Pathology of Eupatorium adenophorum (Sticky snakeroot) toxicity in mice

The leaves of Eupatorium adenophorum Spreng were powdered and extracted with methanol.  An acute oral toxicity study was conducted in male Swiss albino mice and a LD50 of 3501 mg/kg was obtained during 14 days observation period. Twenty Swiss albino mice (male) randomly divided into four groups were administered orally with vehicle (5% tween 80), 1/20th (i.e. 175 mg/kg), 1/10th (i.e. 350 mg/kg) and 1/5th (i.e. 750 mg/kg) LD50 doses of methanolic leaf extract of E. adenophorum Spreng; respectively for a period of 30 days. The mice were sacrificed on day-31 and the liver dissected out freed from adherent tissue weighed to nearest milligram. The  liver histology, estimations of biochemical contents and enzyme activities were carried out. Treatment of the mice with methanolic extract of E. adenophorum at the dose level of 750 mg/kg (i.e. 1/5th LD50) elicited hepatotoxicity and the animals had yellow discoloration of liver, subcutaneous tissue and musculature indicating jaundice. Study on liver enzymes revealed marked increase in the activities of alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST) and lactate dehydrogenase (LDH), while significant increase in serum bilirubin level. Histopathological examination of the livers of the group IV animals had focal areas of necrosis and bile duct proliferation. Elevation in plasma bilirubin concomitant with alterations in enzyme profile and histopathological lesions are consistent with liver injury and cholestasi

Particle density fluctuations

Event-by-event fluctuations in the multiplicities of charged particles and photons at SPS energies are discussed. Fluctuations are studied by controlling the centrality of the reaction and rapidity acceptance of the detectors. Results are also presented on the event-by-event study of correlations between the multiplicity of charged particles and photons to search for DCC-like signals.Comment: Talk presented at Quark Matter 2002, Nantes, Franc

cAMP increases liver Na+-taurocholate cotransport by translocating transporter to plasma membranes

Adenosine 3',5'-cyclic monophosphate (cAMP), acting via protein kinase A, increases transport maximum of Na+-taurocholate cotransport within 15 min in hepatocytes (S. Grüne, L. R. Engelking, and M. S. Anwer. J. Biol. Chem. 268: 17734-17741, 1993); the mechanism of this short-term stimulation was investigated. Cycloheximide inhibited neither basal nor cAMP-induced increases in taurocholate uptake in rat hepatocytes, indicating that cAMP does not stimulate transporter synthesis. Studies in plasma membrane vesicles showed that taurocholate uptake was not stimulated by the catalytic subunit of protein kinase A but was higher when hepatocytes were pretreated with cAMP. Immunoblot studies with anti-fusion protein antibodies to the cloned Na+-taurocholate cotransport polypeptide (Ntcp) showed that pretreatment of hepatocytes with cAMP increased Ntcp content in plasma membranes but not in homogenates. Ntcp was detected in microsomes, endosomes, and Golgi fractions, and cAMP pretreatment resulted in a decrease only in endosomal Ntcp content. It is proposed that cAMP increases transport maximum of Na+-taurocholate cotransport, at least in part, by translocating Ntcp from endosomes to plasma membranes