Nutritive value, fermentation characteristics, and in situ disappearance kinetics of ensiled warm-season legumes and bahiagrass.

This study determined the nutritive value, ensiling characteristics, and in situ disappearance kinetics of bahiagrass (Paspalum notatum Flügge 'Tifton 9'), perennial peanut (Arachis glabrata Benth. 'Florigraze'), annual peanut [Arachis hypogaea (L.) 'FL MDR 98'], cowpea [Vigna unguiculata (L.) Walp. 'Iron clay'], and pigeonpea [Cajanus cajan (L.) Millsp. 'GA-2']. All forages were harvested at maturity stages that optimized dry matter (DM) yield and nutritive value. After harvest, forages were wilted to 45% DM, and 4 replicate bales of each legume and 8 bales of bahiagrass were wrapped in polyethylene and ensiled for 180 d. After each bale was opened, the forage was thoroughly mixed, and representative subsamples were taken for laboratory analysis and in situ incubation. Wilting and ensiling decreased the rumen-undegradable protein, water-soluble carbohydrate, crude protein (CP), and in vitro true digestibility (IVTD) of bahiagrass, perennial peanut, and cowpea, and increased their neutral detergent fiber (NDF) concentrations. Among haylages, CP concentration was greatest for annual peanut, followed by perennial peanut and cowpea, and least for bahiagrass. In contrast, NDF concentration was greater in bahiagrass than in legumes. Pigeonpea had the greatest NDF concentration among legumes and lowest IVTD of all haylages. All haylages were aerobically stable for at least 84 h, but pH was lower in perennial peanut and cowpea than in pigeonpea. Ammonia-N concentrations tended to be greater in legume haylages than in bahiagrass haylage. Butyrate concentration was greater in annual and perennial peanut than in bahiagrass. Total VFA concentration was greater in annual and perennial peanut and cowpea haylages than in bahiagrass haylage. Undegradable DM fractions were greater and extent of DM degradation was lower in bahiagrass and pigeonpea than in other haylages but lag time and degradation rates did not differ. Annual and perennial peanut and cowpea haylages were as aerobically stable and had greater CP, IVTD, and extent of degradation than did bahiagrass haylage; therefore, they are promising forages for dairy cow diets in the southeastern United States.

Effects of Silicon Applications on Soybean Rust Development Under Greenhouse and Field Conditions.

Soybean rust (SBR), caused by Phakopsora pachyrhizi, is one of the most destructive fungal diseases affecting soybean production. Silicon (Si) amendments were studied as an alternative strategy to control SBR because this element was reported to suppress a number of plant diseases in other host-pathogen systems. In greenhouse experiments, soybean cultivars inoculated with P. pachyrhizi received soil applications of wollastonite (CaSiO3) (Si at 0, 0.96, and 1.92 t ha-1) or foliar applications of potassium silicate (K2SiO3) (Si at 0, 500, 1,000, or 2,000 mg kg-1). Greenhouse experiment results demonstrated that Si treatments delayed disease onset by approximately 3 days. The area under disease progress curve (AUDPC) of plants receiving Si treatments also was significantly lower than the AUDPC of non-Si-treated plants. For field experiments, an average 3-day delay in disease onset was observed only for soil Si treatments. Reductions in AUDPC of up to 43 and 36% were also observed for soil and foliar Si treatments, respectively. Considering the natural delayed disease onset due to the inability of the pathogen to overwinter in the major soybean production areas of the United States, the delay in disease onset and the final reduction in AUDPC observed by the soil Si treatments used may lead to the development of SBR control practices that can benefit organic and conventional soybean production systems.

Intake, digestibility, and nitrogen retention by sheep supplemented with warm-season legume haylages or soybean meal.

The high cost of commercial supplements necessitates evaluation of alternatives for ruminant livestock fed poor quality warm-season grasses. This study determined how supplementing bahiagrass haylage (Paspalum notatum Flügge cv. Tifton 9) with soybean [Glycine max (L.) Merr.] meal or warm-season legume haylages affected the performance of lambs. Forty-two Dorper x Katadhin lambs (27.5 +/- 5 kg) were fed for ad libitum intake of bahiagrass haylage (67.8% NDF, 9.6% CP) alone (control) or supplemented with soybean meal (18.8% NDF, 51.4% CP) or haylages of annual peanut [Arachis hypogaea (L.) cv. Florida MDR98; 39.6% NDF, 18.7% CP], cowpea [Vigna unguiculata (L.) Walp. cv. Iron clay; 44.1% NDF, 16.0% CP], perennial peanut (Arachis glabrata Benth. cv. Florigraze; 40.0% NDF, 15.8% CP), or pigeonpea [Cajanus cajan (L.) Millsp. cv. GA-2; 65.0% NDF, 13.7% CP]. Haylages were harvested at the optimal maturity for maximizing yield and nutritive value, wilted to 45% DM, baled, wrapped in polyethylene plastic, and ensiled for 180 d. Legumes were fed at 50% of the dietary DM, and soybean meal was fed at 8% of the dietary DM to match the average CP concentration (12.8%) of legume haylage-supplemented diets. Lambs were fed each diet for a 14-d adaptation period and a 7-d data collection period. Each diet was fed to 7 lambs in period 1 and 4 lambs in period 2. Pigeonpea haylage supplementation decreased (P < 0.01) DM and OM intake and digestibility vs. controls. Other legume haylages increased (P < 0.05) DM and OM intake vs. controls; however, only soybean meal supplementation increased (P = 0.01) DM digestibility. All supplements decreased (P = 0.05) NDF digestibility. Except for pigeonpea haylage, all supplements increased (P < 0.01) N intake, digestibility, and retention, and the responses were greatest (P = 0.04) with soybean meal supplementation. Microbial N synthesis was reduced (P = 0.02) by pigeonpea haylage supplementation, but unaffected (P = 0.05) by other supplements. Efficiency of microbial protein synthesis was unaffected (P = 0.05) by diet. Ruminal ammonia concentration was increased (P = 0.01) by all supplements, but only soybean meal and annual peanut haylage increased (P < 0.03) plasma urea-N concentrations. Perennial peanut, annual peanut, and cowpea haylages are promising protein supplements for growing lambs.

Intake, digestibility, and nitrogen retention by sheep supplemented with warm-season legume hays or soybean meal.

The increasing cost of feed supplements necessitates evaluation of alternatives for ruminant livestock grazing poor quality warm-season grasses. This study determined how supplementing bahiagrass hay (Paspalum notatum Flügge cv. Pensacola) with soybean [Glycine max (L.) Merr.] meal or warm-season legume hays affected intake, digestibility, and N utilization by lambs. Dorper x Katadhin crossbred lambs (30.6 +/- 5.5 kg; n = 42) were fed bahiagrass hay (73.8% NDF, 8.1% CP) for ad libitum intake and supplemented with nothing (control), soybean meal, or hays of annual peanut [Arachis hypogaea (L.) cv. Florida MDR98; 46.2% NDF, 14.7% CP], cowpea [Vigna unguiculata (L.) Walp. cv. Iron clay; 62.2% NDF, 11.7% CP], perennial peanut (Arachis glabrata Benth. cv. Florigraze; 43.3% NDF, 15.2% CP), pigeonpea [Cajanus cajan (L.) Millsp. cv. GA-2; 78.6% NDF, 12.2% CP], or soybean (cv. Pioneer 97B52; 59.0% NDF, 13.5% CP). Legume hays were supplemented at 50% of total diet DM, and soybean meal was supplemented at a level (4.25% of diet DM) that matched the average dietary CP content (10.8%) of the legume hay-supplemented diets. The cowpea, pigeonpea, and soybean were harvested at respective maturities that maximized DM yield and nutritive value, and the peanuts were first cuttings. Diets were fed to 6 lambs per treatment for 2 consecutive 21-d periods. Supplementation with hays of annual and perennial peanut, cowpea, and soybean increased (P < 0.01) DMI vs. control, but apparent DM digestibility was only increased (P = 0.03) by supplementation with annual or perennial peanut hay. Compared with the control, N intake, digestibility, and retention were increased (P < 0.01) by supplementation with legume hay or soybean meal. Responses were greatest when annual or perennial peanut hays were fed. Ruminal ammonia concentration was increased (P < 0.01) by all legume hay supplements vs. the control. Microbial N synthesis and ruminally degraded OM were increased (P = 0.03) by perennial and annual peanut hay supplementation, but efficiency of microbial synthesis was not different (P = 0.52) among diets. Unlike other supplements, annual and perennial peanut hays increased DM and N intake and digestibility and improved microbial N synthesis; therefore, they were the best supplements for the bahiagrass hay under the conditions of this study.

First Report of Peanut stunt virus in Perennial Peanut in North Florida and Southern Georgia.

In spring 2001, symptoms similar to aphid-vectored peanut stunt disease caused by Peanut stunt virus (PSV) were observed on perennial peanut (Arachis glabrata) cv. Floragraze in Jackson and Gulf counties, FL and Lowndes County, GA. Symptoms observed in commercial hay fields and at the North Florida Research and Education Center in Marianna and Quincy included malformed leaves, plant chlorosis, leaf mottling, and stunted plants, which resulted in reduced foliage yield. Leaf symptoms were visible throughout the growing season. Stunting was more common in spring and early summer. No symptoms were seen on rhizomes. Diagnosis of PSV (genus Cucumovirus) from symptomatic leaves and rhizome materials of 12 plants was confirmed by a direct antigen-coated enzyme-linked immunosorbent assay (DAC-ELISA). ELISA tests were repeated three times. Antibodies specific to the Clemson isolate, serotype E, were obtained from Clemson University, Clemson, SC. DAC-ELISA (1) values of 0.1 A405 above the healthy control for perennial peanut were considered positive for foliage and rhizome material tested. ELISA values ranged from 0.4 to 2.1. The mean ELISA value of the positive controls was 2.65. Symptomatic plants were also tested with ELISA using available antibodies from Agdia Inc., Elkart, IN, for Tomato spotted wilt virus, from ATCC for Peanut stripe virus, and from Clemson University (Cowpea isolate) for Cucumber mosaic virus, but all results were negative. To our knowledge, this is the first report of PSV on perennial peanut in Florida and southern Georgia. At this time, it is not known what role perennial peanut may play as a reservoir of the virus in the vicinity of peanut fields. Little is known about the potential for forage production loss and stand longevity. Next season, molecular detection techniques and epidemiological studies on peanut and perennial peanut will be conducted to ascertain the incidence and possible impact of PSV in Georgia and Florida. Reference: (1) A. G. Gillaspie, Jr. et al. Plant Dis. 79:388, 1995.

Identification of urocortin III, an additional member of the corticotropin-releasing factor (CRF) family with high affinity for the CRF2 receptor.

The corticotropin-releasing factor (CRF) family of neuropeptides includes the mammalian peptides CRF, urocortin, and urocortin II, as well as piscine urotensin I and frog sauvagine. The mammalian peptides signal through two G protein-coupled receptor types to modulate endocrine, autonomic, and behavioral responses to stress, as well as a range of peripheral (cardiovascular, gastrointestinal, and immune) activities. The three previously known ligands are differentially distributed anatomically and have distinct specificities for the two major receptor types. Here we describe the characterization of an additional CRF-related peptide, urocortin III, in the human and mouse. In searching the public human genome databases we found a partial expressed sequence tagged (EST) clone with significant sequence identity to mammalian and fish urocortin-related peptides. By using primers based on the human EST sequence, a full-length human clone was isolated from genomic DNA that encodes a protein that includes a predicted putative 38-aa peptide structurally related to other known family members. With a human probe, we then cloned the mouse ortholog from a genomic library. Human and mouse urocortin III share 90% identity in the 38-aa putative mature peptide. In the peptide coding region, both human and mouse urocortin III are 76% identical to pufferfish urocortin-related peptide and more distantly related to urocortin II, CRF, and urocortin from other mammalian species. Mouse urocortin III mRNA expression is found in areas of the brain including the hypothalamus, amygdala, and brainstem, but is not evident in the cerebellum, pituitary, or cerebral cortex; it is also expressed peripherally in small intestine and skin. Urocortin III is selective for type 2 CRF receptors and thus represents another potential endogenous ligand for these receptors.

Actions of activins, inhibins and follistatins: implications in anterior pituitary function.

1. The anterior pituitary is well documented to be under the control of central and peripheral factors that dynamically interact to affect cell-specific modulation of pituitary functions. However, it is becoming increasingly evident that these extrinsic factors work in concert with a variety of local products that exert autocrine/paracrine control on pituitary cells. 2. These factors modulate the activity of their target pituitary cells by altering the synthesis and secretion of cell-specific hormones and by exerting control on the growth and differentiation of cells of this tissue. Included in the list of growth factors and bioactive peptides known to be products of pituitary cells are the activins, possibly inhibins and follistatins. 3. These protein factors play an important role in the local modulation of several pituitary cell types and are crucial for the maintenance of normal follicle-stimulating hormone production and, thus, reproductive function and fertility.

Regulation and actions of Smad7 in the modulation of activin, inhibin, and transforming growth factor-beta signaling in anterior pituitary cells.

Activins and transforming growth factor-beta (TGF beta) are crucial autocrine, paracrine, and endocrine modulators of anterior pituitary function. Activins regulate most pituitary cells and lactotropes are targets of TGF beta. Smad2 and Smad3 are two cellular mediators of activin/TGF beta signaling, whereas Smad7 is as an inducible, negative modulator of the pathway. This study was undertaken to evaluate Smad7 regulation in the pituitary. Activin A rapidly and transiently increased Smad7 messenger RNA (mRNA) levels of rat anterior pituitary (RAP), clonal gonadotrope (alpha T 3-1 and L beta T2), and corticotrope (AtT20) cells with an EC(50) of 0.1-0.2 nM. In RAP cells, activin A or TGF beta 1 had equivalent effects that were additive. Follistatin, known to bind and inactivate activins, prevented Smad7 induction by activin. Inhibin A partially antagonized activin A, perhaps reflecting gonadotrope-selective actions. This antagonism was also evident with alpha T 3-1 and L beta T2 gonadotropes. Forskolin had no measurable effect in RAP cells, but increased Smad7 mRNA levels in alpha T3-1 cells and decreased them in L beta T2 cells. Transient transfection of Smad7 along with 3TPLux, an activin/TGF beta-responsive reporter, blocked activin-mediated promoter activation in alpha T3-1 and AtT20 cells. In alpha T3-1 cells, which express endogenous follistatin mRNA, a follistatin-luciferase reporter, rFS(rin3)-Luc, was transcriptionally activated by activin A, or when cotransfected with a constitutively active ActRIB [Alk4(T>D)], Smad2, or Smad3. Smad7 blocked rFS(rin3)-Luc activation by activin A or Alk4(T>D). Together, these results point to a role of Smad7 in modulating activin/TGF beta signaling in the pituitary.

First Report of a Furovirus Infecting Field-Grown Rye in North America.

Viral symptoms were present in a dwarf recurrent population (99RP17) of rye (Secale cereale) at the North Florida Research and Education Center in Quincy, Gadsden County, FL, during the winter and spring of 2000. Symptoms and distribution of the infected plants in the field were similar to those caused by Soilborne wheat mosaic virus (SBWMV; acronym WSBMV), which was first recognized in North America in 1919 (4) and found in Florida in wheat in 1970 (3). SBWMV has been observed based on symptoms in rye in North America (4). Interveinal, non-continuous, chlorotic areas of leaves and stunting of plants in patchy patterns occurred in four locations (0.8 to 1.6 km between locations). Incidences of the disease ranged from 3 to 15%. Leaves and roots of more than 25 plants were assessed. Using light microscopy, after staining with Calcomine Orange 2RS/Luxol Brilliant Green BL (1), amorphous, vacuolate inclusions were observed in all assayed leaves. With electron microscopy, rigid rods were present with a bimodal distribution of particle lengths that conformed to size distributions found originally in wheat in 1970 in Florida. Leaves with symptoms were sent to Agdia Inc. (Elkhart, IN) and samples were strongly positive for SBWMV using enzyme-linked immunosorbent assay. Cystosori of Polymyxa graminis were detected from a few roots from symptomatic plants. While these associations are suggestive of SBWMV, and rye is a reported host of SBWMV, the possibility of this virus being soilborne rye mosaic virus exists (2). Such a differentiation will require nucleotide sequence analysis. To our knowledge, this is the first report of a furovirus infecting field-grown rye in Florida and in North America. References: (1) R. G. Christie and J. R. Edwardson. 1994. Light and Electron Microscopy of Plant Virus Inclusions Monogr. 9. University of Florida, Quincy. (2) R. Koenig et al. 1999. Arch. Virol. 144:2125-2140. (3) T. A. Kucharek and J. H. Walker. Plant Dis. Rep. 58:763-765, 1974. (4) H. H. McKinney. J. Agric. Res. 23:771-800, 1923.

Betaglycan binds inhibin and can mediate functional antagonism of activin signalling.

Activins and inhibins, structurally related members of the TGF-beta superfamily of growth and differentiation factors, are mutually antagonistic regulators of reproductive and other functions. Activins bind specific type II receptor serine kinases (ActRII or IIB) to promote the recruitment and phosphorylation of the type I receptor serine kinase, ALK4 (refs 7-9), which then regulates gene expression by activating Smad proteins. Inhibins also bind type II activin receptors but do not recruit ALK4, providing a competitive model for the antagonism of activin by inhibin. Inhibins fail to antagonize activin in some tissues and cells, however, suggesting that additional components are required for inhibin action. Here we show that the type III TGF-beta receptor, betaglycan, can function as an inhibin co-receptor with ActRII. Betaglycan binds inhibin with high affinity and enhances binding in cells co-expressing ActRII and betaglycan. Inhibin also forms crosslinked complexes with both recombinant and endogenously expressed betaglycan and ActRII. Finally, betaglycan confers inhibin sensitivity to cell lines that otherwise respond poorly to this hormone. The ability of betaglycan to facilitate inhibin antagonism of activin provides a variation on the emerging roles of proteoglycans as co-receptors modulating ligand-receptor sensitivity, selectivity and function.

Identification of a binding site on the type II activin receptor for activin and inhibin.

Type II activin receptors (ActRII and ActRIIB) are single-transmembrane domain serine/threonine kinase receptors that bind activin to initiate the signaling and cellular responses triggered by this hormone. Inhibin also binds type II activin receptors and antagonizes many activin effects. Here we describe alanine scanning mutagenesis of the ActRII extracellular domain. We identify a cluster of three hydrophobic residues (Phe(42), Trp(60), and Phe(83)) that, when individually mutated to alanine in the context of the full-length receptor, cause the disruption of activin and inhibin binding to ActRII. Each of the alanine-substituted ActRII mutants retaining activin binding maintains the ability to form cross-linked complexes with activin and supports activin cross-linking to the type I activin receptor ALK4. Unlike wild-type ActRII, the three mutants unable to bind activin do not cause an increase in activin signaling when transiently expressed in a corticotroph cell line. Together, our results implicate these residues in forming a critical binding surface on ActRII required for functional interactions with both activin and inhibin. This first identification of a transforming growth factor-beta family member binding site may provide a general basis for characterizing binding sites for other members of the superfamily.

Urocortin messenger ribonucleic acid: tissue distribution in the rat and regulation in thymus by lipopolysaccharide and glucocorticoids.

Urocortin (Ucn), a new mammalian member of the CRF family, is a candidate endogenous ligand for type 2 CRF receptors. In a survey of peripheral tissues from adult male rats, we found that Ucn messenger RNA (mRNA) was abundant in the gastrointestinal tract and immune tissues such as thymus and spleen. We next tested the hypothesis that levels of Ucn mRNA levels in thymus and spleen would be altered after immune activation. As measured by ribonculease protection assay, lipopolysaccharide (LPS) induced a 2-fold time-dependent increase in thymic Ucn mRNA levels within 6 h. By contrast, splenic Ucn mRNA levels decreased after LPS. Because LPS activates the hypothalamus-pituitary-adrenal (HPA) axis, we examined whether the effects of LPS on Ucn mRNA might be mediated through changes in HPA axis hormones. Ucn mRNA in thymus, but not spleen, was significantly increased after ACTH injection; however, LPS did not increase Ucn expression in the thymus of adrenalectomized rats with corticosterone replacement, despite substantial increases in ACTH. Finally, sc injection of corticosterone stimulated Ucn mRNA comparably to that of LPS. Together, these results suggest that Ucn mRNA expression can increase after immune activation in a corticosterone-dependent manner, and that such changes in Ucn mRNA may be an additional consequence of HPA axis activation.

Race and differences in breast cancer survival in a managed care population.

BACKGROUND: African-American women with breast cancer have poorer survival than European-American women. After adjustment for socioeconomic variables, survival differences diminish but do not disappear, possibly because of residual differences in health care access, biology, or behavior. This study compared breast cancer survival in African-American and European-American women with similar health care access. METHODS: We measured survival in women with breast cancer who are served by a large medical group and a metropolitan Detroit health maintenance organization where screening, diagnosis, treatment, and follow-up are based on standard practices and mammography is a covered benefit. We abstracted data on African-American and European-American women who had been diagnosed with breast cancer from January 1986 through April 1996 (n = 886) and followed these women for survival through April 1997 (137 deaths). RESULTS: African-American women were diagnosed at a later stage than were European-American women. Median follow-up was 50 months. Five-year survival was 77% for African-American and 84% for European-American women. The crude hazard ratio for African-American women relative to European-American women was 1.6 (95% confidence interval [CI] = 1.1-2.2). Adjusting only for stage, the hazard ratio was 1.3 (95% CI = 0.9-1.9). Adjusting only for sociodemographic factors (age, marital status, and income), the hazard ratio was 1.2 (95% CI = 0.8-1.9). After adjusting for age, marital status, income, and stage, the hazard ratio was 1.0 (95% CI = 0.7-1.5). CONCLUSION: Among women with similar medical care access since before their diagnoses, we found ethnic differences in stage of breast cancer at diagnosis. Adjustment for this difference and for income, age, and marital status resulted in a negligible effect of race on survival.

Interleukin-1beta regulates pituitary follistatin and inhibin/activin betaB mRNA levels and attenuates FSH secretion in response to activin-A.

Activins and follistatins regulate all levels of the reproductive axis, including the pituitary where they stimulate and inhibit FSH production, respectively. Gonadotropes are known to express inhibin/activin betaB and activin-B (betaBbetaB) functions as an autocrine modulator of FSH production. By contrast, the mRNA for the activin-binding protein, follistatin, is present in most pituitary cells and folliculo-stellate cells may be the major source of the protein secreted by the anterior pituitary. Interleukin-1beta (IL-1beta) is one of several cytokines known to also influence the reproductive axis. IL-1beta inhibits the hypothalamo-pituitary-gonadal (HPG) axis by suppressing GnRH and gonadal steroid production. Because several pituitary cell types, including follistatin-producing folliculo-stellate cells, are targets of IL-1beta, cytokine effects on gonadotrope function were evaluated using cultured rat anterior pituitary cells. Activin-A (0.01 to 1 nM; 24h) increased basal FSH secretion approximately 2-fold. IL-1beta (0.005 to 0.5 nM) by itself had no effect on basal FSH secretion. However, IL-1beta attenuated FSH secretion in response to all concentrations of activin-A. These results suggest that the cytokine might stimulate the local production of a factor, such as follistatin, that antagonizes the action of activin-A. RNase protection analysis indicated that IL-1beta (0.005 to 5 nM) stimulated follistatin and inhibin/activin betaB mRNA accumulation in a time-dependent manner. These in vitro effects of IL-1beta were blocked by the specific IL-1 receptor antagonist (IL-lra) and were not mimicked by either rhIL-6 or lipopolysaccharide (LPS). Treatment of intact male rats with LPS (50 microg, i.v.), which increases plasma IL-1beta and induces IL-1beta expression in many tissues, including the pituitary, produced similar time-dependent increases in pituitary follistatin and inhibin/activin subunit mRNA levels. These results suggest that IL-1beta can modulate gonadotrope responses to activins by influencing the local balance of activin-B and follistatin within the pituitary.

Ventilatory strategies affect gas exchange in a pig model of closed-chest cardiac compression.

STUDY OBJECTIVE: To identify the arterial and mixed venous blood gas changes caused by different ventilatory strategies during resuscitation from ventricular fibrillation in a pig model of closed-chest cardiac compression. METHODS: A prospective randomized animal study was performed using 27 domestic pigs (body weight, 30 to 35 kg). Pentobarbital-anesthetized pigs were assigned to receive one of three treatments: (1) chest compression without assisted ventilation (n = 8), (2) assisted ventilation with room air (n = 8), and (3) assisted ventilation with 100% oxygen (n = 8). A fourth group, with the airway completely blocked, was added at the end of the experiment (n = 3). After instrumentation, the ventricles were fibrillated, and chest compression was begun 30 seconds after fibrillation with the use of the Thumper Mechanical CPR system (Michigan Instruments). Arterial and mixed venous blood gas samples were collected at 1, 3, 10, and 20 minutes of resuscitation. Defibrillation was attempted after the 20-minute sample was taken. RESULTS: Fibrillation followed by chest compression alone caused a significant drop in arterial and mixed venous partial pressure of oxygen (PO2) and a significant increase in arterial and mixed venous partial pressure of carbon dioxide (PCO2). Compared with the chest compression only, ventilation with room air significantly increased arterial and mixed venous PO2 and decreased arterial and mixed venous PCO2. Ventilation with 100% oxygen further increased arterial and mixed venous PO2 but did not affect PCO2, when compared with room air ventilation. The only successful defibrillations (3 animals) occurred in the group receiving 100% oxygen. CONCLUSION: This study indicates that passive air movement during chest compression does not allow physiologically significant pulmonary gas exchange and that room air ventilation alone is not sufficient to maintain mixed venous PO2.

Performance of Frogeye Leaf Spot-Resistant and -Susceptible Near-Isolines of Soybean.

Frogeye leaf spot (FLS) caused by Cercospora sojina Hara is a disease of soybean (Glycine max (L.) Merr.) that causes significant seed yield losses in warm, humid environments of southeastern United States. The Rcs3 gene in soybean has been reported to condition resistance to all known races of C. sojina. The objectives of this study were to determine the effectiveness of Rcs3 in limiting seed yield loss due to FLS and to compare the seed yield of the resistant and susceptible near-isolines (NILs) in the absence of significant FLS disease. Four pairs of NILs-Colquitt/Colquitt-Rcs3, Gordon/Gordon-Rcs3, Thomas/Thomas-Rcs3, and Wright/Wright-Rcs 3-were evaluated in 23 field experiments in Alabama, Florida, Georgia, Louisiana, Mississippi, and South Carolina during 1992 to 1994. The amount of damage to susceptible soybean caused by FLS was dependent on the specific environment. All four of the Rcs3 NILs were resistant to the prevalent races of FLS in all environments. In the absence of significant FLS disease, each of the Rcs3 NILs was at least equal to the respective susceptible line in its seed yield. In the presence of FLS infestation, the susceptible lines suffered significant seed yield loss (up to 31%) compared to their Rcs3 NILs. The effect of FLS on seed yield was dependent on cumulative disease severity over the growing season. Thus, the area under disease progress curve was more useful than percent of leaf area infected at the end of the growing season (R7 stage of development) in explaining the seed yield loss due to FLS.

Racial differences in surgically staged patients with endometrial cancer.

This study examined whether differences in survival for endometrial cancer attributed to race are primarily associated with socioeconomic status, comorbid illnesses, molecular genetic alterations, and other disease-related characteristics identified as poor prognostic factors. One hundred fifty-two surgically staged patients with endometrial cancer (37 African-American and 115 European-American women) treated from 1990 to 1994 were analyzed for differences in demographics, disease-related characteristics, and survival. Survival was poorer for African-American women than for European-American women. African-American women had lower socioeconomic status and a higher prevalence of poor prognostic factors. Surgical stage, positive peritoneal cytology, angiolymphatic invasion, cervical stromal involvement, and a history of other malignancies were similar between the two groups. The most important predictors of survival were age at diagnosis, surgical stage, myometrial invasion, positive peritoneal cytology, cervical stromal involvement, tumor grade, aneuploidy, histology, S-phase fraction, number of poor prognostic factors, and race. Racial differences in survival were not explained by socioeconomic status, comorbid illnesses, or estrogen use. When incorporating the number of poor prognostic factors in a survival model with race and surgical stage, race ceased to be of significant prognostic value. In an analysis restricted to women with poor prognostic factors, this phenomena also occurred after adjusting for the number of poor prognostic factors. These findings suggest that the cumulative number of poor prognostic factors, not race, is a more important predictor of survival in endometrial cancer.

Pituitary follistatin and inhibin subunit messenger ribonucleic acid levels are differentially regulated by local and hormonal factors.

Follistatins, activins, and inhibins are expressed in a wide range of tissues where they function as autocrine and/or paracrine factors. Activin B (beta B beta B) and inhibin B (alpha beta B) are the predominant forms expressed in the rat anterior pituitary. This study was designed to evaluate the regulation of the messenger RNAs (mRNAs) for inhibin alpha and beta B, and follistatin, relative to each other, using cultured rat anterior pituitary cells. Activin A stimulated follistatin (a maximal 4-fold stimulation by 6 h) and beta B (a maximal 1.7-fold stimulation after 2 h) mRNA levels. Although inhibin A dramatically decreased follistatin mRNA levels (34% of the control value after 24 h), it only marginally affected those of beta B (86% of the control value after 2 h). Follistatin inhibited the accumulation of its own mRNA (46% of the control value after 6 h), but had no statistically significant effect on beta B or alpha mRNA levels. Inhibin A was the only treatment that had an effect on alpha mRNA levels, causing a slight decrease (82% of the control value by 24 h). The effects of activin A and inhibin A on follistatin and beta B mRNA levels were dose dependent. Moreover, follistatin and inhibin A blocked the effects of activin A. Immunoneutralization experiments were performed to determine whether locally secreted activin B regulates the expression of these three mRNAs. A monoclonal antibody to activin B reduced follistatin and beta B mRNA levels (37% and 73% of the control value, respectively) and enhanced the stimulatory effect of exogenous activin A on these mRNAs (840% vs. 300% and 170% vs. 145% of the control value, respectively); there was no change in alpha mRNA accumulation. GnRH and activators of the protein kinase A (forskolin) and protein kinase C (12-O-tetradecanoylphorbol acetate) pathways also had differential effects on follistatin, beta B, and alpha mRNA levels. GnRH stimulated follistatin mRNA levels, but suppressed those of beta B. 12-O-Tetraphorbol acetate had no effect on beta B, but stimulated follistatin mRNA levels to the same extent as forskolin. Of these agents, only forskolin produced a marginal inhibitory effect on alpha mRNA accumulation. Testosterone decreased both follistatin and beta B mRNA levels without affecting those of alpha. The results of this study demonstrate that the local production of rat anterior pituitary follistatin, activin B, and inhibin B is regulated by hypothalamic, peripheral, and local factors in such a way that the ratios between activin B and its two inactivators, follistatin and inhibin B, are very tightly maintained.

Corticotropin-releasing factor (CRF) and glucocorticoids modulate the expression of type 1 CRF receptor messenger ribonucleic acid in rat anterior pituitary cell cultures.

Previous studies involving radioreceptor and functional assays have shown that CRF and glucocorticoids are able to modulate CRF receptors of the brain and anterior pituitary. In this study, we analyzed the effects of CRF, vasopressin (AVP), dexamethasone (DEX), and corticosterone on the regulation of CRF receptor (CRF-R1) messenger RNA (mRNA) levels in cultured rat anterior pituitary cells. CRF decreased CRF-R1 mRNA levels in a time- and concentration-dependent manner. In the presence of 10 nM CRF, CRF-R1 mRNA levels decreased within 1 h (to 65 +/- 3% of the control value; P < 0.01) with a maximal effect after 3 h (to 28 +/- 1% of the control value; P < 0.001). The concentration dependence of the inhibitory effect of CRF at 3 h correlated with that required for ACTH secretion (half-maximal at approximately 0.03 nM). Treatment with a maximal (100 nM) dose of AVP or a submaximal (0.1 nM) dose of CRF for 3 h reduced CRF-R1 mRNA levels to 66 +/- 3% and 53 +/- 6% of the control value, respectively. In the presence of both AVP and CRF, CRF-R1 mRNA levels were 32 +/- 3% of the control value. The incubation of cells for 3 h with 10 microM forskolin to activate adenylate cyclase or with 20 nM 12-0-tetradecanoylphorbol-13-acetate to activate protein kinase C resulted in a decrease in receptor mRNA levels to 40 +/- 9% (P < 0.01) and 28 +/- 8% (P < 0.001) of the control value, respectively, suggesting that the effects of CRF and AVP may be mediated by these pathways. DEX (20 nM) also caused a dose- and time-dependent decrease in mRNA levels. Maximal inhibition was observed after 3 h (to 31 +/- 6% of the control value; P < 0.001), with a partial recovery of mRNA levels at 24 or 48 h. Corticosterone similarly inhibited the accumulation of CRF-R1 mRNA in a dose- and time-dependent manner, but, in contrast to DEX, CRF-R1 mRNA levels returned almost to control levels after 24 h. These results indicate that the ability of CRF, AVP, and glucocorticoids to modulate the responses of corticotropes to CRF may be due in part to the actions of these agents on CRF-R1 mRNA accumulation.