The relationship of Helicobacter pylori positivity with age, sex, and ABO/Rhesus blood groups in patients with gastrointestinal complaints in Turkey

BACKGROUND: To determine the magnitude of Helicobacter pylori infection in patients with gastrointestinal complaints in Turkey. METHODS: We studied 1680 patients with variable gastrointestinal complaints. The H. pylori infection status was determined using C-14 urea breath test (UBT). Overall, 1567 patients (548 male, 1019 female; age range 4-80 years, mean 29.37 +/- 17.30 years) were included in this study. The relationship between H. pylori positivity and age, sex, sociodemographic characteristic, blood groups, and gastrointestinal diagnosis was determined. RESULTS: H. pylori positivity was found to be 68%. The difference in positivity rates between age groups 4-9 years and other groups was statistically significant (p = .001). H. pylori positivity was 67.7% in males and 68.2% in females (p = .865). H. pylori positivity was 72.1, 65.1, 70, and 68.4% in blood groups A, B, AB, and O (p = .703), and 68.9% and 76.3% in Rh (+) and Rh (-) blood subgroups, respectively (p = .292). There was no statistically significant difference between H. pylori positivity and gastrointestinal diagnosis (p = .980). There was significant association between increased number of household members and low socioeconomic status, and H. pylori positivity (p < .001). Living in rural and suburban area was significantly associated with H. pylori positivity compared with living in urban. CONCLUSIONS: H. pylori infection positivity rate was 68% in symptomatic subjects in Turkey and the positivity rate was significantly lower at age 4-9 years than the other age groups. It was not related to gender, ABO, and Rh blood groups and gastrointestinal diagnosis. Low socioeconomic conditions and living in rural and suburban area were significantly associated with H. pylori positivity.     

DNA adducts in human placenta exposed to ambient environment and passive cigarette smoke during pregnancy

BACKGROUND: The risk of human diseases and abnormal development under the relatively reduced toxic environmental exposure conditions of passive cigarette smoke and urban pollution is emerging as significant. To assess the genotoxic potential of such exposure, we analyzed the DNA adducts of polynuclear aromatic hydrocarbons (PAH), a proven marker of genotoxicity, in human placental DNA samples of pregnancies monitored for passive cigarette smoke exposure. METHODS: Maternal exposure to active and passive cigarette smoke was evaluated by verbal disclosure and urinary nicotine and cotinine measurements. PAH-DNA adducts were assayed by ELISA using a polyclonal antibody against benzo[alpha]pyrene-diol-epoxide-DNA in placental DNA. Birth weights of infants were recorded in these monitored pregnancies. RESULTS: Urinary nicotine and cotinine values were reduced in the passive smoke-exposed group compared to smokers and similar to those in the nonsmoker ambient exposure group. PAH-DNA and nicotine/cotinine values were not correlated with birth weight of the infant. PAH-DNA adducts were present in approximately 25% of samples exposed to passive cigarette smoke and ambient environment. CONCLUSIONS: The study has revealed that a subpopulation of humans is predisposed to accumulating PAH adducts independent of high levels of PAH sources (e.g., maternal cigarette smoke exposure). Because DNA adducts promote genomic changes, it is likely that this subpopulation is susceptible to diverse changes in the genome that may influence human development.     

Diagnostic performance of lactate dehydrogenase (LDH) isoenzymes levels for the severity of COVID-19

BackgroundLactate dehydrogenase (LDH) levels predict coronavirus disease 2019 (COVID-19) severity. We investigated LDH isoenzyme levels to identify the tissue responsible for serum LDH elevation in patients with COVID-19.MethodsHospitalised COVID-19 patients with serum LDH levels exceeding the upper reference limit included. LDH isoenzymes were detected quantitatively on agarose gels. The radiological severity of lung involvement on computed tomography was scored as 0-5 for each lobe (total possible score, 0-25). Disease severity was determined using the World Health Organization (WHO) clinical progression scale.ResultsIn total, 111 patients (mean age, 59.96 ± 16.14), including 43 females (38.7%), were enrolled. The serum levels of total LDH and all five LDH isoenzymes were significantly higher in the severe group. The levels of all LDH isoenzymes excluding LDH5 positively correlated with the WHO score. LDH3 levels correlated with chest computed tomography findings (r² = 0.267, p = 0.005). On multivariate analysis, LDH3 was an independent risk factor for the deterioration of COVID-19.ConclusionsLDH3 appears to be an independent risk factor for deterioration in patients with COVID-19. LDH elevation in patients with COVID-19 predominantly resulted from lung, liver and muscle damage.     

Triterpene saponins from Cyclamen hederifolium

Five triterpene saponins never reported before, hederifoliosides A-E, and four known triterpene saponins were isolated from the tubers of Cyclamen hederifolium. The structures of hederifoliosides A-E were determined as 3β,16α-dihydroxy-13β,28-epoxyolean-30-oic acid 3-O-{[β-D-glucopyranosyl-(1 → 2)-O]-β-D-xylopyranosyl-(1 → 2)-O-β-D-glucopyranosyl-(1 → 4)-O-α-L-arabinopyranoside}, 3β,16α-dihydroxy-13β,28-epoxyolean-30-oic acid 3-O-{[β-D-glucopyranosyl-(1 → 2)-O]-β-D-xylopyranosyl-(1 → 2)-O-[β-D-glucopyranosyl-(1 → 3)]-O-β-D-glucopyranosyl-(1 → 4)-O-α-L-arabinopyranoside}, 3β,16α-dihydroxy-13β,28-epoxyolean-30-al 3-O-{[β-D-glucopyranosyl-(1 → 2)-O]-β-D-xylopyranosyl-(1 → 2)-O-[β-D-glucopyranosyl-(1 → 3)]-O-[β-D-glucopyranosyl-(1 → 6)]-O-β-D-glucopyranosyl-(1 → 4)-O-α-L-arabinopyranoside}, 30-O-β-D-glucopyranosyl-(1 → 2)-O-β-D-glucopyranosyl-3β,16α,30-trihydroxyolean-12-en-28-al 3-O-{[β-D-glucopyranosyl-(1 → 2)-O]-β-D-xylopyranosyl-(1 → 2)-O-β-D-glucopyranosyl-(1 → 4)-O-α-L-arabinopyranoside}, 30-O-β-D-glucopyranosyl-(1 → 2)-O-β-D-glucopyranosyl-3β,16α,28,30-tetrahydroxyolean-12-en 3-O-{[β-D-glucopyranosyl-(1 → 2)-O]-β-D-xylopyranosyl-(1 → 2)-O-[β-D-glucopyranosyl-(1 → 3)]-O-β-D-glucopyranosyl-(1 → 4)-O-α-L-arabinopyranoside}, by a combination of one- and two-dimensional NMR techniques, and mass spectrometry. The cytotoxic activity of the isolated compounds was evaluated against a small panel of cancer cell lines including Hela, H-446, HT-29, and U937. None of the tested compounds, in a range of concentrations between 1 and 50 μM, caused a significant reduction of the cell number.     

Magnesite Enrichment with Pseudomonas oryzihabitans Isolated from Magnesite Ore

Magnesite is a primary source of magnesium and its compounds. The major problem in its practical use are the impurities such as silicon, iron and calcium carbonate. Some magnesite ores in Turkey cannot be used due to a high amount of CaCO₃ (≥3%). In this study, bacterial isolates from magnesite quarries in Mersin were tested by plate assay for their ability to decalcify magnesite. A bacterial strain producing the largest clear zones in the plate assay was identified as Pseudomonas oryzihabitans by 16S rDNA-PCR and applied to magnesite ore. It was found to be effective in decalcifying magnesite ore without significant concurrent dissolution of the magnesium carbonate.     

Neuropathology in mice expressing mouse alpha-synuclein

α-Synuclein (αSN) in human is tightly linked both neuropathologically and genetically to Parkinson's disease (PD) and related disorders. Disease-causing properties in vivo of the wildtype mouse ortholog (mαSN), which carries a threonine at position 53 like the A53T human mutant version that is genetically linked to PD, were never reported. To this end we generated mouse lines that express mαSN in central neurons at levels reaching up to six-fold compared to endogenous mαSN. Unlike transgenic mice expressing human wildtype or mutant forms of αSN, these mαSN transgenic mice showed pronounced ubiquitin immunopathology in spinal cord and brainstem. Isoelectric separation of mαSN species revealed multiple isoforms including two Ser129-phosphorylated species in the most severely affected brain regions. Neuronal Ser129-phosphorylated αSN occurred in granular and small fibrillar aggregates and pathological staining patterns in neurites occasionally revealed a striking ladder of small alternating segments staining either for Ser129-phosphorylated αSN or ubiquitin but not both. Axonal degeneration in long white matter tracts of the spinal cord, with breakdown of myelin sheaths and degeneration of neuromuscular junctions with loss of integrity of the presynaptic neurofilament network in mαSN transgenic mice, was similar to what we have reported for mice expressing human αSN wildtype or mutant forms. In hippocampal neurons, the mαSN protein accumulated and was phosphorylated but these neurons showed no ubiquitin immunopathology. In contrast to the early-onset motor abnormalities and muscle weakness observed in mice expressing human αSN, mαSN transgenic mice displayed only end-stage phenotypic alterations that manifested alongside with neuropathology. Altogether these findings show that increased levels of wildtype mαSN does not induce early-onset behavior changes, but drives end-stage pathophysiological changes in murine neurons that are strikingly similar to those evoked by expression of human wildtype or mutant forms.