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Fatty acids resources:

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Burns. 1999 Mar;25(2):171-8.
Acute renal failure in severely burned patients.

Holm C, Horbrand F, von Donnersmarck GH, Muhlbauer W.

Department of Plastic and Reconstructive Surgery, Hand Surgery, Burn Center, Krankenhaus Munchen-Bogenhausen, Academic Teaching Hospital, Technical University Munich, Germany. wmuehlbaue-online.de

Acute renal failure (ARF) is a well known complication of severe burns and is an important factor leading to an increase in mortality. In order to analyze possible pathogenetic and prognostic factors associated with ARF in burned patients we reviewed in a retrospective study the files of 328 patients with burns > 10% body surface area (BSA), admitted to our burn unit between 01.01.94 and 01.05.98. We found 48 patients with acute renal failure corresponding with an incidence of 14.6%. Patients with ARF had a mean burned surface area of 48% (13-95) and an abbreviated burn severity index score (ABSI) of 9.8 (4-15). Thirty eight (79%) of these patients had an inhalation injury diagnosed. Renal insufficiency was divided in a late and an early form depending on its time of onset and we found 15 (31%) patients with ARF occurring within the first 5 days of the hospital stay and 33 (69%) patients with ARF developing >5 days following the thermal injury. The incidence of myoglobinuria and hypotension during the resuscitation phase was significantly higher in the group with early ARF, whereas patients with late ARF presented sepsis more frequently than patients with early occurring renal failure. Accordingly, potential nephrotoxic antibiotics were administered more often in patients with late ARF. Patients with ARF were treated by continuous arteriovenous hemofiltration (CAVH) for a mean period of 10.5 days (1-47) and CAVH was associated with a complication rate of 10%. Most of the complications were associated with the vascular access in the femoral artery. The mortality rate in patients with ARF was 85% and death was due to multiple organ failure in 83% of the cases. Only burned BSA and inhalation injury proved to be significantly correlated with the development of ARF, whereas age, third degree burn or electric injury were not significantly different between the two groups. Neither age, TBSA, day of onset of ARF nor duration of the renal replacement therapy proved to be significantly different comparing survivors with non-survivors, and thus predictive for the survival rate.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10208394&dopt=Abstract



Biophys J. 2003 Aug;85(2):1176-85.
Molecular dynamics simulation of dimeric and monomeric forms of human prion protein: insight into dynamics and properties.

Sekijima M, Motono C, Yamasaki S, Kaneko K, Akiyama Y.

Computational Biology Research Center, National Institute of Advanced Industrial Science and Technology, 2-41-6 Aomi, Koto-ku, Tokyo 135-0064, Japan. sekijimbrc.jp

A central theme in prion protein research is the detection of the process that underlies the conformational transition from the normal cellular prion form (PrP(C)) to its pathogenic isoform (PrP(Sc)). Although the three-dimensional structures of monomeric and dimeric human prion protein (HuPrP) have been revealed by NMR spectroscopy and x-ray crystallography, the process underlying the conformational change from PrP(C) to PrP(Sc) and the dynamics and functions of PrP(C) remain unknown. The dimeric form is thought to play an important role in the conformational transition. In this study, we performed molecular dynamics (MD) simulations on monomeric and dimeric HuPrP at 300 K and 500 K for 10 ns to investigate the differences in the properties of the monomer and the dimer from the perspective of dynamic and structural behaviors. Simulations were also undertaken with Asp178Asn and acidic pH, which is known as a disease-associated factor. Our results indicate that the dynamics of the dimer and monomer were similar (e.g., denaturation of helices and elongation of the beta-sheet). However, additional secondary structure elements formed in the dimer might result in showing the differences in dynamics and properties between the monomer and dimer (e.g., the greater retention of dimeric than monomeric tertiary structure).


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12885661&dopt=Abstract [PubMed - in process]



Circulation. 2003 Aug 12;108(6):767-71. Epub 2003 Jul 28.
Prophylactic efficacy of topical temporin A and RNAIII-inhibiting peptide in a subcutaneous rat Pouch model of graft infection attributable to staphylococci with intermediate resistance to glycopeptides.

Cirioni O, Giacometti A, Ghiselli R, Dell'Acqua G, Gov Y, Kamysz W, Lukasiak J, Mocchegiani F, Orlando F, D'Amato G, Balaban N, Saba V, Scalise G.

Institute of Infectious Diseases and Public Health, University of Ancona, Ancona, Italy.

BACKGROUND: Bacteria that adhere to implanted medical devices play an important role in industry and in modern medicine. Staphylococci are among the most common pathogens that cause biomaterial infections. Vascular prosthetic graft infection is one of the most feared complications that the vascular surgeon treats, frequently resulting in prolonged hospitalization, organ failure, amputation, and death. A rat model was used to investigate the topical efficacies of temporin A and the quorum-sensing inhibitor RNAIII-inhibiting protein (RIP) as prophylactic agents of vascular prosthetic graft infections caused by Staphylococcus aureus and Staphylococcus epidermidis with intermediate resistance to glycopeptides. METHODS AND RESULTS: Graft infections were established in the back subcutaneous tissue of adult male Wistar rats by implantation of Dacron prostheses 1 cm2 followed by topical inoculation with 2x10(7) colony-forming units of bacterial strains. The study included, for each staphylococcal strain, a control group (no graft contamination), a contaminated group that did not receive antibiotic prophylaxis, and 6 contaminated groups that received grafts soaked with temporin A, RIP, rifampin, temporin A plus RIP, RIP plus rifampin, or temporin A plus RIP. The infection was evaluated by quantitative agar culture. When tested alone, temporin A and RIP showed comparable efficacies, and their efficacies were significantly higher than that of rifampin against both strains. All combinations showed efficacies significantly higher than that of each single compound. The combinations of temporin A and RIP exerted the strongest antistaphylococcal efficacies, eliminating infection by 100%. CONCLUSIONS: The results of the present study make these molecules potentially useful for antimicrobial chemoprophylaxis in vascular surgery.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12885754&dopt=Abstract [PubMed - in process]



Circulation. 2003 Aug 12;108(6):754-9. Epub 2003 Jul 28.
Disruption of leptin signaling contributes to cardiac hypertrophy independently of body weight in mice.

Barouch LA, Berkowitz DE, Harrison RW, O'Donnell CP, Hare JM.

Department of Medicine, Division of Cardiology, Johns Hopkins Hospital, 600 North Wolfe St, Baltimore, Md 21287, USA.

BACKGROUND: Whether left ventricular hypertrophy (LVH) in obesity results from increased hemodynamic load or altered neurohormonal signaling remains controversial. Dysregulation of leptin, a neurohormone essential to energy homeostasis, is implicated in the pathogenesis of obesity. Because leptin has cardiovascular bioactivity, we hypothesized that disruption of leptin signaling mediates the development of obesity-associated LVH. METHODS AND RESULTS: We measured left ventricular (LV) wall thickness and LV mass with echocardiography in mice lacking leptin (ob/ob, n=15) or functional receptor (db/db, n=10) and controls at 2, 4, and 6 months of age. None of the mice had LVH at 2 months. Progressive obesity developed in ob/ob and db/db mice. At 6 months, LVH occurred in ob/ob and db/db compared with controls. We observed corresponding myocyte hypertrophy by light microscopy. To separate the direct contribution of leptin deficiency from mechanical effects of obesity, we induced weight loss in 6- to 8-month-old ob/ob mice either by leptin infusion or caloric restriction. Mice in both groups lost similar weight compared with placebo-treated controls. Leptin infusion completely reversed the increase in wall thickness with partial resolution of myocyte hypertrophy, whereas calorie-restricted mice had no decrease in wall thickness and a lesser change in myocyte size. CONCLUSIONS: Together these data show that the effect of leptin on LV remodeling is not attributable to weight loss alone, indicating that leptin has antihypertrophic effects on the heart, either directly or through a leptin-regulated neurohumoral pathway. Disruption of leptin signaling may represent a novel mechanism in LVH and related cardiovascular disorders.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12885755&dopt=Abstract [PubMed - in process]



J Exp Med. 2003 Aug 4;198(3):379-89. Epub 2003 Jul 28.
Multiple T cell subsets control Francisella tularensis LVS intracellular growth without stimulation through macrophage interferon gamma receptors.

Cowley SC, Elkins KL.

Division of Bacterial, Parasitic, and Allergenic Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Rockville, MD 20852, USA. cowleber.fda.gov

A variety of data suggest that in vivo production of interferon (IFN)-gamma is necessary, but not sufficient, for expression of secondary protective immunity against intracellular pathogens. To discover specific IFN-gamma-independent T cell mediated mechanisms, we took advantage of an in vitro culture system that models in vivo immune responses to the intracellular bacterium Francisella tularensis live vaccine strain (LVS). LVS-immune lymphocytes specifically controlled 99% of the growth of LVS in wild-type murine bone marrow-derived macrophages. Surprisingly, LVS-immune lymphocytes also inhibited LVS intracellular growth by as much as 95% in macrophages derived from IFN-gamma receptor knockout (IFNgammaR KO) mice. CD8+ T cells, and to a lesser degree CD4+ T cells, controlled LVS intracellular growth in both wild-type and IFNgammaR KO macrophages. Further, a unique population of Thy1+alphabeta+CD4-CD8- cells that was previously suggested to operate during secondary immunity to LVS in vivo strongly controlled LVS intracellular growth in vitro. A large proportion of the inhibition of LVS intracellular growth in IFNgammaR KO macrophages by all three T cell subsets could be attributed to tumor necrosis factor (TNF) alpha. Thus, T cell mechanisms exist that control LVS intracellular growth without acting through the IFN-gamma receptor; such control is due in large part to TNF-alpha, and is partially mediated by a unique double negative T cell subpopulation.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12885873&dopt=Abstract [PubMed - in process]








Beautiful, dense hair is a dream for many people. Hair growth is a sophisticated biological process, which has not yet been understood. A multitude of therapeutic measures, including drugs, surgery, and suppelements have been developed. However, due to the diversity of the problems underlying hair loss, there is no single solution that can address all hair loss cases. Another problem is that most of chemical drugs and hair transplantation surgeries are not free from varying degrees of undesirable side effects on health.

Hair Million is an alternative solution to cope with hair loss problems. Anecdotally, it shows prositive results and improvement especially for age-related hair thinning and hair loss for a large group of people who take it as suggested. Although personal experiences and anecdotal evidences indicate that it works, we still do not understand the mechanisms of action as to how Hair Million works to help stop hair loss, and promote hair growth. There has been no clinical trials nor placebo controlled statistical analysis on the efficacy of Hair Million on hair loss and hair growth. R & D costs dearly, and no one would afford to research complex herbal ingredients, which are often not patentable at all because they are made by mother nature.














DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.







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