(Benzoato-κ2 O,O′)(quinoline-2-carboxyl­ato-κ2 N,O)(quinoline-2-carboxylic acid-κ2 N,O)manganese(II)

The crystal structure of the title compound, [Mn(C7H5O2)(C10H6NO2)(C10H7NO2)], contains manganese(II) ions six-coordinated in a distorted octa­hedral environment. The equatorial plane is occupied by four O atoms, two from the carboxyl­ate group of the benzoate ion, the other two from carboxyl­ate/carboxyl groups of the quinaldate/quinaldic acid mol­ecules. The axial positions are occupied by the N atoms of the quinoline ring systems. The metal ion lies on a twofold rotation axis that bisects the benzoate ligand; the quinaldate and quinaldic acid ligands are therefore equivalent by symmetry, and the carboxylate/carboxyl groups are disordered. The complexes are joined together by hydrogen bonds between the carboxyl­ate/carboxyl groups of adjacent quinaldate/quinaldic acid mol­ecules, forming zigzag chains that run along the c axis

Wettability and reactivity of ZrB2 substrates with liquid Al

Wetting characteristics of the Al/ZrB2 system were experimentally determined by the sessile drop method with application of separate heating of the ZrB2 and Al samples and combined with in situ cleaning of Al drop from native oxide film directly in vacuum chamber. The tests were performed in ultrahigh vacuum of 10−6 mbar at temperatures 710, 800, and 900 °C as well as in flowing inert gas (Ar) atmosphere at 1400 °C. The results evidenced that liquid Al does not wet ZrB2 substrate at 710 and 800 °C, forming high contact angles (θ) of 128° and 120°, respectively. At 900 °C, wetting phenomenon (θ < 90°) occurs in 29th minute and the contact angle decreases monotonically to the final value of 80°. At 1400 °C, wetting takes place immediately after drop deposition with a fast decrease in the contact angle to 76°. The solidified Al/ZrB2 couples were studied by scanning and transmission electron microscopy coupled with x-ray energy diffraction spectroscopy. Structural characterization revealed that only in the Al/ZrB2 couple produced at the highest temperature of 1400 °C new phases (Al3Zr, AlB2 and α-Al2O3) were formed

Bis[(2-quinol­yl)methane­diol-κ2 N,O](sulfato-κO)copper(II) dihydrate

In the title compound, [Cu(SO4)(C10H9NO2)2]·2H2O, the CuII ion is chelated by two (2-quinol­yl)methane­diol ligands and coordinated by a monodentate sulfate ligand in a distorted trigonal–bipyramidal environment, with O atoms occupying the equatorial sites and N atoms in the axial sites. The dihedral angle between the two essentially planar quinoline ring systems is 45.02 (9)°. In the crystal structure, an extensive O—H⋯O hydrogen-bonding network forms layers parallel to the ab plane

(Benzoato-κ2 O,O′)(quinoline-2-carboxyl­ato-κ2 N,O)(quinoline-2-carboxylic acid-κ2 N,O)copper(II)

The crystal structure of the title compound, [Cu(C10H6NO2)(C7H5O2)(C10H7NO2)], contains copper(II) ions five-coordinated in a distorted trigonal-bipyramidal environment. The equatorial plane is occupied by three O atoms, one from the carboxyl­ate group of the benzoate ion considered as occupying a single coordination site, the other two from two carboxyl­ate groups of the quinaldic acid and quinaldate ligands. The axial positions are occupied by the N atoms of the quinoline ring system. The metal ion lies on a twofold axis that bisects the benzoate ion. The quinaldate and quinaldic acid ligands are equivalent by symmetry, and the carboxyl­ate/carboxyl groups are disordered. The disordered H atom is shared between the carboxyl­ate groups of adjacent quinaldic acid mol­ecules. Such hydrogen bonds delineate zigzag chains that run along the c axis. The structure is very similar to that of the MnII analog

Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development

Glutathione is the most abundant thiol in the vast majority of organisms and is maintained in its reduced form by the flavoenzyme glutathione reductase. In this work, we describe the genetic and functional analysis of the Caenorhabditis elegans gsr-1 gene that encodes the only glutathione reductase protein in this model organism. By using green fluorescent protein reporters we demonstrate that gsr-1 produces two GSR-1 isoforms, one located in the cytoplasm and one in the mitochondria. gsr-1 loss of function mutants display a fully penetrant embryonic lethal phenotype characterized by a progressive and robust cell division delay accompanied by an aberrant distribution of interphasic chromatin in the periphery of the cell nucleus. Maternally expressed GSR-1 is sufficient to support embryonic development but these animals are short-lived, sensitized to chemical stress and have increased mitochondrial fragmentation and lower mitochondrial DNA content. Furthermore, the embryonic lethality of gsr-1 worms is prevented by restoring GSR-1 activity in the cytoplasm but not in mitochondria. Given the fact that the thioredoxin redox systems are dispensable in C. elegans, our data support a prominent role of the glutathione reductase/glutathione pathway in maintaining redox homeostasis in the nematode

Changes in Phospholipid Composition Studied by HPLC and Electric Properties of Liver Cell Membrane of Ethanol-Poisoned Rats

Ethanol introduced into the organism undergoes rapid metabolism to acetaldehyde and then to acetic acid. The process is accompanied by formation of reactive oxygen species (ROS), which damage mainly lipids of membrane cells. The effects of ROS can be neutralized by administering preparations with antioxidant properties. The natural preparations of this kind are teas

DNA damage in circulating leukocytes measured with the comet assay may predict the risk of death

The comet assay or single cell gel electrophoresis, is the most common method used to measure strand breaks and a variety of other DNA lesions in human populations. To estimate the risk of overall mortality, mortality by cause, and cancer incidence associated to DNA damage, a cohort of 2,403 healthy individuals (25,978 person-years) screened in 16 laboratories using the comet assay between 1996 and 2016 was followed-up. Kaplan-Meier analysis indicated a worse overall survival in the medium and high tertile of DNA damage (p < 0.001). The effect of DNA damage on survival was modelled according to Cox proportional hazard regression model. The adjusted hazard ratio (HR) was 1.42 (1.06-1.90) for overall mortality, and 1.94 (1.04-3.59) for diseases of the circulatory system in subjects with the highest tertile of DNA damage. The findings of this study provide epidemiological evidence encouraging the implementation of the comet assay in preventive strategies for non-communicable diseases

Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.

Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability

Frequency of micronuclei in reticulocytes of Male mice expose to bisphenol A and a combination of X-rays and bisphenol A

Celem pracy było zbadanie wpływu bisfenolu A oraz skojarzonego działania promieniowania X i bisfenolu A na indukcję mikrojąder w retikulocytach krwi obwodowej i szpiku kostnego samców myszy. Myszy Pzh:Sfis przez 2 tygodnie napromieniano promieniowaniem X (0,05 Gy i 0,10 Gy) lub podawano im bisfenol A (5 mg/kg mc, 10 mg/kg mc, 15 mg/kg mc, 20 mg/ kg mc, 40 mg/kg mc) lub poddawano skojarzonemu działaniu obu czynników (0,05 Gy + 5 mg/kg mc BPA lub 0,10 Gy + 10 mg/kg mc BPA). Bisfenol A i promieniowanie X zastosowane osobno stymulowały powstawanie mikrojąder w retikulocytach szpiku kostnego i krwi obwodowej. Skojarzone działanie promieniowania X i bisfenolu A zwiększało częstość występowania mikrojąder w porównaniu do efektów notowanych w następstwie działania samego bisfenolu A. Niekiedy, szczególnie po zastosowaniu skojarzenia obu czynników w małych dawkach, efekty skojarzonego działania przewyższały również rezultaty uzyskane po działaniu samego promieniowania jonizującego. Promieniowanie jonizujące jest prawdopodobnie czynnikiem decydującym o pękaniu lub nierównomiernej dystrybucji chromosomów w wyniku skojarzonego działania z bisfenolem A, który jest słabszym mutagenem.The aim of the study was to estimate the effects of bisphenol A and combined exposure to X-rays and bisphenol A on the induction of micronuclei in the blood and bone marrow reticulocytes. Pzh:Sfis male mice were irradiated (0.05 Gy and 0.10 Gy) or/and treated with bisphenol A (5 mg/kg mc, 10 mg/kg mc, 15 mg/kg mc, 20 mg/kg mc, 40 mg/kg mc) or exposed to combination of both (0,05 Gy + 5 mg/kg mc BPA lub 0,10 Gy + 10 mg/kg mc BPA) for 2 weeks. Bisphenol A as well as ionizing radiation alone stimulated induction of micronuclei in peripheral blood and bone marrow reticulocytes. Combined exposure of X-rays and bisphenol A induced higher frequency of micronuclei compared to effect produced by BPA alone. Sometimes, especially after combined exposure to low doses of both agents, observed effects enhanced that obtained following exposure to X-rays alone. Ionising radiation is probably the agent which decided about damage and/or unequal distribution of chromosomes following combined exposure together with bisphenol A, which seems to be weak mutagen

THe influence of bisphenol A and of combined exposure to X-rays and bisphenol A to somatic cells of the bone marrow and liver of mice

Celem pracy było zbadanie wpływu bisfenolu A (BPA) i skojarzonego działania promieniowania X i BPA na komórki somatyczne szpiku kostnego i wątroby myszy. Samce myszy szczepu Pzh: Sfis przez 8 tygodni napromieniano dawką 0,05 Gy lub podawano im bisfenol A (5 mg/kg mc, 10 mg/kg mc, 20 mg/kg mc) albo poddawano skojarzonemu działaniu obu czynników (0,05 Gy + 5 mg/kg BPA). Próby pobierano po 24h, 1, 4 i 8 tygodniach po zakończeniu ekspozycji. Niniejsze badania wykazały, że BPA może indukować, mierzone testem kometowym, uszkodzenia DNA w limfocytach szpiku kostnego. Natomiast nie stwierdzono zmian w DNA w komórkach somatycznych wątroby. Po zastosowaniu obu czynników jednocześnie zaobserwowano w obu narządach większą migrację DNA niż po podaniu samego bisfenolu A. Prawdopodobnie promieniowanie X potęguje genotoksyczność BPA.The aim of study was to estimate the effects of bisphenol A (BPA) and combined exposure to X-rays and BPA to somatic cells of the bone marrow and liver of mice. Male mice Pzh: Sfis were irradiated with 0.05 Gy or treated with BPA (5 mg/kg mc, 10 mg/kg mc, 20 mg/kg mc) or exposed to a combination of both (0.05 Gy + 5 mg/kg BPA) for 8 weeks. Samples were taken at 24h, 1, 4 and 8 weeks after the end of exposure. Our study showed, that BPA can induce, measured by Comet assay, DNA damage in limphocytes of the bone marrow. The induction of DNA damage in somatic cells of the liver was not detected. After combined exposure to both agents a greater migration of DNA in cells of both organs than after the exposure to bisphenol A alone was observed. Probably the X-rays intensify the genotoxicity of BPA