Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FOWLS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources

Deduction of a model for sperm storage in the oviduct of the domestic fowl (Gallus domesticus).

The mechanism of sperm storage in the fowl oviduct has remained a mystery since the 1960s, when sperm storage tubules (SST) were discovered between the shell gland and vagina. Previously, it was known that only motile sperm could ascend the vagina and enter these tubules. However, the means by which sperm resided therein was not clear. Research with computer-assisted sperm motion analysis has demonstrated that 1) seminal plasma glutamate acts as a motility agonist via N-methyl-d-aspartate receptors; 2) motility depends on extracellular Ca2+ and Na+; 3) straight-line velocity is a variable with a skewed distribution; 4) sperm cell trajectory is a function of straight-line velocity; and 5) specific inhibition of phospholipase A2 renders sperm immotile. An additional experiment demonstrated that Ca2+ acts as a second messenger and thereby modulates the content of long-chain acylcarnitine within sperm. Therefore, it is proposed that 1) the release of endogenous fatty acids fuels sperm as they ascend the vagina; (2) on entering the SST, motile sperm maintain position against a fluid current generated by SST epithelial cells; 3) resident sperm metabolize exogenous fatty acids released from lipid-laden epithelial cells; (4) motile sperm emerge from the SST when their velocity declines to a threshold at which retrograde movement begins; and 5) the skewed distribution of straight-line velocity accounts for the exponential pattern of sperm emergence from the SST. In summary, sperm residence within and emergence from the SST are phenomena most likely explicable in terms of sperm cell motility.

Animals↗

Episodic gonadotropin secretion in the mature fowl: serial blood sampling from unrestrained male broiler breeders (Gallus domesticus).

Forty-week-old male broiler breeders were used in two experiments. Males were reared as recommended by the breeder, housed in individual cages, and cannulated to facilitate blood sampling. In experiment 1, blood samples were collected at 10- min intervals for 4 h commencing the day of cannulation (Day 0) and for 12 h on each of Days 1 and 2. In experiment 2, blood samples were collected at 10-min intervals for 8 h on Day 1. After centrifugation, plasma was stored at -20 degrees C until LH, FSH (experiment 1 and 2), testosterone, and corticosterone (experiment 1) concentrations were determined by RIA. Different statistical methods used to identify hormone secretion profiles revealed a characteristic pulsatile pattern of LH and FSH in plasma. However, LH pulses were more frequent and had greater amplitude than FSH pulses. Less than 32% of the FSH pulses were associated with LH episodes. Conversely, the association between LH and testosterone pulses averaged 83% in birds with testis weight greater than 10 g. Concentrations of corticosterone tended to increase after cannulation and remained elevated for only 3-4 h. Our data indicate that LH, FSH, and testosterone secretion is pulsatile in male broiler breeders. Additionally, LH pulses are associated with testosterone episodes but not with FSH pulses. The pulsatile pattern of FSH secretion, which is unique from those of LH, in adult males suggests that FSH secretion is independently regulated in the adult male fowl.

Animals↗

Spinal kyphosis causes demyelination and neuronal loss in the spinal cord: a new model of kyphotic deformity using juvenile Japanese small game fowls.

STUDY DESIGN: Histologic changes in the spinal cord caused by progressive spinal kyphosis were assessed using a new animal model. OBJECTIVES: To evaluate the effects of chronic compression associated with kyphotic deformity of the cervical spine on the spinal cord. SUMMARY OF BACKGROUND DATA: The spinal cord has remarkable ability to resist chronic compression, however, delayed paralysis is sometimes seen following the development of spinal kyphosis. In the past, no animal model to clarify the mechanism of spinal cord damage due to spinal kyphotic deformity has been available. METHODS: Laminectomy and bilateral facetectomy at the C4-C5 level was performed in 52 Japanese small game fowls. Histologic changes in the spinal cord associated with progressive kyphotic deformity were examined at different time points after surgery in each animal. The degree of spinal cord flattening and the severity of demyelination in histologic sections were quantitatively evaluated using an image analyzer, and their association with the kyphotic angle was analyzed. Changes in the microvascular distribution in the spinal cord were also examined by microangiography. RESULTS: In all operated animals, progressive kyphosis developed reproducibly. The kyphotic angle increased gradually until 3 weeks after surgery and stabilized thereafter. There was a significant correlation between the kyphotic angle and the degree of spinal cord flattening. The spinal cord was compressed most intensely at the apex of the kyphosis, where demyelination of the anterior funiculus as well as neuronal loss and atrophy of the anterior horn were observed. Demyelination progressed as the kyphotic deformity became more severe, initially affecting the anterior funiculus and later extending to the lateral and then the posterior funiculus. Angiography revealed a decrease of the vascular distribution at the ventral side of the compressed spinal cord. CONCLUSIONS: Progressive kyphosis of the cervical spine resulted in demyelination of nerve fibers in the funiculi and neuronal loss in the anterior horn due tochronic compression of the spinal cord. These histologic changes seem to be associated with both continuous mechanical compression and vascular changes in the spinal cord.

Animals↗

Modeling the anxiety-depression continuum hypothesis in domestic fowl chicks.

Anxiety and depression are currently classified as separate clinical syndromes despite considerable similarities in their symptoms, pathophysiological substrates and response to treatment interventions. An alternative hypothesis views anxiety and depression along a temporal continuum, a construct that the current research attempts to model in a preclinical setting. In experiment 1, socially raised domestic fowl chicks separated from conspecifics demonstrated a pattern of distress vocalizations that sequentially models anxiety-like and depressive-like states. In addition, administration of the benzodiazepine anxiolytic chlordiazepoxide and the tricyclic antidepressant imipramine provided pharmacological validation for the model in that they were capable of dissociating the anxiety-like and depressive-like states. In experiment 2, corticosterone levels were quantified across the isolation test session to provide convergent validity to the model. These findings fit well with the human clinical literature on the anxiety-depression continuum perspective, and suggest the consideration of a nosology that emphasizes the inter-relatedness of these clinical states rather than their boundaries.

Animals↗

The relative fracture strengths of the inner and outer surfaces of the eggshell of the domestic fowl.

A method is described for comparing the strength of the material near the inner and outer surfaces of the eggshell of the domestic fowl. Half eggs with blunt poles, obtained by cutting the egg around the equator, were subjected to concentric loading through neoprene O-rings, respectively 7 mm and 15.5 mm diameter. A finite element solution for the stress distribution showed that the point of maximum tensile stress lay on the line of the smaller ring. For downward loading on the smaller ring, the maximum stress occurred on the inner surface of the shell. For upward loading it moved to the outer surface. Upward loading gave a value for the average fracture stress of the outer surface of the shell (27.3 Nmm-2). For downward loading fracture occurred on the outer surface at the larger ring before the fracture stress was reached on the inner surface. This measurement gave a lower bound to the average fracture stress of the inner surface (30.4 Nmm-2). The fracture stress of the inner surface was measured using concentric loading along the axis of the whole egg. The average fracture stress was 36.7 Nmm-2 so the inner surface is 34% stronger than the outer surface.

Animals↗

Sperm mobility determines the outcome of sperm competition in the domestic fowl.

The aim of this study was to establish whether the mobility of sperm of the domestic fowl, as measured by an in vitro assay, predicted the outcome of sperm competition. Thirteen pairs of New Hampshire roosters, comprising one male categorized as having high-mobility sperm and the other as having average-mobility sperm, were used. Each male provided 25 x 10(6) sperm, which were mixed and artificially inseminated into between four and seven New Hampshire hens, each of which produced 2-11 offspring. The experiment was conducted twice, such that the same pair of males inseminated the same females. Paternity was assigned by using microsatellite markers. There was a clear effect of sperm-mobility phenotype on the outcome of sperm competition: in all 13 pairs the high-mobility male fathered the majority of offspring (75.3% overall; p < 0.0001). The proportion of offspring fathered by the high-mobility male within pairs varied significantly between male pairs (p < 0.0005). This effect was associated with the difference in sperm-mobility scores between males within pairs; there was a significant positive relationship between the proportion of offspring fathered by the high-mobility male and the ratio of mobility scores between males (p < 0.05). In addition, compared with their success predicted from the non-competitive situation, in the competitive situation high-mobility males were disproportionately successful in fertilizing eggs compared with average-mobility males. This may occur because female sperm storage is limited in some way and a greater proportion of high-mobility sperm gain access to the female's sperm storage tubules. There was no evidence that female effects accounted for any of the variation in paternity.

Animals↗

Sperm mobility: mechanisms of fertilizing efficiency, genetic variation and phenotypic relationship with male status in the domestic fowl, Gallus gallus domesticus.

When females are sexually promiscuous, sexual selection continues after insemination through sperm competition and cryptic female choice, and male traits conveying an advantage in competitive fertilization are selected for. Although individual male and ejaculate traits are known to influence paternity in a competitive scenario, multiple mechanisms co-occur and interact to determine paternity. The way in which different traits interact with each other and the mechanisms through which their heritability is maintained despite selection remain unresolved. In the promiscuous fowl, paternity is determined by the number of sperm inseminated into a female, which is mediated by male social dominance, and by the quality of the sperm inseminated, measured as sperm mobility. Here we show that: (i) the number of sperm inseminated determines how many sperm reach the female sperm-storage sites, and that sperm mobility mediates the fertilizing efficiency of inseminated sperm, mainly by determining the rate at which sperm are released from the female storage sites, (ii) like social status, sperm mobility is heritable, and (iii) subdominant males are significantly more likely to have higher sperm mobility than dominant males. This study indicates that although the functions of social status and sperm mobility are highly interdependent, the lack of phenotypic integration of these traits may maintain the variability of male fitness and heritability of fertilizing efficiency.

Animals↗

Studies on mutation lesions and physiology of fowl plague virus ts mutants.

Temperature-sensitive (ts) mutants of fowl plague virus (FPV) were divided into six complementation groups. Experiments with ts mutants having defects of transcription showed that in FPV strain Weybridge, protein P1 coded by gene N2 takes part in primary transcription, and protein P3 coded for by gene N1 takes part in secondary transcription. Ts mutants of FPV with lower pathogenicity were present in all six complementation groups under study. Simultaneous inoculation of chickens with two pathogenic ts mutants of FPV caused death of the chickens and a pathogenic virus with ts+ phenotype was isolated from their organs. By recombination of ts multimutant FPV with human influenza virus a recombinant was obtained that contained genes coding for the haemagglutinin and neuraminidase of human influenza virus; all other genes were derived from FPV. In experiments on volunteers this recombinant appeared to be non-reactogenic but capable of inducing antibody formation.

Animals↗

A genetic approach to studies on the synthesis of the complementary RNA's of fowl plague virus.

The rate of incorporation of 5-fluorouracil into complementary strands of replicating RNA of fowl plague virus (FPV) has been studied. The efficiency of incorporation was estimated by determination of the reversion frequency in s-mutants with known types of base transitions in the RNA of the virus particle. It was established that maximum incorporation of 5-fluorouracil into progeny virus particle RNA took place between 2 and 4 h after infection. The maximum incorporation of the mutagen into complementary RNA (plus strands) occurred when the cells were exposed to 5-fluorouracil from 1 to 2 h after infection.

Base Sequence↗

Characterization of virus-specific messenger RNAs from avian fibroblasts infected with fowl plague virus.

In cell-free protein synthesizing systems from wheat embryos, messenger RNAs extracted from chick embryo fibroblasts infected with fowl plague virus direct the synthesis of nine virus-specific polypeptides, two of which may be related to the virus-specific glycopolypeptides. All of the mRNAs are complementary in sequence to virion RNA, and RNAs which do not contain poly A appear to be translated as efficiently as their polyadenylated counterparts. Under certain conditions of incubation, virion RNA also directs the synthesis of discrete polypeptides but these products are not detected in infected cells.

Animals↗

Investigation of recombinants of human influenza and fowl plague viruses.

Recombinants of human influenza type A viruses, A/Krasnodar/101/1959 (H2N2) or A/Habarovsk/15/1976 (H3N2), and fowl plague virus (FPV), strain Weybridge (Hav1Neq1) were obtained. The genome of the recombinant obtained by recombination of influenza A/Habarovsk/15/1976 virus and FPV contained the genes 4 (HA) and 6 (NA) derived from the influenza A/Habarovsk virus and all the other genes [1, 2, 3, 5 (NP), 7 (M), 8 (NS)] from FPV. The genome of the recombinant of A/Krasnodar/101/1959 virus and FPV contained the genes 2, 4 (HA) and 6 (NA) derived from influenza A/Krasnodar virus and all the other genes [1, 3, 5, (NP), 7 (M), 8 (NS)] from FPV. The recombinants, like FPV, gave high virus yields in chick embryos and could multiply at high temperatures (40 and 42 degrees C), but, like human influenza viruses, were non-pathogenic for chickens and did not replicate in chick embryo fibroblast culture, but did replicate in a human conjunctiva cell line, clone 1-5C-4. The virion transcriptase of the recombinants, in a number of properties determined in vitro, was similar to FPV transcriptase but not to the human influenza virus enzyme.

Animals↗

Ultrastructural changes in cells induced by temperature-sensitive mutants of fowl plague virus at permissive and non-permissive temperature.

Ultrastructural changes developing in chick embryo fibroblast cultures infected with a wild-type strain of fowl plague virus (FPV) or one of six FPV temperature-sensitive (ts) mutants belonging to different complementation groups were studied. Cells infected with wild-type FPV and incubated at optimal (36 degrees C) or nonpermissive temperature (42 degrees C) displayed changes similar to those described for orthomyxoviruses. The same patterns of changes were observed at 36 degrees C in cells infected with ts mutants belonging to five of the complementation groups. Mutant ts 303, possessing mutation-altered haemagglutinin, induced at 36 degrees C the formation of virions carrying a considerably reduced number of spikes on their surfaces. At 42 degrees C, cells infected with ts mutant 131, with a defective primary transcription stage, showed no morphological changes and no formation of electron-dense inclusions. Cells infected with ts mutants with defective secondary transcription or replication displayed nuclear inclusions but no formation of filamentous cytoplasmic structures or virions. Mutant ts 5 with defective late morphogenesis induced formation of considerably enhanced numbers of nuclear inclusions.

Animals↗

Productive and abortive infection of L cells by fowl plague virus (FPV): comparison of in vivo and in vitro translation products of the virus mRNAs.

The abortive infection of L cells by the Dobson strain of fowl plague virus (FPV) and the productive infection by a mammalian cell-adapted mutant have been compared. The mRNA population during the abortive cycle is characterized by a lower production compared to the productive system of mRNA 7 (which codes for the M polypeptide) early in the cycle, and a lower production of mRNAs 4, 6 and 7 (which code for HA, NA and M) late in the cycle. Differences in the amounts of the corresponding polypeptides can also be detected when these mRNA populations are used to programme a wheat germ cell-free system. However, analysis of the polypeptides synthesized in vivo by the two viruses show that equivalent amounts of all virus polypeptides are synthesized during the productive and the abortive cycles. Possible reasons for differences between in vivo and in vitro translation of the virus mRNAs during the abortive cycle are discussed.

Animals↗

Evidence for intracistronic complementation of the product of the influenza virus gene Ptra (P3 of fowl plague virus).

The ts lesion of the fowl plague virus (FPV) mutants ts 18 and ts 236 has been located in RNA segment 2 (Ptra gene, corresponding to P3). After double-infection with these mutants and ts 90 or ts 93, which also carry a ts lesion in segment 2, plaques were formed at the non-permissive temperature (40 degrees C). These plaques cannot be passaged at 40 degrees C and exhibit a morphology which differs from those formed by the wild-type virus. The yield of infectious particles after double-infection shows a non-linear correlation between the plaque number and dilution, indicating that at least two particles are needed for infection of a cell. All experimental evidence points to an intracistronic complementation within the P3 protein.

Animals↗

Genotypic and phenotypic characterization of a mammalian cell-adapted mutant of fowl plague virus (FPV).

A mammalian cell-adapted mutant of the Dobson strain of fowl plague virus (FPV-B) was characterized. Genetic analyses of recombinants between a ts mutant of this virus and either the non-adapted Dobson strain or the Rostock strain of FPV showed that the gene coding for the P3 protein of the adapted Dobson strain was sufficient to enable any recombinant to grow in L cells. The abortive cycle of wild-type Dobson strain (FPV+) was compared to the productive cycle of the mutant. By using 100 p.f.u./cell, no quantitative difference could be detected in infected L cells between polypeptides and cRNAs induced by FPV+ and FPV-B. However, the maturation of virions at the plasma membrane did not proceed correctly. At a lower m.o.i. the amounts of virus polypeptides decreased with the m.o.i. This decrease was not the same for all polypeptides and cRNA segments: HA, M and NA and their mRNAs decreased to a greater extent than the others. These results are discussed in relation to a possible biological activity of polypeptide P3.

Animals↗

Extragenic suppression of a ts phenotype during recombination between ts mutants of two fowl plague virus strains with a ts mutation in gene 1.

Fowl plague virus (FPV) ts mutants belonging to six recombination groups and obtained from the Weybridge strain (in the U.S.S.R.) or the Rostock strain (in the U.K.) have been studied in a recombination test. Temperature-sensitive mutants obtained from different FPV strains were revealed which had a ts mutation in gene 1; however, their crossing resulted in ts+ recombinants which appeared with a high frequency. This phenomenon was due not to intragenic complementation but to extragenic suppression, when the expression of a ts phenotype of the Rostock strain mutant gene 1 is suppressed by gene 2 products of the Weybridge strain.

Gene Expression Regulation↗

Studies of fowl plague virus temperature-sensitive mutants with defects in transcription.

Two fowl plague virus temperature-sensitive (ts) mutants belonging to different complementation groups were studied. Both were defective in the syntheses of unpolyadenylated complementary RNA [A(-)cRNA] and virus RNA (vRNA) at non-permissive temperature whereas primary transcription was unaffected. In addition, ts 29, in which the ts mutation is in gene 1 coding for polypeptide P3, has a defect in 'secondary' synthesis of mRNA at non-permissive temperature whereas inhibition of mRNA synthesis by ts 131, in which the ts mutation is in gene 2 coding for polypeptide P1, appeared to result from a defect in vRNA synthesis. These results indicate, therefore, that different enzymes are responsible for the syntheses of virus mRNAs and A(-)cRNAs, which is consistent with the apparent differences in initiation and termination of transcription in the two reactions. The patterns of synthesis of the various types of virus RNA during infection are discussed.

Cycloheximide↗

Temperature-sensitive mutants of fowl plague virus (influenza A) generated by undiluted passages at 33 degrees C.

Temperature-sensitive (ts) mutants obtained by undiluted passages of fowl plague virus at 33 degrees C have their defects located mainly in RNA segments 3, 4 and 8 as determined by rescue to wild-type with standard ts mutants. This result is different from that obtained after treatment of virus with mutagens, where the frequency of mutations follows roughly the target size of the RNA segments. Many isolates generated after undiluted passages at 33 degrees C, which seem to have mutations in RNA segments 3 and 4, can be rescued to wild-type. This occurs, however, with certain defined standard ts mutants having a defect in RNA segment 4, but not by other segment 4 mutants. One such mutant, ts 1/93 (ts defect in segment 3), interferes with the multiplication of ts 227 (ts defect in segment 4) at the permissive temperature, presumably at the level of vRNA synthesis, preventing reassortment to wild-type. Similarly, ts 263 (ts defect in segment 3) interferes with the multiplication of ts 1/1 (ts defect in segment 4). For other such interfering mutants, the mechanism preventing reassortment to wild-type is different from that of ts 1/93 or ts 1/1, but is not yet understood. Thus, the number of mutations as determined by rescue with standard ts mutants in isolates obtained by undiluted passages is overestimated due to intrinsic interference.

Animals↗