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J Cutan Med Surg. 2003 Jan-Feb;7(1):38-42. Epub 2002 Oct 09.
Foreign body granuloma: a new manifestation of immune restoration syndrome.
Murray CA, DeKoven J, Spaner DE.
Division of Dermatology, University of Toronto, Toronto, Ontario, Canada.
BACKGROUND: People with human immunodeficiency virus may experience an immune restoration syndrome during the lymphocyte recovery period following effective highly active antiretroviral therapy. In this syndrome, antigens that previously were ignored by the immune system now induce an exaggerated response with obvious clinical effects. Most cases have been associated with infectious agents such as cytomegalovirus or mycobacterium avium intracellulare. However, the sudden onset of sarcoidal granulomatous reactions have also been described in this setting. OBJECTIVE: We report a 66-year-old HIV-positive man who presented with exacerbation of multiple foreign body granulomas decades after the original injuries. The presentation coincided with a significant rise in CD4 count after beginning highly active antiretroviral therapy. CONCLUSION: We propose that this case demonstrates another manifestation of the immune restoration syndrome and postulate that an uncontrolled Th1 response is the causative mechanism.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12362265&dopt=Abstract
Acta Biochim Pol. 2002;49(2):295-302.
Tumors and the danger model.
Kowalczyk DW.
Department of Cancer Immunology, K Marcinkowski University School of Medical Sciences, GreatPoland Cancer Center, Poznan. dkowalczyco.pl
This article reviews the evidence for the danger model in the context of immune response to tumors and the insufficiency of the immune system to eliminate tumor growth. Despite their potential immunogenicity tumors do not induce significant immune responses which could destroy malignant cells. According to the danger model, the immune surveillance system fails to detect tumor antigens because transformed cells do not send any danger signals which could activate dendritic cells and initiate an immune response. Instead, tumor cells or antigen presenting cells turn off the responding T cells and induce tolerance. The studies reviewed herein based on model tumor antigens, recombinant viral vectors and detection of tumor specific T cells by MHC/peptide tetramers underscore the critical role of tumor antigen presentation and the context in which it occurs. They indicate that antigen presentation only by activated but not by cancer or resting dendritic cells is necessary for the induction of immune responses to tumor antigens. It becomes apparent that the inability of dendritic cells to become activated provides a biological niche for tumor escape from immune destruction and seems to be a principal mechanism for the failure of tumor immune surveillance.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12362970&dopt=Abstract [PubMed - in process]
Acta Biochim Pol. 2002;49(2):313-21.
Antiangiogenic gene therapy in inhibition of metastasis.
Szala S, Szary J, Cichon T, Sochanik A.
Department of Molecular Biology, Center of Oncology-Maria Sklodowska-Curie Memorial Institute, Gliwice, Poland. sszalo.gliwice.pl
This short review attempts to demonstrate the usefulness of antiangiogenic gene therapy in achieving inhibition of growth in experimentally-induced metastases. Certain normal tissues (for example skeletal muscle) may be used in vivo, after genetic modification, as a "bioreactor", able to produce and secrete into the bloodstream proteins known to exert antiangiogenic effects. By inhibiting neoangiogenesis these proteins would thus prevent the development of metastases. The review discusses also the perspectives of antimetastatic therapy based on certain types of allogenic cells (for example myoblasts and fibroblasts) that had been genetically modified and then microencapsulated. The strategy of encapsulation is aimed at protecting the modified cells secreting antiangiogenic factors from being eliminated by the immune system. Secretion of antiangiogenic proteins by these microencapsulated cells can be controlled with inducible promoters. Antiangiogenic genes remaining under the transcriptional control of such promoters may be switched on and off using antibiotics, such as tetracycline derivatives, or steroid hormones.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12362972&dopt=Abstract [PubMed - in process]
Immunol Rev. 2002 Sep;187:48-64.
Human hematopoietic lineage commitment.
Payne KJ, Crooks GM.
Childrens Hospital Los Angeles, Division of Research Immunology/Bone Marrow Transplantation, Los Angeles, CA, USA. kpaynhla.usc.edu
The ultimate goal of developmental immunology is to understand the normal processes that give rise to the immune system in order to diagnose and develop effective treatments for diseases that occur as a consequence of immune system defects. Central to achieving this goal is understanding the complex interplay between microenvironmental signals and transcription factors that direct human hematopoietic differentiation and lineage commitment. The ability to isolate highly purified populations of human hematopoietic cells at critical points in differentiation make it possible to answer very specific questions about the hematopoietic process and lineage restriction. This review describes the use of surface immunophenotypes to identify human hematopoietic cells at particular points in differentiation or with particular patterns of lineage restriction. Culture models are discussed in the context of the ability to detect, characterize and determine the lineage potential of human hematopoietic stem cells and progenitors. Variations in hematopoeises that correspond to ontogeny will be examined. Potential roles for the HOX and Ikaros proteins in human lineage commitment will be considered. Also included will be discussion of a number of factors that provide challenges to experimental design, to experimental interpretation, and to the development of a comprehensive model of human hematopoiesis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12366682&dopt=Abstract [PubMed - in process]
Mol Microbiol. 2002 Oct;46(1):157-68.
Proteinases of common pathogenic bacteria degrade and inactivate the antibacterial peptide LL-37.
Schmidtchen A, Frick IM, Andersson E, Tapper H, Bjorck L.
Section for Dermatology, Department of Medical Microbiology, Dermatology and Infection, Biomedical Center, B14, Tornavagen 10, S-22184 Lund, Sweden. artur.schmidtcheerm.lu.se
Effectors of the innate immune system, the anti-bacterial peptides, have pivotal roles in preventing infection at epithelial surfaces. Here we show that proteinases of the significant human pathogens Pseudomonas aeruginosa, Enterococcus faecalis, Proteus mirabilis and Streptococcus pyogenes, degrade the antibacterial peptide LL-37. Analysis by mass spectrometry of fragments generated by P. aeruginosa elastase in vitro revealed that the initial cleavages occurred at Asn-Leu and Asp-Phe, followed by two breaks at Arg-Ile, thus inactivating the peptide. Proteinases of the other pathogens also degraded LL-37 as determined by SDS-PAGE. Ex vivo, P. aeruginosa elastase induced LL-37 degradation in human wound fluid, leading to enhanced bacterial survival. The degradation was blocked by the metalloproteinase inhibitors GM6001 and 1, 10-phenantroline (both of which inhibited P. aeruginosa elastase, P. mirabilis proteinase, and E. faecalis gelatinase), or the inhibitor E64 (which inhibited S. pyogenes cysteine proteinase). Additional experiments demonstrated that dermatan sulphate and disaccharides of the structure [DeltaUA(2S)-GalNAc(4,6S)], or sucroseoctasulphate, inhibited the degradation of LL-37. The results indicate that proteolytic degradation of LL-37 is a common virulence mechanism and that molecules which block this degradation could have therapeutic potential.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12366839&dopt=Abstract
The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes
Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs.
However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals.
The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime.
Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.
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.
Our bodies produce decreasing amount of DHEA as we get older.
various health benefits: To deter aging,
improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance,
facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions,
and treat depression.
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