.38-0.7% among all lymphomas. Primary breast lymphomas are usually of B-cell phenotype. T-cell phenotype has been published in the literature as case reports. In this report, a 22-year-old female patient with breast mass is presented. Upon detection of primary T-cell lymphoma of the breast on biopsy, 4 courses of CHOP followed by radiotherapy was administered to the patient. The patient, who entered remission after treatment is under follow-up for approximately a year and is still in remission. A patient presenting with breast mass may have lymphoma and differentiation with breast masses should be made. [ABSTRACT FROM AUTHOR]

Copyright of Turkish Journal of Surgery / Ulusal Cerrahi Dergisi is the property of Turkish Surgery Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Turkish Journal of Oncology / Türk Onkoloji Dergisi is the property of KARE Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lytic phages control the timepoint of host cell lysis by timing the holin-mediated release of cell wall-degrading endolysins. In phage T4, the antiholin RI inhibits the holin T, thereby preventing the early release of the T4 endolysin and lysis. The antiholin achieves lysis inhibition (LIN) in response to phage superinfections, thereby increasing the chance for lysis in an environment with a lower phage concentration. The holin T consists of a small N-terminal cytoplasmic domain, a transmembrane helix, and a periplasmic C-terminal domain. The antiholin is targeted to the periplasm by a cleavable signal peptide. Recently, the periplasmic soluble domains of the holin and the antiholin were found to form T2/RI2 tetramers in crystals. To investigate the functional relevance of this complex, we reconstituted LIN in a phage-free system, using only RI, T, and endolysin, and combined targeted mutagenesis with functional analyses. Inactivation of the RI signal peptide cleavage site did not abolish LIN, indicating that RI can function in a membrane-bound state, which argued against the tetramer. This led to analyses showing that only one of the two T/RI interfaces in the tetramer is physiologically relevant, which is also the only interaction site predicted by AlphaFold2. Some holin mutations at this interaction site prevented lysis, suggesting that the RI interaction likely acts by blocking the holin oligomerization required for hole formation. We conclude that LIN is mediated by a dimeric T/RI complex that, unlike the tetramer, can be easily formed when both partners are membrane-anchored. [ABSTRACT FROM AUTHOR]

Copyright of Xinjiang Agricultural Sciences is the property of Xinjiang Agricultural Sciences Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Malaria can infect erythrocytes and hence cause different pathogenesis episodes leading to death mostly in pregnant women and children under the age of 5 years. The selective pressure of these parasites leads to the production of new human genetic diseases. The most prevalent genetic alterations in the human genome are thalassemia and hemoglobinopathies (Hb E, Hb S), which are recognized throughout the world, including Saudi Arabia. Methods: From May 2018 to August 2019, 13972 Saudi citizens from King Fahd Central Hospital and premarital facilities in the Saudi Arabian province of Jazan participated in this study. This study aims to compare the prevalence of Hb E and other hemoglobinopathies in positive versus negative cases of malaria. So, CBC, malaria test, Hb-electrophoresis, and molecular study were investigated. Result: For thalassemias and Hb disorders, 36% with abnormal Hb (47% of them) carried Hb S in their blood, 37% with α-thalassemia, 11% for β-thalassemia and 4% of Hb E. Significant variations in CBC parameters were observed in Hb E patients. There was significant decrease in MCV, MCH and MCHC and slightly increase in WBCs, RBCs, RDW and PLT as compared to controls. [ABSTRACT FROM AUTHOR]

The ribonuclease H (RNase H) active site of HIV-1 reverse transcriptase (RT) is the only viral enzyme not targeted by approved antiretroviral drugs. Using a fluorescence-based in vitro assay, we screened 65,239 compounds at a final concentration of 10 µM to identify inhibitors of RT RNase H activity. We identified 41 compounds that exhibited 50% inhibitory concentration (i.e., IC50) values < 1.0 µM. Two of these compounds, 2-(4-methyl-3-(piperidin-1-ylsulfonyl)phenyl)benzo[d]isothiazol-3(2H)-one (1) and ethyl 2-(2-(3-oxobenzo[d]isothiazol-2(3H)-yl)thiazol-4-yl)acetate (2), which both share the same benzisothiazolone pharmacophore, demonstrate robust antiviral activity (50% effective concentrations of 1.68 ± 0.94 µM and 2.68 ± 0.54, respectively) in the absence of cellular toxicity. A limited structure–activity relationship analysis identified two additional benzisothiazolone analogs, 2-methylbenzo[d]isothiazol-3(2H)-one (3) and N,N-diethyl-3-(3-oxobenzo[d]isothiazol-2(3H)-yl)benzenesulfonamide (4), which also resulted in the inhibition of RT RNase H activity and virus replication. Compounds 1, 2 and 4, but not 3, inhibited the DNA polymerase activity of RT (IC50 values~1 to 6 µM). In conclusion, benzisothiazolone derivatives represent a new class of multifunctional RT inhibitors that warrants further assessment for the treatment of HIV-1 infection. [ABSTRACT FROM AUTHOR]

Copyright of Boletín de la Sociedad Argentina de Botánica is the property of Sociedad Argentina de Botanica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: This study aimed to investigate whether a genetic-based algorithm derived from ACE (rs1799752) and ACTN3 (rs1815739) polymorphisms could be utilized to predict the magnitude of improvements in vertical jump performance following high-intensity resistance training. Methods: Twenty male professional footballers (age 18.7 ± 0.6 year; height 169.8 ± 2.7 cm, body mass 62.3 ± 6.0 kg) were recruited and allocated into "low" and "high" weighted total genotype score (TGS) groups based on the number of power/strength-associated ACE and ACTN3 polymorphisms. Explosive power of the lower limb was assessed by vertical jump test before and after an eight-week high-intensity resistance training. Results: The magnitude of improvement was found to be significantly different between the high and low TGS groups (p = 0.042; d = 0.98) with greater improvement being observed in the high TGS group (15.4%) as compared to the low TGS group (2.8%) following the resistance training intervention. Further stratification of the players into tertiles based on the percentage change score in vertical jump showed that a large proportion of footballers among the high responders belonged to the high TGS group (83.3%). Conclusions: In conclusion, this study showed the combined influence of ACE and ACTN3 polymorphisms on the magnitude of improvements in vertical jump performance following high-intensity resistance training. This finding may contribute towards the development of a more personalised resistance training regime that targets explosive power adaptations. [ABSTRACT FROM AUTHOR]

Copyright of Goya is the property of Fundacion Lazaro Galdiano and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background and Aim: Rheumatoid arthritis (RA) is a chronic autoimmune disorder primarily affecting the joints. Interleukin-10 (IL-10) is an important immunoregulatory cytokine involved in regulating the immune response and inflammation. Polymorphism in the promoter region of the IL-10 can affect the expression of the gene. This study aims to investigate the association of human IL-10 rs1800896 (-1082 A/G), rs1800871 (-824 C/T), and rs1800872 (-597 C/A) promoter single nucleotide polymorphisms (SNPs) with susceptibility to RA in the Iraqi women population. Methods: Here, 280 RA female patients who referred to the AL-Hussein Teaching Hospital in Karbala, Iraq between November 2022 to April 2023, and 120 healthy agematched subjects were examined. The two groups were genotyped for rs1800896, rs1800871, and rs1800872 by tetra-primer ARMS--PCR. Statistical analyses were performed using IBM SPSS windows version 25 Results: All the genotypes did not deviate from Hardy-Weinberg Equilibrium (HWE) expectations in both groups. No positive association was found between allele and genotype frequencies of three SNPs and the incidence of rheumatoid arthritis (all p>0.05). Only the ACC haplotype showed an association with disease susceptibility (pvalue= 0.0004). Conclusion: Based on the results, promoter SNPs of the IL-10 gene cannot be used as a suitable marker to determine the susceptibility to rheumatoid arthritis in the Iraqi women population and to prevent its progression. [ABSTRACT FROM AUTHOR]

Simple Summary: DNA polymerases are essential enzymes for the growth and survival of a cell. These enzymes replicate and/or repair the cellular genome. Some DNA polymerases have been associated with specific diseases. For example, Y-family DNA polymerases have been associated with cancer. Family A polymerases (typified by E. coli DNA polymerase I) have been extensively studied, primarily to understand the mechanism of DNA replication. Human mitochondrial DNA polymerase γ and DNA polymerase θ are exceptions as they have roles in genetic diseases and cancer, respectively. However, recent studies have uncovered novel roles of Family A polymerases. Thus, polymerase θ has been shown to conduct reverse transcriptase activity, an activity displayed by retroviruses' (such as HIV) reverse transcriptases. The association of these polymerases with diseases makes them attractive therapeutic targets against diseases such as cancer and bacterial/parasitic infections. This perspective is focused on Family A polymerases as potential therapeutic targets for the development of new classes of antibiotics, antimalarial, and anticancer drugs. These new drugs could be used either alone or in combination with current interventions to circumvent drug-resistance. Modern techniques, such as artificial intelligence and docking of millions of drug-like compounds, can expedite the discovery of new interventions targeting Family A polymerases. DNA polymerases replicate cellular genomes and/or participate in the maintenance of genome integrity. DNA polymerases sharing high sequence homology with E. coli DNA polymerase I (pol I) have been grouped in Family A. Pol I participates in Okazaki fragment maturation and in bacterial genome repair. Since its discovery in 1956, pol I has been extensively studied, primarily to gain deeper insights into the mechanism of DNA replication. As research on DNA polymerases advances, many novel functions of this group of polymerases are being uncovered. For example, human DNA polymerase θ (a Family A DNA pol) has been shown to synthesize DNA using RNA as a template, a function typically attributed to retroviral reverse transcriptase. Increased interest in drug discovery against pol θ has emerged due to its roles in cancer. Likewise, Pol I family enzymes also appear attractive as drug-development targets against microbial infections. Development of antimalarial compounds targeting apicoplast apPOL, an ortholog of Pol I, further extends the targeting of this family of enzymes. Here, we summarize reported drug-development efforts against Family A polymerases and future perspective regarding these enzymes as antibiotic targets. Recently developed techniques, such as artificial intelligence, can be used to facilitate the development of new drugs. [ABSTRACT FROM AUTHOR]

Neutrophil-lymphocyte (NLR), platelet-lymphocyte (PLR), eosinophil-lymphocyte (ELR), and monocyte-lymphocyte (MLR) ratios are systemic inflammatory markers related to myocardial infarction. The aim of this study is to investigate the association of Src homology 2-B adapter protein 3 (SH2B3) C784 T and methylenetetrahydrofolate reductase (MTHFR) C677 T polymorphisms (SNP) with systemic inflammatory markers and the severity of coronary artery disease (CAD) in 150 ST-elevation myocardial infarction (STEMI) patients. Single nucleotide polymorphisms were genotyped using the tetra-primer amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR) method. The inflammatory markers were calculated. An interventional cardiologist blinded to other data assessed the SYNTAX (SX) Score. Eosinophil and platelet counts were significantly higher in SH2B3 variants than in the wild type. Additionally, SH2B3 variants had significantly higher ELR than the wild type (.12 ±.19 vs.25 ±.34, p =.018). NLR, PLR, ELR, and MLR were considerably higher in MTHFR variants than in the wild type (p <.05). The SX score was significantly higher in both SH2B3 C784 T (21.24 ± 8.90 vs 15.29 ± 9.40, p =.00) and MTHFR C677 T (20.34 ± 10.21 vs 16.08 ± 8.39, p =.00) variants when compared with wild type. In conclusion, these polymorphisms are associated with several markers of systemic inflammation as well as the severity of CAD. [ABSTRACT FROM AUTHOR]

Copyright of Journal for the Critique of Science, Imagination & New Anthropology / Časopis za Kritko Znanosti, Domišljijo in Novo Antropologijo is the property of Institute for the Critique of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Turkish Journal of Geriatrics / Türk Geriatri Dergisi is the property of Turkish Geriatrics Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Fragment-based screening methods can be used to discover novel active site or allosteric inhibitors for therapeutic intervention. Using saturation transfer difference (STD) NMR and in vitro activity assays, we have identified fragment-sized inhibitors of HIV-1 reverse transcriptase (RT) with distinct chemical scaffolds and mechanisms compared to nonnucleoside RT inhibitors (NNRTIs) and nucleoside/ nucleotide RT inhibitors (NRTIs). Three compounds were found to inhibit RNA- and DNA-dependent DNA polymerase activity of HIV-1 RT in the micromolar range while retaining potency against RT variants carrying one of three major NNRTI resistance mutations: K103N, Y181C, or G190A. These compounds also inhibit Moloney murine leukemia virus RT but not the Klenow fragment of Escherichia coli DNA polymerase I. Steady-state kinetic analyses demonstrate that one of these fragments is a competitive inhibitor of HIV-1 RT with respect to deoxyribonucleoside triphosphate (dNTP) substrate, whereas a second compound is a competitive inhibitor of RT polymerase activity with respect to the DNA template/primer (T/P), and consequently also inhibits RNase H activity. The dNTP competing RT inhibitor retains activity against the NRTI-resistant mutants K65R and M184V, demonstrating a drug resistance profile distinct from the nucleotide competing RT inhibitors indolopyridone-1 (INDOPY-1) and 4-dimethylamino- 6-vinylpyrimidine-1 (DAVP-1). In antiviral assays, the T/P competing compound inhibits HIV-1 replication at a step consistent with an RT inhibitor. Screening of additional structurally related compounds to the three fragments led to the discovery of molecules with improved potency against HIV-1 RT. These fragment inhibitors represent previously unidentified scaffolds for development of novel drugs for HIV- 1 prevention or treatment. [ABSTRACT FROM AUTHOR]

Rice (Oryza sativa L.) is one of themost important crops around theworld. MATERIALS AND METHODS Plant materials Two Egyptian rice cultivars(Oryza sativa L.), Giza 179 and Sakha 101were obtained from the, Rice Department,Field Crops Research Institute (FCRI),Agriculture Research Center (ARC), Giza,Egypt. Differential display polymerasechain reaction (DD-PCR) All DNA primers used in PCR reactions(Table 1) were purchased fromOperon Molecular for Life (Germany). SCP4-4 did not show any significanthomology to known sequence neitherin blast N nor blast X database.SAP3-1 fragment The expression of SAP3-1 wasfound to be up regulated by droughttreatment in Egyptian G179 rice cultivar,but did not appear in SK101 rice cultivar. [Extracted from the article]

Background: Diabetic retinopathy (DR) is expanding to epidemic levels globally due to the progressing prevalence of diabetes mellitus (DM). In this study, the association between factor V Leiden (FVL), MTHFRC677T, and FXIIIVal34Leu polymorphisms and diabetic retinopathy was investigated in Eastern Iran. Methods: This case-control study enlisted the participation of 300 people (diabetic patients=100, diabetic retinopathy patients=100, healthy controls=100), and polymorphisms were examined by Tetra primer ARMS-PCR. Results: The frequency of FVL (p=0.294) and FXIIIVal34Leu (P=0.349) polymorphism showed no significant results between the genotype frequency in the mentioned groups. In contrast, MTHFRC677T SNP was significantly different in diabetic patients and controls (P=0.008). The MTHFRC677T polymorphism was found to be connected with increased systolic blood pressure in patients who had the TT genotype (130.96±11.92mm/Hg; P=0.011). Conclusion: Our study recommended that the MTHFRC677T polymorphism may offer to DR development. Studies with larger sample sizes and a wider spectrum of populations are authorized to verify this finding. [ABSTRACT FROM AUTHOR]