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S A Moore

Publications and source records attributed to S A Moore.

At least 55 records · Page 3Linked to original sources
PubMed1998

Expression of monocyte chemoattractant protein (MCP-1) and nitric oxide synthase-2 following cerebral trauma.

Traumatic injury to the brain initiates multiple interrelated processes that involve parenchymal, vascular, and infiltrating inflammatory cells. Nitric oxide (NO) and chemokines have been implicated as regulators of the central nervous system injury response. Following a cryogenic lesion of the cerebral cortex in mice, mRNA for NO synthase (NOS)-2 was detected by reverse transcriptase polymerase chain reaction ipsilaterally 12 h after injury and persisted for 2 weeks. While mRNA was also detected contralaterally, the time course of expression was shorter (1 week). By immunohistochemistry, NOS-2 protein was initially detected ipsilaterally 12 h after injury in infiltrating inflammatory cells. Astroglial cells expressed NOS-2 from 24 to 72 h after injury. The expression of monocyte chemoattractant protein (MCP-1) mRNA peaked at 6 h on the lesion side, remained for 24 h and then declined by 48 h. On the unlesioned side, MCP-1 mRNA was expressed to a much lesser extent and had declined by 24 h. The up-regulation of MCP-1 was relatively specific as a closely related mRNA encoding IP-10 was not significantly increased. These findings implicate a role for NOS-2 and MCP-1 as potential regulators of cellular events following cryogenic cerebral trauma.

Animals↗
PubMed1998

14,15-Epoxyeicosatrienoic acid inhibits prostaglandin E2 production in vascular smooth muscle cells.

14,15-Epoxyeicosatrienoic acid (EET), a cytochrome P-450 epoxygenase product of arachidonic acid (AA), reduced PGE2 formation by 40-75% in porcine aortic and murine brain microvascular smooth muscle cells. The inhibition was reversed 6-10 h after removal of 14,15-EET from the medium and was regioisomeric specific; 8,9-EET produced a smaller effect, whereas 11,12- and 5,6-EET were ineffective. Although the cells converted 14,15-EET to 14, 15-dihydroxyeicosatrienoic acid (14,15-DHET), 14,15-DHET did not inhibit PGE2 formation, and the 14,15-EET-induced inhibition was potentiated by 4-phenylchalcone oxide, an epoxide hydrolase inhibitor. The inhibition occurred when substrate amounts of AA were used and was not accompanied by enhanced production of other PGs, suggesting an effect on PGH synthase; however, in murine cells, 14, 15-EET did not reduce PGH synthase mRNA or protein. Moreover, the 14, 15-EET-induced decrease in PGE2 production was overcome by increasing the concentration of AA, but not oleic acid (which is not a substrate for PGH synthase). These findings suggest that 14,15-EET competitively inhibits PGH synthase activity in vascular smooth muscle cells. The 14,15-EET-induced inhibition of PGE2 production resulted in potentiation of platelet-derived growth factor-induced smooth muscle cell proliferation, suggesting that the competitive inhibition of PGH synthase by 14,15-EET can affect growth responses in smooth muscle cells.

8,11,14-Eicosatrienoic Acid↗
PubMed1998

Presentation, management and follow-up of Schilder's disease.

Schilder's diffuse myelinoclastic sclerosis is a rare demyelinating disease which often mimics intracranial neoplasm or abscess. We have treated 3 patients with this disorder in the past 5 years and followed their postoperative course. Certain distinct features of this disease will allow neurosurgeons to preoperatively entertain this diagnosis. We discuss postoperative treatment and propose a new hypothesis regarding the variable prognoses of this disorder. Schilder's disease constitutes an important diagnosis for any neurosurgeon to be aware of (especially those treating the pediatric age group) which has not received adequate coverage in the neurosurgical literature.

Adolescent↗
PubMed1998

Expression and vascular effects of cyclooxygenase-2 in brain.

BACKGROUND AND PURPOSE: Cyclooxygenase-2 (COX-2) is an inducible isoform of cyclooxygenase. Several types of brain cells in culture can express COX-2 when treated with lipopolysaccharide (LPS) or some cytokines. LPS produces dilatation of cerebral arterioles in vivo through a mechanism that is partially inhibited by indomethacin. In the present study we examined the hypothesis that LPS causes increased expression of COX-2 in brain as well as COX-2-dependent dilatation of cerebral arterioles. METHODS: Cranial windows were implanted in anesthetized rats and used to measure diameter of cerebral arterioles under control conditions and during topical application of various agonists and antagonists. Windows were flushed every 30 minutes for 4 hours with vehicle (artificial cerebrospinal fluid; n=5), LPS (100 ng/mL; n=8), LPS and NS-398 (100 micromol/L; n=8), a selective inhibitor of COX-2, or LPS and dexamethasone (1 micromol/L; n=5), which attenuates expression of COX-2. To examine expression of COX-2 protein in vivo, other animals were injected intracisternally with artificial cerebrospinal fluid (n=3) or LPS (40 ng; n=4). Four hours after injection, the leptomeninges were harvested and analyzed by Western blot for expression of COX-2 protein. In a third group of experiments, COX-2 expression and prostaglandin E2 (PGE2) production were determined in leptomeningeal tissue treated for 4 hours ex vivo with vehicle (n=4), LPS (100 ng/mL; n=4), LPS and NS-398 (100 micromol/L; n=4), or LPS and dexamethasone (1 micromol/L; n=4). RESULTS: LPS caused marked, progressive dilatation of cerebral arterioles, with a maximum increase in diameter of 55+/-9% (mean+/-SEM) at 4 hours. Coapplication of either NS-398 or dexamethasone with LPS reduced dilatation of cerebral arterioles at hours 2 through 4 (P<0.05). In contrast, NS-398 did not inhibit dilatation of cerebral arterioles in response to bradykinin or ADP. In animals injected intracisternally with vehicle, COX-2 protein was expressed at a very low level in leptomeningeal tissue. Intracisternal injection of LPS increased COX-2 protein expression by approximately 20-fold (P<0.05). In leptomeningeal tissue treated ex vivo with LPS, there was also expression of COX-2. Both dexamethasone and NS-398 markedly reduced COX-2 protein expression in ex vivo LPS-treated tissue. PGE2 production was detectable under control conditions in leptomeningeal tissue incubated in vehicle ex vivo for 4 hours (6.5+/-1.1 pmol/mg protein). LPS treatment significantly increased PGE2 production to 12.8+/-1.1 pmol/mg protein (P<0.05). Both dexamethasone and NS-398 significantly attenuated LPS-induced PGE2 production (P<0.05). CONCLUSIONS: LPS increased expression of COX-2 protein in leptomeningeal tissue and caused COX-2-dependent dilatation of cerebral arterioles in vivo. Ex vivo, both NS-398 and dexamethasone suppressed LPS-induced PGE2 production and COX-2 expression in leptomeningeal tissue. Inhibition of LPS-induced dilatation of cerebral arterioles in vivo by NS-398 and dexamethasone suggests that the dilatation was dependent on expression and activity of COX-2. These findings support the concept that exposure of brain to LPS causes cerebral vasodilatation that is dependent in part on expression and activity of COX-2.

Adenosine Diphosphate↗
PubMed1997

Three-dimensional structure of diferric bovine lactoferrin at 2.8 A resolution.

The three-dimensional structure of diferric bovine lactoferrin (bLf) has been determined by X-ray crystallography in order to investigate the factors that influence iron binding and release by transferrins. The structure was solved by molecular replacement, using the coordinates of diferric human lactoferrin (hLf) as a search model, and was refined with data to 2.8 A resolution by simulated annealing (X-PLOR) and restrained least squares (TNT). The final model comprises 5310 protein atoms (residues 5 to 689), 124 carbohydrate atoms (from ten monosaccharide units, in three glycan chains), 2 Fe3+, 2 CO32- and 50 water molecules. This model gives an R-factor of 0.232 for 21440 reflections in the resolution range 30.0 to 2.8 A. The folding of the bLf molecule is essentially the same as that of hLf, but bLf differs in the extent of closure of the two domains of each lobe, and in the relative orientations of the two lobes. Differences in domain closure are attributed to amino acid changes in the interface, and differences in lobe orientations to slightly altered packing of two hydrophobic patches between the lobes. Changed interdomain interactions may explain the lesser iron affinity of bLf, compared with hLf, and two lysine residues behind the N-lobe iron site of bLf offer new insights into the "dilysine trigger" mechanism proposed for iron release by transferrins. The bLf structure is also notable for several well-defined oligosaccharide units which demonstrate the structural factors that stabilise carbohydrate structure. One glycan chain, attached to Asn545, appears to contribute to interdomain interactions and may modulate iron release from the C-lobe.

Animals↗
PubMed1997

Novel inhibitors of cytokine-induced IkappaBalpha phosphorylation and endothelial cell adhesion molecule expression show anti-inflammatory effects in vivo.

We have identified two compounds that inhibit the expression of endothelial-leukocyte adhesion molecules intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin. These compounds act by inhibiting tumor necrosis factor-alpha-induced phosphorylation of IkappaB-alpha, resulting in decreased nuclear factor-kappaB and decreased expression of adhesion molecules. The effects on both IkappaB-alpha phosphorylation and surface expression of E-selectin were irreversible and occurred at an IC50 of approximately 10 microM. These agents selectively and irreversibly inhibited the tumor necrosis factor-alpha-inducible phosphorylation of IkappaB-alpha without affecting the constitutive IkappaB-alpha phosphorylation. Although these compounds exhibited other activities, including stimulation of the stress-activated protein kinases, p38 and JNK-1, and activation of tyrosine phosphorylation of a 130-140-kDa protein, these effects are probably distinct from the effects on adhesion molecule expression since they were reversible. One compound was evaluated in vivo and shown to be a potent anti-inflammatory drug in two animal models of inflammation. The compound reduced edema formation in a dose-dependent manner in the rat carrageenan paw edema assay and reduced paw swelling in a rat adjuvant arthritis model. These studies suggest that inhibitors of cytokine-inducible IkappaBalpha phosphorylation exert anti-inflammatory activity in vivo.

Animals↗
PubMed1997

Regulation of cytokine-induced iNOS expression by a hairpin oligonucleotide in murine cerebral endothelial cells.

Inducible nitric oxide synthase (iNOS) is expressed in response to cytokines by a number of cell types participating in CNS inflammation, including brain cerebral endothelial cells. NF-kappaB, a transcription factor, mediates effector actions of pro-inflammatory cytokines. A combination of tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) enhanced the expression of iNOS in murine cerebral endothelial cells (MCECs). In an attempt to modulate TNF-alpha+IFN-gamma induced expression of iNOS in MCECs, we designed a double-strand hairpin (hp) oligonucleotide carrying the NF-kappaB motif. This hp oligonucleotide inhibited NF-kappaB binding activity and decreased both iNOS mRNA and protein expression induced by TNF-alpha+IFN-gamma. As a control, a mutant hp oligonucleotide was without effect. The present study confirms the role of transcription factor NF-kappaB in iNOS expression induced by TNF-alpha+IFN-gamma in MCECs. More importantly, it demonstrates that an appropriately designed hp oligonucleotide is an effective tool to modulate iNOS expression and may be of potential pharmacological use.

Animals↗
PubMed1997

Changes in mononuclear phagocyte microtubules after endotoxin stimulation. I. Changes in microtubule stability.

Microtubules are in a dynamic equilibrium of polymerization and depolymerization. In monocytes and macrophages, microtubules bind endotoxin and partly regulate inflammatory events such as cytokine production. To characterize the morphologic differences between alveolar macrophage and blood monocyte microtubules after LPS stimulation, cells were examined by immunofluorescent microscopy and laser confocal microscopy. Fresh monocytes contained an average of 26 microtubules per cell which significantly increased to 31 microtubules per cell following a 30-min exposure to LPS (P < 0.001). Using a nocodazole-based assay of microtubule dynamic instability, the half-life of fresh unstimulated human monocyte microtubules was approximately 18 s and extended to 26 s following a 30-min exposure to LPS. In vitro maturation of monocytes for 18 h increased microtubule stability but not number. Compared to monocytes, alveolar macrophage microtubules were longer, more numerous, and much more stable. These results suggest that alveolar macrophage microtubules are more numerous and stable than blood monocyte microtubules and that LPS causes an increase in monocyte microtubule number and stability.

Female↗
PubMed1997

Changes in mononuclear phagocyte microtubules after endotoxin stimulation. II. Changes in microtubule composition.

Microtubules are integral components of the cytoskeleton of human cells and are composed of alpha- and beta-tubulin as well as a variable number of microtubule-associated proteins. In monocytes and macrophages, microtubules bind endotoxin and partly regulate endotoxin-induced inflammatory events such as cytokine production. Endotoxin causes a rapid alteration in monocyte microtubule stability. To characterize the effect of endotoxin on mononuclear phagocyte microtubule composition, Western blots and flow cytometry were performed on human monocytes and the monocyte/macrophage-like cell line THP-1. Compared to unstimulated monocytes, monocytes stimulated with endotoxin for 18 h had increased quantities of alpha-, beta-, and tyrosinated alpha-tubulin as well as microtubule-associated protein-2. PMA-differentiated THP-1 cells had increased levels of alpha-tubulin, beta-tubulin, microtubule-associated protein-5, microtubule-associated protein-2, and tau after endotoxin stimulation. These results indicate that endotoxin can alter mononuclear phagocyte microtubules by causing an increase in certain microtubule component proteins.

Blotting, Western↗
PubMed1997

Comparing two strategies to modify dietary behavior and serum cholesterol.

AIM: To test the hypothesis that a strategy including cholesterol screening and dietary education is more effective than dietary education alone in changing dietary behavior and serum cholesterol levels. METHODS: Individuals at four worksites were enrolled in a randomized trial with a 'full intervention' condition in which subjects were told their serum cholesterol value and also received a dietary change kit (n = 236), and a 'partial intervention' condition in which subjects received the same dietary change kit, but were not told their serum cholesterol value (n = 284). Individuals (n = 115) in two worksites served as a nonrandomized 'untreated control group'. Subjects were tested for serum cholesterol and completed a questionnaire at baseline, and 3 and 6 months later. RESULTS: Dietary changes occurred in seven of nine categories in individuals subjects to the full and partial interventions but in only one of nine categories in those studied in the control condition. Mean dietary intake differed between the full and partial intervention conditions for only three of nine dietary categories. Cholesterol level dropped in the full, partial and control conditions by 4.9, 3.9 and 9.6%, respectively. CONCLUSIONS: Dietary education has favorable effects on the dietary behaviors of individuals. Being told one's cholesterol level at the outset of this educational intervention has little effect on dietary change.

Adult↗
PubMed1997

Chymopapain-induced reduction of proinflammatory phospholipase A2 activity and amelioration of neuropathic behavioral changes in an in vivo model of acute sciatica.

The mechanism of action underlying chymopapain (Chymodiactin) chemonucleolysis remains obscure. Radiographic studies suggest that chymopapain does not alter disc fragment size acutely; nonetheless, patients often report symptom resolution within a few days, even hours, of treatment. The authors postulate that, in addition to its chemonucleolytic action, chymopapain may possess antiinflammatory properties. To test this hypothesis, the authors assessed the ability of chymopapain to modulate the activity of the proinflammatory enzyme phospholipase A2 (PLA2) and to ameliorate behavioral changes associated with inflammatory neuropathy in an in vivo model of sciatica. Thirty-nine male Fischer rats were randomly assigned to one of three treatment groups: 1) saline, 2) betamethasone, or 3) chymopapain. All of the rats underwent unilateral sciatic nerve ligation with loose chromic gut suture to induce inflammatory mononeuropathy. The animals were tested for thermal and mechanical hyperalgesia on Days 0 (preoperation), 7 (pretreatment), and 14 (prior to death). Three animals were killed on Day 0 to determine the baseline PLA2 activity within unmanipulated rat sciatic nerves. On Day 7, three animals from each group were killed to assess PLA2 activity prior to treatment. The remainder were given a single infusion of saline, betamethasone (0.3 mg/kg), or chymopapain (100 pKat U) around the inflamed nerve. On Day 14, the remaining animals were killed and their sciatic nerves were removed. The tissue was homogenized and the PLA2 activity was determined using [14C]arachidonate-labeled Escherichia coli phospholipid membrane as a substrate. Lipids were extracted and separated by thin-layer chromatography. All animals developed behavioral changes consistent with inflammatory mononeuropathy 24 to 72 hours postoperatively; these included gait disturbance, flexion deformity, and hyperalgesia of the involved hindlimb. The degree of mechanical and thermal hyperalgesia was comparable between groups at Day 7. By Day 14, the thermal hyperalgesia had resolved; the mechanical hyperalgesia was less evident in the betamethasone- and chymopapain-treated groups than in the saline-treated controls (p = 0.003; saline- vs. chymopapain-treated groups p = 0.004; saline- vs. betamethasone-treated groups p = 0.008). The mean PLA2 activity at baseline (Day 0) was 11.6 +/- 4.9 nmol phospholipid hydrolyzed per minute per milligram of protein. The PLA2 activity at Day 7 was 74.4 +/- 18.2 (ligated side) and 21.2 +/- 11.7 (nonligated side). At Day 14, PLA2 activity was reduced in the chymopapain- (47.8 +/- 12.3) and betamethasone- (39.7 +/- 9.5) treated groups compared with the saline control group (62.3 +/- 11.2), (saline- vs. chymopapain-treated groups p < 0.05; saline- vs. betamethasone-treated groups p < 0.01). The PLA2 activity in nonligated specimens was 18.6 +/- 10.1. These data indicate that chymopapain exhibits antiinflammatory properties in vivo, reducing PLA2 activity and ameliorating mechanical hyperalgesia in this model of inflammatory sciatic neuropathy.

Acute Disease↗
PubMed1996

Estrogenic triarylethylene acetic acids: effect of structural variation on estrogen receptor affinity and estrogenic potency and efficacy in MCF-7 cells.

Triarylethylenecarboxylic acids exemplified by (E,Z)-2-{4-[1-(p-hydroxyphenyl)-2-phenyl]-1-butenyl}phenoxyacetic acid (8) are a new class of estrogen receptor (ER) ligands capable of tissue selective estrogen agonist and antagonist effects. We report the syntheses of 8 and of analogues incorporating structural features known or anticipated to facilitate ER affinity in triarylethylenes. These studies revealed that the p-hydroxyphenyl moiety, ethylenic bond, and ether oxygen of 8 were all critical for high ER affinity. Although a 1,1-bisphenolic analogue bearing the p-(oxyacetic acid) moiety on its 2-phenyl ring, 12, had low ER affinity, it exhibited estrogenic potency approaching that of 8 in MCF-7 cells. Unlike 8 which was a partial agonist with weak antagonist potency, 12 was a full agonist. A similar profile of potency/efficacy in MCF-7 cells was seen in 9, an ethylenic bond saturated analogue of 8. Growth-promoting effects of 8, 9, and 12 were fully antagonized by the antiestrogen tamoxifen, suggesting that such effects were mediated solely via ER. Thus, our studies in MCF-7 cells have confirmed the estrogenicity of 8 and have enabled identification of two analogues with favorable estrogenic potency and full estrogen efficacy. On this basis, these three (triarylethylene)acetic acids have been selected for more intensive animal studies of their extrareproductive tract estrogenic effects.

Animals↗
PubMed1996

Detection of IL-5 and IL-1 receptor antagonist in bronchoalveolar lavage fluid in acute eosinophilic pneumonia.

BACKGROUND: Acute eosinophilic pneumonia is an idiopathic cause of respiratory failure, characterized by very high numbers of alveolar eosinophils without significant blood eosinophilia. OBJECTIVE: The purpose of this study was to determine which cytokines are associated with acute eosinophilic pneumonia. METHODS: Soluble IL-1 type II receptor and the cytokines IL-1 beta, IL-1ra, IL-3, IL-5, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-alpha were measured in serum and in bronchoalveolar lavage fluid from two patients with acute eosinophilic pneumonia during both acute and convalescent phases. RESULTS: Compared with patients with adult respiratory distress syndrome, the patients with acute eosinophilic pneumonia had high bronchoalveolar lavage fluid levels of IL-5, IL-1ra, and soluble type II IL-1 receptor but not IL-1 beta, tumor necrosis factor-alpha, IL-3, or granulocyte-macrophage colony-stimulating factor. Bronchoalveolar lavage fluid levels of IL-5 and IL-1ra fell after resolution of symptoms. In the serum of patients with acute eosinophilic pneumonia, IL-5 was not detectable, and IL-1ra was initially high but fell after corticosteroid treatment. CONCLUSION: Acute eosinophilic pneumonia is characterized by locally high levels of IL-5, IL-1ra, and soluble type II IL-1 receptor in the alveolar space.

Acute Disease↗
PubMed1996

Expression of heat shock protein 70 in rat spleen lymphocytes is affected by age but not by food restriction.

The purpose of this study was to determine if food restriction alters the age-related decline in heat shock protein 70 (hsp70) expression in lymphocytes from male Fischer 344 rats. Spleen lymphocytes were isolated from young (6 mo) and old (24 mo) rats that had free access to food (control group) and from food-restricted old (24 mo) rats that, beginning at 6 wk of age, were fed 60% (40% food restriction) of the diet consumed by the control rats. Lymphocytes were either heat shocked (42.5 degrees C for 1 h) or maintained at 37 degrees C (control). The levels of hsp70 protein and mRNA and the induction of interleukin-2 (IL-2) mRNA by concanavalin A (conA) were measured in these rats. In addition, the percentage of viability (as an index of thermosensitivity) of the lymphocytes from these rats was also measured after exposure of cells to different temperatures (first at 42.5 degrees C and then 45 degrees C). We found that the induction of hsp70 protein and mRNA in lymphocytes isolated from control old rats and food-restricted old rats was lower (P < 0.001) than that in control young rats. However, the levels of hsp70 and mRNA in lymphocytes isolated from food-restricted old rats were similar to the levels in age-matched control rats. Lymphocytes from both control old rats and food-restricted old rats were more thermosensitive than lymphocytes from control young rats; however, thermosensitivity of lymphocytes from food-restricted old rats was similar to that of age-matched control rats. The induction of IL-2 mRNA levels by conA was significantly (P < 0.001) lower in old than in young control rats. In contrast to hsp70, which was not affected by food restriction, the induction of IL-2 mRNA was higher (P < 0.05) in food-restricted old rats than in age-matched control rats. Therefore, food restriction has a differential effect on gene expression.

Aging↗
PubMed1996

Prostaglandin production in cultured cerebral microvascular smooth muscle is serum dependent.

To expand the understanding of cerebrovascular eicosanoid metabolism, the ability of smooth muscle isolated from murine cerebral microvessels to produce prostaglandins (PGs) was studied in vitro. Cultures from SJL and BALB/c mice produced primarily prostaglandin E2 (PGE2) and I2 (PGI2) in response to exogenous arachidonate and calcium ionophore as well as the agonists acetylcholine and epinephrine. Subconfluent smooth muscle cultures demonstrated a two- to threefold increased capacity to produce PG compared with confluent cultures. In contrast, serum deprivation of smooth muscle caused an 80-90% diminution in both PGE2 and PGI2 production but had no effect on PG release in cerebromicrovascular endothelium. Reintroduction of serum to smooth muscle restored PG production within 6h, and the restoration was inhibited by 1 microM dexamethasone. Message for both prostaglandin H synthase (PGHS)-1 and -2 was detectable in smooth muscle grown in the presence of serum, but PGHS-2 message was not present in serum-deprived cultures. Furthermore, readdition of serum induced a massive increase in PGHS-2 mRNA with only a small increase in PGHS-1 message. The serum induction of PGHS-2 was corroborated by immunohistochemistry and Western blotting. Thus cerebromicrovascular smooth muscle may contribute significantly to the formation of PG under circumstances likely to be present during central nervous system pathologies. The induction of PGHS, particularly PGHS-2, may play a key role in this process.

Animals↗
PubMed1996

Factors affecting dystocia in Brahman-cross heifers in subtropical southeastern United States.

This study was conducted to determine relative relationships among factors affecting dystocia in Brahman-cross heifers. Body and pelvic measurements were obtained in mid-June (when heifers were approximately 17 mo old), 45 d after a 60-d breeding season. Heifers studied were 207 Red Brangus, 209 Simbrah, and 250 Braford bred to Black Angus bulls; calving began on December 1. Heifers grazed stockpiled bahia and hemarthria grass or ryegrass supplemented with 0.9 kg of 32% protein cottonseed meal and 1.8 kg of mill-run black strap molasses daily during calving. Calvings were scored (1 = no difficulty to 4 = major difficulty). A random sample of birth weights were obtained on 131 and 210 calves in 1992 and 1993. Data were analyzed within year by SAS procedures. Breed differences in dam size and pelvic measurements were highly significant. Residual correlations between body weight and pelvic area were .20 and .35 (both P < .01) for 1991 and 1992. Dystocia incidence was 6.9% in 1992 and 10.5% in 1993, with higher incidence in males than in females (1992, 10.6 vs 3.1%, P = .08; 1993, 15.6 vs 4.2%, P < .01, male vs female, respectively). Male birth weight exceeded (P < .01) that of females (26.7 vs 24.3 kg, 1992; 28.1 vs 26.1 kg, 1993). Correlations among dam size and calf birth weight were not significant. Birth weight was significantly correlated with dystocia score (.19 and .49, 1992 and 1993). Path analyses of influences on dystocia found birth weight, dam heart girth, and body weight significant in 1992, but only birth weight significant in 1993. Regression of calving score on birth weight was curvilinear and significant in both years, with the birth weight inflection point at 22 kg. We conclude that dam body size data obtained following the breeding season were of minor value in determining dystocia, but birth weight was consistently important.

Animals↗
PubMed1995

Monocyte Fc gamma receptor cross-linking induces IL-8 production.

In response to bacterial cell wall products such as LPS, monocytes produce IL-8, a powerful neutrophil chemotaxin. However, in the absence of bacterial pathogens, immune complex-mediated diseases such as rheumatoid arthritis are associated with high levels of IL-8 in monocyte-rich compartments. Since it is known that IgG-containing immune complexes can recruit neutrophils via an Fc gamma R-dependent process, we hypothesized that cross-linking of monocyte Fc gamma receptors may induce IL-8. To test this hypothesis, peripheral blood mononuclear cells were evaluated for IL-8 induction in response to immobilized LPS-free pooled human IgG. Immobilized IgG, but not soluble IgG, induced IL-8 in a dose-dependent manner (p < 0.05, r = 0.99). This induction corresponded with an up-regulation in IL-8 steady state mRNA levels that peaked at 4 h. The released IL-8 was functional, since supernatants induced concentration-dependent neutrophil migration that was inhibited by a monoclonal anti-IL-8 Ab. Evaluation of purified monocytes for IL-8 production, as well as FACS analysis of IgG-stimulated PBMC preparations, demonstrated that monocytes are the principal IL-8 producer cell. Thus, monocyte Fc gamma R cross-linking induces biologically active IL-8, which may participate in the pathogenesis of immune complex-mediated diseases.

Cells, Cultured↗