A Study of the Air Space Volatiles Present in a Boll Weevil Mass Rearing Facility12

1975 ◽  
Vol 68 (5) ◽  
pp. 592-594 ◽  
Author(s):  
P. A. Hedin ◽  
O. H. Lindig ◽  
R. C. Gueldner ◽  
A. C. Thompson
Keyword(s):  
Boll Weevil ◽  
Mass Rearing ◽  
Air Space

Host size-dependent sex allocation behaviour in a parasitoid: implications forCatolaccus grandis(Hymenoptera: Pteromalidae) mass rearing programmes

1998 ◽  
Vol 88 (1) ◽  
pp. 37-45 ◽  
Author(s):  
K.M. Heinz
Keyword(s):  
Biological Control ◽  
Sex Ratio ◽  
Sex Allocation ◽  
Sex Ratios ◽  
Boll Weevil ◽  
Mass Rearing ◽  
Host Size ◽  
Offspring Sex Ratio ◽  
Offspring Sex ◽  
Control Programmes

AbstractAn often encountered problem associated with augmentative and inundative biological control programmes is the high cost of producing sufficient numbers of natural enemies necessary to suppress pest populations within the time constraints imposed by ephemeral agroecosystems. In many arrhenotokous parasitoids, overproduction of males in mass-rearing cultures inflates costs (per female) and thus limits the economic feasibility of these biological control programmes. Within the context of existing production technologies, experiments were conducted to determine if the sex ratio ofCatolaccus grandis(Burks), an ectoparasitoid of the boll weevilAnthonomous grandisBoheman, varied as a function of boll weevil larval size. Results from natural and manipulative experiments demonstrate the following behavioural characteristics associated with C.grandissex allocation behaviour: (i) femaleC. grandisoffspring are produced on large size hosts and male offspring are produced on small hosts; (ii) whether a host is considered large or small depends upon the overall distribution of host sizes encountered by a female parasitoid; and (iii) female parasitoids exhibit a greater rate of increase in body size with host size than do male parasitoids. The observed patterns cannot be explained by sex-specific mortality of immature parasitoids developing on the different host size categories. In subsequent experiments, laboratory cultures ofC. grandisexposed daily to successively larger sizes ofA. grandislarvae produced successively greater female biased offspring sex ratios, cultures exposed daily to successively smaller sizes of host larvae produced successively greater male biased offspring sex ratios, and cultures exposed daily to equivalent host size distributions over time maintained a uniform offspring sex ratio. By increasing the average size ofA. grandislarval hosts exposed toC. grandisby 2.5 mg per day in mass rearing cultures, the percentage of male progeny can be reduced from 33% to 23% over a period of four consecutive exposure days.

Boll Weevil 1 Development in Mass Rearing: Effects of Temperature 23

1980 ◽  
Vol 9 (1) ◽  
pp. 72-74
Author(s):  
J. G. Griffin ◽  
J. Roberson ◽  
O. L. Malone
Keyword(s):  
Boll Weevil ◽  
Mass Rearing ◽  
Effects Of Temperature ◽  
Rearing Effects

Quantitative Microscopic Comparison of the Organization of the Lung in Transgenic Mice Expressing Transforming Growth Factor-α (TGF-α)

1996 ◽  
Vol 54 ◽  
pp. 14-15
Author(s):  
C. G. Plopper ◽  
C. Helton ◽  
A. J. Weir ◽  
J. A. Whitsett ◽  
T. R. Korfhagen
Keyword(s):  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Transgenic Mice ◽  
Blood Vessels ◽  
Lung Parenchyma ◽  
Lung Maturation ◽  
Alveolar Air ◽  
Parenchymal Tissue ◽  
Air Space ◽  
Conducting Airways

A wide variety of growth factors are thought to be involved in the regulation of pre- and postnatal lung maturation, including factors which bind to the epidermal growth factor receptor. Marked pulmonary fibrosis and enlarged alveolar air spaces have been observed in lungs of transgenic mice expressing human TGF-α under control of the 3.7 KB human SP-C promoter. To test whether TGF-α alters lung morphogenesis and cellular differentiation, we examined morphometrically the lungs of adult (6-10 months) mice derived from line 28, which expresses the highest level of human TGF-α transcripts among transgenic lines. Total volume of lungs (LV) fixed by airway infusion at standard pressure was similar in transgenics and aged-matched non-transgenic mice (Fig. 1). Intrapulmonary bronchi and bronchioles made up a smaller percentage of LV in transgenics than in non-transgenics (Fig. 2). Pulmonary arteries and pulmonary veins were a smaller percentage of LV in transgenic mice than in non-transgenics (Fig. 3). Lung parenchyma (lung tissue free of large vessels and conducting airways) occupied a larger percentage of LV in transgenics than in non-transgenics (Fig. 4). The number of generations of branching in conducting airways was significantly reduced in transgenics as compared to non-transgenic mice. Alveolar air space size, as measured by mean linear intercept, was almost twice as large in transgenic mice as in non-transgenics, especially when different zones within the lung were compared (Fig. 5). Alveolar air space occupied a larger percentage of the lung parenchyma in transgenic mice than in non-transgenic mice (Fig. 6). Collagen abundance was estimated in histological sections as picro-Sirius red positive material by previously-published methods. In intrapulmonary conducting airways, collagen was 4.8% of the wall in transgenics and 4.5% of the wall in non-transgenic mice. Since airways represented a smaller percentage of the lung in transgenics, the volume of interstitial collagen associated with airway wall was significantly less. In intrapulmonary blood vessels, collagen was 8.9% of the wall in transgenics and 0.7% of the wall in non-transgenics. Since blood vessels were a smaller percentage of the lungs in transgenics, the volume of collagen associated with the walls of blood vessels was five times greater. In the lung parenchyma, collagen was 51.5% of the tissue volume in transgenics and 21.2% in non-transgenics. Since parenchyma was a larger percentage of lung volume in transgenics, but the parenchymal tissue was a smaller percent of the volume, the volume of collagen associated with parenchymal tissue was only slightly greater. We conclude that overexpression of TGF-α during lung maturation alters many aspects of lung development, including branching morphogenesis of the airways and vessels and alveolarization in the parenchyma. Further, the increases in visible collagen previously associated with pulmonary fibrosis due to the overexpression of TGF-α are a result of actual increases in amounts of collagen and in a redistribution of collagen within compartments which results from morphogenetic changes. These morphogenetic changes vary by lung compartment. Supported by HL20748, ES06700 and the Cystic Fibrosis Foundation.

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