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Am J Gastroenterol. 2000 Oct;95(10):2966-8.
Transjugular intrahepatic portosystemic shunt for bleeding stomal varices associated with chronic portal vein occlusion: long-term angiographic, hemodynamic, and clinical follow-up.
Morris CS, Najarian KE.
Department of Radiology, Fletcher Allen Health Care, University of Vermont College of Medicine, Burlington, USA.
The efficacy of the transjugular intrahepatic portosystemic shunt procedure (TIPS) in controlling refractory hemorrhage from stomal varices at the mucocutaneous junction has been previously described, but the durability of this procedure for this indication is unknown. Conservative therapy may be unsuccessful in preventing recurrent hemorrhage. Some authors believe that portosystemic shunting is the treatment of choice for patients with bleeding stomal varices who are good surgical candidates, because of the low incidence of recurrent bleeding and the longest survival. We report the 39-month angiographic and hemodynamic follow-up, and the 48-month clinical follow-up of a patient with refractory hemorrhage from stomal varices and coexistent chronic portal vein occlusion successfully treated with a TIPS procedure.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11051377&dopt=Abstract hemorrhage
Vet Radiol Ultrasound. 2000 Sep-Oct;41(5):396-402.
The computed tomographic appearance of acute thoracolumbar intervertebral disc herniations in dogs.
Olby NJ, Munana KR, Sharp NJ, Thrall DE.
Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh 27606, USA.
The appearance of herniated intervertebral disc material in the thoracolumbar vertebral canal was evaluated in 23 dogs using computed tomography (CT). The images were then compared with the myelographic and surgical findings. The normal spinal cord, outlined by epidural fat over intervertebral disc spaces, was of intermediate attenuation on transverse CT images. Herniated disc material was identified in all animals as a heterogeneous hyperattenuating extradural mass. The attenuation of the disc material increased with the degree of mineralization. In seven dogs, the herniated material was only slightly more attenuating than the spinal cord. In these dogs, small fragments of mineralized disc material and significant hemorrhage were found in the epidural space at surgery. In dogs with a long standing history of disc herniations, disc material identified in the vertebral canal had a more hyperattenuating and homogeneous appearance than recently herniated disc material. We conclude that mineralized, herniated disc material and hemorrhage can be identified quickly and safely in dogs using CT.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11052360&dopt=Abstract hemorrhage
Toxicol Sci. 2000 Nov;58(1):109-17.
Protection against Fas receptor-mediated apoptosis in hepatocytes and nonparenchymal cells by a caspase-8 inhibitor in vivo: evidence for a postmitochondrial processing of caspase-8.
Bajt ML, Lawson JA, Vonderfecht SL, Gujral JS, Jaeschke H.
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA.
Lymphocytes can kill target cells including hepatocytes during various inflammatory diseases by Fas receptor-mediated apoptosis. Caspase-8 is activated at the receptor level, thereby initiating the processing of downstream effector caspases. The aim of this study was to investigate the time course of caspase-8 activation and to evaluate the efficacy of the caspase-8 inhibitor IETD-CHO in a model of Fas-induced apoptosis in vivo. C3Heb/FeJ mice were treated with the anti-Fas antibody Jo-2 (0.6 mg/kg). Western blot analysis demonstrated increased cytochrome c in the cytosol (20 min), which was followed by the progressive activation of caspase-3, -9 (40-120 min), and caspase-8 (120 min). At 90 and 120 min, extensive hemorrhage was observed, indicating damage to sinusoidal lining cells. In addition, high plasma ALT levels (997 +/- 316 U/L) and histological evaluation indicated severe parenchymal cell injury. Parenchymal and nonparenchymal cells showed a similar increase in caspase-3 activity and DNA fragmentation. Treatment with IETD-CHO (10 mg/kg) attenuated the increase in caspase-3 activity and DNA fragmentation by 80-90% and completely prevented hemorrhage and parenchymal cell damage. IETD-CHO also prevented the early release of mitochondrial cytochrome c and the processing of caspase-3, -8, and -9. Thus, our data support the hypothesis that Fas-mediated apoptosis is dependent on caspase-8 activation in hepatocytes and nonparenchymal cells. However, the bulk of procaspase-8 is processed late, suggesting that only a small amount of procaspase-8 may actually be activated at the Fas receptor. This initial signal may be amplified by further activation of caspase-8 by effector caspases, i.e., after mitochondrial activation. Caspase-8 is a promising therapeutic target for inhibition of Fas-mediated apoptosis.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11053547&dopt=Abstract hemorrhage
Thromb Res. 2000 Oct 1;100(1):61-72.
Activation of coagulation in C57BL/6 mice given verotoxin 2 (VT2) and the effect of co-administration of LPS with VT2.
Sugatani J, Igarashi T, Munakata M, Komiyama Y, Takahashi H, Komiyama N, Maeda T, Takeda T, Miwa M.
Department of Pharmaco-Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan.
To obtain better insight into the pathogenesis of verotoxin-producing Escherichia coli-associated diseases, in this study, we explored the effect of verotoxin 2 (VT2) on coagulation in an animal model. After being given VT2 (50 ng/kg, lethal dose), C57BL/6 mice showed progressively increasing expression of TF mRNA in the kidney and brain and elevated plasma levels of thrombin-antithrombin III complex (TAT), normotest, fibrinogen, and PAI-1 paralleling the disease course over 24 hours; platelet counts were decreased at 48 hours with hemorrhage in the kidney and brain. Co-administration of lipopolysaccharide (LPS, 0.5 mg/kg) with VT2 (50 ng/kg) exhibited more prominant and/or prolonged increase in not only expression of TF and PAI-1 mRNAs in the kidney and brain but also plasma levels of TAT, fibrinogen, and PAI-1 and was associated with more remarkable hemorrhage in the tissues. Although VT2 (5 ng/kg) was not a lethal dose, co-administration of LPS (0.5 mg/kg) with VT2 (5 ng/kg) enhanced the susceptibility to VT2, resulting in more prolonged elevation of TAT levels during the first 24 hours than that in the LPS group and a second elevation at 72 hours, followed by death. Plasma IL-1beta level reached a maximum at 24 hours after VT2 (50 ng/kg) injection prior to the increase in TAT levels, whereas the increase in TNFalpha level immediately after injection was associated with the increase in PAI-1 mRNA. These observations indicate that the activation of coagulation by VT2 may occur through a mechanism different from that used by LPS, since plasma TAT levels rose in the mice immediately after LPS injection and returned to normal over 36 hours.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11053618&dopt=Abstract hemorrhage
Free Radic Biol Med. 2000 Oct 15;29(8):764-74.
Resuscitative effects of polynitroxylated alphaalpha-cross-linked hemoglobin following severe hemorrhage in the rat.
Buehler PW, Mehendale S, Wang H, Xie J, Ma L, Trimble CE, Hsia CJ, Gulati A.
Department of Pharmaceutics and Pharmacodynamics, The University of Illinois, Chicago, IL 60612, USA.
alphaalpha-Cross-linked hemoglobin (alphaalphaHb) is an example of a hemoglobin-based oxygen carrier (HBOC) with significant cardiovascular activity. This may compromise the safety and efficacy of this HBOC by causing systemic hypertension and reducing blood flow to some organs. The present work is based on the hypothesis that incorporating antioxidant activity into an HBOC in the form of a covalently attached nitroxide may prevent these effects. We have tested this hypothesis by adding antioxidant activity to alphaalphaHb with 2,2,6,6-tetramethyl-piperidinyl-1-oxyl (Tempo) to create polynitroxylated alphaalphaHb (PN-alphaalphaHb). The new compound PN-alphaalphaHb acts as an antioxidant in our in vitro and in vivo assays. In this study urethane-anesthetized rats were hemorrhaged to a mean arterial pressure (MAP) of 35-40 mmHg and maintained for 30 min. Animals were resuscitated with solutions of (1) 10% PN-alphaalphaHb (43 mmHg), (2) 10% alphaalphaHb (43 mmHg), (3) 7.5% albumin (43 mmHg), (4) 300% Ringers lactate (RL), and (5) 0. 9% normal saline equal to the shed blood volume (SBV). Hemodynamics and regional blood circulation was measured at baseline, following hemorrhage, and at 30 and 60 min postresuscitation using a radioactive microsphere technique. Base deficit (BD) was measured at baseline, following hemorrhage, and at 60 min following resuscitative fluid infusion. Finally survival was determined as the time following resuscitation until secession of heart rhythm. Saline and 300% RL resuscitation did not improve BD, systemic hemodynamics, or regional blood circulation. PN-alphaalphaHb, alphaalphaHb, and albumin significantly improved these parameters, however, only PN-alphaalphaHb and alphaalphaHb improved survival. PN-alphaalphaHb was found to be less hypertensive than alphaalphaHb due to blunted increases in both cardiac output and systemic vascular resistance. This study demonstrates that, by using alphaalphaHb as a scaffold for polynitroxylation, improvement in vasoactivity and resuscitative efficacy may be possible. In conclusion, the addition of antioxidant activity in the form of polynitroxylation of a low molecular weight Hb (alphaalphaHb) may create a safe and efficacious resuscitative fluid.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11053778&dopt=Abstract hemorrhage
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