Sociodemographic and clinical risk factors associated with in-hospital tuberculosis mortality in Türkiye, 2008-2018.

Introduction: Tuberculosis (TB) is an infectious disease that can be fatal if left untreated or poorly treated, and it is associated with many morbidities. Deaths may provide better understanding of the associated factors and help guide interventions to reduce mortality. In this study, it was aimed to reveal some of the features that predict hospital mortality in patients with TB and to present some alarming findings for clinicians. Materials and Methods: Patients who had been hospitalized with the diagnosis of TB between January 2008 and December 2018 were included and analyzed retrospectively. In-hospital mortality because of any TB disease after the initiation of treatment in patients admitted to the TB Ward and the primary cause of mortality were taken as endpoint. Result: A total of 1321 patients with a mean age of 50.1 years were examined. Total mortality was 39.4% (521 deaths) and 13.1% were in-hospital deaths (173 deaths). Of the deaths, 61.8% (n= 107) occurred during the first month after TB treatment were started. On univariate analysis, age over 48.5 years, Charlson comorbidity index, extension of radiological involvement, hypoalbuminemia and lymphopenia were most predictive variables with higher odds ratios (respectively, p<0.001 for all). Conclusions: In-hospital tuberculosis disease mortality is related with older age, cavitary or extensive pulmonary involvement, low albumin levels, unemployment, cigarette smoking and especially those with concomitant malignancy and chronic pulmonary disease.

Electrochemical neuron-specific enolase (NSE) immunosensor based on CoFe2O4@Ag nanocomposite and AuNPs@MoS2/rGO.

Small cell lung cancer (SCLC) is highly associated with the risk of early metastasis. Neuron-specific enolase (NSE), a biomarker of SCLC, is directly related to tumor burden and early diagnosis. This biomarker exists in nerve tissue and neuroendocrine tissue. In this study, an electrochemical NSE immunosensor based on gold nanoparticles modified molybdenum disulfide and reduced graphene oxide (AuNPs@MoS2/rGO) as the electrode platform and CoFe2O4@Ag nanocomposite as the signal amplification was developed. The immobilization of anti-NSE capture antibody was successfully performed on AuNPs@MoS2/rGO modified electrode surface by amino-gold affinity and the conjugation of anti-NSE secondary antibody on CoFe2O4@Ag nanocomposite was successfully completed by the strong esterification reaction. The final immunosensor was designed by the specific interactions of electrode platform and signal amplification. The fabricated nanocomposites and electrochemical immunosensor were characterized by both physicochemical characterization techniques including transmission electron microscopy (TEM), scanning electron microscopy (SEM), x-ray diffraction (XRD), x-ray photoelectron spectroscopy (XPS), fourier transform infrared spectroscopy (FTIR), and electrochemical methods such as cyclic voltammetry (CV), square wave voltammetry (SWV), and electrochemical impedance spectroscopy (EIS). The quantification limit (LOQ) and the determination limit (LOD) were computed to be 0.01 pg mL-1 and 3.00 fg mL-1, respectively. In brief, it can be speculated that the constructed electrochemical NSE immunosensor can be successfully utilized in the early diagnosis for lung cancer.

A green and sensitive guanine-based DNA biosensor for idarubicin anticancer monitoring in biological samples: A simple and fast strategy for control of health quality in chemotherapy procedure confirmed by docking investigation.

Drug efficiency can be considerably boosted while adverse effects can be reduced by precisely monitoring the concentration of anti-cancer drugs. Thus, one of the most important parameters for human health is the monitoring and detection of anticancer drugs during chemotherapy treatment. Herein, a glassy carbon electrode (GCE) was modified by Pt- and Pd-incorporated ZnO nanoparticles-decorated single-wall carbon nanotubes (Pt-Pd-ZnO/SWCNTs) nanocomposites, and ds-DNA (Calf Thymus) that was a biological recognition element, and it was aimed to be utilized as an ultrasensitive and effective electroanalytical biosensor for idarubicin (IDR) monitoring. Various physicochemical characterization techniques including transmission electron microscopy (TEM), field-emission scanning electron microscopy (FE-SEM) with energy-dispersive X-ray spectroscopy (EDS) were used to investigate the morphology and structure of the Pt-Pd-ZnO/SWCNTs nanocomposite, which was produced via straightforward chemical precipitation combined with the one-pot method. The layer-by-layer modification technique was implemented to fabricate the ds-DNA/Pt-Pd-ZnO/SWCNTs/GCE to be further utilized as a voltammetric sensor for sensitive monitoring of idarubicin in biological fluids and pharmaceutical substances. The electroanalytical method implemented to detect idarubicin was based to detect the ds-DNA's guanine base signal on the surface of the modified electrode in the absence and presence of the anticancer drug. The results explicated that the developed biosensor performed well in determining idarubicin in concentrations ranging from 1.0 nM to 65 µM, with a detection limit of 0.8 nM. The idarubicin detection ability of the modified electrode in real samples was evaluated, and the recovery data was acquired in the range of 98.0% and 104.75%. In the final step, the preferential intercalative binding mode of idarubicin drug with ds-DNA was approved by molecular docking study. This study paves the way for engineering highly sensitive DNA biosensors to be employed in the monitoring of anticancer drugs by combining the benefits of nanocomposites and valuable information of a molecular docking study.

A molecularly imprinted electrochemical biosensor based on hierarchical Ti2Nb10O29 (TNO) for glucose detection.

A novel molecularly imprinted electrochemical biosensor for glucose detection is reported based on a hierarchical N-rich carbon conductive-coated TNO structure (TNO@NC). Firstly, TNO@NC was fabricated by a novel polypyrrole-chemical vapor deposition (PPy-CVD) method with minimal waste generation. Afterward, the electrode modification with TNO@NC was performed by dropping TNO@NC particles on glassy carbon electrode surfaces by infrared heat lamp. Finally, the glucose-imprinted electrochemical biosensor was developed in presence of 75.0 mM pyrrole and 25.0 mM glucose in a potential range from + 0.20 to + 1.20 V versus Ag/AgCl via cyclic voltammetry (CV). The physicochemical and electrochemical characterizations of the fabricated molecularly imprinted biosensor was conducted by transmission electron microscopy (TEM), scanning electron microscopy (SEM), X-ray diffraction (XRD) method, X-ray photoelectron spectroscopy (XPS), electrochemical impedance spectroscopy (EIS), and CV techniques. The findings demonstrated that selective, sensitive, and stable electrochemical signals were proportional to different glucose concentrations, and the sensitivity of molecularly imprinted electrochemical biosensor for glucose detection was estimated to be 18.93 µA µM-1 cm-2 (R2 = 0.99) at + 0.30 V with the limit of detection (LOD) of 1.0 × 10-6 M. Hence, it can be speculated that the fabricated glucose-imprinted biosensor may be used in a multitude of areas, including public health and food quality.

Disseminated tuberculosis infection and paradoxical reaction during antimycobacterial treatment related to TNF-alpha blocker agent Infliximab.

Tumor necrosis factor (TNF)-alpha inhibitors play an important role in the treatment of immun-mediated diseases such as Crohn's disease. But they also have been related to increased risk for disseminated Mycobacterium tuberculosis infections and paradoxical response to antimycobacterial treatment. Here we report a disseminated tuberculosis case and a paradoxical response to treatment after receiving TNF-inhibitor agent Infliximab for Crohn's disease. The patient had a severe clinical condition before the antimycobacterial treatment and although proper treatment was initiated his radiological findings were worsened one month after initiation of the treatment. All control microbologic tests for secondary infections were negative and this situation was accepted as a paradoxical response to antimycobacterial treatment and treatment was continued with the same regimen. At the end of the second month of the treatment, most of the symptoms disappeared and chest radiograph findings were better than the previous one. In conclusion, TNF-alpha inhibitor therapy increases risk of mycobacterial infections and patients should be examined carefully about tuberculosis before starting this therapy. Also, it is important for physicians to recognize and know how to manage paradoxical response related to TNF-alpha inhibitors during anti-tuberculosis treatment.