Only in Titles

           Search results for: L    

paperclip

#32061168   // Save this To Up

Percutaneous mechanical thrombectomy in patients with high-risk pulmonary embolism and contraindications for thrombolytic therapy.

Background High-risk pulmonary embolism is associated with a high early mortality rate. We report our experience with percutaneous mechanical thrombectomy in patients with high-risk pulmonary embolism and contraindications for thrombolytic therapy. Patients and methods This was a retrospective analysis of consecutive patients with high-risk pulmonary embolism and contraindications to thrombolytic therapy. They were treated with percutaneous mechanical thrombectomy which included thrombectomy and additional thrombus aspiration when needed. Clinical parameters and survival to discharge were measured. Results From November 2005 to September 2015 we treated 25 patients with a mean age of 62.6 ± 12.7 years, 64% were men. Mean simplified Pulmonary Embolism Severity Index was 2.9. Mean maximum lactate levels were 7.8 ± 6.6 mmol/L, vasopressors were used in 77%, and 59% needed mechanical ventilation. Mechanical treatment included thrombus fragmentation complemented with aspiration (56%) and aspiration using Aspirex®S catheter (44%). Local (5 patients; 20%) and systemic (3 patients; 12%) thrombolytics were used as a salvage therapy. We observed nonsignificant improvements in systemic blood pressure (100 ± 41 mm Hg vs 119 ± 34; p = 0.100) and heart frequency (99 ± 35 min-1 vs 87 ± 31 min-1; p = 0.326) before and after treatment, respectively. Peak systolic tricuspid pressure gradient was significantly lower after treatment (57 ± 14 mm Hg vs 31 ± 3 mm Hg; p = 0.018). Overall the procedure was technically successful in 20 patients (80%) and 17 patients (68%) survived to hospital discharge. Conclusions In patients with high-risk pulmonary embolism who cannot receive thrombolytic therapy, percutaneous mechanical thrombectomy is a promising alternative to reduce pulmonary artery pressure.

1208 related Products with: Percutaneous mechanical thrombectomy in patients with high-risk pulmonary embolism and contraindications for thrombolytic therapy.



Related Pathways

paperclip

#32061159   // Save this To Up

Clinico-pathological features, treatments and survival of malignant insulinomas: a multicenter study.

management of malignant insulinomas is challenging due to the need to control both hypoglycaemic syndrome and tumor growth. Literature data is limited to small series.

2802 related Products with: Clinico-pathological features, treatments and survival of malignant insulinomas: a multicenter study.



Related Pathways

paperclip

#32061156   // Save this To Up

GHR gene transcript heterogeneity may explain phenotypic variability in GHR pseudoexon (6Ψ) patients.

The homozygous GH receptor (GHR) pseudoexon (6Ψ) mutation leads to growth hormone insensitivity (GHI) with clinical and biochemical heterogeneity. We investigated whether transcript heterogeneity (6Ψ-GHR to WT-GHR transcript ratio) and/or concurrent defects in other short stature (SS) genes contribute to this.

1845 related Products with: GHR gene transcript heterogeneity may explain phenotypic variability in GHR pseudoexon (6Ψ) patients.

Ghrelin Antibody Rabbit Anti-Ghrelin Polyc Mouse Epstein-Barr Virus Rabbit Anti-Ghrelin Polyc Rabbit Anti-Ghrelin Polyc Native Human GHRH Protein Human Ghrelin DNA (cytosine 5) methyltr Rabbit Anti-Ghrelin Polyc Rabbit Anti-Ghrelin Polyc Rabbit Anti-Human Bcl-2 I Rabbit Anti-Human GHRF An

Related Pathways

paperclip

#   // Save this To Up


2553 related Products with:



Related Pathways

  •  
  • No related Items
paperclip

#32061153   // Save this To Up

Cardiac protection of Bauhinia championii against reperfusion injury.

This study aims to investigate the protective effects of the Bauhinia championii (BC) against ischemia/reperfusion (I/R)-induced injury in an isolated heart model. Langendorff-perfused C57BL/6JNarl mice hearts were performed with 30 minutes ischemia and 60 minutes reperfusion by left anterior descending artery ligation. Before reperfusion, boiling water extracts of BC (10 mg/L) was pretreated for 15 minutes. During reperfusion, BC significantly decreased the occurrence of ventricular arrhythmias by lead II electrocardiogram (ECG). Electrophysiological effect of BC was further determined in isolated ventricular myocytes by whole-cell patch clamp technique. The underlying mechanism may result from its Na channel blocking activity characterized with reduced rise slope of action potential and Na current density. Moreover, BC dramatically reduced I/R-caused infarct size, which was accessed by 2,3,5-triphenyltetrazolium chloride (TTC) assay. Since BC decreased I/R-induced myoglobin release and oxidation of Ca -calmodulin-dependent protein kinase, inhibition of myocardial necroptosis may account for the protective effects of BC on myocytes lose. This study indicated that BC may prevent I/R induced ventricular arrhythmias and myocyte death by blocking Na channels and decreasing necroptosis, respectively. Since most of the available antiarrhythmic remedies have unwanted adverse actions, BC could be a novel candidate for the treatment of myocardial infarction and ventricular arrhythmia.

2926 related Products with: Cardiac protection of Bauhinia championii against reperfusion injury.

Mouse Anti-Human Troponin Picro-Sirius Red Stain K Ofloxacin CAS Number [824 Recombinant Troponin I-C Mouse Anti-Troponin-I (Ca Recombinant Human Cardiac Mouse Anti-Troponin-T (Ca Rabbit Anti-Nkx2.5 Cardia Rabbit Anti-Nkx2.5 Cardia Rabbit Anti-phospho-cardi Rabbit Anti-phospho-cardi Mouse Anti-Human Myosin T

Related Pathways

paperclip

#32061134   // Save this To Up

NOS1AP polymorphisms reduce NOS1 activity and interact with prolonged repolarization in arrhythmogenesis.

NOS1AP SNPs correlate with QT prolongation and cardiac sudden death in patients affected by long QT syndrome type 1 (LQT1). NOS1AP targets NOS1 to intracellular effectors. We hypothesize that NOS1AP SNPs cause NOS1 dysfunction and this may converge with prolonged action potential duration (APD) to facilitate arrhythmias.

2444 related Products with: NOS1AP polymorphisms reduce NOS1 activity and interact with prolonged repolarization in arrhythmogenesis.



Related Pathways

paperclip

#32061126   // Save this To Up

Metabolism and Effects on Endogenous Metabolism of Paracetamol (Acetaminophen) in a Porcine Model of Liver Failure.

The metabolic fate, toxicity and effects on endogenous metabolism of paracetamol (acetaminophen, APAP) in 22 female Landrace cross large white pigs were evaluated in a model of acute liver failure (ALF). Anaesthetized pigs were initially dosed at 250 mg/kg via an oroduodenal tube with APAP serum concentrations maintained above 300 mg/L using maintenance doses of 0.5-4g/h until ALF. Studies were undertaken to determine both the metabolic fate of APAP and its effects on the endogenous metabolic phenotype of ALF in using 1H NMR spectroscopy. Increased concentrations of citrate combined with pre-ALF increases in circulating lactate, pyruvate and alanine in plasma suggest mitochondrial dysfunction and a switch in hepatic energy metabolism to glycolysis in response to APAP treatment. A specific liquid chromatography-tandem mass spectrometry assay was used to quantify APAP and metabolites. The major circulating and urinary metabolite of APAP was the phenolic glucuronide (APAP-G), followed by p-aminophenol glucuronide (PAP-G) formed from N-deacetylated APAP. The PAP produced by N-deacetylation was the likely cause of the methaemoglobinemia and kidney toxicity observed in this, and previous, studies in the pig. The phenolic sulfate of APAP, and the glutathione-derived metabolites of the drug were only found as minor components (with the cysteinyl conjugate detected but not the mercapturate). Given its low sulfation, combined with significant capacity for N-deacetylation the pig may represent a poor translational model for toxicology studies for compounds undergoing significant metabolism by sulfation, or which contain amide bonds which when hydrolysed to unmask an aniline lead to toxicity. However, the pig may provide a useful model where extensive amide hydrolysis is seen for drugs or environmental chemicals in humans, but not in e.g., the rat and dog which are the pre-clinical species normally employed for safety assessment.

2630 related Products with: Metabolism and Effects on Endogenous Metabolism of Paracetamol (Acetaminophen) in a Porcine Model of Liver Failure.

Liver cancer tissue array Mid advanced stage liver Liver cancer tissue array Liver cancer tissue array Liver carcinoma and norma Liver cancer survey tissu Liver cancer tissue array Alkaline Phospatase (ALP) Liver cancer and normal t Human Bone Metabolism Ar Liver late stage tumor ti Liver cancer test tissue

Related Pathways

paperclip

#32061110   // Save this To Up

Melatonin and circadian rhythms in liver diseases: Functional roles and potential therapies.

Circadian rhythms and clock gene expressions are regulated by the suprachiasmatic nucleus in the hypothalamus, and melatonin is produced in the pineal gland. Although the brain detects the light through retinas and regulate rhythms and melatonin secretion throughout the body, the liver has independent circadian rhythms and expressions as well as melatonin production. Previous studies indicate the association between circadian rhythms with various liver diseases, and disruption of rhythms or clock gene expression may promote liver steatosis, inflammation, or cancer development. It is well known that melatonin has strong antioxidant effects. Alcohol drinking or excess fatty acid accumulation produces reactive oxygen species and oxidative stress in the liver leading to liver injuries. Melatonin administration protects these oxidative stress-induced liver damage and improves liver conditions. Recent studies have demonstrated that melatonin administration is not limited to antioxidant effects and it has various other effects contributing to the management of liver conditions. Accumulating evidence suggests that restoring circadian rhythms or expressions as well as melatonin supplementation may be promising therapeutic strategies for liver diseases. This review summarizes recent findings for the functional roles and therapeutic potentials of circadian rhythms and melatonin in liver diseases.

2937 related Products with: Melatonin and circadian rhythms in liver diseases: Functional roles and potential therapies.

Multiple diseases of live Liver cancer tissue array LIVER DISEASES 5' Nucleot Liver cancer tissue array (5α,16β)-N-Acetyl-16-[2 Liver cancer test tissue Liver cancer tissue array (5α)-Androst-2-en-17-one HIV Self Test Kit, 1Test 1,4 Androstadiene 3,17 di ELISA 5α-Androstane-3α, ∆1-Androstene-3α,17β-

Related Pathways

paperclip

#32061077   // Save this To Up

Concurrent Hepatotoxicity and Neutropenia Induced by Clozapine.

Clozapine is known as one of the atypical antipsychotics which is placed in the second line of medical treatment for schizophrenia due to its hematologic complications. It is used in cases of resistance to treatment. Some side effects of clozapine include leukopenia, granulocytopenia, fever, hepatotoxicity, sedation, dizziness, hypotension, weight gain, constipation, and seizure. Neutropenia and hepatotoxicity have been separately reported after taking atypical antipsychotics, including clozapine. However, simultaneous occurrence of these two complications is rare and has not been reported with clozapine use. This study reports a case of concurrent hepatotoxicity and neutropenia induced by clozapine. The patient was a 58-year-old man who started taking clozapine for the first time in March 2017, about seven weeks before his recent admission, because of a history of treatment-resistant schizophrenia. He had been referred to the emergency department of a general hospital with symptoms of weakness, lethargy, fever, and chills. The laboratory results showed neutropenia with a frequency of 352 × 103 (17.5%) and hepatotoxicity with alanine transferase (ALT) = 139 u/L, aspartate transferase (AST) = 214 u/L, total bilirubin = 11.5 mg/dL, and direct bilirubin = 9.3 mg/Dl, caused by taking clozapine. The symptoms were attenuated within eight days after discontinuation of clozapine. Moreover, the patient's para-clinical complications including neutropenia, and raised transaminases and bilirubin returned to normal. It was concluded that clozapine can simultaneously cause neutropenia and hepatotoxicity; physicians are recommended to be aware of this issue to prevent mortality through appropriate and timely diagnosis.

1658 related Products with: Concurrent Hepatotoxicity and Neutropenia Induced by Clozapine.



Related Pathways