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PubMed1998

Roles of extracellular Ca++ and calmodulin in roxatidine-stimulated secretion and synthesis of mucus by cultured rabbit gastric mucosal cells.

We found that roxatidine stimulates mucus secretion and synthesis by cultured rabbit gastric mucosal cells. In this study, we examined the roles of the extracellular Ca++ and calmodulin in these effects of roxatidine. Reduction of the extracellular Ca++ concentration decreased the roxatidine-induced increases in mucus secretion and synthesis by gastric mucosal cells. Roxatidine concentration-dependently promoted Ca++ influx and caused an increases in intracellular Ca++. After the addition of roxatidine, the increases in the secretion and synthesis reflected those in Ca++ influx and intracellular Ca++ concentration and then disappeared as Ca++ influx and intracellular Ca++ concentration returned to the control level. The roxatidine-stimulated Ca++ influx and intracellular Ca++ mobilization were abolished by reduction of the extracellular Ca++ concentration. Nifedipine and diltiazem inhibited both the effects of roxatidine, but even at 10 microM, the inhibition was partial. Furthermore, W-7 (a calmodulin antagonist) completely abolished the effects of roxatidine on mucus secretion and synthesis without causing a reduction of the stimulated Ca++ influx. Taken together, these results suggest that roxatidine promotes Ca++ influx through both voltage-sensitive Ca++ channels and other Ca++ entry gates and the subsequent intracellular Ca++ mobilization, leading to potentiation of mucus secretion and synthesis by rabbit gastric mucosal cells. In addition, Ca(++)-activated calmodulin may play a pivotal role in these stimulatory effects of roxatidine.

Animals↗
PubMed2006

Characterization of the transient receptor potential channels mediating lysophosphatidic acid-stimulated calcium mobilization in B lymphoblasts.

Altered 1-oleoyl-lysophosphatidic acid (LPA, 100 microM)-stimulated calcium responses occur in B-lymphoblast cell lines from bipolar disorder patients, but the mechanism(s) involved is uncertain. Lysophosphatidic acid shares a structurally similar fatty acid side chain with the diacylglycerol analogue, 1-oleoyl-2-acetyl-sn-glycerol (OAG), a known activator of subtypes 3, 6 and 7 of the canonical transient receptor potential (TRPC) cation channel subfamily. Accordingly, the objective of this study was to determine whether the LPA-stimulated calcium response in B-lymphoblasts is mediated, in part, through this TRPC channel subfamily. Divalent cation selectivity in response to thapsigargin, LPA and OAG were used to distinguish TRPC-like character of the responses to these agents in BLCLs. The sensitivity to gadolinium, an inhibitor of capacitative calcium channels, was used to determine the store-operated nature of the responses. The TRPC isoforms that are present in BLCLs as identified by immunoblotting and/or PCR include TRPC1, 3 and 5. Minimal barium influx in calcium-free buffer was observed following thapsigargin stimulation. However, LPA stimulated barium influx of a magnitude similar to that induced by OAG. Thapsigargin-provoked calcium influx was completely inhibited by gadolinium (10 microM), whereas LPA and OAG-stimulated responses were partially inhibited and potentiated, respectively. The results suggest that 100 microM LPA stimulates calcium entry through channels with characteristics similar to TRPC3, as TRPC6 and 7 are absent in B-lymphoblasts.

B-Lymphocytes↗
PubMed2004

Residential mobility during pregnancy.

In epidemiological studies of environmental exposures and adverse pregnancy outcomes, maternal residence at delivery is often used to assign an exposure level, based on routinely collected data. In order to examine the potential for exposure misclassification due to residential mobility, we examined maternal mobility according to changes in residence overall, as well as changes in municipality and county. The potential for mobility to be related to pregnancy outcomes was considered by examining the relationship between mobility and risk factors commonly included in investigations of adverse pregnancy outcomes. Previously collected data were studied from 398 population-based control subjects from a case-control study of stillbirths. We compared demographic, lifestyle, medical, pregnancy and environmental factors of women who moved during pregnancy with those who did not. Bivariable and multivariable log binomial regressions were used to identify risk factors that were associated with mobility during pregnancy. Twelve per cent of subjects moved at least once during their pregnancy. Among women who moved, the majority (62%) moved within the same municipality. In bivariable analyses, we found that low family income, lower maternal age, unmarried status and tobacco use were associated with an increased likelihood of moving during pregnancy, whereas women who used folic acid before conception and who had a higher prepregnancy body mass index (BMI) were less likely to move during pregnancy. In multivariable analyses, only family income, age and prepregnancy BMI were independently predictive of mobility. These results indicate that in studies using maternal residence at delivery to assign environmental exposures, mobility during pregnancy is likely to be prevalent enough to introduce exposure misclassification. The potential for differential exposure misclassification should be considered should any of the risk factors for moving identified by this study also be risk factors for the outcome under study.

Adult↗
PubMed2003

Large-scale isolation of CD133+ progenitor cells from G-CSF mobilized peripheral blood stem cells.

We have evaluated the feasibility of large-scale isolation of CD133+ progenitors from healthy mobilized adult donors for potential clinical use in autologous and allogeneic transplantation. A total of 11 healthy volunteer adult donors were mobilized with G-CSF. CD133+ stem cells were isolated from a single leukapheresis using the Clinimacs method. The median percentage of CD133 before positive selection was 0.75% (range 0.39-2.03%). After selection, the median purity and recovery was 94% (range 85.2-98.0%) and 69% (range 44-100%), respectively. The median log10 T-cell depletion obtained by CD133+ positive selection was 4.2 (range 3.8-4.7). The CD133+ progenitors were highly enriched in colony-forming units (CFU) and transplantation into NOD/SCID mice resulted in a high engraftment rate. Transplantation of sorted CD133+/CD34+ cells into NOD/SCID mice showed a higher engraftment compared to CD133-/CD34+ cells. Mobilized peripheral CD133+ stem cells can be purified in large scale for potential clinical use. The biological function of the cells is not impaired. The majority of the NOD/SCID repopulating cells are within the CD133+/CD34+ subpopulation. Therefore, clinical studies using purified CD133+ stem cells can be envisoned to further clarify the role of CD133+ stem cells in hematopoietic reconstitution after transplantation.

AC133 Antigen↗
PubMed1993

Multiple mechanisms by which protein kinase A potentiates inositol 1,4,5-trisphosphate-induced Ca2+ mobilization in permeabilized hepatocytes.

The mobilization of Ca2+ from intracellular stores by Ins(1,4,5)P3 in suspensions of permeabilized rat hepatocytes was potentiated by preincubating intact cells with adenosine 3':5'-cyclic phosphorothioate (cpt-cAMP), or by addition of the catalytic subunit of cyclic-AMP-dependent protein kinase (PKA) after cell permeabilization. This action of PKA involved both an enhancement in Ins(1,4,5)P3 sensitivity and an increase in the size of the Ins(1,4,5)P3-releasable Ca2+ pool. Inclusion of the protein phosphatase inhibitor okadaic acid in the permeabilization medium augmented the effects of PKA. Treatment with PKA catalytic subunit also increased the rate of ATP-dependent Ca2+ sequestration. To determine whether the effects of PKA on the Ca(2+)-release mechanism were secondary to alterations in the Ca2+ load of the Ins(1,4,5)P3-sensitive stores, a method was developed using Mn2+ as a Ca2+ surrogate to examine the permeability properties of the Ins(1,4,5)P3-gated channels independent of Ca2+ fluxes. This approach utilized the ability of Mn2+ to quench the fluorescence of fura-2 compartmentalized within intracellular Ca2+ stores in an Ins(1,4,5)P3-dependent manner, with thapsigargin added to block the ATP-activated Ca2+ pump and to ensure that the Ca2+ stores were fully depleted of Ca2+. The initial rate and extent of Mn2+ quenching of compartmentalized fura-2 was increased in a dose-dependent manner by Ins(1,4,5)P3. PKA activation increased both the initial rate and the extent of Mn2+ quenching at sub-maximal Ins(1,4,5)P3 doses, but there was no effect on the quench rate in the presence of saturating Ins(1,4,5)P3. However, the amount of compartmentalized fura-2 that could be quenched by Mn2+ in the presence of maximal Ins(1,4,5)P3 was increased by PKA. These data suggest two distinct actions of PKA on the Ins(1,4,5)P3-sensitive Ca2+ stores. (1) Modification of the ion-permeability properties of the Ins(1,4,5)P3 receptor/channel through an increase in the sensitivity to Ins(1,4,5)P3 for channel opening. (2) A recruitment of Ca2+ stores from the Ins(1,4,5)P3-insensitive pool. Both actions were independent of the Ca(2+)-loading state of the stores. Imaging studies of single permeabilized hepatocytes showed that the Ins(1,4,5)P3-sensitive stores were distributed throughout the cell and PKA enhanced the rate of Ins(1,4,5)P3-stimulated Mn2+ quench in individual cells, without modifying the subcellular distribution of Ins(1,4,5)P3-sensitive stores.

Animals↗
PubMed1996

Normal human peripheral blood mononuclear cells mobilized with granulocyte colony-stimulating factor have increased osteoclastogenic potential compared to nonmobilized blood.

Single-cell suspensions of granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood mononuclear cells (G-PBMC) cultured in alpha minimal essential medium (alphaMEM) containing 10% fetal bovine serum formed multicellular aggregates within 24 hours. In six separate experiments, formation of aggregates appeared to be dependent on cell density per surface area, so that 5.8 +/- 1.3 aggregates formed per 1 x 10(5) cells when G-PBMC were cultured at densities greater than or equal to 1 x 10(5) cells/cm2. The frequency of aggregate formation was less than 1 per 10(5) cells when G-PBMC were cultured at densities less than 1 x 10(5) cells/cm2. Once formed, aggregates became adherent within 72 hours, and then, over the course of 21 days, released CD3/CD4/CD25-positive cells into the supernatant. This T-cell production peaked between days 7 and 14, reaching a total of 1,269 +/- 125.9 cells released per aggregate by day 21. Between days 14 and 21, the aggregates also generated macroscopic clusters of adherent mononuclear and giant multinucleated cells that stained positive for tartrate-resistant acid phosphatase (TRAP). At 4 weeks, the macroscopic foci coalesced into monolayers. Multinucleated TRAP-positive cells were distinguished from macrophage polykaryons by the absence of CD14 expression and the presence of osteoclast-specific membrane receptors for calcitonin and alphavbeta3-vitronectin. The osteoclast nature of these cells was further demonstrated by their ability to form resorption lacunae on dentine slices. Comparable osteoclast formation was not detected in cultures of normal marrow or normal nonmobilized peripheral blood.

Acid Phosphatase↗
PubMed1990

A career mobility program for skilled nursing facilities.

This article reports the results of a 3-year demonstration project in career mobility for nursing personnel in skilled nursing facilities. The goal of the project was to demonstrate the effectiveness of a career mobility program in addressing service delivery challenges such as recruitment, retention, and satisfaction of nursing personnel in skilled nursing facilities. The project was a joint effort between an educational department of a large university and a major long-term care corporation. The project evaluation addressed the effectiveness of this career mobility program in attracting and retaining nursing personnel, the satisfaction of nursing personnel with their jobs, and whether the additional training affected the quality of care. Five pilot and three comparison sites were designated in Southern California. Survey, self-report, and interview data were collected at yearly intervals and at the completion of the project. Descriptive statistics and analysis of variance formed the basis for data analysis and interpretation. Overall, the findings suggested that the career mobility program has the potential to retain staff who benefit from a career development program. The career mobility program was a valuable strategy, but its success was only as good as the management team's authority to support the program and emphasize its goals.

California↗
PubMed2002

A requirement of nuclear factor-kappaB activation in fear-potentiated startle.

Previous studies have shown that biochemical changes that occur in the amygdala during fear conditioning in vivo are similar to those occur during long term potentiation (LTP) in vitro. Electrophoretic mobility shift assay of nuclear extracts from startle-potentiated rats showed a selective increase in the amygdala of nuclear factor-kappaB (NF-kappaB) DNA binding activity. Supershift experiments further indicated that p65 and p50 subunits but not c-Rel were involved in DNA binding. The protein levels of IkappaB-alpha were reduced by treatments that reliably induced LTP in this area of the brain. This was accompanied by a decrease of NF-kappaB in the cytoplasm concomitant with an increase in the nucleus. Quantitative analysis of IkappaB kinase activity demonstrated that fear training led to an increase in kinase activity, and this effect was inhibited by thalidomide. Paralleled behavioral tests revealed that thalidomide inhibited fear-potentiated startle. Intra-amygdala administration of kappaB decoy DNA prior to training impaired fear-potentiated startle as well as LTP induction. Similarly, NF-kappaB inhibitors blocked IkappaB-alpha degradation and startle response. These results provide the first evidence of a requirement of NF-kappaB activation in the amygdala for consolidation of fear memory.

Animals↗
PubMed1980

Current uses of mobility aids.

Developmental milestones are a key indicator in determining a proper mobility aid. Proper positioning is essential if the individual is to utilize the mobility aid to its fullest potential, thereby maximizing independence. This article deals with mobility aids available, as well as techniques for providing supportive yet comfortable positioning.

Child↗
PubMed2006

[The potential mechanism on signal transduction pathway in regulation of mRNA expression of high mobility group box-1 protein in septic rats].

OBJECTIVE: To investigate the potential role of Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway in regulation of gene expression of high mobility group box-1 protein (HMGB1) in various tissues in rats with sepsis. METHODS: A sepsis model reproduced by cecal ligation and puncture (CLP), and 128 male Wistar rats were randomly divided into normal control group (n = 10), sham operation group (n = 10), CLP group (n = 60), AG490 treatment group (n = 24), and rapamycin (RPM) treatment group (n = 24). At serial time points animals in each group were sacrificed after CLP, then tissue samples were harvested to determine HMGB1 mRNA expression and STAT1/3 DNA binding activity. RESULTS: STAT1 activities increased rapidly in the liver, lungs and small intestine after CLP, peaking at 6 - 12 h, while it increased slowly, and still kept at mild level from 2 to 48 h in the kidneys. Compared with STAT1, lower STAT3 activities were detected only in the liver and lungs, with negative detection in the small intestine and kidneys. HMGB1 mRNA levels significantly increased in liver, lungs and small intestine at various time points after CLP respectively (P < 0.05 or P < 0.01), while they didn't change in the kidneys. Treatment with AG490 could markedly inhibit HMGB1 mRNA expression in the liver and small intestine at 24 and 48 h (P < 0.05 or P < 0.01), and in lungs at 2 h following CLP (P < 0.01). Similarly, treatment with RPM significantly decreased HMGB1 mRNA expression in the lungs at 2, 6, 24 and 48 h, in the liver at 6 and 24 h, and in the small intestine at 24 and 48 h (P < 0.05 or P < 0.01). In addition, STAT1 and STAT3 activities in the liver and lungs were significantly correlated with corresponding tissue HMGB1 mRNA expression. CONCLUSIONS: Peritoneal infection could extensively activate STAT1 and limitedly activate STAT3 in vital organs. Activation of JAK/STAT pathway might be involved in up-regulating the gene expression of HMGB1 and systemic inflammation secondary to severe septic challenge.

Animals↗
PubMed2005

Insulin, glucagon and fatty acid treatment of hepatocytes does not result in phosphorylation or changes in activity of triacylglycerol hydrolase.

It is recognized that the majority of very low density lipoprotein (VLDL) associated triacylglycerol (TG) is synthesized from fatty acids and partial acylglycerols generated by lipolysis of intra-hepatic storage rather than made de novo. Triacylglycerol hydrolase (TGH) is involved in mobilizing stored TG. Modulating the ability of TGH to hydrolyze stored lipids represents a potentially regulated and rate limiting step in VLDL assembly. Phosphorylation of lipases and carboxylesterases trigger diverse but functionally significant events. We explored the potential for regulating the mobilization of hepatic TG through phosphorylation of TGH. Insulin is known to suppress VLDL secretion from liver, and glucagon can be considered an opposing hormone. However, neither insulin nor glucagon treatment of hepatocytes led to phosphorylation of TGH or changes in its activity. Augmenting intracellular TG stores by incubations with oleic acid also did not lead to changes in TGH activity. Therefore, changes in phosphorylation state are not a mechanism for regulating TGH activity, access to TG substrate pools or for TGH-mediated contributions to VLDL assembly and secretion.

Alkaline Phosphatase↗
PubMed2001

Unique signaling properties of B cell antigen receptor in mature and immature B cells: implications for tolerance and activation.

Immature B cells display increased sensitivity to tolerance induction compared with their mature counterparts. The molecular mechanisms underlying these differences are poorly defined. In this study, we demonstrate unique maturation stage-dependent differences in B cell Ag receptor (BCR) signaling, including BCR-mediated calcium mobilization responses. Immature B cells display greater increases in intracellular calcium concentrations following Ag stimulation. This has consequences for the induction of biologically relevant responses: immature B cells require lower Ag concentrations for activation than mature B cells, as measured by induction of receptor editing and CD86 expression, respectively. BCR-induced tyrosine phosphorylation of CD79a, Lyn, B cell linker protein, and phospholipase Cgamma2 is enhanced in immature B cells and they exhibit greater capacitative calcium entry in response to Ag. Moreover, B cell linker protein, Bruton's tyrosine kinase, and phospholipase Cgamma2, which are crucial for the induction of calcium mobilization responses, are present at approximately 3-fold higher levels in immature B cells, potentially contributing to increased mobilization of calcium. Consistent with this possibility, we found that the previously reported lack of inositol-1,4,5-triphosphate production in immature B cells may be explained by enhanced inositol-1,4,5-triphosphate breakdown. These data demonstrate that multiple mechanisms guarantee increased Ag-induced mobilization of calcium in immature B cells and presumably ensure elimination of autoreactive B cells from the repertoire.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Tollbooth workers and mobile source-related hazardous air pollutants: how protective is the indoor environment?

Tollbooth workers are potentially exposed to high levels of mobile source-related air pollutants due to the proximity and intensity of the source. To evaluate this worker hazard, we measured the concentration of air toxins including volatile organic compounds (VOCs) and particle-bound polycyclic aromatic hydrocarbons (PAHs) inside and outside a Baltimore Harbor Tunnel tollbooth during the summer of 2001. Mean outdoor benzene and 1,3-butadiene concentrations varied by shift with the morning (10.7 and 19.8 microg/m3) exceeding afternoon (7.2 and 14.9 microg/m3) and the lowest levels observed during the night (3.7 and 4.9 microg/m3, respectively) when traffic volume was the lowest. In comparison, considerable protection was provided to workers bythe indoor environment where lower concentrations of 1,3-butadiene and benzene were observed for all three shifts (2.9 and 6.7, 0.9 and 3.2, and 0.9 and 2.4 microg/m3, respectively). The greatest protection offered by the tollbooth was observed during the afternoon shift (5-8-fold reduction in indoor concentration), whereas the morning and night shifts experienced similar protection (2-4-fold reduction). Chlorinated hydrocarbons were observed at higher concentrations within the tollbooth, indicating the presence of indoor sources and the opportunity for exposure mitigation. Levels of PAHs were similarly reduced from outdoors (50 ng/m3) to indoors (15.4 ng/m3). The protective nature of the tollbooth highlighted in this study is likely due to the positive pressure control ventilation system that was present at this specific facility, which represents 55% of tollbooths in Maryland. This study provides an estimate of tollbooth workers potential exposures to various mobile source-related pollutants and highlights the protective nature of tollbooths equipped with positive pressure control ventilation systems.

Air Pollution, Indoor↗
PubMed1990

Potentiation of angiotensin II-stimulated phosphoinositide hydrolysis, calcium mobilization and contraction of renal mesangial cells upon down-regulation of protein kinase C.

Long-term pretreatment of rat mesangial cells with 12-O-tetradecanoylphorbol 13-acetate (TPA) down-regulated protein kinase C activity and potentiated the angiotensin II-induced inositol trisphosphate (InsP3) formation. This increased response to angiotensin II occurred without a significant change in the receptor number or Kd value of angiotensin II binding to the cells. The biologically inactive phorbol ester 4 alpha-phorbol 12,13-didecanoate was without effect on angiotensin II-stimulated InsP3 generation. Long-term pretreatment with TPA also increased the angiotensin II-induced mobilization of Ca2+ and the subsequent contraction of mesangial cells.

Angiotensin II↗
PubMed2002

Chi(1) rotamer populations and angles of mobile surface side chains are accurately predicted by a torsion angle database potential of mean force.

The equilibrium angles and distributions of chi(1) rotamers for mobile surface side chains of the small, 63-residue, B1 domain of protein L have been calculated from the static crystal structure by rigid body/torsion angle simulated annealing using a torsion angle database potential of mean force and compared to those deduced by Monte Carlo analysis of side chain residual dipolar couplings measured in solution. Good agreement between theory and experiment is observed, indicating that for side chains undergoing rotamer averaging that is fast on the chemical shift time scale, the equilibrium angles and distribution of chi(1) rotamers are largely determined by the backbone phi/psi torsion angles.

Bacterial Proteins↗
PubMed2006

Fractional Fokker-Planck dynamics: Numerical algorithm and simulations.

Anomalous transport in a tilted periodic potential is investigated numerically within the framework of the fractional Fokker-Planck dynamics via the underlying continuous-time random walk. An efficient numerical algorithm is developed which is applicable for an arbitrary potential. This algorithm is then applied to investigate the fractional current and the corresponding nonlinear mobility in different washboard potentials. Normal and fractional diffusion are compared through their time evolution of the probability density in state space. Moreover, we discuss the stationary probability density of the fractional current values.

Journal Article↗
PubMed1987

Mobile blood-derived components in rat renal allograft contain significant immunogenic potential.

Using a modified 'primed rejection assay' (PRA), we have investigated the immunogenic potential of different rat renal allograft components. Temporary transplantation of an extensively perfused DA kidney to a WF recipient can sensitize the WF recipient in less than 10 min; consequently, the survival of a subsequent DA heart allograft is significantly reduced. Irradiation of the renal allograft donor significantly reduces the immunogenic potential of the first allograft, but does not deplete it entirely. When the first allograft was made chimeric with regard to the (capillary) blood compartment, it was found that in vivo perfusion of an irradiated DA kidney with WF blood did not alter the immunogenic potential in WF recipients, whereas perfusion of irradiated DA kidneys with DA blood increased the immunogenicity. On the other hand, short in vivo perfusion of irradiated WF kidneys with DA blood make the first WF kidney allograft strongly immunogenic in the WF recipient, whereas perfusion of the kidney with WF blood has no effect. The rapid rate of sensitization observed, coupled with the induction and alteration of the allograft immunogenic potential by manipulation of blood-derived capillary compartment, suggests that mobile blood-derived components, which are outside the reach of extensive perfusion, contain significant immunogenic potential.

Animals↗
PubMed2003

Parathyroid hormone increases the sensitivity of inositol trisphosphate receptors by a mechanism that is independent of cyclic AMP.

1 In fura 2-loaded HEK-293 cells stably expressing human type 1 parathyroid hormone (PTH) receptors, PTH potentiated the Ca(2+) mobilization evoked by carbachol by >4 fold without itself increasing the intracellular [Ca(2+)]. 2 PTH potentiated the Ca(2+) release evoked by a cell-permeant analogue of inositol 1,4,5-trisphosphate (InsP(3)BM). 3 Prolonged incubation with InsP(3)BM emptied the Ca(2+) stores as effectively as PTH in combination with a maximal concentration of carbachol, indicating that PTH did not increase the size of the InsP(3)-sensitive Ca(2+) pool. 4 Responses to PTH were unaffected by disruption of the cytoskeleton. 5 The EC(50) for carbachol-evoked Ca(2+) release and InsP(3) formation were indistinguishable (approximately 40 microM), consistent with even the highest concentrations of carbachol generating insufficient InsP(3) to release the entire InsP(3)-sensitive Ca(2+) pool. 6 Inhibition of cyclic AMP-dependent protein kinase A (PKA), using H89 or CMIQ, did not affect potentiation of carbachol-evoked Ca(2+) signals by PTH. 7 SQ22536 or DDA, inhibitors of adenylyl cyclase, inhibited PTH-evoked cyclic AMP formation and IBMX, an inhibitor of cyclic nucleotide phosphodiesterase, increased the amount of cyclic AMP detected after stimulation by PTH. None of these drugs affected the potentiation of Ca(2+) signals by maximal or submaximal concentrations of PTH. 8 We conclude that PTH potentiates the Ca(2+) release evoked by receptors that stimulate InsP(3) formation by sensitizing InsP(3) receptors through a cyclic AMP-independent mechanism.

Calcium↗