Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of reconstituting a murine monoclonal IgG1 antibody kit with pertechnetate technetium 99m on antibody distribution in the liver, spleen and sternal bone marrow of patients was examined. The 99mTc-labelled antibody used is directed against non-specific cross-reacting antigen (NCA-95) and carcinoembryonic antigen (CEA) and has been successfully applied for imaging tissue inflammation and bone marrow scanning. Radioactivity uptake was determined in the liver, spleen, bone marrow and a precordial background region in a consecutive series of 25 patients, examined with an antibody preparation, routinely radiolabelled according to the manufacturer's recommendations and in 14 patients, in whom the antibody was reconstituted with special care, avoiding bubble formation and dropping of buffer into the antibody-containing vial. Gentle compared with routine antibody reconstitution caused a highly significant reduction of the antibody uptake in the liver, as determined by count densities, normalized to injected dose and acquisition time (13.2 +/- 5.5 vs 20.1 +/- 6.0 cpm per pixel, means +/- SD, P = 0.008). The liver to background ratio was reduced from 3.4 +/- 1.4 to 1.9 +/- 0.5 (P less than 0.001). Spleen, sternal bone marrow and precordial background count rates were not significantly affected. These results clearly demonstrate that gentle antibody reconstitution can decrease non-specific antibody uptake in the liver by 34% +/- 6.4% (means +/- SEM). Thus, scan quality is improved, and the potential deleterious camouflage of underlying structures is avoided.
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PMID:Reduced technetium 99m labelled NCA-95/CEA-antibody uptake in liver due to gentle antibody reconstitution. Technical note. 196 40

Cell-mediated and humoral immune responses of streptozotocin-induced diabetic mice were evaluated using in vivo and in vitro immunological assays. C57BL/6 mice were rendered diabetic by a single intraperitoneal injection of 125-200 mg/kg of streptozotocin. Immunological studies were performed after the mice were diabetic (mean +/- SEM serum glucose 537 +/- 14 mg/dl) for a minimum of 4 weeks. Spleen cells from streptozotocin-induced diabetic mice exhibited significantly diminished direct IgM plaque-forming cell (PFC) responses following either in vivo or in vitro immunization with sheep erythrocytes, markedly impaired cytotoxic cell responses following in vivo or in vitro allogeneic stimulation, and diminished blastogenic response to the T-cell mitogens phytohemagglutinin and concanavalin A. In contrast the blastogenic response of diabetic spleen cells to lipopolysaccharide, a B-cell mitogen, was normal. The defects in in vivo PFC responses and in vivo cytotoxic cell responses were corrected by islet cell transplantation, suggesting that the abnormalities in immunological function of streptozotocin-induced diabetic mice are a consequence of the diabetic state and not of direct streptozotocin toxicity to lymphoid cells.
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PMID:Alterations in immunological function in streptozotocin-induced murine diabetes mellitus: correction by islet cell transplantation. 643 88

The kinetics of 111In platelets have been investigated in human subjects using a gamma camera and computer system. Time activity curves were recorded over the spleen, chest and liver, following intravenous bolus injection of autologous radio-labelled platelets. Splenic blood flow expressed as the percentage of total blood volume entering the spleen in unit time, and intrasplenic platelet transit time were calculated from the time activity curves. Spleen size was recorded from the camera images. Splenic blood flow increased with increasing spleen size (r = 0.56, P less than 0.001). Platelet transit time showed an inverse relationship with a semi-quantitative estimate of splenic perfusion (i.e. splenic blood flow per unit volume spleen; r = 0.64, P less than 0.001) but was not related to spleen size. At high rates of estimated splenic perfusion transit time appeared to reach a minimum value of about 7 min, whereas at low rates of estimated perfusion, transit time rose sharply to reach levels greater than 20 min. The effect of polycythaemia, taken to indicate high intrasplenic haematocrit on platelet transit time, was also investigated. Patients with secondary polycythaemia had elevated transit times (19 min SEM 1.6, n = 10) compared with primary polycythaemia (9.7 min SEM 0.8, n = 5) and normals (9.6 min SEM 0.5, n = 5). It was concluded that splenic perfusion was important in determining the duration of platelet transit.
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PMID:Factors controlling the intrasplenic transit of platelets. 680 67

Xiang-sha Warming (XSW) and Shashen Nourishing Decoction (SSN) were used in treating Yang Deficiency Syndrome (YaDS) and Yin Deficiency Syndrome (YiDS) of chronic atrophic gastritis (CAG) respectively. 121 cases with Spleen YaDS, and 29 cases with Spleen YiDS were selected. 26 and 30 specimens were taken from gastric mucosa for observation under the SEM and TEM, including 12 and 12 YaDS cases, 14 and 12 Spleen Qi Deficiency cases respectively, 2 cases of YiDS were also observed with TEM. The specimens were taken from the same site of the gastric mucosa directly under the gastroscope pre- and post-treatment. 43 patients (35.6%) with spleen YaDS and 5 cases (17.2%) in Spleen YiDS showed marked effect after 3-month treatment. It showed that the effect in Spleen YaDS was better than YiDS. The XSW was superior than that of SSN. The effects were related to the syndromes and the degrees of pathologic change. This showed that the recipe could somewhat reverse and restore the abnormal glands of gastric mucosa.
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PMID:[Pathomorphologic changes on 150 chronic atrophic gastritis patients by treatment based on syndrome differentiation]. 833 30

Antibodies to Schistosoma mansoni soluble egg antigens (SEA) generated in outbred rabbits from two different sources were used to study cross-reactive idiotype/anti-idiotype (Id/anti-Id) interactions in S. mansoni-infected mice in two different locations. Immunoaffinity purified rabbit polyclonal anti-SEA antibody preparations (RabId) were predominantly Ig by SDS-PAGE and demonstrated anti-SEA activity by ELISA and Western blot. RabId prepared from three separate rabbits and used at 40 micrograms/ml in vitro stimulated lymphocyte proliferative responses of spleen cells from mice with eight week infections (Mean +/- SEM [E-C]) of 3869 +/- 764, 18594 +/- 3046 and 8962 +/- 1734 cpm. Spleen cells from uninfected mice exposed to the same RabId preparations in vitro had respective [E-C] values of 206 +/- 144, 494 +/- 154 and 363 +/- 180. Lymph node cells from mice infected for 8 weeks demonstrated [E-C] of 123 +/- 400, 5073 +/- 828 and 2361 +/- 656 upon exposure to these 3 RabId preparations. Lymph node cells from uninfected mice had [E-C] of 220 +/- 76, 194 +/- 82 and 143 +/- 72 when exposed to these RabId. Maximum in vitro proliferative response to Ig from unimmunized rabbits was 761 +/- 400 by spleen cells from mice with eight week infections. These data indicate the presence of cross-reactive Id on rabbit anti-SEA antibodies from different rabbits that can stimulate in vitro lymphoproliferative responses of spleen or lymph node cells from S. mansoni-infected mice.
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PMID:Cross-reactive idiotypes on rabbit anti-SEA antibodies stimulate anti-idiotype spleen and lymph node cell responses of mice infected with Schistosoma mansoni. 922 53

The effect of systemic complement depletion by cobra venom factor (CVF) was evaluated in adoptive transfer experimental allergic neuritis (AT-EAN). Spleen cells of rats immunized with a neuritogenic peptide SP26 were injected into naive rats. On days 3 and 6 after cell transfer AT-EAN rats were treated with CVF or saline intraperitoneally. AT-EAN rats treated with CVF had significantly lower scores for histological inflammation (0.25 +/- 0.25 vs 1.9 +/- 0.4, mean +/- SEM, P < 0.03) and demyelination (0.13 +/- 0.13 vs 1.6 +/- 1.4, P < 0.02) than saline-treated AT-EAN rats. Immunocytochemistry of lumbosacral nerve roots showed significantly less ED1-positive macrophages (0.5 +/- 0.3 vs 1.6 +/- 0.6, P < 0.04) and CD11bc-positive (expressing complement receptor 3 or CR3) inflammatory cells (0.6 +/- 0.4 vs 1.7 +/- 0.5, P < 0.03). Our data suggest that complement plays a crucial role in inflammatory demyelination since systemic complement depletion significantly reduces recruitment of macrophages into the nerve and subsequent macrophage-mediated demyelination.
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PMID:Systemic complement depletion reduces inflammation and demyelination in adoptive transfer experimental allergic neuritis. 954 96

Phex is the gene whose mutation is the cause of X-linked hypophosphatemia in humans and mice. The organs expressing Phex in normal animals, and their possible sensitivity to stimulation by low phosphate diets, are unknown. In this study, Phex expression was measured in 6-wk-old normal B6C3H male and female mice and in 135 g Sprague-Dawley rats fed a normal phosphate diet or a low phosphate diet with deionized water ad libitum for 7 d. The animals were then anesthetized, and a variety of organs were collected and frozen in liquid nitrogen. Phex mRNA expression was measured in each organ by reverse transcription-polymerase chain reaction (RT-PCR) with primers specific for both Phex and glyceraldehyde-3-phosphate dehydrogenase (G3PDH). Southern blots were prepared, hybridized with 32P-labeled internal oligonucleotides, and quantified with a phosphor imager. The Phex/G3PDH ratio was computed, and the data were compiled as the mean +/- SEM. In these growing animals, the highest Phexexpression levels were found in the gonads, brain, and lung. In contrast, Phex expression in calvaria and femur was markedly less. Two significant changes were found in animals that were fed a low phosphate diet. Spleen showed a significant decrease in Phex mRNA levels on low phosphate diet (60+/-10% of normal P diet, n = 12/group, p = 0.002). The pituitary gland showed a significant increase in Phex expression with low phosphate diet (851+/-127% of G3PDH) over normal P diet (569+/-78%, n = 24 - 25/group, p = 0.03). No significant change was found in femur, calvaria, or a variety of soft tissues. In summary, Phex mRNA was found in most tissues examined. Expression levels varied by two orders of magnitude from highest to lowest with more in gonads, brain, and lung and with less in bone. Increased Phex mRNA was found in the pituitary gland of animals that were fed a low phosphate diet.
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PMID:MRNA expression of Phex in mice and rats: the effect of low phosphate diet. 1105 Oct 50