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To evaluate the effect of potassium citrate administration on the composition of encrusted material on the ureteral stent after Double-J insertion.

We designed a randomized clinical trial for our study; 65 patients that underwent transurethral lithotripsy and Double-J stent insertion were included in the study after informed consent and divided into two groups. In the first group (33 patients) potassium citrate was prescribed after surgery till stent removal and the second group (32 patients) followed without prescribing this medication. After stent removal, encrusted materials on removed stents were analyzed then the type and composition of encrusted material compared with the primary stone that was removed.

Our results revealed that the type and composition of primary stone and encrusted stone were similar in patients that do not receive potassium citrate (p-value of 0.073, 0.251 and 0.944 for calcium oxalate, uric acid, and calcium phosphate respectively). In patients that taking potassium citrate rate of calcium oxalate (p-value < 0.001) and uric acid (p-value < 0.001) material on encrusted stent significantly decreased compared with the non-intervention group.

Results of this study revealed that taking of potassium citrate after ureteral stent insertion significantly decreases the formation of calcium oxalate and uric acid encrusted material on Double-J stent so it could be recommended for prevention of stent encrustation in patients that primary stone analysis are calcium oxalate and uric acid stone.

Results of this study revealed that taking of potassium citrate after ureteral stent insertion significantly decreases the formation of calcium oxalate and uric acid encrusted material on Double-J stent so it could be recommended for prevention of stent encrustation in patients that primary stone analysis are calcium oxalate and uric acid stone.

Nowadays, due to the lack of an effective vaccine to prevent the toxoplasmosis, chemotherapy with the combination of pyrimethamine and sulfadiazine is considered as the "gold standard" treatment for toxoplasmosis. Recent reports have exhibited that these synthesized chemical drugs are associated with some serious side effects. The present study aims to evaluate the prophylactic effects of copper nanoparticles (CuNPs) green synthesized by Capparis spinosa fruit methanolic extract alone and combined with atovaquone against chronic toxoplasmosis induced by the Tehran strain of Toxoplasma gondii in mice METHODS Mice were then orally administrated with CuNPs at the doses of 2 and 4mg/kg/day and in combined with atovaquone 50mg/kg for 14days. Male BALB/c mice were divided into two seven groups include C1 (non-treated non-infected); C2 (treated with normal saline); C3 (Infected mice treated with atovaquone 100mg/kg/day); Ex1 (treated with CuNPs 2mg/kg/day); Ex2 (treated with CuNPs 4mg/kg/day); Ex3 (treated with CuNO was increased in all mice of experimental groups in comparison with the control group C2; however, a significant enhancement was detected in mRNA level of IFN-γ, IL-12, and iNO in the tested groups of Ex3 and Ex4 when compared with control group C3.

The obtained results revealed the high potency of CuNPs alone and combined with atovaquone to prevent toxoplasmosis in mice. Although, the prophylactic effects of CuNPs and other properties, such as improved cellular immunity and low toxicity, are positive topics; however, more studies are required to approve these findings especially in clinical settings.

The obtained results revealed the high potency of CuNPs alone and combined with atovaquone to prevent toxoplasmosis in mice. Although, the prophylactic effects of CuNPs and other properties, such as improved cellular immunity and low toxicity, are positive topics; however, more studies are required to approve these findings especially in clinical settings.Gastric cancer is one of the malignant tumors of the gastrointestinal tract that, despite its decrease in recent years, is still the fourth most common cancer and the second leading cause of cancer-related death. Various strategies including chemotherapy are used to keep cancer cells from spreading and induce apoptotic death in them. Recent studies have shown that dihydropyrimidinones (DHPMs) are privileged structures in medicinal chemistry due to their pharmacological effects. A number of new 2-aminothiazolyl/benzothiazolyl derivatives of 3,4-DHPMs (3-8) were synthesized and structurally identified, and then their effects on the migration behavior of human AGS cells (gastric cancer cells) were investigated. Molecular docking and molecular dynamics (MD) simulations were applied to explore binding potential and realistic binding model of the assessed derivatives through identification of key amino acid residues within L5/α2/α3 allosteric site of kinesin 5 (Eg5) as a validated microtubule-dependent target for monastrol as a privileged DHPM derivative.Background Non-ventilator associated hospital-acquired pneumonia accounts for significant antibiotic use and is associated with a high rate of resistance emergence. However, the optimal duration of antibiotic treatment is uncertain, especially in cases of non-fermenting gram-negative bacilli. Objective To compare a short course (5-7 days) to a prolonged course (10-14 days) of antibiotics for non-ventilator associated hospital-acquired pneumonia. Methods Data collected retrospectively on patients completed treatment in a Malaysian tertiary hospital from January 2017 till December 2018. Regression analysis determined variables independently associated with clinical outcome. Main outcome measures Clinical resolution, superinfection, 30-day and 90-day all-cause mortality between short and prolonged courses. Results Of the 167 patients included, 112 patients were treated with a short course antibiotic, whereas 55 patients received a prolonged course of therapy. Neither short nor prolonged course group has a significantly higher rate of clinical resolution. Short course group had significantly higher mean ± SD antibiotic-free days (21.9 ± 3.5 versus 15.1 ± 6.2 days, p  less then  0.001). Higher rate of superinfection was observed in prolonged course group compared to short course group (6.3% versus 18.2%, p = 0.027). For non-ventilator associated hospital-acquired pneumonia caused by non-fermenting gram-negative bacilli, the superinfection rate was higher in prolonged course group (35.7% versus 15.4%, p = 0.385) while 30-day mortality rate was higher in the short course group (38.5% versus 14.3%, p = 0.209). Non-fermenting gram-negative bacilli cause higher rate of superinfection (p = 0.010). Conclusion We found no clinical benefit as defined by clinical resolution and reduction in all-cause mortality in prolonging antimicrobial therapy. Superinfections emerge more frequently in prolonged course of antibiotic therapy and more likely to develop in non-fermenting gram-negative bacilli.Tardigrada (also known as "water bears") are hydrophilous microinvertebrates with a bilaterally symmetrical body and four pairs of legs usually terminating with claws. Water bears are quite complex animals and range from 50 to 1200 μm in length. Their body is divided into a head segment and four trunk segments, each bearing a pair of legs. They inhabit almost all terrestrial and aquatic environments, from the ocean depths to highest mountains ranges. BMS-986365 datasheet However, one of their best known and unusual features is their capability for cryptobiosis. In this state tardigrades are able to survive extremely low and high temperatures and atmospheric pressures, complete lack of water, high doses of radiation, high concentrations of toxins and even a cosmic vacuum. The cellular mechanisms enabling cryptobiosis are poorly understood, although it appears the synthesis of certain types of molecules (sugars and proteins) enable the prevention of cellular damage at different levels. The endoplasmic reticulum (ER) is a morphologically and functionally diverse organelle able to integrate multiple extracellular and internal signals and generate adaptive cellular responses. However, the ER morphology and activity in the case of tardigrades has been studied rarely and in the context of oogenesis, functioning of the digestive system, and in the role and function of storage cells. Thus, there are no direct studies on the contribution of the ER in the ability of this organism to cope with environmental stress during cryptobiosis. Nevertheless, it is highly probable that the ER has a crucial role in this uncommon process. Since water bears are easy to handle laboratory animals, they may represent an ideal model organism to uncover the important role of the ER in the cell response to extreme environmental stress conditions.The unfolded protein response (UPR) is an evolutionarily conserved adaptive regulatory pathway that alleviates protein-folding defects in the endoplasmic reticulum (ER). Physiological demands, environmental perturbations and pathological conditions can cause accumulation of unfolded proteins in the ER and the stress signal is transmitted to the nucleus to turn on a series of genes to respond the challenge. In metazoan, the UPR pathways consisted of IRE1/XBP1, PEK-1 and ATF6, which function in parallel and downstream transcriptional activation triggers the proteostasis networks consisting of molecular chaperones, protein degradation machinery and other stress response pathways ((Labbadia J, Morimoto RI, F1000Prime Rep 67, 2014); (Shen X, Ellis RE, Lee K, Annu Rev Biochem 28893-903, 2014)). The integrated responses act on to resolve the ER stress by increasing protein folding capacity, attenuating ER-loading translation, activating ER-associated proteasomal degradation (ERAD), and regulating IRE1-dependent decay of mRNA (RIDD). Therefore, the effective UPR to internal and external causes is linked to the multiple pathophysiological conditions such as aging, immunity, and neurodegenerative diseases. Recent development in the research of the UPR includes cell-nonautonomous features of the UPR, interplay between the UPR and other stress response pathways, unconventional UPR inducers, and noncanonical UPR independent of the three major branches, originated from multiple cellular and molecular machineries in addition to ER. Caenorhabditis elegans model system has critically contributed to these unprecedented aspects of the ER UPR and broadens the possible therapeutic targets to treat the ER-stress associated human disorders and time-dependent physiological deterioration of aging.Endoplasmic reticulum (ER) stress is a prominent cellular alteration of diseases impacting the nervous system that are associated to the accumulation of misfolded and aggregated protein species during aging. The unfolded protein response (UPR) is the main pathway mediating adaptation to ER stress, but it can also trigger deleterious cascades of inflammation and cell death leading to cell dysfunction and neurodegeneration. Genetic and pharmacological studies in experimental models shed light into molecular pathways possibly contributing to ER stress and the UPR activation in human neuropathies. Most of experimental models are, however, based on the overexpression of mutant proteins causing familial forms of these diseases or the administration of neurotoxins that induce pathology in young animals. Whether the mechanisms uncovered in these models are relevant for the etiology of the vast majority of age-related sporadic forms of neurodegenerative diseases is an open question. Here, we provide a systematic analysis of the current evidence linking ER stress to human pathology and the main mechanisms elucidated in experimental models.

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