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Cholesterol Crystals (cholesterol + crystal)
Selected AbstractsGallbladder Na+/H+ exchange activity is up-regulated prior to cholesterol crystal formationEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2005S. C. Narins Abstract Background, Gallbladder Na+ and H2O absorption are increased prior to gallstone formation and may promote cholesterol nucleation. Na+/H+ exchange (NHE) isoforms NHE2 and NHE3 are involved in gallbladder Na+ transport in prairie dogs. We examined whether increased gallbladder Na+ absorption observed during early gallstone formation is the result of NHE up-regulation. Materials and methods, Native gallbladder and primary cultures of gallbladder epithelial cells (GBECs) harvested from prairie dogs fed nonlithogenic (CON) or 1·2% cholesterol diet for varying lengths of time to induce cholesterol-saturated bile (PreCRYS), cholesterol crystals (CRYS), or gallstones (GS) were used. NHE activity was assessed by measuring dimethylamiloride-inhibitable 22Na+ uptake under H+ gradient in primary GBECs. HOE-694 was used to determine NHE2 and NHE3 contributions. NHE protein and mRNA expression were examined by Western and Northern blots, respectively. Results, Gallbladder total NHE activity was 25·1 ± 1·3 nmol mg protein,1 min,1 in the control and increased during gallstone formation peaking at the PreCRYS stage (98·4 ± 3·9 nmol mg protein,1 min,1). There was a shift in NHE activity from NHE2 to NHE3 as the animals progressed from no stones through the PreCRYS and CRYS stages to gallstones. The increase in NHE activity was partly caused by an increased Vmax without any change in KNam. Both NHE2 and NHE3 protein increased moderately during the PreCRYS stage without increases in mRNA expression. Conclusions, Increased gallbladder Na+ absorption observed prior to crystal formation is in part caused by an increase NHE activity which is not fully accounted for by an increase in NHE proteins and mRNA levels but may be explained by enhanced localization in the membranes and/or altered regulation of NHE. [source] Case Report: Atheroembolic renal disease in a 72-year-old patient through coronary intervention after myocardial infarctionHEMODIALYSIS INTERNATIONAL, Issue 4 2008Anna Laura HERZOG Abstract Cholesterol embolization or atheroembolic renal disease (AERD) is an often underdiagnosed issue in patients featuring a prevalent risk profile. It is a multisystemic disease with progressive renal insufficiency due to foreign body reaction of cholesterol crystals flushed into a small vessel system of the kidneys from the arteriosclerotic plaques. The most common setting in which it occurs is iatrogenic after vascular catheterization and less frequent spontaneously. Typical clinical symptoms are delayed impairment of renal function, cutaneous manifestations such as livedo reticularis or purple toes with persistingly palpable arterial pulse, myalgia, systemic symptoms such as weight loss and fever, and abdominal and neurological symptoms. Diagnosis is generally made by clinical appearance, risk profile, and interval of time from intervention; a definitive diagnosis can only be made by renal biopsy. Even though the exact incidence is not known because most patients do not undergo biopsy due to older age, comorbidity, and other explanations for loss of renal function, it is estimated to be 4% after vascular intervention. Patient and renal outcome is dependent on comorbidity, risk profile, and preexisting chronic kidney disease (CKD). About 30% of patients are estimated to require maintenance dialysis and these patients have a high risk of death within 24 months after the first renal replacement therapy. Prognosis is also influenced by severity. The case reported is a 72-year-old male patient with preexisting CKD stage 3 undergoing percutaneous coronary intervention after myocardial infarction and consecutive AERD with typical clinical appearance 6 weeks after the event. [source] Review: low caloric intake and gall-bladder motor functionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000D. Festi Summary Cholelithiasis is the primary expression of obesity in the hepatobiliary system. In obese subjects the risk of developing gallstones is increased due to a higher cholesterol saturation of gall-bladder bile. During weight reduction with very low calorie diets (VLCD) the incidence of gallstones increases, but the mechanism for gallstone formation is not completely understood and several pathogenetic mechanisms have been suggested: increased saturation of bile, increased gall-bladder secretion of mucin and calcium, increased presence of prostaglandins and arachidonic acid. Alterations in gall-bladder motility may contribute to gallstone formation, but few studies have addressed the issue of gall-bladder motility during rapid weight loss and its possible role in gallstone formation. VLCD have been associated with a gall-bladder stasis, as a consequence of reduced gall-bladder stimulation by low fat content of the diets. A threshold quantity of fat (10 g) has been documented to obtain efficient gall-bladder emptying. Ursodeoxycholic acid administered during VLCD seems to have a protective role in developing a biliary cholesterol crystals. Gall-bladder emptying was lower in response to low fat meals with respect to relative higher fat meals, before as well as during the VLCD. This may account the possibility of an adaptative response of the gall-bladder motility to a given diet regimen. Adequate fat content of the VLCD may prevent gallstone formation, maintaining adequate gall-bladder motility and may be more economic and physiologically acceptable than administration of a pharmacological agent. [source] Microemboli may link spreading depression, migraine aura, and patent foramen ovaleANNALS OF NEUROLOGY, Issue 2 2010Ala Nozari MD Objective Patent foramen ovale and pulmonary arteriovenous shunts are associated with serious complications such as cerebral emboli, stroke, and migraine with aura. The pathophysiological mechanisms that link these conditions are unknown. We aimed to establish a mechanism linking microembolization to migraine aura in an experimental animal model. Methods We introduced particulate or air microemboli into the carotid circulation in mice to determine whether transient microvascular occlusion, insufficient to cause infarcts, triggered cortical spreading depression (CSD), a propagating slow depolarization that underlies migraine aura. Results Air microemboli reliably triggered CSD without causing infarction. Polystyrene microspheres (10,m) or cholesterol crystals (<70,m) triggered CSD in 16 of 28 mice, with 60% of the mice (40% of those with CSD) showing no infarcts or inflammation on detailed histological analysis of serial brain sections. No evidence of injury was detected on magnetic resonance imaging examination (9.4T; T2 weighted) in 14 of 15 selected animals. The occurrence of CSD appeared to be related to the magnitude and duration of flow reduction, with a triggering mechanism that depended on decreased brain perfusion but not sustained tissue damage. Interpretation In a mouse model, microemboli triggered CSD, often without causing microinfarction. Paradoxical embolization then may link cardiac and extracardiac right-to-left shunts to migraine aura. If translatable to humans, a subset of migraine auras may belong to a spectrum of hypoperfusion disorders along with transient ischemic attacks and silent infarcts. ANN NEUROL 2010;67:221,229 [source] | ||||||||||