Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0393754 (HSA)
 2,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to evaluate 99mTc-DTPA-HSA as an iliopelvic lymphoscintigraphic agent in 5 normal volunteers and 10 patients with metastases of malignant tumors (cancer, 9; and malignant lymphoma, 1) to the iliopelvic lymph nodes. The subjects underwent intradermal injection of 185 MBq of 99mTc-DTPA-HSA into digital web spaces of the feet. Massage was applied at the injection sites for 30 sec; the subjects then walked around for 2 min. Whole-body scintigrams were obtained 5 min after injection. The whole-body scanning speed was 20 cm/min. The tracer transport was prompt. Within 15 min after injection, the tracer reached the termination of the thoracic duct in all normal volunteers. Normal whole-body images of excellent quality delineated the lymph nodes and channels almost without background radioactivity. The images of 9 patients with metastases of cancer showed clearly the following abnormal patterns: a) obstruction of lymphatic system (5/9, 55.6%); b) absence of visualization of the thoracic duct (44.4%); c) decreased uptake in lymph nodes (88.9%); d) visualization of collateral circulation (44.4%); e) tracer extravasation into more proximal soft tissue (22.2%). The image in the patient with malignant lymphoma showed increased uptake in the enlarged lymph nodes in addition to the all abnormal findings mentioned above. We concluded that 99mTc-DTPA-HSA is an excellent radiopharmaceutical for iliopelvic lymphoscintigraphy.
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PMID:[Lymphoscintigraphy with 99mTc-DTPA-HSA: detection of metastases to iliopelvic lymph nodes]. 192 Sep 55

We conducted a randomized crossover study comparing the hemopoietic effect of partially purified human urinary colony-stimulating factor (CSF-HU, an active drug) and human serum albumin (HSA, a control drug) in 24 patients with malignant lymphoma, solid tumors, or multiple myeloma who were receiving two consecutive courses of the same chemotherapeutic regimen. Patients received daily 2-4 X 10(6) units of CSF-HU or an equal amount of protein HSA for five days after the end of the courses of chemotherapy. Assignment to CSF-HU or HSA was determined by the envelope method. The average number of blood granulocytes of 24 cases on day 7 after chemotherapy was 2116 +/- 1649 in CSF-HU-infused courses, which was significantly higher than in HSA-infused courses (1520 +/- 1022) (p less than 0.05). The average time that patients had fewer than 2000 granulocytes/mm3 was 7.6 +/- 4.4 days in CSF-HU-infused courses and 10.3 +/- 5.0 days in HSA-infused courses (p less than 0.02). Fever greater than 38 degrees C was the most frequent side effect, occurring in 32% of the patients receiving CSF-HU infusions. A reduction in the neutropenic interval in CSF-HU-infused courses was observed in patients with fever, as well as in those without fever. Infusions of CSF-HU did not change the number of other hematological parameters, such as erythrocytes, platelets, monocytes, and lymphocytes. These results suggest that CSF-HU infusions may partially protect the patients from granulocytopenia after anticancer chemotherapy.
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PMID:Protective effect of partially purified human urinary colony-stimulating factor on granulocytopenia after antitumor chemotherapy. 349 Sep 92

Dominant second signals for T cell activation can be generated through interactions between CD28 and CTLA-4 on T cells with their co-stimulatory ligands B7-1 and B7-2 on APC. Nevertheless, some B7-negative cell lines appear capable of providing second signals to T cells, illustrating that B7-independent co-stimulatory pathways may exist. One such cell line, the peptide-transporter defective T lymphoma RMA-S, was investigated in the present study, to determine the origin of the co-stimulatory effects it provides. RMA-S can support clonal expansion of purified CD4 or CD8 T cells from unprimed mice activated with concanavalin A (ConA) or immobilized anti-CD3. Nevertheless, RMA-S does not express B7-1 or B7-2, nor does it express other known co-stimulatory molecules, i.e. CD40, gp39, CD70 and HSA. Also, co-stimulation provided by RMA-S could not be blocked by antibodies or fusion proteins specific for these co-stimulatory molecules, excluding their participation. However, RMA-S' co-stimulatory activity is dependent on adhesive interactions. RMA-S is incapable of IL-2 production in the presence of ConA or anti-CD3, but T cells co-stimulated by RMA-S produce IL-2 and IFN-gamma upon anti-CD3- or ConA-induced activation. Furthermore, co-stimulation of antigen-specific T cell proliferation of both class I- and class II-restricted T cell clones can be provided by RMA-S, and RMA-S can preclude induction of anergy by 1-ethyl-3-(3-dimethyl amino propyl)carboiimide-fixed APC in a class II-restricted T cell clone. The results suggest that potent co-stimulatory pathways can be induced by cellular interactions between a T lymphoma, RMA-S and T cells, not involving gp39, CD40, CD70, HSA, B7-1 (CD80) or B7-2 (CD86). Characterization of the molecules involved is in progress.
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PMID:A T cell lymphoma can provide potent co-stimulatory effects to T cells that are not mediated by B7-1, B7-2, CD40, HSA or CD70. 858 81

CD22 is a B cell-restricted surface molecule which may play an important role in interactions between B cells and other cells and in regulating signals through the B cell receptor (BCR) complex. Here we have examined whether the mouse is a suitable in vivo model for studying CD22 functions. In primary and secondary lymphoid organs of adult mice CD22 is on all mature B cells, including resting IgM+IgD+ B cells, IgG+ HSA(lo) memory B cells, syndecan+ plasma cells and CD5+ B cells, but it is not on immature IgM+IgD- B cells. Biochemical analysis revealed that murine CD22 is associated with the IgM receptor in some, but not all, CD22+ B leukemic and lymphoma cell lines; as with human CD22, murine CD22 is rapidly phosphorylated on tyrosine after ligation of the BCR. In the CD22- murine pro-B cell line, FEMCL, CD22 expression was inducible by treatment with phorbol 12-myristate 13-acetate. A genomic fragment of the cd22b allele containing 1.3 kb 5' of exon 1 was sequenced in order to identify potential DNA regulatory elements in the CD22 promoter region. Consensus sequences for transcription factor binding sites including PU.1, AP-1, AP-2, C/EBP and SP-1 were present, but no classical TATA elements or initiator motifs were evident at relevant positions. The 1.3-kb promoter fragment 5' of exon 1 was sufficient for directing basal promoter activity in B and T cells. There was no significant sequence similarity between the murine and human cd22 gene promoters, although both contain repetitive elements and Sp-1 and AP1 binding sites. Thus, murine CD22 shares a number of features with human CD22 and the mouse provides a suitable model system for elucidating the function of CD22 in vivo.
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PMID:Characterization of the expression and gene promoter of CD22 in murine B cells. 897 19

The Hodgkin's-like Type B neoplasms which arise spontaneously in aging C57L mice (25% incidence at 21 months of age) were first reported over 40 years ago, but since then relatively little has been published about these lymphomas. Based on previous studies in SJL mice, we investigated the phenotypic and functional properties of C57L-derived lymphomas in relation to Mtv29-encoded vSAg expression by the tumor cells, and their ability to stimulate TCR Vbeta-restricted T cells. The cell surface phenotype of the C57L lymphomas indicates a B cell origin (sIg(+), MHC II(+)). These B lymphoma cells also express co-stimulatory molecules [B7-1 (CD80) and HSA (CD24)], and stimulate marked proliferation of syngeneic CD4(+) T cells. C57L B lymphoma cells exhibit Mtv-encoded mRNA by northern analysis, and also stimulate IL-2 production from Vbeta16(+) T cell hybrids, suggesting a role for Mtv 29 in this syngeneic T cell response. After transfer to syngeneic recipients, primary C57L lymphomas grow slowly, if at all. However, tumor growth is greatly accelerated by pretreatment of C57L recipients with anti-asialo GM1 antibody (but not anti-CD8 mAb), suggesting that NK cells play a major role in inhibiting lymphoma growth. If, in addition to anti-asialo GM1, the mice are also pretreated with anti-CD4 mAb, tumor growth is markedly inhibited, indicating that the lymphoma-responsive syngeneic CD4(+) T cells promote tumor growth. Therefore, although the vSAg-induced response stimulated by vSAg29 expressing lymphoma cells in syngeneic TCR Vbeta-restricted CD4(+) T cells is an important etiologic factor in this type of B cell neoplasm both in C57L and in SJL mice, the final outcome of the spontaneous neoplastic process appears strongly influenced by endogenous NK activity in aging mice.
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PMID:B cell lymphomas of C57L/J mice; the role of natural killer cells and T helper cells in lymphoma development and growth. 1097 82

Down's syndrome (DS) in humans is caused by trisomy of chromosome 21 (HSA 21). DS patients have a variety of pathologies, including mental retardation and an unusually high incidence of leukemia or lymphoma such as megakaryocytic leukemia. Individuals with DS develop the characteristic neuropathological hallmarks of Alzheimer's disease (AD) in early adulthood, generally by the fourth decade of life. There are several mouse models of DS that have a segmental trisomy of mouse chromosome 16 (MMU 16) with triplicated genes orthologous to HSA 21. These mice display neurodegeneration similar to DS. Although brain pathology in DS models is known, little information is available about other organs. We studied the extraneural pathology in aged DS mice (Ts65Dn, Ts2 and Ts1Cje aged 8 to 24 months) as well as other mouse models of neurodegeneration, including presenilin (PS), amyloid-beta precursor protein (APP), and tau (hTau and JNPL) transgenic mice. An increased incidence of peripheral amyloidosis, positive for amyloid A (AA) but not amyloid-beta peptide (A beta), was found in APP over-expressing and tauopathic mice as compared to non-transgenic (ntg) littermates or to DS mouse models. A higher incidence of lymphoma was found in the DS models, including Ts1Cje that is trisomic for a small segment of MMU 16 not including the App gene, but not in the APP over-expressing mice, suggesting that high APP expression is not the cause of lymphoma in DS. The occurrence of lymphomas in mouse DS models is of interest in relation to the increased incidence of malignant conditions in human DS.
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PMID:Systemic pathology in aged mouse models of Down's syndrome and Alzheimer's disease. 1904 4