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Antioxid Redox Signal. 2002 Oct;4(5):711-20.
Hepatic redox regulation of transcription factors activator protein-1 and nuclear factor-kappaB after hemorrhagic shock in vivo.
Paxian M, Bauer I, Kaplan D, Bauer M, Rensing H.
Department of Anesthesiology and Critical Care Medicine, University of the Saarland, D-66421 Homburg, Germany.
Ischemia and reperfusion result in a hepatocellular stress gene response, characterized by a zonal heterogeneity with pericentral hepatocytes being the primary target. In the present study, we assessed cell type-specific and zonal pattern of activation of redox-sensitive transcription factors nuclear factor-kappaB (NFkappaB) and activator protein-1 (AP-1) in a graded model of hemorrhage and their modulation by the antioxidants trolox and tempol. Hemorrhagic hypotension (35-40 mm Hg) up to 3 h without subsequent resuscitation led to an only moderate activation of NFkappaB and AP-1. In contrast, fluid resuscitation after 1 or 2 h of hemorrhage induced a profound activation of AP-1 within the first hour of reperfusion. Consistent with a regulation by oxygen free radicals, activation of AP-1 was substantially attenuated by antioxidants. The faint activation of NFkappaB with various intervals of hemorrhage was unaffected by antioxidants and did not exceed activation with sham operation. Immunohistochemistry for the AP-1 subunit c-Jun revealed a predominant expression in nuclei of pericentral and midzonal hepatocytes. These data suggest activation of AP-1 in hepatocytes most susceptible to injury and reprogramming of gene expression in low-flow ischemia. Whereas activation of NFkappaB is weak in this model and is not modulated by either reperfusion or antioxidants, regulation of AP-1 after hemorrhage and subsequent resuscitation seems to depend on oxygen free radical formation because it requires reperfusion and is inhibitable by antioxidants.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12470498&dopt=Abstract hemorrhage
Antioxid Redox Signal. 2002 Oct;4(5):733-40.
Reactive oxygen as modulator of TNF and fas receptor-mediated apoptosis in vivo: studies with glutathione peroxidase-deficient mice.
Bajt ML, Ho YS, Vonderfecht SL, Jaeschke H.
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205-7199, USA. Bajtjaeschkemaryams.edu
Reactive oxygen species (ROS) can directly induce or enhance tumor necrosis factor (TNF)-mediated apoptosis in a number of different cell lines. To test the relevance of intracellular ROS in modulating apoptotic signaling in vivo, we evaluated hepatocellular apoptosis mediated by the TNF or Fas receptor in wild-type and glutathione peroxidase-1 (Gpx1-/-)-deficient mice (129SV/B6 background). Apoptosis developed in livers of wild-type animals 4-6 h after intraperitoneal administration of 700 mg/kg galactosamine/100 micro g/kg endotoxin. Apoptosis was indicated by processing of procaspases-3 (assessed by western blotting), a fivefold increase in caspase-3 activity (DEVD-AMC as substrate), and a 44-fold increase in DNA fragmentation (ELISA). The time course and magnitude of apoptosis were the same in Gpx1-/- mice. In contrast, Gpx1-/- mice had higher plasma alanine aminotransferase (ALT) levels and more severe hemorrhage compared to wild-type animals at 6 h. Treatment of wild-type mice with the anti-Fas antibody Jo-2 (0.6 mg/kg i.v.) resulted in processing of procaspase-3 and a sevenfold increase in caspase-3 activity in both wild-type and Gpx1-/- mice. However, higher plasma ALT values in Gpx1-/- mice at 3 h may reflect a trend to develop more rapidly secondary necrosis. These data suggest that, under our experimental conditions, intracellular ROS did not modulate the death receptor-initiated apoptotic signaling cascade in hepatocytes. As Gpx1 is located in the cytosol and in mitochondria, which are the main cellular compartments involved in apoptotic signaling, our findings indicate that the oxidant stress in vivo was insufficient to modulate these signaling pathways. However, Gpx1 deficiency enhances the susceptibility for secondary necrosis or neutrophil-induced cell injury.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12470500&dopt=Abstract hemorrhage
Am J Ophthalmol. 2002 Dec;134(6):911-2.
Ophthalmodynamometric diagnosis of unilateral ischemic ophthalmopathy.
Jonas JB, Niessen A.
Department of Ophthalmology, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Mannheim, Germany. Jost.Jonaugen.ma.uni-heidelberg.de
PURPOSE: To describe a patient presenting with typical signs of vascular occlusive retinopathy. DESIGN: Observational case report. METHODS: A 65-year-old man experienced painless unilateral loss of vision to 4/20 in his left eye. Ophthalmoscopy of the left eye showed pronounced attenuation of the retinal arterioles, ischemic retinal edema, and a few intraretinal hemorrhages. Fluorescein angiography revealed a diffusely reduced retinal perfusion typical of retinal occlusive disease. Using a new ophthalmodynamometer with a pressure sensor at the mounting support of a conventional Goldmann contact lens, we additionally measured the diastolic central retinal artery collapse pressure. RESULTS: The diastolic central retinal artery collapse pressure was significantly lower in the left eye than in the right eye (14.7 +/- 2.4 relative units vs 51.7 +/- 4.3 relative units; P <.001). Both values were significantly (P =.03) lower than those in a control group (80.9 +/- 6.9 relative units). Doppler sonography revealed a total occlusion of the left carotid artery and a nonrelevant stenosis of the right carotid artery. CONCLUSIONS: A new ophthalmodynamometric device consisting of a pressure sensor at the mounting support of a Goldmann contact lens was helpful in detecting carotid artery occlusion leading to ischemic ophthalmopathy.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12470765&dopt=Abstract hemorrhage
Am J Ophthalmol. 2002 Dec;134(6):920-2.
Morphometric change analysis of the optic nerve head in unilateral disk hemorrhage cases.
Ahn JK, Park KH.
Department of Ophthalmology, Seoul National University College of Medicine, Chongno-gu, South Korea.
PURPOSE: To measure the changes in optic disk morphology after unilateral disk hemorrhage and to compare the changes between eyes. DESIGN: Observational case series. METHODS: Ten glaucoma patients who had a unilateral disk hemorrhage were enrolled. The baseline measurements obtained by Heidelberg Retina Tomograph (HRT) were performed on both eyes when a disk hemorrhage was detected, and the second measurements were done after an average of 32 +/- 19 months. The amount of change and the percent change in the HRT parameters from the baseline measurements of the hemorrhagic eyes were compared with those of the contralateral nonhemorrhagic eyes. RESULTS: The reduction in the neuroretinal rim area and the decrease in volume were significantly greater in the octant with the disk hemorrhage than measured in the contralateral eyes (P =.002, Wilcoxon signed rank test). CONCLUSIONS: This study demonstrated quantitatively that the progression of optic disk damage in glaucoma is faster in eyes with disk hemorrhage than in eyes without disk hemorrhage.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12470770&dopt=Abstract hemorrhage
Am J Ophthalmol. 2002 Dec;134(6):927-9.
Recurrent episodes of spontaneous subconjunctival hemorrhage in patients with factor XIII Val34Leu mutation.
Incorvaia C, Costagliola C, Parmeggiani F, Gemmati D, Scapoli GL, Sebastiani A.
Department of Ophthalmology, University of Ferrara, Ferrara, Italy. sbns.unife.it
PURPOSE: To report on the occurrence of frequent episodes of spontaneous subconjunctival hemorrhage (SCH) in patients with the Leu 34 allele of the coagulation factor XIII (FXIII), known to be associated with high hemorrhagic risk. DESIGN: Observational case series. METHODS: Five young adults who had suffered from recurrent idiopathic SCH not associated with any recognized ocular and systemic hemorrhagic risk factor were investigated. Accurate anamnestic, ophthalmologic, hematologic, and serologic examinations were performed, together with blood pressure measurements, electrocardiogram (ECG), and 24-hour Holter ECG recordings. FXIII Val34Leu polymorphism was studied by DNA chain polymerase reaction. RESULTS: DNA analyses showed that the hemorrhagic mutated Leu34 allele was present in four of our selected patients: two mutated homozygotes (Leu/Leu) and two heterozygotes (Val/Leu). In the last subject this polymorphism was not detected. All the other clinical evaluations did not disclose any significant abnormality. CONCLUSIONS: The FXIII Val34Leu mutation may be associated with an increased risk for spontaneous episodes of SCH.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12470774&dopt=Abstract hemorrhage
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