[Animal products and products of animal origin (fish and other products of fishing)].
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Quality of biotechnological products: analysis of the expression construct in cell lines used for production of r-DNA derived protein products. ICH Harmonised Tripartite Guideline.
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Animals↗
Quality of biotechnological products: stability testing of biotechnological/biological products. Annex to the ICH Harmonised Tripartite Guideline for the Stability Testing of New Drug Substances and Products.
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Animals↗
Quality of biotechnological products: derivation and characterisation of cell substrates used for production of biotechnological/biological products. ICH Harmonised Tripartite Guideline.
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Animals↗
Beta 2-adrenergic receptor agonist induces IL-18 production without IL-12 production.
Endogenous catecholamine, epinephrine and norepinephrine, and isoproterenol concentration-dependently induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma, and inhibited that of IL-10 in human peripheral blood mononuclear cells (PBMC). All responses by these stimulations were antagonized by the selective beta 2-adrenergic receptor (AR) antagonist, butoxamine, but not by alpha 1-, alpha 2- and beta 1-AR antagonists. The selective beta 2-AR agonists, salbutamol and terbutaline, induced a similar pattern of cytokine production, indicating that the effect of these AR agonists on cytokine production was through beta 2-AR stimulation. Anti-IL-18 Ab or caspase-1 inhibitor prevented all increase/decrease effects, suggesting that IL-18 might affect the production of all other cytokines. While endogenous IL-18 produced by salbutamol and terbutaline reached a sufficient concentration to induce IL-12 production, these beta 2-AR agonists did not induce the production of IL-12 at all. Epinephrine/norepinephrine/isoproterenol/beta 2-AR agonists increased the production of IL-18 in monocytes, but had no effect on IL-12, TNF-alpha, IFN-gamma and IL-10 production. The lack of beta 2-AR-induced effect on IL-12 production was due to a beta 2-AR-induced inhibition of an IL-18-elicited upregulation of both CD40 and CD40 ligand (CD40L/CD154) expressions on monocytes. The sympathetic innervating lymphoid organs may be under the control of beta2-AR stimulation, maintaining the basal cytokine environment in the tissues.
Adrenergic Antagonists↗
Visual product evaluation: exploring users' emotional relationships with products.
This paper discusses an industrial designer's approach to eliciting user perceptions and emotional responses to products through visual evaluation and stimuli. Whilst the authors accept that product functionality is crucial for product success, the appearance, use of materials, shape and form provide the most immediate product data for the user. Less tangible issues such as emotional bonding of users with products, cultural perceptions and social value systems, provide valuable insights for the product developer to help expand knowledge and understanding of the users' need beyond the functional. This paper presents product personality profiling as a new technique for design researchers/designers, and discusses it alongside other emerging approaches such as mood boards and visual product evaluation. The authors have used these techniques during focus group sessions with users to elicit individuals' needs and aspirations towards products. Such a user-centred approach is fundamental to applied ergonomics. Experiences, benefits, and limitations of these techniques are outlined as well as the opportunities for further development.
Emotions↗
Inhibition of aldosterone production by alpha-human atrial natriuretic polypeptide is associated with an increase in cGMP production.
Synthetic alpha-human atrial natriuretic polypeptide caused rapid and marked inhibition of aldosterone production in dispersed rat adrenal capsular cells. The polypeptide also slightly, but significantly, decreased cAMP production in the adrenal dispersed capsular cells, while markedly stimulating cGMP production. The cGMP production was accelerated at the concentration of alpha-human atrial natriuretic polypeptide lower than the threshold level to stimulate aldosterone production. These findings suggest that alpha-human atrial natriuretic polypeptide possibly plays a regulatory role in aldosterone production and an additional role in natriuresis through inhibition of aldosterone production. The stimulation of cGMP production by alpha-human atrial natriuretic polypeptide may be involved in the inhibitory effect of this peptide on aldosterone production.
Adrenal Glands↗
The effects of noradrenaline and alpha-2 adrenoceptor agents on the production of monocytic products.
There are some reports that catecholamines may modulate the production of monocytic cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF alpha). The present study was carried out in order to examine the effects of noradrenaline (10(-5), 10(-6) and 10(-7) M), clonidine (10(-5), 10(-6) and 10(-7) M), an alpha2-adrenoceptor agonist, and yohimbine (10(-5), 10(-6) and 10(-7) M), an alpha 2-adrenoceptor antagonist, on the production of IL-6, the IL-1 receptor antagonist (IL-1RA) and TNF alpha by stimulated whole blood of normal humans. We measured the in vitro production of IL-6, TNF alpha and IL-1RA by stimulated (phytohemagglutinin+lipopolysaccharide), diluted whole blood of 16 normal volunteers. The results show that noradrenaline, 10(-5) M, significantly suppressed the production of IL-6; noradrenaline, 10(-5) and 10(-6) M, significantly suppressed the production of IL-1RA and TNF alpha; clonidine, 10(-5) M, significantly suppressed the production of TNF alpha; and yohimbine, 10(-5) and 10(-6) M, significantly suppressed the production of IL-1RA. It is concluded that (1) noradrenaline has significant negative immunoregulatory effects in humans through suppression of the production of (monocytic) proinflammatory cytokines, e.g. IL-6 and TNF alpha, and (2) the suppression of the production of TNF alpha may be related to alpha(2)-adrenoceptor-related mechanisms.
Adrenergic alpha-2 Receptor Agonists↗
Staphylococcal enterotoxin A induced interferon (IFN)-gamma production in spleen cells from BCG-immunized mice: the IFN production is dependent on leukotriene C4 but not dependent on interleukin 2.
In our previous paper, we showed that IFN was induced in sera by injection of staphylococcal enterotoxin A (SEA) in Bacillus Calmette-Guérin (BCG) immunized C57BL/6 (B6) mice. In analyzing the phenomenon in vitro, we showed that SEA induced IFN-gamma in the supernatant of the spleen cell culture from BCG immunized B6 mice and that leukotriene C4 (LTC4) from BCG activated macrophages in the spleen was involved in the IFN production from Ly 1+ T cells. On the other hand, interleukin-2 (IL-2) has reported to play an important role in the regulation of synthesis of IFN-gamma by T cells. In the present study, we examined whether IL-2 is involved in SEA-induced IFN production. The result showed that the SEA-induced IFN-gamma production was observed in spite of suppression of SEA-induced IL-2 production in spleen cells from BCG-immunized B6 mice. On the contrary, the depressed IFN production was observed in spite of high SEA-induced IL-2 production in spleen cells from their control mice. On the other hand, LTC4 production was 8 times higher in spleen cells from BCG-immunized B6 mice, high producer of SEA-induced IFN, than in that from BCG-immunized C3H mice, the low producer. We also observed that the IFN and the LTC4 production of spleen cells from BCG-immunized B6 mice was suppressed in the presence of caffeic acid and nordihydroguaiaretic acid, non-specific lipoxygenase inhibitors, and that LTC4 augmented the IFN production of normal B6 mouse spleen cells in the presence of 2-mercaptoethanol. Therefore, involvement of LTC4 rather than of IL-2 was supported in our experimental system.
Animals↗
Inhibition of steroid production in Leydig cells by non-steroidal anti-inflammatory and related compounds: evidence for the involvement of lipoxygenase products in steroidogenesis.
The effect of inhibitors of the cyclo-oxygenase and lipoxygenase pathways of arachidonic acid metabolism on steroidogenesis in rat testis Leydig cells and rat tumour Leydig cells has been investigated. In the presence of nordihydroguaiaretic acid [NDGA; 4,4'-(2,3- dimethylbutan -1,4- diyl )bis[1,2- benzendiol ]], 5,8,11,14-eicosatetraynoic acid (ETYA), BW 755C [3-amino-1-[3-(trifluoromethyl)phenyl]-2-pyrazoline hydrochloride] and benoxaprofen [ Opren ; 2-(2-p-chlorophenyl- benzoxazol -5-yl)propionic acid)] (which inhibit lipoxygenase activity), but not indomethacin and aspirin (which inhibit cyclo-oxygenase activity), a dose-related inhibition of lutropin (LH)-stimulated testosterone and pregnenolone production was obtained (ID50 values of 2.5, 30, 25 and 30 microM for NDGA, ETYA, BW 755C and benoxaprofen were obtained, respectively). BW 755C and benoxaprofen had no significant effect on LH-stimulated cyclic AMP production except at the highest concentrations examined (330 and 380 microM, respectively), whereas NDGA and ETYA inhibited LH-stimulated cyclic AMP production in a dose-dependent manner (ID50 7.0 and 22 microM respectively). However, NDGA and ETYA also caused a dose-dependent inhibition of dibutyryl cyclic AMP-stimulated testosterone and pregnenolone production. The metabolism of exogenous ( 22R )-hydroxycholesterol or pregnenolone to testosterone by Leydig cells was not inhibited by either NDGA, ETYA or indomethacin. At low concentrations of NDGA and ETYA a significant increase in the conversion of both pregnenolone and ( 22R )-hydroxycholesterol to testosterone was obtained. Studies in which the metabolism of [14C]arachidonic acid by purified rat tumour Leydig cells was investigated indicate that products are formed by tumour Leydig cells that have similar mobilities in a thin layer chromatography system to 5-L-hydroxy-6,8,11,14-eicosatetraenoic acid, 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid and leukotriene B4. The formation of these products was inhibited to varying degrees by NDGA, BW 755C and benoxaprofen but not by aspirin and indomethacin. These studies demonstrate for the first time that inhibition of lipoxygenase activity but not cyclo-oxygenase activity causes an inhibition of LH- and dibutyryl cyclic AMP-stimulated steroid production and suggest a stimulatory role for products of the lipoxygenase pathway of arachidonic acid metabolism in steroidogenesis. The site of this stimulation is apparently distal to the production of cyclic AMP and before the side chain cleavage of cholesterol.
4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
Reduced IFNgamma production in response to IL-12 stimulation and/or reduced IL-12 production in atopic patients.
BACKGROUND: Several studies have shown that interleukin (IL)-4 and interferon-gamma (IFNgamma) are important for the regulation of IgE production and that IL-12 induces IFNgamma. OBJECTIVE: IFNgamma production in response to IL-12 stimulation and IL-12 production were investigated in peripheral blood mononuclear cells (PBMCs) of atopic patients with various levels of serum IgE. METHODS: Cytokine production from PBMCs was measured following stimulation with a nonspecific stimulator (phytohemagglutinin: PHA), a specific stimulator (Der f 1) and IL-12 in 17 healthy controls and 23 atopic patients with various serum IgE levels. RESULTS: The IFNgamma production by IL-12-stimulated PBMCs in the atopic group was lower than that in the control group. Furthermore, the serum IgE level was negatively correlated with IFNgamma production by PBMCs stimulated with IL-12 (P < 0.001), and with IL-12 production by PBMCs stimulated with Der f 1 (P < 0.001). Although the IFNgamma concentrations by PHA-stimulated PBMCs were correlated with those by IL-12-stimulated PBMCs, there were differences in several patients. CONCLUSIONS: Our results indicated that atopic patients may have some abnormality in the IL-12-IFNgamma loop. It was shown that the elevation in IgE levels in atopic patients may be due to reduced IFNgamma production in response to IL-12 stimulation and/or due to reduced IL-12 production.
Adolescent↗
Balance between cytokine production by peripheral blood mononuclear cells and reactive oxygen species production by monocytes in patients with chronic kidney disease.
Hemodialysis (HD) and peritoneal dialysis are associated with inflammatory events and immunological incompetence. The purpose of this study was to evaluate the effect of both uremia and dialysis modality on the production of cytokines and reactive oxygen species (ROS) by monocytes. four groups of subjects were studied: 28 chronic kidney disease (CKD) patients, 14 chronic HD patients, 14 patients on continuous ambulatory peritoneal dialysis (CAPD) patients, and 14 healthy volunteers, peripheral blood mononuclear cells (PBMC) were isolated from blood samples and incubated for 24 hr with or without lipopolysaccharide (LPS). TNF-alpha and IL-10 production by PBMC and serum levels of these cytokines were quantified by ELISA. Aliquots of whole blood were incubated in vitro and ROS production and phagocytosis were quantified by flow cytometry. Compared to the control group, Staphylococcus aureus-stimulated ROS production by monocytes was significantly lower in the HD group. The highest levels of unstimulated TNF-alpha production in vitro were observed in the HD group. In the CKD group, as well as in the whole population, there were a negative correlation between TNF-alpha production by unstimulated PBMC and ROS production by S. aureus-stimulated monocytes and a positive correlation between PMA-stimulated ROS production by monocytes and unstimulated and LPS-stimulated IL-10 production by PBMC suggesting that the pro-inflammatory state in CKD patients is associated with decreased response to infectious challenges.
Adult↗
Regulation of HIV production by blood mononuclear cells from HIV-infected donors: II. HIV-1 production depends on T cell-monocyte interaction.
Cell-cell interactions induced between T cells and monocytes by certain soluble anti-CD3 monoclonal antibodies (MAbs) were previously shown to be required for high-level production of HIV-1 by peripheral blood mononuclear cells (PBMCs) from infected donors. Staphylococcal enterotoxin or superantigen (SAg) is another mitogen inducing monocytes-T cell interactions that exhibit potent induction of HIV-1 production. Antibodies to several adhesion molecules were used to test the requirements for T cell- and monocyte-associated adhesion molecules in HIV-1 production following activation with anti-CD3 or SAg. Blocking of either CD2-LFA-3, or CD18-ICAM-1, inhibited anti-CD3- or SAg-induced HIV-1 production by more than 90% without inhibiting CD4+ T cell proliferation. Inhibition of HIV production was observed when either the T cell or monocyte coreceptor was bound by MAbs to these adhesion molecules. Blocking of CD28-B7 interactions by soluble CTLA-4 fusion protein, a CD28 homolog, inhibited both HIV-1 production and CD4+ T cell proliferation. Fc binding was not required for HIV-1 inhibition by MAbs to CD2 and CD18, because Fab or F(ab')2 fragments of these MAbs inhibited HIV-1 production by more than 80%. A chimeric single-chain MAb to CD2 was produced, containing heavy and light chain variable regions from MAb 35.1 to CD2 linked to the constant regions of human IgG1 (CD2 SFv-Ig). This humanized CD2 SFv-Ig inhibited HIV-1 production by 30% to > 98%. These results thus indicate that simultaneous engagement of multiple adhesion pathways between T cells and monocytes are required for HIV production by patients PBMCs and may have implications for therapy of HIV infections.
Abatacept↗
Interleukin-1beta induces interleukin-6 production through the production of prostaglandin E(2) in human osteoblasts, MG-63 cells.
This study was conducted to investigate the mechanism of interleukin-1beta (IL-1beta)-induced IL-6 production in human osteoblasts (MG-63 cells). Stimulation with IL-1beta resulted in the production of IL-6 and prostaglandin E(2) (PGE(2)). IL-6 production gradually increased and peaked 96 h after stimulation. IL-6 mRNA was detected between 4 and 72 h after IL-1beta stimulation. The patterns of PGE(2) production and the expression of cyclooxygenase-2 (COX-2) mRNA were biphasic after stimulation. Actinomycin D, cycloheximide, indomethacin, and NS-398 (COX-2 inhibitor) suppressed the production of IL-6 and PGE(2). Anti-PGE(2) antibody markedly reduced the production of IL-6. In addition, stimulation with 17-phenyl-PGE(2), a PGE receptor-1 (EP-1 receptor) agonist, led to the expression of IL-6 mRNA after pretreatment with IL-1beta. These findings indicate that IL-1beta-induced IL-6 production in MG-63 cells involves the following sequence of steps: IL-1beta-induced COX-2 activation, PGE(2) production, and EP-1 receptor signaling prior to IL-6 production.
Antibodies↗
The relationships between leukotoxin production, growth rate and the bicarbonate concentration in a toxin-production-variable strain of Actinobacillus actinomycetemcomitans.
Actinobacillus actinomycetemcomitans, a Gram-negative periodontopathic bacterium, produces a leukotoxin belonging to the RTX family. The production of leukotoxin varies greatly among different strains of this species. In this paper the effects of growth rate and bicarbonate on the leukotoxin production by a toxin-production-variable strain (301-b) during growth in a chemostat were examined. When the bacterium was grown in anaerobic fructose-limited chemostat cultures (pH 7.0 and 37 degrees C) at dilution rates (D) ranging from 0.04 to 0.20 h-1 in the absence and presence of 10 mM bicarbonate, it produced leukotoxin as a cluster of two polypeptides (M(r) 113,000 and 120,000) and complexed with nucleic acids on the bacterial cell surface. The relationship between leukotoxin production and specific growth rate was analysed by plotting the specific rate of leukotoxin production [qLT, in microgram (mg dry wt)-1 h-1] against D. The plots were approximated to the linear relationships qLT = 2.7D-0.058 and qLT = 9.3D-0.407 without and with bicarbonate, respectively. These relationships suggest that the apparent leukotoxin production is a result of both growth-rate-dependent production and growth-rate-independent decomposition. The cellular leukotoxin level was also followed after the change from chemostat to batch culture in the same fermenter. In batch culture leukotoxin production stopped immediately and the cellular toxin level rapidly decreased, suggesting toxin decomposition. From the slopes of the approximated linear relationships between qLT and D, a theoretical maximum leukotoxin yield (YLT) was estimated as 2.7 and 9.3 micrograms (mg dry wt)-1 in the absence and presence of 10 mM bicarbonate, respectively. The increased YLT value in the cultures containing bicarbonate indicated that the addition stimulated the efficiency of leukotoxin synthesis up to about threefold. Further increases of bicarbonate concentration to between 20 and 40 mM had no effect on the total leukotoxin production, but the amount of extracellular leukotoxin increased with higher bicarbonate concentrations.
Actinobacillus Infections↗
Content and reactivity to product perfumes in fragrance mix positive and negative eczema patients. A study of perfumes used in toiletries and skin-care products.
The aim of the study was to investigate the elicitation potential of perfumes from 17 commonly sold lower-price cosmetic products. 8 of the perfumes were from stay-on cosmetics and 9 were from wash-off cosmetics. Each perfume was tested in 500 consecutive eczema patients, who also were tested with the European standard patch test series. 4.2% reacted to 1 or more of the wash-off product perfumes and 3.2% to 1 or more of the stay-on product perfumes. Concordant positive reactions between the fragrance mix and the product perfumes were found in 81.3% of positive reactions to the stay-on product perfumes and in 52.4% of the reactions to the wash-off product perfumes. Compared to the fragrance mix alone, only 1 additional case of contact allergy to the product perfumes was detected by balsam of Peru. Chemical analysis revealed that between 1 and 5 of the chemically-defined constituents of the fragrance mix were present in all of the product perfumes. Geraniol was found in 12 of the 17 perfumes and was most often detected. The concentration of the target fragrance materials ranged from 0.005%-1.35 w/v%. It is concluded that the allergenic constituents of the fragrance mix are impossible to avoid if perfumed cosmetics are used. Furthermore, patients suspected of perfume allergy need to be tested with their own perfumed products, as far from all cases of perfume allergy are detected by the fragrance mix and/or balsam of Peru in the European standard patch test series.
Acyclic Monoterpenes↗
High glucose increases inducible NO production in cultured rat mesangial cells. Possible role in fibronectin production.
BACKGROUND/AIM: Increased nitric oxide (NO) generation and action have been suggested to be associated with glomerular hyperfiltration and increased vascular permeability early in diabetes. However, previous studies have primarily focused on the constitutive nitric oxide synthase (cNOS) pathway present in endothelial cells, and the role of the inducible NOS (iNOS) pathway in diabetic nephropathy has remained unclear. This study examined whether high glucose modulates NO synthesis by the iNOS pathway in rat mesangial cells. In addition, the effect of inhibition of the iNOS pathway on fibronectin production was determined to examine the role of the iNOS pathway in high glucose-induced extracellular expansion by mesangial cells. METHODS: NO synthesis by the iNOS pathway was evaluated by nitrite and iNOS mRNA and protein productions. The effects of protein kinase C (PKC) inhibitor and aldose reductase inhibitor on the iNOS mRNA expression and aminoguanidine, a relatively specific inhibitor of the iNOS on fibronectin protein production were examined. RESULTS: High 30 mM glucose concentration led to significant increases in nitrite production of rat mesangial cells upon stimulation with lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma) compared with control 5.6 mM glucose concentration. Mesangial iNOS mRNA expression and protein production also increased significantly in response to high glucose. The addition of calphostin C, a PKC inhibitor, and 6-bromo-1,3-dioxo-1H-benz[d,e]isoquinoline-2(3H)-acetic acid, an aldose reductase inhibitor, significantly suppressed the enhancement of iNOS mRNA expression in high glucose concentration. High glucose also significantly increased fibronectin protein production of mesangial cells upon stimulation with LPS plus IFN-gamma compared to control glucose. Aminoguanidine reversed this high glucose-induced fibronectin production at dose inhibiting iNOS mRNA expression. CONCLUSIONS: These results indicate that high glucose enhances cytokine-induced NO production by rat mesangial cells, and that the activation of PKC and aldose reductase pathway may play a role in this enhancement. In addition, high glucose-induced NO production by the iNOS pathway may promote extracellular matrix accumulation by mesangial cells under certain condition.
Acetates↗
Cyclooxygenase products stimulate carbon monoxide production by piglet cerebral microvessels.
Products of arachidonic acid (AA) metabolism by cyclooxygenase (Cox) are important in regulation of neonatal cerebral circulation. The brain and cerebral microvessels also express heme oxygenase (HO) that metabolizes heme to carbon monoxide (CO), biliverdin, and iron. The purpose of this study in newborn pig cerebral microvessels was to address the hypothesis that Cox products affect HO activity and HO products affect Cox activity. AA (2.0-20 microM) increased prostaglandin E2 (PGE2) measured by radioimmunoassay (RIA) and also CO measured by gas chromatography/mass spectrometry (GC/MS). Further, 10(-4) M indomethacin, which inhibited Cox, reduced both AA and heme-induced CO production. Conversely, neither exogenous 2 x 10(-6) M heme, which markedly increased CO production, nor the inhibitor of HO, chromium mesoporphyrin, altered PGE2 synthesis. Because AA metabolism by Cox generates both prostanoids and superoxides, we determined the effects of the predominant prostanoid and superoxide on CO production. Although PGE2 caused a small increase in CO production, xanthine oxidase plus hypoxanthine, which produces superoxide, strongly stimulated the production of CO by cerebral microvessels. This increase was mildly attenuated by catalase. These data suggest that Cox-catalyzed AA metabolites, most likely superoxide and/or a subsequent reactive oxygen species, increase cerebrovascular CO production. This increase seems to be caused, at least in part, by the elevation of HO-2 catalytic activity. Conversely, Cox activity is not affected by HO-catalyzed heme metabolites. These data suggest that some cerebrovascular functions attributable to Cox activity could be mediated by CO.
Animals↗