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Kidney stone, also known as calcium oxalate nephrolithiasis, is one of the most common diseases worldwide. Calculi usually forms when urine becomes supersaturated with particular calcium salts such as calcium oxalate. In the present study, we investigated the ameliorative potential of the root extract of the Common golden thistle, Scolymus hispanicus L. (SH) on rats with ethylene glycol (EG) induced kidney stone disease. Sprague-Dawley rats, each weighing 250-300 g, were divided into three groups (n=6 per group): (i) Control (C); (ii) EG; and (iii) EG+SH. To induce nephrolithiasis, the rats received 1% of EG with drinking water, while the C group received normal drinking water during the study. SH extract 2 g/kg was added to the treatment from the 4th week onwards in EG+SH group. At the end of each experiment, rats were decapacitated and serum levels of calcium, magnesium, phosphorus, creatinine, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were assessed in all groups at 0, 4, and 8 weeks. Oxalic acid and creatininelevels were measured in urine samples collected at 24 h in metabolic cages. Renal tissues were evaluated histopathologically at the end of the experiment. After 8 weeks, serum creatinine levels were found decreased in the SH group while increased in the EG group. Serum magnesium and AST levels were also found decreased in the EG group, however, SH treatment reversed these values. The SH treatment also increased urinary oxalic acid levels. When the kidney tissue of EG group was examined, there was a high level of crystal/stone, especially in the renal cortex. In kidney tissues of the SH group, only small amounts of crystal/stone were observed. Our experimental findings have demonstrated the ameliorative potential of the aqueous extracts of S. hispanicus roots and shells on EG-induced in the kidney stones in rats. Isolation of active compounds of SH would be desirable to understand the biochemical mechanism behind the process better.
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ABSTRACT Objective: Right-heart function is a major determinant of clinical outcome in patients with elevated pulmonary artery pressure due to pulmonary venous hypertension (PVH) and pulmonary arterial hypertension (PAH). Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase. This study aimed to evaluate if different types of pulmonary hypertension (PH) would cause the same effect on right-heart functions and serum ADMA levels in female patients. Methods: This study included patients with PAH as group I, patients with PVH due to mitral stenosis (mitral valve area ≤ 1.5 cm2, without any additional valve or left-heart disease and systolic pulmonary artery pressure ≥ 50 mmHg in transthoracic echocardiography) as group II, and healthy control subjects as group III. Transthorasic echocardiographic evaluations for right-heart functions were performed according to the guidelines of the American Society of Echocardiography. Venous blood samples were collected, and the serum ADMA concentrations were obtained with the ELISA kit (DRG® International Inc., Springfield, NJ, USA). Results: Patients in groups I and II had higher ADMA levels than healthy control subjects. Right-atrium area and dimensions, right-ventricular (RV) volumes, grade of tricuspid regurgitation, systolic pulmonary arterial pressure, RV wall thickness, and RV outflow tract diameters were significantly higher in group I patients than in group II patients. Right-ventricular myocardial performance index was lower, and RV fractional area change and tricuspid valve systolic tissue Doppler velocity were higher in group II patients than in group I patients. Conclusion: This study demonstrated that both PAH and PVH caused increase in right-heart dimensions and impairment in right-heart functions.
Subject(s)
Humans , Female , Adolescent , Adult , Middle Aged , Aged , Young Adult , Arginine/analogs & derivatives , Nitric Oxide Synthase , Hypertension, Pulmonary/physiopathology , Echocardiography , Ventricular Dysfunction, RightABSTRACT
ABSTRACT Objective: Dyspepsia, one of the most commonly seen symptoms, can be due to organic dyspepsia (OD) or functional dyspepsia (FD). The aim of this study is to evaluate neutrophil-tolymphocyte ratio (NLR) for the predictability of OD due to peptic ulcer disease (PUD) and gastric cancer (GC). Methods: We investigated retrospectively the patients with dyspepsia who underwent endos-copy. The study included 119 patients with OD (41 patients with biopsy-proven GC and 78 patients with PUD) and 100 patients with FD diagnosed. Results: The NLR among the patients with GC and PUD was significantly higher than FD subject (p < 0.001 each). The NLR in patients with GC was also significantly higher than that in patients with PUD (p < 0.005). When OD was compared with FD, NLR and white blood cell were statistically significantly higher (p < 0.001 and p < 0.05 respectively). The best predictive cut-off value of NLR was 1.72 with a specificity of 63% and a sensitivity of 66% for OD, on receiver-operating characteristic curve analysis. Conclusion: Neutrophil-to-lymphocyte ratio was higher in patients with OD compared with those with FD, and even higher in patients with GC. Our findings suggest that NLR should be calculated in patients with dyspepsia and patients with high levels of NLR should undergo endoscopy.
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Dendritic cells (DCs) play a crucial role as central orchestrators of immune system response in atherosclerosis initiation and progression. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is involved in the immune maturation of DCs, but the underlying mechanisms remain unclear. We isolated mouse bone marrow progenitors and stimulated them with granulocyte-macrophage colony-stimulating factor and interleukin (IL)-4 to induce immature DCs. We then treated DCs with oxidized low-density lipoprotein (oxLDL) to induce maturation. LOX-1 siRNA was used to investigate the modulation of LOX-1 on the development of DCs and the underlying signal pathways. CD11c-positive DCs were successfully derived from mouse bone marrow progenitors. OxLDL promoted the expressions of DCs maturation markers and pro-inflammatory cytokines. OxLDL also upregulated LOX-1 expression and activated MAPK/NF-κB pathways. LOX-1 siRNA could attenuate the expression of MAPK/NF-κB pathways and inflammatory cytokines. In conclusion, oxLDL induced the maturation of DCs via LOX-1-mediated MAPK/NF-κB pathway, which contributed to the initiation and progression of atherosclerosis.
Subject(s)
Animals , Rats , Dendritic Cells , NF-kappa B , MAP Kinase Signaling System , Scavenger Receptors, Class E , Lipoproteins, LDLABSTRACT
This study evaluated the effect of muscle satellite cells (MSCs) overexpressing myogenin (MyoG) on denervated muscle atrophy. Rat MSCs were isolated and transfected with the MyoG-EGFP plasmid vector GV143. MyoG-transfected MSCs (MTMs) were transplanted into rat gastrocnemius muscles at 1 week after surgical denervation. Controls included injections of untransfected MSCs or the vehicle only. Muscles were harvested and analyzed at 2, 4, and 24 weeks post-transplantation. Immunofluorescence confirmed MyoG overexpression in MTMs. The muscle wet weight ratio was significantly reduced at 2 weeks after MTM injection (67.17±6.79) compared with muscles injected with MSCs (58.83±5.31) or the vehicle (53.00±7.67; t=2.37, P=0.04 and t=3.39, P=0.007, respectively). The muscle fiber cross-sectional area was also larger at 2 weeks after MTM injection (2.63×103±0.39×103) compared with MSC injection (1.99×103±0.58×103) or the vehicle only (1.57×103±0.47×103; t=2.24, P=0.049 and t=4.22, P=0.002, respectively). At 4 and 24 weeks post-injection, the muscle mass and fiber cross-sectional area were similar across all three experimental groups. Immunohistochemistry showed that the MTM group had larger MyoG-positive fibers. The MTM group (3.18±1.13) also had higher expression of MyoG mRNA than other groups (1.41±0.65 and 1.03±0.19) at 2 weeks after injection (t=2.72, P=0.04). Transplanted MTMs delayed short-term atrophy of denervated muscles. This approach can be optimized as a novel stand-alone therapy or as a bridge to surgical re-innervation of damaged muscles.
Subject(s)
Animals , Male , Muscular Atrophy/rehabilitation , Myogenin/metabolism , Cell Transplantation , Muscle, Skeletal/innervation , Satellite Cells, Skeletal Muscle/transplantation , Muscle Denervation/rehabilitation , Organ Size/genetics , Plasmids , Muscular Atrophy/etiology , Transfection , Gene Expression , Fluorescent Antibody Technique , Rats, Sprague-Dawley , Myogenin/genetics , Satellite Cells, Skeletal Muscle/cytology , Real-Time Polymerase Chain ReactionABSTRACT
Purpose: To assess whether vancomycin minimum inhibitory concentration (MIC) creeps among clinical isolates of methicillin‑resistant Staphylococcus aureus (MRSA) in a regional hospital in China. Furthermore, to analyze the causes of vancomycin MIC creeps and the relationship between vancomycin MICs and the outcome among patients with MRSA infection. Materials and Methods: All clinical isolates of MRSA from 2006-2010 were retrieved and tested by the broth microdilution procedure to determine their vancomycin MIC. Meanwhile, related patient records were analyzed. Results: While all isolates were susceptive to vancomycin, the percentage of isolates with a vancomycin MIC = 1 mg/L increased significantly from 2006 (37.0%) to 2010 (75.7%). Meanwhile, vancomycin usage density (DDDs/1000 bed‑days) had increased significantly from 2006-2010. Mean linear correlation analysis showed a statistically significant positive correlation (r = 0.905, P < 0.05) between the consumption of vancomycin and the percentage of MRSA isolates with a vancomycin MIC = 1 mg/L. Clinical records revealed high vancomycin MIC was associated with a higher microbiologic failure rate in MRSA bloodstream infections. Conclusions: The data demonstrated vancomycin MIC creep among clinical isolates in our hospital, and the MIC creep may be caused by the increasing usage of vancomycin. Furthermore, the analysis strongly suggested this shift of vancomycin MIC within the susceptible range may be associated with an increasing probability of treatment failure.
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We report a case of successful treatment with erlotinib of a patient with non-small cell lung cancer (stage IV) and meningeal metastasis. Combined treatment with whole brain radiotherapy (WBRT) and erlotinib mitigated neurologic symptoms of the patient. Magnetic resonance imaging showed reduction of the brain metastasis. Partial remission was observed by chest computed tomography (CT) scan after six months of erlotinib therapy.
Reportamos un caso de tratamiento exitoso con el erlotinib de un paciente con cáncer pulmonar de células no pequeñas (fase IV) y metástasis meníngea. El tratamiento combinado con la radioterapia total del cerebro (WBRT) y erlotinib mitigaron los síntomas neurológicos del paciente. Las imágenes de resonancia magnética mostraron una reducción de la metástasis del cerebro. La remisión parcial fue observada mediante CT scan de tórax tras seis meses de terapia con erlotinib.