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PubMed1980

Properties of the factor VIII after DDAVP (1-deamino-8-D-arginine vasopressin) infusion in normal subjects.

The factor VIII response to DDAVP (1-deamino-8-D-arginine vasopressin) was examined in 6 healthy volunteers. Following intravenous DDAVP infusion, each subject showed a marked increase in factor VIII procoagulant activity (VIII:C), factor VIII related antigen (VIIIR:AG) and von Willebrand factor activity (VIIIR:WF). But there were differences among augmentation index of each activity. Further investigations were performed whether there was a qualitative abnormality in the factor VIII after DDAVP infusion. Between factor VIII activities before and after DDAVP, there was no difference in a thermostability of VIII:C in vitro, gel chromatographic pattern on Sepharose 2B or 4B, a precipitation with concanavalin A (Con A) and a recovery in cryoprecipitate. The increase of VIIIR:AG, however, was mostly brought about by the augmentation of relatively slowly migrating portion as demonstrated by crossed immunoelectrophoresis (CIE). From these results it was assumed that there was no remarkable abnormalities in the factor VIII after DDAVP administration, and the elevated factor VIII could function efficiently in vivo. The findings in cryoprecipitation showed that DDAVP could be applied to blood donation for the preparation of cryoprecipitate.

Arginine Vasopressin↗
PubMed2006

Expansion of functionally immature transitional B cells is associated with human-immunodeficient states characterized by impaired humoral immunity.

X-linked lymphoproliferative disease (XLP) is a severe immunodeficiency associated with a marked reduction in circulating memory B cells. Our investigation of the B cell compartment of XLP patients revealed an increase in the frequency of a population of B cells distinct from those previously defined. This population displayed increased expression of CD10, CD24, and CD38, indicating that it could consist of circulating immature/transitional B cells. Supporting this possibility, CD10+CD24highCD38high B cells displayed other immature characteristics, including unmutated Ig V genes and elevated levels of surface IgM; they also lacked expression of Bcl-2 and a panel of activation molecules. The capacity of CD24highCD38high B cells to proliferate, secrete Ig, and migrate in vitro was greatly reduced compared with mature B cell populations. Moreover, CD24highCD38high B cells were increased in the peripheral blood of neonates, patients with common variable immunodeficiency, and patients recovering from hemopoietic stem cell transplant. Thus, an expansion of functionally immature B cells may contribute to the humoral immunodeficient state that is characteristic of neonates, as well as patients with XLP or common variable immunodeficiency, and those recovering from a stem cell transplant. Further investigation of transitional B cells will improve our understanding of human B cell development and how alterations to this process may precipitate immunodeficiency or autoimmunity.

ADP-ribosyl Cyclase 1↗
PubMed1998

RAGE-Abeta interactions in the pathophysiology of Alzheimer's disease.

RAGE is a cell surface molecule primarily identified for its capacity to bind advanced glycation end-products and amphoterin. Immunocytochemical studies demonstrated that in Alzheimer's Disease (AD) the expression of RAGE is elevated in neurons close to neuritic plaque beta-amyloid (Abeta) deposits and in the cells of Abeta containing vessels. Cross-linking of surface bound Abeta 1-40 to endothelial cells, yielded a band of 50 kDa identified as RAGE. Using the soluble extracellular domain of recombinant human RAGE, we found that Abeta binds to RAGE with a Kd = 57 +/- 14 nM, a value close to those found for mouse brain endothelial cells and rat cortical neurons. The interaction of Abeta with RAGE in neuronal, endothelial, and RAGE-transfected COS-1 cells induced oxidative stress, as assessed by the TBARS and MTT assays. ELISA demonstrated a 2.5 times increase of RAGE in AD over control brains. Activated microglia also showed elevated expression of RAGE. In the BV-2 microglial cell line, RAGE bound Abeta in dose dependent manner with a Kd of 25 +/- 9 nM. Soluble Abeta induced the migration of microglia along a concentration gradient, while immobilized Abeta arrested this migration. Abeta-RAGE interaction also activated NF-kappaB, resulting in neuronal up-regulation of macrophage-colony stimulating factor (M-CSF) which also induced microglial migration. Taken together, our data suggest that RAGE-Abeta interactions play an important role in the pathophysiology of Alzheimer's Disease.

Journal Article↗
PubMed1989

Thrombocytopenia associated with hypersensitivity to ranitidine: possible cross-reactivity with cimetidine.

A rare case of thrombocytopenia associated with ranitidine is described. The thrombocytopenia was accompanied by eosinophilia and slightly elevated serum IgE. The platelet and eosinophilic counts returned to normal as soon as the drug was stopped. Cell-mediated immunity (CMI) determined in vitro by the leukocyte migration inhibition factor test was found against ranitidine and cimetidine. IgE antibody response against both drugs was also found by the mast cell degranulation test. These data suggest an association between the ranitidine-induced thrombocytopenia and both humoral antibody response and CMI. Cross-reactivity between the two H2-receptor antagonists is suggested, as well.

Cell Migration Inhibition↗
PubMed1995

The cancer burden of southern-born African Americans: analysis of social-geographic legacy.

Southern-born black Americans, especially those who migrated to the Northeast and Midwest, had much higher cancer mortality rates during the period 1979 to 1991 than their counterparts who were born and died outside the South. Elevated rates were apparent for the 35- to 44-year-old age group, and were highest among the elderly. The largest and most consistent differences between Southern-born and Northeastern, Midwestern, and Western-born African Americans were for cancer of the breast (female), esophagus, larynx, and lung (male), pancreas, prostate, and stomach. The combined effects of nutritional imbalances, cigarette smoking, high-risk jobs, limited access to medical screening and care, and other factors associated with poverty are suggested as etiologic factors common to the high-risk, Southern-born black population. It is also possible that the Southern-born excess of cancer deaths is at least partly an artifact of the data and the ecological level of the analysis.

Adult↗
PubMed1996

Elevated concentration and biologic activity of monocyte chemotactic protein-1 in the peritoneal fluid of patients with endometriosis.

OBJECTIVE: To estimate the concentration and the biologic activity of monocyte chemotactic protein-1 (MCP-1) in the peritoneal fluid (PF) of women with and without endometriosis. DESIGN: A case control study was conducted. SETTING: Gynecology clinic and Laboratories of endocrinology of reproduction and immunology. PATIENTS: Women presenting for infertility, pelvic pain, or tubal ligation in which endometriosis was diagnosed at laparoscopy (n = 36) and normal fertile controls presenting for tubal ligation (n = 21). INTERVENTIONS: Collection of PF via laparoscopy. MAIN OUTCOME MEASURES: Determination of PF concentrations of MCP-1 by an ELISA and evaluation of its monocyte chemotactic activity using a human hystiocytic cell line (U937). RESULTS. The concentration of MCP-1 (median, range of values) was increased in the PF of endometriosis patients (283, 0 to 1,930 pg/mL; conversion factor to SI unit, 0.155) compared with the control group (140, 0 to 435 pg/mL). The most significant elevation of MCP-1 levels was found in the stage II of the disease (371, 200 to 1,930 pg/mL). An increased chemotactic activity for monocytes (mean number of migrating cells/mm2 +/- SD) also was found in stages I (1,460 +/- 312) and II (1,541 +/- 336) of the disease when compared with fertile controls (393 +/- 56). Forty percent to 53% of this activity was inhibited in the presence of an antibody specific to MCP-1. CONCLUSIONS: These observations are consistent with previous data indicating increased leukocyte chemotaxis in the PF of patients with endometriosis and suggest that MCP-1 may play a relevant role in the peritoneal inflammatory reaction associated with the disease.

Adult↗
PubMed1991

Rap1A is a substrate for cyclic AMP-dependent protein kinase in human neutrophils.

The Ras-related protein, Rap1B, has previously been shown to serve as a PKA substrate in vitro and to be phosphorylated by cAMP elevating agents in human platelets. We have purified a Rap1 protein that serves as a PKA substrate from human neutrophils, and we now identify this protein as Rap1A. A 23-kDa protein that co-migrated with recombinant Rap1A was phosphorylated in electroporated human neutrophils upon stimulation by cAMP in the presence of [gamma-32P]ATP. This protein could be immunoprecipitated by the Rap1A/B-specific antibody, R61. The 23-kDa phosphoprotein was monitored during the purification of Rap1 from neutrophil membrane extracts and was shown to copurify with Rap1 during the DEAE Sephacel, heptylamine Sepharose, and MonoQ chromatography steps utilized. The purified protein was phosphorylated to an extent of 1 mol phosphate/mol GTP gamma S bound. This protein was identified as Rap1A by: 1) amino acid sequence analysis; and 2) immunoblotting with a Rap1A-specific antibody. The amino acid phosphorylated on Rap1A by PKA was a serine residue. The site of phosphorylation was indicated by carboxypeptidase digestion and confirmed using a mutant recombinant Rap1A lacking the relevant serine (serine-180). Rap1A, not Rap1B, appears to be the major 23-kDa PKA substrate in human neutrophils. It is possible that Rap1A plays a role in human neutrophils in mediating the inhibitory effects of cAMP-elevating agents upon chemoattractant-stimulated cell activation.

Electrophoresis, Gel, Two-Dimensional↗
PubMed1985

Intracellular pH shift leads to microtubule assembly and microtubule-mediated motility during sea urchin fertilization: correlations between elevated intracellular pH and microtubule activity and depressed intracellular pH and microtubule disassembly.

The regulation of the microtubule-mediated motions within eggs during fertilization was investigated in relation to the shift in intracellular pH (pHi) that occurs during the ionic sequence of egg activation in the sea urchins Lytechinus variegatus and Arbacia punctulata. Microtubule assembly during formation of the sperm aster and mitotic apparatus was detected by anti-tubulin immunofluorescence microscopy, and the microtubule-mediated migrations of the sperm and egg nuclei were studied with time-lapse video differential interference contrast microscopy. Manipulations of intracellular pH were verified by fluorimetric analyses of cytoplasmic fluorescein incorporated as fluorescein diacetate. The ionic sequence of egg activation was manipulated i) to block the pHi shift at fertilization or reduce the pHi of fertilized eggs to unfertilized values, ii) to elevate artificially the pHi of unfertilized eggs to fertilized values, and iii) to elevate artificially or permit the normal pHi shift in fertilized eggs in which the pHi shift at fertilization was previously prevented. Fertilized eggs in which the pHi shift was suppressed did not assemble microtubules or undergo the normal microtubule-mediated motions. In fertilized eggs in which the pHi was reduced to unfertilized levels after the assembly of the sperm aster, no motions were detected. If the intracellular pH was later permitted to rise, normal motile events leading to division and development occurred, delayed by the time during which the pH elevation was blocked. Microtubule-mediated events occurred in eggs in which the intracellular pH was elevated, even in unfertilized eggs in which the pH was artificially increased. These results indicate that the formation and normal functioning of the egg microtubules is initiated, either directly or indirectly, by the shift in intracellular pH that occurs during fertilization.

Animals↗
PubMed1998

No evidence for elevated numbers of mononuclear cells expressing MCP-1 and RANTES mRNA in blood and CSF in multiple sclerosis.

The perivascular accumulation of mononuclear cells (MNC) in brain white matter is critical in the development of active lesions in multiple sclerosis (MS). Chemokines contribute to leukocyte recruitment by increasing the adhesiveness of integrins expressed on leukocytes and by promoting migration through endothelium and extracellular matrix. By using an in situ hybridization technique, it was possible to enumerate blood and CSF MNC expressing mRNA for the two CC chemokines monocyte chemoattractant protein-1 (MCP-1) and RANTES (regulated upon activation, normal T cells, expressed and secreted) in MS patients and controls. No differences in numbers of blood MNC expressing MCP-1 or RANTES could be found in MS patients compared to healthy individuals or patients with acute aseptic meningoencephalitis (AM). High numbers of CSF MNC expressing MCP-1 and RANTES were found in some MS patients, but also in patients with AM. This shows that elevated numbers of MCP-1 and RANTES mRNA expressing CSF MNC are not specific for the inflammatory process in MS. We conclude that there is no evidence for a systemic dysregulation of the CC chemokines MCP-1 and RANTES in MS.

Adult↗
PubMed2002

Significant increases in serum and plasma concentrations of matrix metalloproteinases 3 and 9 in patients with rapidly destructive osteoarthritis of the hip.

OBJECTIVE: Rapidly destructive osteoarthritis (OA) of the hip is an uncommon subset of OA that affects mainly elderly women. Previous studies indicate that elevated levels of matrix metalloproteinases (MMPs) are produced within the tissue of patients with the condition. In the present study, we sought to determine whether serum and plasma levels of MMPs and tissue inhibitors of metalloproteinases (TIMPs) are also elevated. METHODS: Blood samples were obtained from 16 patients with rapidly destructive hip OA and from 20 patients with OA before total hip arthroplasty was performed. Synovial specimens were obtained during surgery. Synovial fibroblasts that had migrated sufficiently from explants were subcultured in vitro for 72 hours after confluency, and harvested supernatants were collected. Blood, tissue samples, and fibroblasts were assayed for MMPs 1, 2, 3, and 9, and TIMPs 1 and 2 by sandwich enzyme immunoassay. RESULTS: In blood samples, the levels of MMP-3 and MMP-9 in the group with rapidly destructive hip OA were significantly higher than the normal range and were also significantly higher than those in the OA group. In tissue samples, the levels of MMP-1, MMP-3, MMP-9, and TIMP-1 in the group with rapidly destructive hip OA were significantly higher than those in the OA group. CONCLUSION: The results of this study show that serum and plasma levels of MMP-3 and MMP-9 are significantly increased in patients with rapidly destructive hip OA. Significantly large amounts of these MMPs produced in synovial tissues within the hip joint could contribute in part to elevation of blood levels. Detection of increased levels of MMP-3 and MMP-9 in patients with painful, disabling hip OA may be of diagnostic value for rapidly destructive hip OA.

Aged↗
PubMed2000

Increase of macrophage migration inhibitory factor in sera of patients with iridocyclitis.

AIMS: To determine whether macrophage migration inhibitory factor (MIF) levels were increased in sera of the patients with iridocyclitis. METHODS: Sera were obtained from 41 patients with acute iridocyclitis, 13 patients with chronic iridocyclitis, and 44 healthy control subjects. MIF levels were determined by a human MIF ELISA. RESULTS: The average levels of MIF in the sera of patients with both acute and chronic iridocyclitis were significantly higher than that of healthy subjects. CONCLUSION: Uveitis induces the elevation of serum MIF, which may affect various inflammatory symptoms in uveitis.

Acute Disease↗
PubMed2000

Vascular endothelial growth factor-A-induced chemotaxis of monocytes is attenuated in patients with diabetes mellitus: A potential predictor for the individual capacity to develop collaterals.

BACKGROUND: Vascular endothelial growth factor-A (VEGF-A) acts on endothelial cells and monocytes, 2 cell types that participate in the angiogenic and arteriogenic process in vivo. Thus far, it has not been possible to identify differences in individual responses to VEGF-A stimulation because of the lack of an ex vivo assay. METHODS AND RESULTS: We report a chemotaxis assay using isolated monocytes from individual diabetic patients and from healthy, age-matched volunteers. The chemotactic response of individual monocyte preparations to VEGF-A, as mediated via Flt-1, was quantitatively assessed using a modified Boyden chamber. Although the migration of monocytes from healthy volunteers could be stimulated with VEGF-A (1 ng/mL) to a median of 148.4% of the control value (25th and 75th percentiles, 136% and 170%), monocytes from diabetic patients could not be stimulated with VEGF-A (median, 91.1% of unstimulated controls; 25th and 75th percentiles, 83% and 98%; P<0.0001). In contrast, the response of monocytes to the chemoattractant formylMetLeuPhe remained intact in diabetic patients. The VEGF-A-inducible kinase activity of Flt-1, as assessed by in vitro kinase assays, remained intact in monocytes from diabetic patients. Moreover, the serum level of VEGF-A, as assessed by immunoradiometric assay, was significantly elevated in diabetic patients. CONCLUSIONS: The cellular response of monocytes to VEGF-A is attenuated in diabetic patients because of a downstream signal transduction defect. These data suggest that monocytes are important in arteriogenesis and that their ability to migrate might be critical to the arteriogenic response. Thus, we resolved a fundamental mechanism involved in the problem of impaired collateral formation in diabetic patients.

Aged↗
PubMed2004

S100A4 regulates cell motility and invasion in an in vitro model for breast cancer metastasis.

Elevated levels of the calcium-binding protein S100A4 are associated with poor patient survival in breast cancer patients and induce metastasis in rodent models. To investigate the effects of S100A4 on different components of the metastatic process, epithelial cells lines have been isolated from nonmalignant tumours in neu transgenic mice and from malignant tumours in neu/S100A4 double transgenic mice. Additional cell lines expressing both Neu and S100A4 have also been derived by transfection of rat S100A4 cDNA into tumour cell lines cloned from neu single transgenic mice. Using these cells in transfilter migration assays, it has been shown that increases in either motility or invasive properties correlate with each other and with the level of S100A4 protein. Injection of three of the cell lines separately into the mammary fat pads of nude mice showed that elevated levels of S100A4 correlated with the degree of metastasis to the lungs. In contrast, changes in cell proliferation and cell-substrate adhesion did not correlate with S100A4 levels. Neither motility nor invasiveness correlated with proteolytic degradation of gelatin as measured by zymography. Thus, the results suggest that the main effect of increases in S100A4 levels in metastasis is to generate increased cell motility and invasion and that this latter change is not dependent upon an increased ability to degrade the intercellular matrix.

Animals↗
PubMed2004

Enhancement of migration and invasion of hepatoma cells via a Rho GTPase signaling pathway.

AIM: Intrahepatic extension is the main cause of liver failure and death in hepatocellular carcinoma patients. The small GTPase Rho and one of its effector molecules ROCK regulate cytoskeleton and actomyosin contractility, and play a crucial role in cell adhesion and motility. We investigated the role of small GTPase Rho in biological behaviors of hepatocellular carcinoma to demonstrate the importance of Rho in cancer invasion and metastasis. METHODS: Using Western blotting, we quantitated Rho protein expression in SMMC-7721 cells induced by Lysophosphatidic acid (LPA). Furthermore, we examined the role of Rho signaling in regulating the motile and invasive properties of tumor cells. RESULTS: Rho protein expression was stimulated by LPA. Using the Rhotekin binding assay to assess Rho activation, we observed that the level of GTP-bound Rho was elevated transiently after the addition of LPA, and Y-27632 decreased the level of active Rho. LPA enhanced the motility of tumor cells and facilitated their invasion. Rho played an essential role in the migratory process, as evidenced by the inhibition of migration and motility of cancer cells by a specific inhibitor of ROCK, Y-27632. CONCLUSION: The finding that invasiveness of hepatocellular carcinoma is facilitated by the Rho/Rho-kinase pathway is likely to be relevant to tumor progression and Y-27632 may be a new potential effective agent for the prevention of intrahepatic extension of human liver cancer.

Amides↗
PubMed2003

Aggretin, a snake venom-derived endothelial integrin alpha 2 beta 1 agonist, induces angiogenesis via expression of vascular endothelial growth factor.

Aggretin, a collagen-like alpha 2 beta 1 agonist purified from Calloselasma rhodostoma venom, was shown to increase human umbilical vein endothelial cell (HUVEC) proliferation and HUVEC migration toward immobilized aggretin was also increased. These effects were blocked by A2-IIE10, an antibody raised against integrin alpha 2. Aggretin bound to HUVECs in a dose-dependent and saturable manner, which was specifically inhibited by A2-IIE10, as examined by flow cytometry. Aggretin elicited significant angiogenic effects in both in vivo and in vitro angiogenesis assays, and incubation of HUVECs with aggretin activated phosphatidylinositol 3-kinase (PI3K), Akt, and extracellular-regulated kinase 1/2 (ERK1/2); these effects were blocked by A2-IIE10 or vascular endothelial growth factor (VEGF) monoclonal antibody (mAb). The angiogenic effect induced by aggretin may be via the production of VEGF because the VEGF level was elevated and VEGF mAb pretreatment inhibited Akt/ERK1/2 activation as well as the in vivo angiogenesis induced by aggretin. The VEGF production induced by aggretin can be blocked by A2-IIE10 mAb pretreatment. In conclusion, aggretin induces endothelial cell proliferation, migration, and angiogenesis by interacting with integrin alpha 2 beta 1 leading to activation of PI3K, Akt, and ERK1/2 pathways, and the increased expression of VEGF may be responsible for its angiogenic activity.

Biocompatible Materials↗
PubMed2002

Expression of ROCK-1 in human pancreatic cancer: its down-regulation by morpholino oligo antisense can reduce the migration of pancreatic cancer cells in vitro.

INTRODUCTION: Invasion and metastasis of cancer cells require cell motility and adhesion. The small GTPase Rho and one of its effector molecules ROCK regulate cytoskeleton and actomyosin contractility, and play a crucial role in cell adhesion and motility. Results of previous studies showed that the elevated activity of ROCK-1, one of the isomers of ROCK kinases, led to an increase in the activity of invasion and metastasis of cancer cell lines. AIM: To investigate the importance of ROCK-1 in cancer invasion and metastasis. METHODOLOGY: We investigated the expression of ROCK-1 in two cancer cell lines and 31 human pancreatic tissues (21 pancreatic cancers [PC] and 10 histologically normal tissues) by immunoblotting and immunohistochemistry. We also examined by haptotaxis assay whether the migratory activity of PC cells could be suppressed by treatment with the morpholino antisense oligonucleotide in vitro. RESULTS: The expression of ROCK-1 was found in 18 of 21 PC tissues (85.7%), but not in normal pancreatic tissues by immunoblotting and immunohistochemistry. Antisense oligo against ROCK-1 significantly inhibited the haptotaxis of Panc-1 in a dose-dependent manner, compared with the control oligo. CONCLUSION: These results suggest that ROCK-1 may contribute to pancreatic cancer cell invasion and/or metastasis by facilitating cancer cell migration.

Cell Movement↗
PubMed2007

Isotopic evidence for age-related immigration to imperial Rome.

Oxygen stable isotope ratios (delta(18)O) have been determined in carbonate in paired first and third molar teeth from individuals (N = 61) who lived in the town of Portus Romae ("Portus") and who were buried in the necropolis of Isola Sacra (First to Third centuries AD) near Rome, Italy. We compare these analyses with data for deciduous teeth of modern Roman children. Approximately one-third of the archaeological sample has first molar (M1) values outside the modern range, implying a large rate of population turnover at that time, consistent with historical data. Delta (18)O(ap) values suggest that a group within the sample migrated to the area before the third molar (M3) crown had completely formed (i.e., between 10 and 17.5 years of age). This is the first quantitative assessment of population mobility in Classical antiquity. This study demonstrates that migration was not limited to predominantly single adult males, as suggested by historical sources, but rather a complex phenomenon involving families. We hypothesize that migrants most likely came from higher elevations to the East and North of Rome. One individual with a higher delta(18)O value may have come (as a child) from an area isotopically similar to North Africa.

Climate↗
PubMed2006

TGF beta-mediated RhoA expression is necessary for epithelial-mesenchymal transition in the embryonic chick heart.

Endothelia in the atrioventricular canal (AVC) of the embryonic heart undergo an epithelial-mesenchymal transition (EMT) and migrate into the underlying extracellular matrix. We explore here whether RhoA mediates this EMT. RhoA was detected in all cells of the chick heart during the stages studied. Expression was elevated when EMT was actively occurring. Explants treated with C3 exoenzyme in collagen gel cultures showed a significant decrease in mesenchymal cell numbers. siRNA was used to inhibit RhoA mRNA, and both activated endothelial and mesenchymal cells decreased significantly with treatment. Loss of RhoA produced a reduction of RhoB, cyclin-b2, and beta-catenin messages showing that these genes are regulated downstream of RhoA. In contrast, runx-2 was not reduced. Inhibition of TGFbeta3 or TGFbeta2 activity caused a large reduction of RhoA message. These data place RhoA in TGFbeta regulated pathways for both endothelial activation and mesenchymal invasion and demonstrate a functional requirement during EMT.

Animals↗