Triflumizole

In the title compound {systematic name: 4-chloro-N-[1-(1H-imidazol-1-yl)-2-propoxyethyl­idene]-2-(trifluoro­meth­yl)aniline}, C15H15ClF3N3O, the dihedral angle between the aniline and imidazole ring planes is 81.80 (4)°. In the crystal structure, weak inter­molecular C—H⋯X (X = N, O or F) hydrogen bonds and C—H⋯π inter­actions help to consolidate the packing

Cases of ethical violation in research publications: through editorial decision making process

Purpose – To improve and strengthen existing publication and research ethics, KODISA has identified and presented various cases which have violated publication and research ethics and principles in recent years. The editorial office of KODISA has been providing and continues to provide advice and feedback on publication ethics to researchers during peer review and editorial decision making process. Providing advice and feedback on publication ethics will ensure researchers to have an opportunity to correct their mistakes or make appropriate decisions and avoid any violations in research ethics. The purpose of this paper is to identify different cases of ethical violation in research and inform and educate researchers to avoid any violations in publication and research ethics. Furthermore, this article will demonstrate how KODISA journals identify and penalize ethical violations and strengthens its publication ethics and practices. Research design, data and methodology – This paper examines different types of ethical violation in publication and research ethics. The paper identifies and analyzes all ethical violations in research and combines them into five general categories. Those five general types of ethical violations are thoroughly examined and discussed. Results – Ethical violations of research occur in various forms at regular intervals; in other words, unethical researchers tend to commit different types of ethical violations repeatedly at same time. The five categories of ethical violation in research are as follows: (1) Arbitrary changes or additions in author(s) happen frequently in thesis/dissertation related publications. (2) Self plagiarism, submitting same work or mixture of previous works with or without using proper citations, also occurs frequently, but the most common type of plagiarism is changing the statistical results and using them to present as the results of the empirical analysis; (3) Translation plagiarism, another ethical violation in publication, is difficult to detect but occurs frequently; (4) Fabrication of data or statistical analysis also occurs frequently. KODISA requires authors to submit the results of the empirical analysis of the paper (the output of the statistical program) to prevent this type of ethical violation; (5) Mashup or aggregator plagiarism, submitting a mix of several different works with or without proper citations without alterations, is very difficult to detect, and KODISA journals consider this type of plagiarism as the worst ethical violation. Conclusions – There are some individual cases of ethical violation in research and publication that could not be included in the five categories presented throughout the paper. KODISA and its editorial office should continue to develop, revise, and strengthen their publication ethics, to learn and share different ways to detect any ethical violations in research and publication, to train and educate its editorial members and researchers, and to analyze and share different cases of ethical violations with the scholarly community

Treatment of instability with scapular notching and glenoid component loosing by partial mixed different implant revision

In general, reverse shoulder arthroplasty revision is performed using the same implant for both the humerus and glenoid components. However, the authors of the present case used different implants from what was used previously for treating instability with scapular notching and glenoid aseptic loosening and report the case

Phyllo-poly[[μ2-1,4-bis­(cyclo­hexyl­sulfanylmeth­yl)benzene-κ2 S:S′](μ2-nitrato-κ2 O:O′)silver(I)]

The title compound, [Ag(NO3)(C20H30S2)]n, was synthesized by the reaction of silver nitrate and 1,4-bis­(cyclo­hexyl­thio­meth­yl)benzene (bctmb) in acetonitrile. The coordination polymer exhibits a two-dimensional layer structure. The layers are wave-like and parallel to the crystallographic ac plane; AgI ions are linked by the bctmb ligands and nitrate anions along the crystallographic a and c directions, respectively. In addition, the crystal structure is stabilized by C—H⋯O hydrogen bonds

Pirimicarb: 2-dimethylamino-5,6-dimethylpyrimidin-4-yl dimethyl­carbamate

In the title compound, C11H18N4O2 (systematic name: 2-dimethyl­amino-5,6-dimethyl­pyrimidin-4-yl N,N-dimethyl­carb­amate), the pyrimidine ring and dimethyl­amino group are almost in the same plane, making a dihedral angle of 1.6 (1)°. The dihedral angle between the mean plane of the pyrimidine ring and that of the dimethyl­carbamate group is 83.42 (5)°. In the crystal structure, inter­molecular C—H⋯O hydrogen bonds contribute to the stabilization of the packing

Methidathion: S-(5-meth­oxy-2-oxo-2,3-dihydro-1,3,4-thia­diazol-3-yl)methyl O,O-dimethyl phospho­rodithio­ate

The title compound, C6H11N2O4PS3, crystallizes with two independent mol­ecules in the asymmetric unit. The dihedral angles between the thia­diazole ring planes and the PS2 planes of the phospho­rodithio­ate group are 86.51 (5) and 56.33 (5)° in the two mol­ecules. In the crystal, weak inter­molecular S⋯S [3.570 (8) Å] inter­actions and C—H⋯O and C—H⋯N hydrogen bonds contribute to the stabilization of the packing

Optic Disc Pit with Peripapillary Retinoschisis Presenting as a Localized Retinal Nerve Fiber Layer Defect

A 59-year-old woman was referred to our clinic for a glaucoma evaluation. The visual acuity and intraocular pressure were normal in both eyes. However, red-free fundus photography in the left eye showed a superotemporal wedge-shaped retinal nerve fiber layer defect, and visual field testing showed a corresponding partial arcuate scotoma. In an optical coherence tomography examination, the macula was flat, but an arcuate-shaped peripapillary retinoschisis was found. Further, the retinoschisis seemed to be connected with a superotemporal optic pit shown in a disc photograph. After 3 months of a topical prostaglandin analogue medication, the intraocular pressure in the retinoschisis eye was lowered from 14 to 10 mmHg and the peripapillary retinoschisis was almost resolved. We report a rare case of an optic disc pit with peripapillary retinoschisis presenting as a localized retinal nerve fiber layer defect

Silibinin induces apoptosis via calpain-dependent AIF nuclear translocation in U87MG human glioma cell death

<p>Abstract</p> <p>Background</p> <p>Silibinin, a natural polyphenolic flavonoid, has been reported to induce cell death in various cancer cell types. However, the molecular mechanism is not clearly defined. Our previous study showed that silibinin induces glioma cell death and its effect was effectively prevented by calpain inhibitor. The present study was therefore undertaken to examine the role of calpain in the silibinin-induced glioma cell death.</p> <p>Methods</p> <p>U87MG cells were grown on well tissue culture plates and cell viability was measured by MTT assay. ROS generation and △ψ_mwere estimated using the fluorescence dyes. PKC activation and Bax expression were measured by Western blot analysis. AIF nuclear translocation was determined by Western blot and immunocytochemistry.</p> <p>Results</p> <p>Silibinin induced activation of calpain, which was blocked by EGTA and the calpain inhibitor Z-Leu-Leu-CHO. Silibinin caused ROS generation and its effect was inhibited by calpain inhibitor, the general PKC inhibitor GF 109203X, the specific PKC_δinhibitor rottlerin, and catalase. Silibinin-induce cell death was blocked by calpain inhibitor and PKC inhibitors. Silibinin-induced PKC_δactivation and disruption of △ψ_mwere prevented by the calpain inhibitor. Silibinin induced AIF nuclear translocation and its effect was prevented by calpain inhibitor. Transfection of vector expressing microRNA of AIF prevented the silibinin-induced cell death.</p> <p>Conclusions</p> <p>Silibinin induces apoptotic cell death through a calpain-dependent mechanism involving PKC, ROS, and AIF nuclear translocation in U87MG human glioma cells.</p