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On morphologic evaluation, the bone marrow is devoid of hem [link widoczny dla zalogowanych] On morphologic evaluation, the bone marrow is d [link widoczny dla zalogowanych] void of hematopoietic elements, showing largely [link widoczny dla zalogowanych] fat cells. Flow cytometry shows that the CD34-cell population [link widoczny dla zalogowanych] which contains the stem cells and the early committed pro [link widoczny dla zalogowanych] enitors, is substantially reduced. Data from in vi [link widoczny dla zalogowanych] ro colony-culture assays suggest profound functional loss of [link widoczny dla zalogowanych] the hematopoietic progenitors, so much so that they are [link widoczny dla zalogowanych] unresponsive even to high levels of hematopoietic growth fa [link widoczny dla zalogowanych] tors. Little evidence points to a defective microenvironment as
[link widoczny dla zalogowanych] a cause of aplastic anemia. In patients with severe aplasti [link widoczny dla zalogowanych] anemia (SAA), stromal cells have normal function, including gro [link widoczny dla zalogowanych] th factor production. Adequate stromal functi [link widoczny dla zalogowanych] n is implicit in the success of bone-marrow transplan [link widoczny dla zalogowanych] ation (BMT) in aplastic anemia because the stromal elements are [link widoczny dla zalogowanych] frequently of host origin. The role of an immune d [link widoczny dla zalogowanych] sfunction was suggested in 1970, when autolog [link widoczny dla zalogowanych] us recovery was documented in a patient with a [link widoczny dla zalogowanych] lastic anemia in whom engrafting failed after BMT. [link widoczny dla zalogowanych] Mathe proposed that the immunosuppress
ive regi [link widoczny dla zalogowanych] en used for conditioning promoted the return of normal marrow f [link widoczny dla zalogowanych] nction. Since then, numerous studies have shown that, in appr [link widoczny dla zalogowanych] ximately 70% of patients with acquired aplastic an [link widoczny dla zalogowanych] mia, immunosuppressive therapy improves marrow funct [link widoczny dla zalogowanych] on. Immunity is genetically regulated (by immu [link widoczny dla zalogowanych] e response genes), and it is also influenced by en [link widoczny dla zalogowanych] ironment (eg, nutrition, aging, previous exposure). Alt [link widoczny dla zalogowanych] ough the inciting antigens that breach immune tolerance wit [link widoczny dla zalogowanych] subsequent autoimmunity are unknown, human leukocyte ant [link widoczny dla zalogowanych] gen (HLA)-DR2 is overrepresented a
mong European an [link widoczny dla zalogowanych] American patients with aplastic anemia. Sup [link widoczny dla zalogowanych] ression of hematopoiesis is likely mediated by an e [link widoczny dla zalogowanych] panded population of the following cytotoxic T lympho [link widoczny dla zalogowanych] ytes (CTLs): CD8 and HLA-DR+, which are detectabl [link widoczny dla zalogowanych] in both the blood and bone marrow of patients [link widoczny dla zalogowanych] with aplastic anemia. These cells produce inh [link widoczny dla zalogowanych] bitory cytokines, such as gamma-interferon and tumor ne [link widoczny dla zalogowanych] rosis factor, which can suppressing progenitor-cell growth. Th [link widoczny dla zalogowanych] se cytokines suppress hematopoiesis by affecting the mit [link widoczny dla zalogowanych] tic cycle and cell killing by inducing
Fas-media [link widoczny dla zalogowanych] ed apoptosis. In addition, these cytokines induce nitric oxide [link widoczny dla zalogowanych] synthase and nitric oxide production by marrow ce [link widoczny dla zalogowanych] ls, which contributes to immune-mediated cytoto [link widoczny dla zalogowanych] icity and the elimination of hematopoietic cells. In the US: [link widoczny dla zalogowanych] o accurate prospective data are available regarding the in [link widoczny dla zalogowanych] idence of aplastic anemia in the United States. Findings from sev [link widoczny dla zalogowanych] ral retrospective studies suggest that the incid [link widoczny dla zalogowanych] nce is 0.6-6.1 cases per million population; this rate was [link widoczny dla zalogowanych] argely based on data from retrospective review
[link widoczny dla zalogowanych] of death registries. Internationally: The annual in [link widoczny dla zalogowanych] idence of aplastic anemia in Europe, as detailed in large, fo [link widoczny dla zalogowanych] mal epidemiologic studies, is similar to that in the United Stat [link widoczny dla zalogowanych] s, with 2 cases per million population. Aplastic [link widoczny dla zalogowanych] nemia is thought to be more common in Asia th [link widoczny dla zalogowanych] n in the West. The incidence was accurately determ [link widoczny dla zalogowanych] ned to be 4 cases per million population in Bangkok [link widoczny dla zalogowanych] but may be closer to 6 cases per million populati [link widoczny dla zalogowanych] n in the rural areas of Thailand and as high as 14 cases per
[link widoczny dla zalogowanych] illion population in Japan, based on prospective studies. This in [link widoczny dla zalogowanych] reased incidence may be related to environmental factors, such [link widoczny dla zalogowanych] s increased exposure to toxic chemicals, rath [link widoczny dla zalogowanych] r than to genetic factors because this increas [link widoczny dla zalogowanych] is not observed in people of Asian ancestry who [link widoczny dla zalogowanych] are presently living in the United States. NHL represe [link widoczny dla zalogowanych] ts a progressive clonal expansion of B cells or T [link widoczny dla zalogowanych] ells and/or natural killer (NK) cells, arising fro [link widoczny dla zalogowanych] the accumulation of genetic lesions that affect proto
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[link widoczny dla zalogowanych] oncogenes or tumor suppressor genes, resulting in cell immor [link widoczny dla zalogowanych] alization. These oncogenes can be activated by [link widoczny dla zalogowanych] chromosomal translocations (ie, the genetic hallmark of lymphoid [link widoczny dla zalogowanych] alignancies), or tumor suppressor loci can be inactivated by chr [link widoczny dla zalogowanych] mosomal deletion or mutation. In addition, the genome of certai [link widoczny dla zalogowanych] lymphoma subtypes can be altered with the introd [link widoczny dla zalogowanych] ction of exogenous genes by various oncogenic [link widoczny dla zalogowanych] iruses. Several cytogenetic lesions are associated with spec [link widoczny dla zalogowanych] fic NHLs, reflecting the presence of specific markers of diagno
[link widoczny dla zalogowanych] tic significance in subclassifying various NHL [link widoczny dla zalogowanych] subtypes. Most NHLs are of B-cell origin (almost 85%); only 1 [link widoczny dla zalogowanych] % are derived from T/NK cells, and the small remainder s [link widoczny dla zalogowanych] em from macrophages. These tumors are character [link widoczny dla zalogowanych] zed by the level of differentiation, the size of th [link widoczny dla zalogowanych] cell of origin, the origin cell's rate of prolifer [link widoczny dla zalogowanych] tion, and the histologic pattern of growth. Fo [link widoczny dla zalogowanych] many of the B-cell NHL subtypes, the pattern of growth [link widoczny dla zalogowanych] and cell size may be important determinants of tumor [link widoczny dla zalogowanych] aggressiveness. Tumors that grow in a
nodular patter [link widoczny dla zalogowanych] , which vaguely recapitulate normal B-cell lymphoid follicular [link widoczny dla zalogowanych] structures, are generally less aggressive than lymphomas t [link widoczny dla zalogowanych] at proliferate in a diffuse pattern. Lymphomas [link widoczny dla zalogowanych] f small lymphocytes generally have a more indolent course com [link widoczny dla zalogowanych] ared with those of large lymphocytes, which may have in [link widoczny dla zalogowanych] ermediate-grade or high-grade aggressiveness. Ho [link widoczny dla zalogowanych] ever, some subtypes of high-grade lymphomas are characterized b [link widoczny dla zalogowanych] small cell morphology. For intermediate-grade lymphomas, [link widoczny dla zalogowanych] HOP chemotherapy remains the standard of care at this tim
[link widoczny dla zalogowanych] . A prospective randomized trial of 4 regimens [link widoczny dla zalogowanych] ie, [1] CHOP versus [2] prednisone, methotrexate, leucovorin, d [link widoczny dla zalogowanych] xorubicin, cyclophosphamide, and etoposide [Pr [link widoczny dla zalogowanych] MACE]–cyclophosphamide, etoposide, Adriamycin, cytarabine, bleo [link widoczny dla zalogowanych] ycin, Oncovin, methotrexate, leucovorin, and prednisone [CytaBOM] [link widoczny dla zalogowanych] versus [3] methotrexate, bleomycin, Adriamyci [link widoczny dla zalogowanych] , cyclophosphamide, Oncovin, and dexamethasone [m-BACOD] versu [link widoczny dla zalogowanych] [4] methotrexate-leucovorin, Adriamycin, cyclophosphamide, Onc [link widoczny dla zalogowanych] vin, prednisone, and bleomycin [MACOP-B]) for pati
[link widoczny dla zalogowanych] nts with diffuse large cell lymphoma showed no difference in res [link widoczny dla zalogowanych] onse rate (RR), OS, or time to treatment failure (TTF) at [link widoczny dla zalogowanych] 3 years. The other 3 regimens were more toxic t [link widoczny dla zalogowanych] an CHOP therapy. However, non-CHOP regimens such as MACOP-B are u [link widoczny dla zalogowanych] ed as first-line therapies in some subtypes of NHL suc [link widoczny dla zalogowanych] as primary mediastinal B large cell NHL. Autologous and [link widoczny dla zalogowanych] llogeneic bone marrow or peripheral stem cell t [link widoczny dla zalogowanych] ansplantation for patients at high risk of relapse are under [link widoczny dla zalogowanych] linical investigation. Innovative approaches to improve the resul
[link widoczny dla zalogowanych] s of CHOP for patients at high risk of relapse, [link widoczny dla zalogowanych] uch as monoclonal antibody therapy, are under clini [link widoczny dla zalogowanych] al investigation. CNS prophylaxis, usually with 4-6 [link widoczny dla zalogowanych] njections of methotrexate intrathecally, is recommended [link widoczny dla zalogowanych] or patients with paranasal sinus or testicular [link widoczny dla zalogowanych] nvolvement, diffuse small noncleaved cell or Burkitt lymphoma, or [link widoczny dla zalogowanych] lymphoblastic lymphoma. CNS prophylaxis for bone marrow in [link widoczny dla zalogowanych] olvement is controversial. Treatment of acute lymphoblastic ly [link widoczny dla zalogowanych] phoma, a very aggressive form of NHL, is usually patte
[link widoczny dla zalogowanych] ned after acute lymphoblastic leukemia (ALL) therapy. Intensi [link widoczny dla zalogowanych] e combination chemotherapy with CNS prophylaxis is the standa [link widoczny dla zalogowanych] d treatment of this aggressive histologic type [link widoczny dla zalogowanych] f NHL. Treatment should be instituted rapidly once di [link widoczny dla zalogowanych] gnosis is confirmed. Other subtypes of high-grade lymphomas are [link widoczny dla zalogowanych] sually treated with more aggressive variations of CHOP chemothera [link widoczny dla zalogowanych] y, including the addition of high-dose methotrexate or [link widoczny dla zalogowanych] other chemotherapy drugs and higher doses of cyclophosphamide. [link widoczny dla zalogowanych] In the Parma trial, the patients with relapse who were randomiz [link widoczny dla zalogowanych] d to autologous bone
marrow transplantation followed by [link widoczny dla zalogowanych] involved field radiation therapy did better than those rand [link widoczny dla zalogowanych] mized to conventional chemotherapy and involved field radiation [link widoczny dla zalogowanych] therapy. After a 5-year median follow-up study, the event-fr