9 research outputs found
Significant impact of +105 A>C promoter polymorphism in IL-18 cytokine in patients with kidney stone disease
Background: Inflammation may be one cause of nephrolithiasis and the interleukin-18 (IL-18) encoding gene  polymorphisms at +105 A>C has been implicated in several inflammation related diseases. The aim of this study was to test whether IL-18+105 A>C polymorphisms could act as genetic marker for renal stone disease. A case-control study was conducted to observe the genotype distribution of IL-18+105 A>C, to elucidate the possible role of this SNP as risk factor in renal stone development and to examine its correlation with the clinico-pathologic variables.Methods: Using the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) technique, we tested the genotype distribution of 160 nephrolithiasis patients in comparison with 200 disease free controls from the same geographical region.  Results: We observed significant differences of IL-18+105 A to C between the controls and patients with odds ratio 5.4 (P = 0.001). The prevalence of the variant genotypes AC + CC in the patients was higher than that in the controls (45% v/s 30%) and showed a significant association (P = 0.003). Moreover, the frequency per copy of the C allele of IL-18+105 A>C was found to be implicated more in patient group 0.27 as against only 0.16 in controls (P = 0.0003). Further, males and subjects with C is implicated in renal stone disease, and that the rare, C related allele is connected with higher susceptibility to nephrolithiasis.
Further Development of the CoSMA-Tool (PEGASUS)
This works focused on the optimisation and programming of a simulation tool for the structural linear analysis of combustor liners made of alloys and ceramic matrix composites
Hyperchloremia and Hypernatremia Decreased Microglial and Neuronal Survival during Oxygen–Glucose Deprivation/Reperfusion
Hyperchloremia and hypernatremia are associated with higher mortality in ischemic stroke, but it remains unclear whether their influence directly contributes to ischemic injury. We investigated the impact of 0.9% sodium chloride (154 mM NaCl), 0.9% sodium acetate (167 mM CH3COONa), and their different combinations (3:1, 2:1, and 1:1) on microglial (HMC-3) and neuronal (differentiated SH-SY5Y) survival during oxygen–glucose deprivation/reperfusion (OGD/R). Further, we assessed the effect of hyperchloremia and hypernatremia-treated and OGD/R-induced HMC-3-conditioned media on differentiated SH-SY5Y cells under OGD/R conditions. We performed cell viability, cell toxicity, and nitric oxide (NO) release assays and studied the alteration in expression of caspase-1 and caspase-3 in different cell lines when exposed to hyperchloremia and hypernatremia. Cell survival was decreased in 0.9% NaCl, 0.9% CH3COONa, combinations of HMC-3 and differentiated SH-SY5Y, and differentiated SH-SY5Y cells challenged with HMC-3-conditioned media under normal and OGD/R conditions. Under OGD/R conditions, differentiated SH-SY5Y cells were less likely to survive exposure to 0.9% NaCl. Expression of caspase-1 and caspase-3 in HMC-3 and differentiated SH-SY5Y cells was altered when exposed to 0.9% NaCl, 0.9% CH3COONa, and their combinations. A total of 0.9% NaCl and 0.9% CH3COONa and their combinations decreased the NO production in HMC-3 cells under normal and OGD/R conditions. Both hypernatremia and hyperchloremia reduced the survival of HMC-3 and differentiated SH-SY5Y cells under OGD/R conditions. Based on the OGD/R in vitro model that mimics human ischemic stroke conditions, it possibly provides a link for the increased death associated with hyperchloremia or hypernatremia in stroke patients
Ultrasonographic Evaluation of Sub-Clinical Synovitis in Juvenile Idiopathic Arthritis: The Disease Classification and Management
Background: Ultrasonography (USG) is a perfect device for analyzing more than one joint in rather brief intervals of time and is well accepted by children with no harmful ionizing radiation, usually does not require sedation, and can be carried out without difficulty in an outpatient setting. Purpose: To demonstrate the ability of ultrasonography (USG) in detecting clinical and subclinical synovitis in children with juvenile idiopathic arthritis (JIA) and compare the USG findings with clinical findings. Methods: 20 patients with JIA diagnosed according to the ILAR criteria were include. A total of 208 joints were examined both clinically and ultrasonographically for detection of synovitis. The presence of subclinical synovitis detected by USG was sought and its effect on the classification of JIA was assessed. USG assessment was done using the High-Resolution Linear probe including both grey scale and Power Doppler assessment. Results: The mean age of patients was 10.2 years with average disease duration of 5.9 months. A total of 49 joints (23.5%) had clinical synovitis and 59 joints (28.4%) had USG synovitis out of a total of 208 joints. A total of 14 joints had subclinical synovitis (8.8% out of the 159 clinically normal joints) upon USG. USG additionally brought about classifying three patients as having poly articular disorder who had been considered as oligo articular upon clinical examination. Conclusion: USG assessment of subclinical synovitis in JIA patients is an essential component of classifying the disease and detects more joints with synovitis than clinical examination; however, both are complimentary and should be used in combination in all patients with JIA
Neuroprotective Potential of Flavonoids in Brain Disorders
Flavonoids are a large subgroup of polyphenols known to be sourced from over 6000 natural products, including fruits, vegetables, bark, and herbs. Due to their antioxidant properties, flavonoids have been implicated as a therapy source for many diseases and conditions, including inflammation, vasculitis, venous insufficiency, and hemorrhoids. Currently, some flavonoids are being researched for their antioxidant ability concerning neuroprotection. These flavonoids can penetrate the blood–brain barrier and, depending on the specific flavonoid, retain adequate bioavailability in certain brain regions. Further data suggest that flavonoids could have a strong anti-inflammatory effect in the brain, which not only could be a robust therapeutic source for known neuroinflammatory diseases such as Alzheimer’s Disease or Parkinson’s Disease but also could be a therapeutic source for ischemic or hemorrhagic conditions such as a stroke. While flavonoid toxicity exists, they are relatively safe and non-invasive drugs from natural origins. As such, exploring the known mechanisms and therapies may highlight and establish flavonoid therapy as a viable source of therapy for stroke patients. As stated, many flavonoids are already being isolated, purified, and implemented in both in vitro and in vivo experiments. As these flavonoids proceed to clinical trials, it will be important to understand how they function as a therapy, primarily as antioxidants, and by other secondary mechanisms. This review aims to elucidate those mechanisms and explore the neuroprotective role of flavonoids