The Effects of Copper Sulfate on Liver Histology and Biochemical Parameters of Term Ross Broiler Chicks

Copper is an essential trace element that is extremely toxic to organisms and organs at high doses. We have investigated the histological and biochemical effects of a toxic dose of copper sulfate on the liver of term Ross broiler chicks. Fertilized eggs were divided into three groups: experimental, injected with 50 mcg/0.1 ml copper sulfate in the air chambers on day 1; sham, injected with 0.1 ml saline; and control, no injection. Term chicks were killed and their livers investigated histologically, with hematoxylin–eosin-stained sections examined under light microscopy, and biochemically, for malondialdehyde and glutathione levels. Histological examinations showed copper-treated samples with granular degeneration and necrosis of hepatocytes and impairment to the cell lining of the remark cords. The samples had a congestive appearance, with blood in the vena centralis and sinusoids, slight connective tissue increase, and lymphocyte infiltration. Control and sham group sections had normal appearances. As oxidative damage parameters, in the copper-treated group, malondialdehyde levels were increased and glutathione levels decreased. In the sham and control groups, there were no significant differences. At this toxic dose, copper sulfate shows oxidative damage according to the histology of term chick liver that are confirmed biochemically by the changes in malondialdehyde and glutathione levels.     

Dependence of pathogen molecule-induced Toll-like receptor activation and cell function on Neu1 sialidase

The signaling pathways of mammalian Toll-like receptors (TLR) are well characterized, but the initial molecular mechanisms activated following ligand interactions with the receptors remain poorly defined. Here, we show a membrane controlling mechanism that is initiated by ligand binding to TLR-2, -3 and-4 to induce Neu1 sialidase activity within minutes in live primary bone marrow (BM) macrophage cells and macrophage and dendritic cell lines. Central to this process is that Neu1 and not Neu2,-3 and-4 forms a complex with TLR-2,-3 and-4 on the cell surface of naïve macrophage cells. Neuraminidase inhibitors BCX1827, 2-deoxy-2,3-dehydro-N-acetylneuraminic acid (DANA), zanamivir and oseltamivir carboxylate have a limited significant inhibition of the LPS-induced sialidase activity in live BMC-2 macrophage cells but Tamiflu (oseltamivir phosphate) completely blocks this activity. Tamiflu inhibits LPS-induced sialidase activity in live BMC-2 cells with an IC₅₀ of 1.2?μM compared to an IC₅₀ of 1015?μM for its hydrolytic metabolite oseltamivir carboxylate. Tamiflu blockage of LPS-induced Neu1 sialidase activity is not affected in BMC-2 cells pretreated with anticarboxylesterase agent clopidogrel. Endotoxin LPS binding to TLR4 induces Neu1 with subsequent activation of NFκB and the production of nitric oxide and pro-inflammatory IL-6 and TNFα cytokines in primary and macrophage cell lines. Hypomorphic cathepsin A mice with a secondary Neu1 deficiency respond poorly to LPS-induced pro-inflammatory cytokines compared to the wild-type or hypomorphic cathepsin A with normal Neu1 mice. Our findings establish an unprecedented mechanism for pathogen molecule-induced TLR activation and cell function, which is critically dependent on Neu1 sialidase activity associated with TLR ligand treated live primary macrophage cells and macrophage and dendritic cell lines.     

Photoluminescence and piezoelectric behaviour of Y2Zr2O7 pyrochlore‐based multifunctional materials and the influence of Eu3+ and Sm3+

Y₂Zr₂O₇‐doped with Eu³⁺ and Sm³⁺ phosphors were prepared for the first time as multifunctional smart materials using a solid‐state reaction method at 1400^oC. Thermal behaviour, crystal structure, surface morphology, and elemental analysis were characterized using thermogravimetric (TG) and differential thermal (DTA) analyses, X‐ray diffraction (XRD) and scanning electron microscope equipped with energy‐dispersive X‐ray spectroscopy (SEM‐EDX). Experimental results revealed that both phosphors have a pyrochlore structure with a cubic crystal system. Photoluminescence properties were also measured and red emission was observed from Y_1.90Eu_0.10Zr₂O₇ and Y_1.90Sm_0.10Zr₂O₇ phosphors. Dielectric constant, loss tangent, piezoelectric charge constant, and Curie temperature of all the samples were determined using an LCR‐meter, d₃₃‐meter, and TG/DTA. Eu doping in Y₂Zr₂O₇ resulted in a high dielectric constant (9.61) and low loss tangent (1.67%) values, whereas high piezoelectric charge constant (0.68 pC/N) and high Curie temperature (820°C) could be obtained using Sm‐doped Y₂Zr₂O₇.     

Identification of miR-17, miR-21, miR-27a,miR-106b and miR-222 as endoplasmic reticulum stress-related potential biomarkers in circulation of patients with atherosclerosis

Molecular Biology Reports - Atherosclerosis and related cardiovascular diseases are among the most common causes of death worldwide. Unfolded protein response, also known as Endoplasmic...     

Utility of the NavX® Electroanatomic Mapping System for Permanent Pacemaker Implantation in a Pregnant Patient with Chagas Disease

Chagas disease is a highly prevalent zoonosis in Mexico, Central, and South America. Early cardiac involvement is one of the most serious complications of this disease, and conduction disturbances may occur at an early age. We describe a young pregnant woman with Chagas disease and a high degree atrioventricular block, who required implantation of a permanent dual chamber pacemaker. Using an electroanatomic navigation EnSite NavX® system the pacemaker was successfully implanted with minimal fluoroscopic exposure. This case demonstrates the safety and feasibility of using an electroanatomic navigation system to guide permanent pacemaker implantation minimizing x-ray exposure in pregnant patients.     

Mutations in TMEM76* cause mucopolysaccharidosis IIIC (Sanfilippo C syndrome)

Mucopolysaccharidosis IIIC (MPS IIIC, or Sanfilippo C syndrome) is a lysosomal storage disorder caused by the inherited deficiency of the lysosomal membrane enzyme acetyl-coenzyme A: alpha -glucosaminide N-acetyltransferase (N-acetyltransferase), which leads to impaired degradation of heparan sulfate. We report the narrowing of the candidate region to a 2.6-cM interval between D8S1051 and D8S1831 and the identification of the transmembrane protein 76 gene (TMEM76), which encodes a 73-kDa protein with predicted multiple transmembrane domains and glycosylation sites, as the gene that causes MPS IIIC when it is mutated. Four nonsense mutations, 3 frameshift mutations due to deletions or a duplication, 6 splice-site mutations, and 14 missense mutations were identified among 30 probands with MPS IIIC. Functional expression of human TMEM76 and the mouse ortholog demonstrates that it is the gene that encodes the lysosomal N-acetyltransferase and suggests that this enzyme belongs to a new structural class of proteins that transport the activated acetyl residues across the cell membrane.     

The chromate-inducible chrBACF operon from the transposable element TnOtChr confers resistance to chromium(VI) and superoxide

Large-scale industrial use of chromium(VI) has resulted in widespread contamination with carcinogenic chromium(VI). The abilities of microorganisms to survive in these environments and to detoxify chromate require the presence of specific resistance systems. Here we report identification of the transposon-located (TnOtChr) chromate resistance genes from the highly tolerant strain Ochrobactrum tritici 5bvl1 surviving chromate concentrations of >50 mM. The 7,189-bp-long TnOtChr of the mixed Tn21/Tn3 transposon subfamily contains a group of chrB, chrA, chrC, and chrF genes situated between divergently transcribed resolvase and transposase genes. The chrB and chrA genes, but not chrF or chrC, were essential for establishment of high resistance in chromium-sensitive O. tritici. The chr promoter was strongly induced by chromate or dichromate, but it was completely unresponsive to Cr(III), oxidants, sulfate, or other oxyanions. Plasmid reporter experiments identified ChrB as a chromate-sensing regulator of chr expression. Induction of the chr operon suppressed accumulation of cellular Cr through the activity of a chromate efflux pump encoded by chrA. Expression of chrB, chrC, or chrF in an Escherichia coli sodA sodB double mutant restored its aerobic growth in minimal medium and conferred resistance to superoxide-generating agents menadione and paraquat. Nitroblue tetrazolium staining on native gels showed that ChrC protein had superoxide dismutase activity. TnOtChr appears to represent a mobile genetic system for the distribution of the chromate-regulated resistance operon. The presence of three genes protecting against superoxide toxicity should provide an additional survival advantage to TnOtChr-containing cells in the environments with multiple redox-active contaminants.     

LGBT+ Individuals’ Perceptions of Healthcare Services in Turkey: A Cross-sectional Qualitative Study

When accessing healthcare services, LGBT+ individuals are often exposed to segregating and marginalizing discourses. Knowledge about how such experiences are reflected in the moral world of LGBT+ individuals living in Turkey is limited. This study examined LGBT+ individuals’ lived experiences when utilizing healthcare services. The findings are discussed in terms of moral discourses related to LGBT+ individuals’ gender identity and sexual orientation. A qualitative field study was conducted using semi-structured interviews with fifty-five LGBT+ individuals from Turkish cities who were in contact with various non-governmental organizations that conduct studies on gender identity and sexual orientation. A questionnaire was administered with items on participants’ demographic information, experiences, behavioural patterns, and knowledge regarding healthcare services. The data were analysed thematically. The findings were evaluated within the framework of “access to healthcare service” theme related to “healthcare service demand” context. Additionally, the “interaction with physicians” theme was addressed in the context of “physician–patient/counselee relationship.” LGBT+ individuals state that they are exposed to stigmatizing and segregating discourses by healthcare professionals, which might pose an obstacle for adaptive health-seeking behaviours. These results suggest that physicians’ professional approach has a considerable influence on LGBT+ individuals’ capacity for utilizing healthcare services.     

Cholecalciferol (vitamin D 3) improves cognitive dysfunction and reduces inflammation in a rat fatty liver model of metabolic syndrome

Aim

The aim of this study was to examine the effects of cholecalciferol on systemic inflammation and memory in the setting of fatty liver disease in rats.

Materials and methods

To induce the development of fatty liver disease, the rats were fed a 35% fructose solution over 8 weeks. Group I (n = 6) was designated as the control group and fed with standard rat chow. Group II (n = 6) was provided with, standard rat chow, and 0.3 μg/kg/day of oral cholecalciferol over a duration of 2 weeks. In addition to standard rat chow, group III (n = 6) and group IV (n = 6) were given 4 mL of the 35% fructose solution per day via oral gavage for 8 weeks. However, group IV was also given 0.3 μg/kg/day of oral cholecalciferol over 2 weeks. After the treatment period, passive avoidance tasks were performed by all groups. The liver and brain were harvested for subsequent biochemical and histopathologic analyses.

Key findings

The development of fatty liver extends the memory latency period of passively avoiding tasks after 1 trial. Moreover, there were increases in brain TNF-α and plasma MDA levels according to two-way analysis of variance. Cholecalciferol supplementation decreased the latency period of passively avoiding tasks in rats with hepatosteatosis, and also significantly reduced brain TNF-α and plasma MDA levels.

Significance

Fatty liver may contribute to the development of systemic inflammation, which affects cognition and causes deficits in memory; however, the anti-inflammatory and antioxidant properties of vitamin D may improve the cognitive function of rats with hepatosteatosis.