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PubMed1979

Induction of ouabain-resistant mutation and sister chromatid exchanges in Chinese hamster cells with chemical carcinogens mediated by human pulmonary macrophages.

Pulmonary macrophages (PAM) metabolically activated benzo[a]pyrene [B(a)P] and its proximate carcinogenic metabolite, (+/-)trans 7,8-dihydroxy-7,8-dihydrobenzo[a]pyrene (7,8-diol), to ultimate mutagens that were detected in cocultivated Chinese hamster V79 cells. Increases in the frequency of ouabainresistant (O(r)) mutations and sister chromatid exchanges were found in V79 cells only when they were cocultivated with both PAM and the chemical procarcinogens. 7,8-Diol caused higher frequencies of both O(r) mutations and sister chromatid exchanges than did the parent compound, B(a)P. When metabolically activated by PAM the mean O(r) mutation frequency caused by B(a)P was 9 O(r) mutants/10(6) surviving V79 cells per 10(6) PAM and a 10-fold interindividual variation (range, 2-21) was found. The mean O(r) mutation frequency caused by 7,8-diol was 64 and a ninefold interindividual variation (range, 14-120) was found. In the absence of PAM, the O(r) mutation frequency in V79 cells was one or less O(r) mutant per 10(6) survivors. 7,8-Benzoflavone, an inhibitor of mixed function oxidases, reduced the frequencies of O(r) mutations and of sister chromatid exchanges in V79 cells caused by 7,8-diol and B(a)P. As expected 7,8-benzoflavone did not influence the frequency of O(r) mutations caused by one of the ultimate mutagens derived from B(a)P and 7,8-diol, (+/-)7beta, 8alpha-dihydroxy-9alpha, 10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene. These data are consistant with the hypothesis that PAM may play a role in the activation of environmental chemical procarcinogens.

Adenocarcinoma↗

PubMed2005

Efficacy of an adenosine A1 receptor agonist compared with atropine and pralidoxime in a rat model of organophosphate poisoning.

The objective of this study was to evaluate the effects of an adenosine A1 agonist, phenylisopropyl adenosine (PIA), on metamidophos poisoning compared to specific antidotes. Rats were poisoned with metamidophos (30 mg/kg, oral) and observed for 24 hours. One group received sodium chloride (1 mL/kg) and four experimental groups received atropine (5 mg/kg), pralidoxime (PAM, 20 mg/kg), atropine/PAM (5/20 mg/kg) or PIA (1 mg/kg) intraperitoneally. Atropine reduced salivation and prevented respiratory distress when compared to sodium chloride-treated rats. Treatment with PAM did not cause any suppression of cholinergic signs. Atropine and PAM combination prevented salivation, convulsion and respiratory distress. PIA delayed initial time of the salivation, convulsion and time to death. However, PIA was found ineffective against the metamidophos-induced cholinergic symptoms and mortality. All treatments, except PIA, lead to survival of these animals. Acetylcholinesterase (AChE) activity was not normalized by PIA or PAM. PIA prevented metamidophos-induced diaphragmatic muscle necrosis as much as PAM. In conclusion, a single dose of PIA was unable to protect the rats from metamidophos toxicity. Further studies are needed involving a combination of PAM and/or atropine with repeated doses of PIA to clarify the efficacy of adenosine agonists in OP poisoning.

Adenosine A1 Receptor Agonists↗

PubMed1993

Interactions of transforming growth factor-alpha and -beta and luteinizing hormone in the regulation of plasminogen activator activity in avian granulosa cells during follicular development.

This study examined the influence of transforming growth factor-alpha (TGF alpha), TGF beta, and LH on progesterone (P4) secretion and plasminogen activator (PA) activity in cultured avian granulosa cells from the first (F1), third (F3), and fifth and sixth (F5-6) preovulatory follicles during a 21-h incubation period. PA activity in the cell (PAc) and the medium (PAm) fractions was measured by fibrinolysis and fibrin overlay methods. P4 was determined by RIA. Basal PAc and PAm activities were highest in cell cultures from the less mature (F5-6) follicles and decreased as follicles matured to the F1 stage of development. PAc activity was greater than PAm activity regardless of the stage of follicular maturation. TGF alpha (0.1-10 ng/ml) increased PA activity in cultures of granulosa cells from F1, F3, and F5-6 follicles in a concentration-dependent manner. TGF alpha-induced PAc and PAm activities were observed by 6 and 15 h of incubation, respectively, and increased rapidly between 15-21 h. LH (100 ng/ml) attenuated TGF alpha-induced PA activity by 15 h in cultures of granulosa cells from F1 and F3, but not F5-6, follicles. Basal PA activities were unaffected by the gonadotropin. TGF beta (2-100 ng/ml) stimulated PAc activity in a dose-dependent manner only in cultures of granulosa cells from F5-6 follicles and significantly enhanced TGF alpha-induced PAc and PAm activities in cell cultures from F3 and F5-6, but not F1, follicles. Basal and growth factor-induced PAc and PAm activities corresponded to a mol wt of about 35 kDa, a value consistent with that of the low mol wt uPA species. TGF alpha and TGF beta, alone or in combination, had no effect on basal P4 secretion at all stages of follicular development. TGF alpha, however, decreased LH-induced P4 secretion in F1 and F3 cultures. These results demonstrate a tightly controlled interaction of TGF alpha, TGF beta, and LH in regulating PA activity and P4 secretion during follicular development in the domestic hen.

Animals↗

PubMed1976

[Inhibition of cholinesterase activity induced by pyridaphenthion].

Inhibitory effects on cholinesterase (ChE) activity in blood of the rabbit induced by pyridaphenthion(PD), an organophosphorus compound, and effects of 2-pyridine aldoxime methiodide(PAM) on this inhibition were examined. 1) Experimental results within 24 hr: An oral administration of each dose of PD(100 approximately 750 mg/kg) gradually decreased ChE activity and ChE activity value decreased to 20.5% in the erythrocytes and 21.5% in the plasma 24 hr after administration of 500 mg/kg of PD. However, this value recovered remarkably with an intravenous injection of PAM. The ChE activity value was 55.5% in the erythrocytes and 41.4% in the plasma with a single injection, and respectively 67.8% and 59.1% when PAM was injected three times. 2) Experimental results for 14 days: Following an increase of the administered dose (100 approximately 400 mg/kg) of PD, a decrease in ChE activity was apparent and a recovery to normal values was delayed. This inhibition could be ameliorated quickly with an injection of PAM. Considering that PAM does not have remarkable detoxicative effects on organophosphorus compounds which have a low toxicity, PAM appears to be a promising antidote against PD.

Administration, Oral↗

PubMed1993

[A study on acute organophosphorus poisoning--changes in the activity and isoenzyme patterns of serum cholinesterase in human poisoning].

Various organophosphorus compounds with low acute toxicity levels are widely used as insecticides. Human acute poisoning by organophosphates has often occurred accidentally. We determined the activity and isoenzyme patterns of serum cholinesterase (ChE) obtained from 13 human patients who attempted suicide with various organophosphates, i.e. Fenitrothion, Malathion, Isoxathion, Pyridaphenthion and Trichlorfon, and studied on the changes in the activity and isoenzyme patterns of serum ChE after ingestion. The following results were obtained. 1) Twenty ChE isoenzyme bands from normal human serum were detected by electrophoretic separation on polyacrylamide gradient gel. The main bands in the ChE isoenzyme pattern in normal serum were bands 4 and 5 which had the highest activity of acetylcholinesterase (AChE) with a molecular weight of 600,000-800,000, and bands 7, 12, 14, 17 and 18. 2) Inhibition of serum ChE activity was more severe as the amount ingested increased in patients who took Fenitrothion and Malathion. Reactivation of serum ChE activity was very slow in patients treated with PAM (2-pyridine aldoxime methiodide) in the late stage of ingestion or whose symptoms reappeared. 3) There were no differences in the patterns of serum ChE isoenzyme by organophosphorus compound. Band 7 disappeared in the serum ChE isoenzyme of almost every patient, and bands 12, 18, 14 and 17 of the serum ChE isoenzyme disappeared successively with the decline of serum ChE activity. Only band 5 of the isoenzyme remained in cases who had serum ChE activity lower than 5% of normal. 4) All 13 patients were treated with PAM and atropine immediately after being admitted to hospitals. We could not clearly determine the efficacy of PAM on reactivation of serum ChE activity and isoenzyme, because it was impossible in human poisoning to compare PAM efficacy with no treatment and with pre- and post-PAM treatment. 5) The activity and isoenzyme patterns of serum ChE recovered rapidly after combined hemoperfusion and hemodialysis treatment (HP-HD treatment) of the patients poisoned with Malathion. But HP-HD treatment had no effect on poisoning by Fenitrothion and Isoxathion. These findings demonstrated the changes in the activity and isoenzyme pattern of serum ChE in patients poisoned with several organophosphates after PAM and HP-HD treatment.

Acute Disease↗

PubMed1990

Defective cytostatic activity of pulmonary alveolar macrophages in primary lung cancer.

Macrophages are thought to play an important immune effector cell role in antitumor host defense. It remains unclear whether PAM antitumor activity in patients with lung cancer is normal or impaired. We examined PAM cytostasis in patients with lung cancer and in control subjects and determined whether the in vitro PAM response could be enhanced by gamma-interferon. Nineteen patients with primary lung carcinoma and 15 control patients underwent BAL. Five patients with cancer underwent lavage of both lungs to assess whether any abnormality found related to tumor proximity or was part of a more generalized defect. Cytostatic activity was assessed by measuring inhibition of incorporation of tritiated thymidine into the target cell U937. There was a significant difference in baseline cytostatic activity between patients with cancer (mean +/- SE, 59 +/- 7 percent) and control patients (92 +/- 2 percent) (p less than 0.0002). The increase in cytostatic function after stimulation with gamma-interferon (1,250 units/ml) was higher in the group with cancer (28 +/- 5 percent increase from baseline) than in controls (5 +/- 1 percent) (p less than 0.0005). Cytostasis after stimulation was not significantly different between the groups. In the bilaterally lavaged group, baseline cytostatic activity was not different between cancerous and noncancerous lungs and was again significantly lower than in control subjects. These results indicate (a) that PAM baseline cytostatic activity in patients with cancer is lower than in controls, (b) that gamma-interferon can significantly augment cytostatic function in patients with cancer, to levels comparable with those achievable in control patients, and (c) that the PAM abnormality is part of a generalized immune defect in lung cancer and does not simply reflect a local response to the carcinoma. It may be inferred from these results that PAMs from patients with primary lung cancer are not fully stimulated in vivo and that a defect of T cell lymphokine production may underlie the macrophage dysfunction.

Adult↗

PubMed2006

Controlling tailwater sediment and phosphorus concentrations with polyacrylamide in the Imperial Valley, California.

External loading of phosphorus (P) from agricultural surface discharge (tailwater) is the main cause of excessive algae growth and the eutrophication of the Salton Sea, California. Continuous polyacrylamide (PAM) applications to agricultural irrigation water inflows were evaluated as a means of reducing sediment and P in tailwater. Zero (control) and 1 mg L(-1) PAM (PAM1) treatments were compared at 17 Imperial Valley field sites. Five and 10 mg L(-1) PAM treatments (PAM5, PAM10) were conducted at one site. The particulate phosphorus (Pp) fraction was determined as the difference between total phosphorus (Pt) and the soluble phosphorus (Ps) fraction. We observed 73, 82, and 98% turbidity reduction with PAM1, PAM5, and PAM10 treatments. Although eight field sites had control tailwater sediment concentrations above the New River total maximum daily loads (TMDL), all but one were made compliant during their paired PAM1 treatments. While PAM1 and PAM10 reduced tail water Pp by 31 and 78%, none of the treatments tested reduced Ps. This may have been caused by high irrigation water Na concentrations which would reduce Ca adsorption and Ca-phosphate bridging on the PAM. The PAM1 treatments resulted in <0.5 mg L(-1) drain water polyacrylamide concentrations 1.6 km downstream of PAM addition, while PAM5 and PAM10 treatments produced > 2 mg L(-1) drain water polyacrylamide concentrations. We concluded that, although PAM practically eliminates Imperial Valley tailwater sediment loads, it does not effectively reduce tailwater Ps, the P fraction most responsible for the eutrophication of the Salton Sea.

Acrylic Resins↗

PubMedDate not supplied

Enhanced biological phosphorus removal from wastewater by biomass with different phosphorus contents, Part III: Anaerobic sources of reducing equivalents.

Laboratory-scale sequencing batch reactors exhibiting enhanced biological phosphorus removal (EBPR) operated at different influent phosphorus/chemical oxygen demand (COD) ratios were analyzed to evaluate possible anaerobic sources of reducing equivalents. Assuming anaerobic glycogen degradation was the sole anaerobic reducing equivalent source, an anaerobic phase carbon balance showed that glycogen-accumulating metabolism (GAM)-dominated systems were nearly carbon-balanced, but that polyphosphate-accumulating metabolism (PAM)-dominated systems had end-anaerobic phase carbon deficits. An anaerobic-phase reducing equivalent balance showed a reducing equivalent excess for the GAM-dominated systems and a deficit for the PAM-dominated systems, suggesting that glycogen degradation was not the sole reducing equivalent source for PAM. Reducing equivalent balances showed that metabolic models including complete anaerobic tricarboxylic acid (TCA) cycle activity, partial TCA cycle activity, and the glyoxylate bypass could provide the reducing equivalents required in PAM. Metabolic precursors produced in glycolysis, the TCA cycle, or modified versions of the TCA cycle could allow anaerobic growth and account for the PAM carbon deficits. The importance of considering both PAM and GAM activity in evaluating EBPR metabolic models was illustrated.

Anaerobiosis↗

PubMed2001

Evaluation of phagocytosis, bactericidal activity, and production of superoxide anion, nitric oxide, and tumor necrosis factor-alpha in Kupffer cells of neonatal pigs.

OBJECTIVE: To evaluate the activity of Kupffer cells (KC) of control neonatal pigs and neonatal pigs treated with endotoxin and to compare activity of KC with that of pulmonary alveolar macrophages (PAM). SAMPLE POPULATION: Kupffer cells and PAM obtained from 24 neonatal pigs (7 to 10 days old). PROCEDURE: Pairs (n = 7) of littermates served as treated (lipopolysaccharide [LPS]) or untreated pigs. Pigs were euthanatized 24 hours after treatment, and cells were isolated. Cells were obtained from 10 other neonatal pigs for other assays. Functional activity of cells was evaluated by use of in vitro assays to evaluate bactericidal activity, phagocytosis, and production of superoxide anion (SOA), nitric oxide (NO), and tumor necrosis factor-alpha (TNF-alpha). Each assay was repeated on cells obtained from 4 to 6 pigs. RESULTS: Phagocytic activity was similar in KC and PAM, but bactericidal activity and production of SDA and TNF-alpha was lower in KC. Neither KC nor PAM produced NO in response to LPS stimulation. Phagocytosis, bactericidal activity, and production of SOA were enhanced for KC obtained from neonatal pigs treated with LPS. The PAM from LPS-treated neonatal pigs had similar bactericidal activity to PAM obtained from untreated pigs. CONCLUSIONS AND CLINICAL RELEVANCE: Functional capacity of KC is affected by endotoxin. This provides additional information of the role the liver plays in immune surveillance. In addition, the response of KC in neonatal pigs exposed to endotoxin is of value for understanding gram-negative bacterial sepsis, which is a major cause of mortality in neonatal pigs.

Animals↗

PubMed2004

In vivo evaluation of pharmacologically active microcarriers releasing nerve growth factor and conveying PC12 cells.

Cell therapy will probably become a major therapeutic strategy in the coming years. Nevertheless, few cells survive transplantation when employed as a treatment for neuronal disorders. To address this problem, we have developed a new tool, the pharmacologically active microcarriers (PAM). PAM are biocompatible and biodegradable microparticles coated with cell adhesion molecules, conveying cells on their surface and presenting a controlled delivery of growth factor. Thus, the combined effect of growth factor and coating influences the transported cells by promoting their survival and differentiation and favoring their integration in the host tissue after their complete degradation. Furthermore, the released factor may also influence the microenvironment. In this study, we evaluated their efficacy using nerve growth factor (NGF)-releasing PAM and PC12 cells, in a Parkinson's disease paradigm. After implantation of NGF-releasing or unloaded PAM conveying PC12 cells, or PC12 cells alone, we studied cell survival, differentiation, and apoptosis, as well as behavior of the treated rats. We observed that the NGF-releasing PAM coated with two synthetic peptides (poly-D-lysine and fibronectin-like) induced PC12 cell differentiation and reduced cell death and proliferation. Moreover, the animals receiving this implant presented an improved amphetamine-induced rotational behavior. These findings indicate that PAM could be a promising strategy for cell therapy of neurological diseases and could be employed in other situations with fetal cell transplants or with stem cells.

Amphetamines↗

PubMed2004

Importance of IL-10 for CTLA-4-mediated inhibition of tumor-eradicating immunity.

In this study, we show that engagement of CTLA-4 on tumor-infiltrating lymphocytes from low-dose melphalan (L-phenylalanine mustard (L-PAM))-treated MOPC-315 tumor bearers led to IL-10 secretion. In addition, the inhibitory activity of CTLA-4 ligation for IFN-gamma secretion following stimulation with anti-CD3 plus anti-CD28 mAb depended on IL-10 production. Consistent with the importance of IL-10 for CTLA-4-mediated inhibition, administration of neutralizing anti-IL-10 mAb to low-dose L-PAM-treated MOPC-315 tumor bearers (administration of blocking anti-CTLA-4 mAb) resulted in enhanced tumor-infiltrating lymphocyte-mediated anti-MOPC-315 cytotoxicity and led to complete tumor eradication in a higher percentage of mice than that observed with low-dose L-PAM alone. The percentage of MOPC-315 tumor-bearing mice cured following administration of neutralizing anti-IL-10 mAb to low-dose L-PAM-treated MOPC-315 tumor bearers was comparable to that observed following administration of blocking anti-CTLA-4 mAb. Moreover, IL-10 neutralization together with CTLA-4 blockade did not provide added therapeutic benefits to low-dose L-PAM-treated MOPC-315 tumor bearers. Taken together, these results indicate that CTLA-4 blockade improves the therapeutic outcome of low-dose L-PAM for MOPC-315 tumor bearers by inhibiting IL-10 secretion as a consequence of blocking CTLA-4 ligation.

Animals↗

PubMed2005

Reciprocal activating interaction between dendritic cells and pamidronate-stimulated gammadelta T cells: role of CD86 and inflammatory cytokines.

We investigated the interactions between human monocyte-derived dendritic cells (DCs) and Ag-activated circulating TCR-gammadelta-expressing lymphocytes (Vdelta2). Coculture of immature DCs (iDCs) with peripheral blood Vdelta2 T cells activated with either pyrophosphomonoesters (isopentenyl pyrophosphate; IPP) or aminobiphosphonates (pamidronate; PAM) led to a significant up-modulation of CD86 and MHC class I molecules and to the acquisition of functional features typical of activated DCs. DC activation induced by both IPP- and PAM-stimulated gammadelta T cells was mostly mediated by TNF-alpha and IFN-gamma secreted by activated lymphocytes. However, the effect of PAM-activated gammadelta T cells, but not that of IPP-activated cells, required cell-to-cell contact. Reciprocally, activation of Vdelta2 T cells by PAM, but not by IPP, was dependent on cell contact with iDCs. In fact, when PAM-stimulated DC-gammadelta T cell cocultures were separated by a semipermeable membrane or treated with blocking anti-CD86 Abs, induction of CD25 and CD69 as well as IFN-gamma and TNF-alpha secretion by Vdelta2 cells were strongly reduced. These results demonstrate for the first time a bidirectional activating interaction between iDCs and PAM-stimulated gammadelta T lymphocytes, thus suggesting a potential adjuvant role of this early cross-talk in the therapeutic activity of aminobiphosphonate drugs.

Anti-Inflammatory Agents↗

PubMed1999

Whole body hyperthermia induction of soluble tumor necrosis factor receptors: implications for rheumatoid diseases.

OBJECTIVE: To test the hypothesis that 41.8 degrees C x 60 min whole body hyperthermia (WBH) induces increased serum levels of soluble necrosis factor receptors (sTNF-R). METHODS: We tested the serum of cancer patients for changes in sTNF-RI and RII levels, as a function of time, pre and post: (1) WBH alone, (2) WBH and chemotherapy, i.e., melphalan (L-PAM), and (3) L-PAM alone. RESULTS: For sTNF-RI there was a marked increase (over pre-treatment values, i.e., 86%) in serum levels after WBH alone (n = 3), which peaked 2.5 h post-WBH; L-PAM (iv) only resulted in a dip in sTNF-RI seen 40 min postadministration; the combination (WBH + L-PAM), resulted in both the dip at 40 min and the increase at 2.5 h post-treatment. For sTNF-RII both WBH alone (n = 3) and WBH + L-PAM (n = 2), there was an increase in receptor serum levels of 25% and 30%, respectively, which peaked 5.5 h post-treatment, and remained elevated at 24 h. L-PAM alone resulted in a dip in levels only at 40 min post-treatment. sTNF-RI and RII levels returned to baseline values within 7 days post-treatment. CONCLUSION: 41.8 degrees C WBH results in transient increases in TNF-RI and RII. These results may have therapeutic implications for the application of WBH to TNF mediated disease processes.

Adult↗

PubMed2002

Glucocorticoids induced the production and gene expression of IL-1alpha through AP-1 and partially NF-kappaB activation in murine epidermal cells.

To investigate the mechanism of the glucocorticoids-induced augmentation of skin response, we have recently reported the modulatory effect of glucocorticoids on the regulation of cytokines production in keratinocytes stimulated with various chemicals in vitro through both NF-kappaB and AP-1 activation. Further to clarify the mechanism in the glucocorticoids-induced augmentation of cytokines production from keratinocytes, we examined the effect of glucocorticoids to keratinocytes without chemical stimulation. Glucocorticoids 10(-4) M inhibited the production of IL-1alpha from Pam 212 cells. However, lower concentration (10(-8)-10(-10) M) of glucocorticoids significantly enhanced the production of IL-1alpha by Pam 212 cells at both the protein and mRNA levels. In contrast, glucocorticoids had no effect on the production of either TNF-alhpa, IL-6, nor GM-CSF by Pam 212 cells cultured for 6 h. Electrophoretic mobility shift assays (EMSA) revealed that 10(-10)-10(-12) M glucocorticoids induced the NF-kappaB activation in Pam 212 cells, however, augmented AP-1 activation by 10(-8)-10(-10) M of glucocorticoids was observed in Pam 212 cells. Furthermore, pyrrolidine dithiocarbamate (PDTC) partially inhibited the IL-1alpha production and completely inhibited NF-kappaB expression by Pam 212 cells. On the other hand, MAP-kinase inhibitors (PD98059, SB202190) completely abrogated not only AP-1 activation but the low concentration glucocorticoids-induced IL-1alpha production. These data indicated that lower concentration of glucocorticoids induced the augmentation of IL-1alpha production from keratinocytes mediated through the AP-1 pathway and partially through NF-kappaB pathway.

Animals↗

PubMedDate not supplied

Immunological characterization of pulmonary intravascular macrophages.

Pulmonary intravascular macrophages (PIMs) are lung macrophages found apposed to the endothelium of pulmonary capillaries. In many species, they are responsible for the clearance of blood-borne particulates and pathogens; however, little else is known about their roles as immunologic effector cells. We compared PIMs with pulmonary alveolar macrophages (PAMs) to determine the relative immunological activities of these two cell populations. Our results suggested that both populations possess similar phagocytic and bactericidal activities. In assays measuring cytotoxicity, PIMs were more cytotoxic than PAMs against virally infected target cells; however, differences between these macrophage populations were not as marked when noninfected targets were used. LPS-stimulated PIMs produced more T-cell proliferative cytokines than PAMs, and both populations of nonstimulated macrophages produced similar amounts of the cytokines. In contrast, PAMs produced more TNF alpha and NO2- than PIMs when both populations were stimulated with LPS; however, nonstimulated PAMs and PIMs produced similar amounts of TNF alpha and NO2. These data suggest that bovine PIMs are immunologically active. Differences between the degrees of activity of PIMs and PAMs indicate that these macrophage populations may have different roles in lung surveillance.

Animals↗

PubMed1992

Stimulation and suppression of the oxygenation activity of porcine pulmonary alveolar macrophages by Actinobacillus pleuropneumoniae and its metabolites.

The effects of Actinobacillus (Haemophilus) pleuropneumoniae and its metabolites on the oxygenation activity of porcine pulmonary alveolar macrophages (PAM) were studied, using a chemiluminescence technique. Actinobacillus pleuropneumoniae strains of serotypes 2, 3, and 9 in a dose of 1, 10, and 100 colony-forming units/macrophage first stimulated the oxygen radical production of PAM. After having reached a peak value, oxygenation activity decreased, finally resulting in total suppression of PAM. All these effects were neutralized by homologous convalescent pig sera that had been adsorbed onto inactivated A pleuropneumoniae strains. Moreover, cross-neutralization was shown between serotypes 2 and 3. Inactivated A pleuropneumoniae strains did not influence the oxidative activity of PAM. Undiluted and lower dilutions of sterile A pleuropneumoniae culture supernatants were toxic for PAM, whereas higher dilutions of the supernatants stimulated oxygen radical production of the macrophages. These effects were heat-sensitive and were neutralized by homologous convalescent pig sera. Cross-neutralization was shown between serotypes 2 and 3. These findings indicated that stimulation and inhibition of the oxygenation activity of PAM are attributable to heat-sensitive metabolites produced by A pleuropneumoniae.

Actinobacillus pleuropneumoniae↗

PubMed2004

[Synthesis and application of the polyacrylamide beads acting as LDL adsorbent's matrices].

This study in pursuit of the synthetic technologies and structure characterization of polyacrylamide-based matrices (PAM beads) for low density lipoprotein (LDL) adsorbent and their adsorbability for LDL was intended for an experimental evidence of developing advanced matrices for LDL adsorbent. PAM beads were synthesized by inverse suspension polymerization, and their structure characterization was characterized by SEM, image analyzer and small angle X-ray scattering. The tripeptide serine-aspartic-glutamic acid (SDE) was coupled on the PAM beads to prepare the LDL adsorbents whose adsorbability for LDL was determined in vitro. The results showed that the PAM beads with the average size diameter 142.1 microm and the average pore diameter 119.8 nm could act as the matrices in accordance with the requirement of adsorbent for LDL. When the amount of acrylamide and the crosslinking agent N,N'-methylene-bis(acrylamide) was fixed, the average pore diameter decreased with the increase of the crosslinking agent content. Although the nonspecific binding of PAM beads for LDL was low, they could selectively adsorb LDL after coupling the SDE on the PAM beads.

Acrylic Resins↗

PubMed2004

Adrenomedullin (AM) and AM receptor type 2 expression is up-regulated in prostate carcinomas (PC), and AM stimulates in vitro growth of a PC-derived cell line by enhancing proliferation and decreasing apoptosis rates.

Adrenomedullin (AM) is a hypotensive peptide, that acts via the calcitonin receptor-like receptor (CRLR), whose interaction with the subtypes 2 and 3 of a family of receptor activity-modifying proteins (RAMP) gives rise to two distinct AM receptors, named AM1 and AM2 receptors. AM derives from the post-translational proteolytic cleavage of pro(p)AM, the last step of which involves the conversion of the inactive AM to active AM by the peptidyl-glycine alpha-amidating monooxigenase (PAM). Compelling evidence suggests that AM, in addition to exerting its well-known regulatory action on blood pressure and water and electrolyte balance, also possesses a growth promoting effect in several normal and neoplastic tissues, including human prostate. Conventional reverse transcription (RT)-polymerase chain reaction (PCR) demonstrated the expression of pAM, PAM, CRLR and RAMP(1-3) mRNAs in both prostate hyperplasias (PH) and carcinomas (PC), and semiquantitative PCR showed that pAM, PAM and RAMP3 mRNA expression was higher in PCs than PHs. Radioimmunoassay measured higher concentrations of immunoreactive AM in PCs than PHs. The expression of pAM, CRLR and RAMP1,2 mRNAs was also detected in the PC-derived cell lines PC-3 and DU-145, RAMP3 expression being restricted to the latter line. AM did not affect the growth rate (duplication time) of PC-3 cells, but it did significantly increase that of DU-145 cells. The growth promoting effect of AM was found to ensue from both the rise in the proliferation rate and the lowering in the apoptosis rate of DU-145 cells. These effects of AM were counteracted by the AM receptor antagonists CGRP(8-37) and AM(22-52), the former antagonist, which is more selective for AM2 than AM1 receptors, being more effective than the latter one. Both antagonists were per se able to induce a slow, but significant decrease in the basal growth rate of DU-145 cells by inhibiting proliferation and enhancing apoptosis, again CGRP(8-37) being more effective than AM(22-52). Taken together, our findings allow us to suggest that: i) endogenous AM system plays an important autocrine-paracrine growth promoting action in the human prostate, being possibly involved in the development of the malignant phenotype of epithelial cells; and ii) the tumor promoting effect of AM in the human prostate is mainly mediated by the AM2 receptor (CRLR/RAMP3) subtype.

Adrenomedullin↗