Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
488.2±45.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:1603-47-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Amyotrophic lateral sclerosis (ALS) is a progressive, fatal neurodegenerative disease characterized by the selective death of motor neurons. While the most common form of ALS is sporadic and has no known cause, a small subset of cases is familial because of underlying genetic mutations. The best-studies example of familial ALS is that caused by mutations in the protein copper-zinc superoxide dismutase. The formation of SOD1-rich inclusions in the spinal cord is an early and prominent feature of SOD1-linked familial ALS in human patients and animal models of this disease. These inclusions have been shown to consist of SOD1-rich fibrils, suggesting that the conversion of soluble SOD1 into amyloid fibrils may play an important role in the etiology of familial ALS. SOD1 is also present in inclusions found in spinal cords of sporadic ALS patients, allowing speculations to arise regarding a possible involvement of SOD1 in the sporadic form of this disease. We here review the recent research on the significance, causes, and mechanisms of SOD1 fibril formation from a biophysical perspective. Antioxid. Redox Signal. 11, 1603-1614.
Aggregation of Copper-Zinc Superoxide Dismutase in Familial and Sporadic ALS
Madhuri Chattopadhyay and Joan Selverstone Valentinecorresponding author
OBJECTIVE: To provide an effective approach for family physicians treating children presenting with urinary tract infections (UTIs). QUALITY OF EVIDENCE: The information presented, and articles quoted, are drawn from both review of the literature and recent consensus guidelines. Data and recommendations come from prospective multicentre trials; retrospective reviews; expert consensus statements; and some smaller trials, commentaries, and editorials. MAIN MESSAGE: Urinary tract infections are often seen in family practice. Diagnosis requires suspicion and a realization that children, especially those younger than 2 years, often have very few, nonspecific signs of infection. Obtaining a proper urine sample is vital, because true infections require radiographic studies. Antibiotic prophylaxis is promoted because of the link between vesicoureteral reflux, recurrent UTIs, and renal scarring and hypertension. We generally provide prophylaxis until children are 3 or 4 years, when risk of damage from reflux is lessened and timely urine samples are easier to obtain for prompt therapy. Surgical opinion is sought only when medical management has failed. Failure is defined as either recurrent infections and pyelonephritis or poor renal growth. CONCLUSION: To diagnose UTIs in children, physicians must suspect them, obtain proper urine samples, order appropriate investigations to rule out underlying anatomic abnormalities, and treat with appropriate antibiotics considering both organism sensitivities and length of therapy.
Children's UTIs in the new millennium. Diagnosis, investigation, and treatment of childhood urinary tract infections in the year 2001.
C. T. White and D. G. Matsell
Purified staphylococcal alpha toxin was found to inhibit the active transport of sodium across the isolated toad bladder when applied to the serosal but not to mucosal surface. Heating or the addition of specific antitoxin abolished this effect. Low temperatures reduced this activity significantly. Application of vasopressin to the bladder serosa shortly after toxin resulted in only weak and transient stimulation of sodium transport; once maximal toxin activity had been established, exposure to the hormone was without effect. Transport in bladders previously stimulated by vasopressin was rapidly inhibited by alpha toxin. Concentrations that suppressed active sodium transport completely within 30-45 min produced a significant increase in oxygen consumption by minced bladder tissue within the same period; antitoxin neutralized this activity. 2,4-dinitrophenol also inhibited sodium transport and stimulated oxygen consumption by the toad bladder. The addition of 2,4 dinitrophenol to bladder tissue in which respiration was maximally stimulated by alpha toxin resulted in a further increase in respiratory rate. The addition of toxin to bladder tissue after its exposure to a concentration of 2,4 dinitrophenol known to uncouple oxidative phosphorylation produced a significant stabilization but no increment in respiratory rate. The data are consistent with the previously suggested action of staphylococcal alpha toxin on cell membranes and suggest that energy-dependent transport processes are inhibited. The stimulation of oxygen consumption may be due to an additional effect on oxidative phosphorylation.
Effect of purified staphylococcal alpha toxin on active sodium transport and aerobic respiration in the isolated toad bladder
James J. Rahal, Jr., Martin E. Plaut, and Louis Weinstein