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Eur J Dermatol. 2000 Oct-Nov;10(7):555-8.
Angiosarcoma arising on rhinophyma.

Gallardo MA, Bosch RJ, Vidal L, Cabra B, Rodrigo AB, De Galvez MV, Herrera E.

Department of Dermatology and Venereology, Catedra de Dermatologia Facultad de Medicina Campus Universitario Teatinos 29010 Malaga, Spain.

We report an 82-year-old man who presented with a tumor which had developed over the previous year on the right nasal ala of a rhinophyma. Histopathological, immunohistochemical, and electron microscopic study confirmed the diagnosis of angiosarcoma on the head and neck. He was treated with radiotherapy of the tumor and cervical adenopathy, which developed later. The possible etiological and pathogenetic role of lymphedema due to inflammatory flares of rosacea on the nose is discussed, together with the histological and immunohistochemical data leading to the diagnosis of this tumor.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056431&dopt=Abstract



Surgery. 2000 Nov;128(5):806-14.
Macrophages infiltrating the tissue in chronic pancreatitis express the chemokine receptor CCR5.

Goecke H, Forssmann U, Uguccioni M, Friess H, Conejo-Garcia JR, Zimmermann A, Baggiolini M, Buchler MW.

Department of Visceral and Transplantation Surgery, the Theodor-Kocher Institute, and the Institute of Pathology, University of Bern, Bern, Switzerland.

BACKGROUND: The immunologic mechanisms involved in the development of chronic pancreatitis (CP) are poorly understood. Chronically inflamed tissues contain increased numbers of mononuclear cells expressing the CC chemokine receptor 5 (CCR5), which is also a coreceptor for HIV entry of macrophagetropic strains. However, whether this receptor is involved in the inflammatory process in CP is not known. In the current study, we analyzed the expression of CCR5 in CP. The detection of chemokine receptors on inflammatory cells would strongly suggest their involvement in the pathogenesis of CP (i.e., attraction and activation of these cells). To further evaluate this, we consecutively analyzed the expression of 2 ligands of CCR5: RANTES and MIP-alpha. METHODS: Pancreatic tissue samples of 22 patients with CP and of 7 healthy pancreas were evaluated. CCR5, RANTES, and MIP-1alpha were analyzed by Northern blot analysis. Consecutive tissue sections were stained for CCR5, CD3, and CD68 to define the leukocyte subtype expressing CCR5 in CP. RESULTS: By Northern blot analysis, CCR5, RANTES, and MIP-1alpha messenger RNA (mRNA) levels were 12.9-fold, 13.3-fold and 9.2-fold higher in CP specimens compared with healthy controls, respectively (P<.01). Immunostaining for CCR5 revealed a 30-fold increase of CCR5-positive cells in CP tissue compared with the healthy pancreas. Staining of consecutive tissue sections revealed that the majority of CCR5-positive cells were also CD68-positive (macrophages). CONCLUSIONS: Our data indicate that a remarkable portion of CCR5-positive cells in CP are macrophages. CCR5 is most likely involved in the attraction and activation of these macrophages, since the CCR5 ligands RANTES and MIP-1alpha are concomitantly upregulated.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056444&dopt=Abstract



Arthritis Res. 1999;1(1):81-91. Epub 1999 Oct 26.
Protection against cartilage and bone destruction by systemic interleukin-4 treatment in established murine type II collagen-induced arthritis.

Joosten LA, Lubberts E, Helsen MM, Saxne T, Coenen-de Roo CJ, Heinegard D, van den Berg WB.

Department of Rheumatology, University Hospital Nijmegen, Nijmegen, The Netherlands. l.joosteeuma.azn.nl

INTRODUCTION: Rheumatoid arthritis (RA) is associated with an increased production of a range of cytokines including tumour necrosis factor (TNF)-alpha and interleukin (IL)-1, which display potent proinflammatory actions that are thought to contribute to the pathogenesis of the disease. Although TNF-alpha seems to be the major cytokine in the inflammatory process, IL-1 is the key mediator with regard to cartilage and bone destruction. Apart from direct blockage of IL-1/TNF, regulation can be exerted at the level of modulatory cytokines such as IL-1 and IL-10. IL-4 is a pleiotropic T-cell derived cytokine that can exert either suppressive or stimulatory effects on different cell types, and was originally identified as a B-cell growth factor and regulator of humoral immune pathways. IL-4 is produced by activated CD4+T cells and it promotes the maturation of TH2 cells. IL-4 stimulates proliferation, differentiation and activation of several cell types, including fibroblasts, endothelial cells and epithelial cells. IL-4 is also known to be a potent anti-inflammatory cytokine that acts by inhibiting the synthesis of proinflammatory cytokines such as IL-1, TNF-alpha, IL-6, IL-8 and IL-12 by macrophages and monocytes. Moreover, IL-4 stimulates the synthesis of several cytokine inhibitors such as interleukin-1 receptor antagonist (IL-1Ra), soluble IL-1-receptor type II and TNF receptors IL-4 suppresses metalloproteinase production and stimulates tissue inhibitor of metalloproteinase-1 production in human mononuclear phagocytes and cartilage explants, indicating a protective effect of IL-4 towards extracellular matrix degradation. Furthermore, IL-4 inhibits both osteoclast activity and survival, and thereby blocks bone resorption in vitro. Of great importance is that IL-4 could not be detected in synovial fluid or in tissues. This absence of IL-4 in the joint probably contributes to the disturbance in the Th1/Th2 balance in chronic RA. Collagen-induced arthritis (CIA) is a widely used model of arthritis that displays several features of human RA. Recently it was demonstrated that the onset of CIA is under stringent control of IL-4 and IL-10. Furthermore, it was demonstrated that exposure to IL-4 during the immunization stage reduced onset and severity of CIA. However, after cessation of IL-4 treatment disease expression increased to control values. AIMS: Because it was reported that IL-4 suppresses several proinflammatory cytokines and matrix degrading enzymes and upregulates inhibitors of both cytokines and catabolic enzymes, we investigated the tissue protective effect of systemic IL-4 treatment using established murine CIA as a model. Potential synergy of low dosages of anti-inflammatory glucocorticosteroids and IL-4 was also evaluated. METHODS: DBA-1J/Bom mice were immunized with bovine type II collagen and boosted at day 21. Mice with established CIA were selected at day 28 after immunization and treated for days with IL-4, prednisolone, or combinations of prednisolone and IL-4. Arthritis score was monitored visually. Joint pathology was evaluated by histology, radiology and serum cartilage oligomeric matrix protein (COMP). In addition, serum levels of IL-1Ra and anticollagen antibodies were determined. RESULTS: Treatment of established CIA with IL-4 (1microgram/day) resulted in suppression of disease activity as depicted in Figure 1. Of great interest is that, although 1 microgram/day IL-4 had only a moderate effect on the inflammatory component of the disease activity, it strongly reduced cartilage pathology, as determined by histological examination (Fig. 1). Moreover, serum COMP levels were significantly reduced, confirming decreased cartilage involvement. In addition, both histological and radiological analysis showed that bone destruction was prevented (Fig. 1). Systemic IL-4 administration increased serum IL-1Ra levels and reduced anticollagen type II antibody levels. Treatment with low-dose IL-4 (0.1 microgram/day) was ineffective in suppressing disease score, serum COMP or joint destruction. Synergistic suppression of both arthritis severity and COMP levels was noted when low-dose IL-4 was combined with prednisolone (0.05 mg/kg/day), however, which in itself was not effective. DISCUSSION: In the present study, we demonstrate that systemic IL-4 treatment ameliorates disease progression of established CIA. Although clinical disease progression of established CIA. Although clinical disease progression was only arrested and not reversed, clear protection against cartilage and bone destruction was noted. This is in accord with findings in both human RA and animal models of RA that show that inflammation and tissue destruction sometimes are uncoupled processes. Of great importance is that, although inflammation was still present, strong reduction in serum COMP was found after exposure to IL-4. (ABSTRACT TRUNCATED)


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056663&dopt=Abstract



Arthritis Res. 1999;2(1):50-58. Epub 1999 Dec 01.
Clonal expansion is a characteristic feature of the B-cell repertoire of patients with rheumatoid arthritis.

Itoh K, Patki V V, Furie RA, Chartash EK, Jain RI, Lane L, Asnis SE, Chiorazzi N.

North Shore University Hospital, New York University School of Medicine, Manhasset, New York, USA.

STATEMENT OF FINDINGS: The present study was designed to analyze the level of B-cell clonal diversity in patients with rheumatoid arthritis by using HCDR3 (third complementarity determining region of the rearranged heavy chain variable region gene) length as a marker. A modified immunoglobulin VH gene fingerprinting method using either genomic DNA or complementary (c)DNA derived from B cells of the peripheral blood, synovial fluid, and tissues of several rheumatoid arthritis patients was employed. These assays permitted the detection and distinction of numerically expanded B-cell clones from activated but not numerically expanded B-cell clones. The present data suggest that B-cell clonal expansion is a common and characteristic feature of rheumatoid arthritis and that it occurs with increasing frequency from the blood to the synovial compartments, resulting in a narrowing of the clonal repertoire at the synovial level. These clonal expansions can involve resting, apparently memory B cells, as well as activated B cells. Furthermore, some of these individual expansions can persist over extended periods of time. These findings support the hypothesis that a chronic ongoing (auto)immune reaction is operative in rheumatoid arthritis and that this reaction, at least at the B-cell level, may be unique to each individual joint. A determination of the targets of these autoimmune reactions may provide valuable clues to help understand the immunopathogenesis of this disease.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056664&dopt=Abstract [PubMed - as supplied by publisher]



Arthritis Res. 1999;1(2):75-84. Epub 1999 Dec 22.
IFN-gamma production in response to in vitro stimulation with collagen type II in rheumatoid arthritis is associated with HLA-DRB1*0401 and HLA-DQ8.

Berg L, Ronnelid J, Sanjeevi CB, Lampa J, Klareskog L.

Karolinska Hospital, Stockholm, Sweden. louise.bermm.ki.se

STATEMENT OF FINDINGS: IFN-gamma was measured in supernatants after in vitro stimulation of peripheral blood mononuclear cells with collagen type II (CII), purified protein derivative or influenza virus. IFN-gamma production in response to CII was similar in rheumatoid arthritis (RA) patients and healthy control individuals. The IFN-gamma response to purified protein derivative and influenza virus was lower in RA patients, reflecting a general T-cell hyporesponsiveness in RA. After recalculating the response to CII taking this hyporesponsiveness into account the CII response was higher in RA patients, and was associated with human leucocyte antigen (HLA)-DRB1*0401 and HLA-DQA1*0301-DQB1*0302 (HLA-DQ8). Rheumatoid arthritis patients with elevated serum levels of immunoglobulin (Ig)G anti-CII antibodies had lower CII-induced IFN-gamma production than patients with low anti-CII levels. The relative increase in CII-reactivity in RA patients as compared with healthy control individuals, and the association of a higher response with RA-associated HLA haplotypes, suggest the existence of a potentially pathogenic cellular reactivity against CII in RA.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056667&dopt=Abstract [PubMed - in process]







Natural Herbal Supplement: Hair Million


Hair loss alone does not pose significant health problems. In fact, there are people who opt for baldness as an alternative hair style. However, in general, however, hair loss is not considered desirable.

The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer a biologically essential part of our body, just like appendix. The hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

While the hair loss and resulting baldness in general have not been proven to be related to underlying health problems, there are certain correlations between hair loss and health problems. For instance, premature hair loss could suggest premature aging or nutritional and hormonal imbalance, stressful life, use of drugs that cause hair loss as a side effect, skin disease, or heart disease. The balding appearance could also impart a subdued impression of integrity in bodily health and youthfulness.












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. 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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