Biomedical subjects

X Ye

Publications and source records attributed to X Ye.

At least 145 records · Page 8Linked to original sources

PubMed1998

Regulatory effects of soluble growth factors on choriocapillaris endothelial growth and survival.

The effects of soluble growth factors on regulating the survival and growth of choriocapillaris endothelial (CCE) cells were investigated in vitro. CCE cells were cultured in a serum-free medium in the presence or absence of various soluble growth factors. Cell growth and cell viability were assessed by counting viable cells. Results showed that acidic fibroblast growth factor (aFGF), basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) significantly stimulated CCE growth in a dose-dependent manner. Platelet-derived growth factor BB (PDGF, 0.4-10 ng/ml), insulin-like growth factor (IGF, 0.4-10 ng/ml) or insulin (0.4-10 micrograms/ml) alone did not affect the growth of CCE cells. In the presence of insulin (10 micrograms/ml), however, PDGF stimulated CCE growth in a dose-dependent manner. By contrast, transforming growth factor beta 1 (TGF-beta 1) induced CCE death in the absence of other growth factors and inhibited the CCE growth induced by aFGF, bFGF or VEGF. When CCE cells had been cultured in media containing aFGF, bFGF, VEGF or the combination of PDGF and insulin for 48 h, withdrawal of aFGF, bFGF or VEGF, but not PDGF, from the media resulted in CCE death. The CCE death induced by either an introduction of TGF-beta 1 or withdrawal of aFGF, bFGF or VEGF was defined as apoptosis based on morphologic characteristics (condensation and fragmentation of nuclei, shrinkage of cells in size) and DNA fragmentation in multiples of approximately 180 base pairs. Phorbol 12-myristate 13-acetate (PMA, 2 or 5 nM) protected CCE cells against apoptosis induced by the introduction of TGF-beta 1 and withdrawal of aFGF, bFGF or VEGF, while H7 (50 microM), but not HA1004 (50 microM), abrogated the protective effect of PMA on CCE apoptosis. However, cycloheximide (0.1 microM), a protein synthesis inhibitor, was only effective to protect CCE cells from apoptosis induced by aFGF, bFGF or VEGF withdrawal, but not that induced by the introduction of TGF-beta 1. Moreover, cycloheximide and a low concentration of PMA (2 nM) showed an additive effect on protecting CCE cells from apoptosis as the result of a growth factor withdrawal. These data may suggest that some growth factors, such as aFGF, bFGF, VEGF and TGF-beta 1, play a more critical role than the others, such as PDGF and IGF, in the regulation of CCE growth and survival. CCE apoptosis as a result of withdrawal of a survival factor or of receiving a death factor such as TGF-beta 1 may involve different mechanisms, which merits further study.

Animals↗

PubMed1998

Astrocytosis and proliferating cell nuclear antigen expression in brains of scrapie-infected hamsters.

Scrapie is a neurodegenerative disease in sheep and goats. Neuropathological examination shows astrocytosis. One issue is whether the astrocytosis seen in scrapie is a function of an increase in reactivity of individual cells, or whether there is actual replication of astrocytes. We used double-label immunohistochemistry for proliferating cell nuclear antigen (PCNA) and for glial fibrillary acidic protein (GFAP) to determine the mitotic state of cells and to confirm their identity as astrocytes. Brain sections from hamsters (strain LVG/LAK) infected with 139H or 263K scrapie isolates were examined. GFAP immunostaining was increased in astrocytes in most regions of the brains of scrapie-infected hamsters. These qualitative observations were confirmed by computerized image analysis quantification. A proportion of the hypertrophic astrocytes (0.5-10.8%, depending on specific location) were PCNA immunoreactive. The PCNA-immunopositive astrocytes were most frequently found in cerebral cortex, corpus callosum, subependymal areas, fimbria, caudate, thalamus, hypothalamus, hippocampus, and dentate gyrus. Our results suggest that the astrocytosis seen in scrapie-infected animals is, at least in part, owing to actual replication of astrocytes in these animals. We hypothesize that the astrocytes may be an important locus for the disease process.

Animals↗

PubMed1998

Analysis of a 69-kb contiguous genomic sequence at a putative tumor suppressor gene locus on human chromosome 6q27.

Multiple neoplasias including B-cell non-Hodgkin's lymphoma, breast carcinoma, and ovarian carcinoma, have been associated with frequent deletions of the distal region on the long arm of human chromosome 6, suggesting the presence of one or more tumor suppressor gene(s) at this locus. Loss of heterozygosity analysis of breast and ovarian tumors has further restricted the minimal region of loss within 6q27. To further characterize this genomic region for gene content including putative tumor suppressor genes as well as other elements that may contribute to tumorigenesis, a 68940-bp contiguous sequence, encompassing markers D6S193 and D6S297, was generated by random shotgun sequencing of a cosmid, P1, and PAC contig. In addition, exon trapping was performed utilizing a subset of these clones. Sixteen trapped exons, ranging in size from 44 to 399 bp, span this approximately 69-kb region. Many other putative exons have been identified computationally. Further analysis has identified 13 potential promoters and 13 putative polyadenylation sites in the region. Northern analysis identified a transcript mapping within this interval that is expressed in ovarian, breast, and lymphoid-derived tumor cell lines. Consideration of these data, together with the demonstration of several regions of high CpG content, suggests the possibility of several genes at this locus.

Alu Elements↗

PubMed1998

[Cervical necrotizing fasciitis].

Necrotizing fasciitis is a severe fatal soft tissue infection characterized by necrosis of fascia. It was caused by polymicrobial infections with aerobe and anaerobe. Although it commonly involved abdomen, extremities and perineum, it might also occur in head and neck. One case of CNF arising from pharyngolaryngitis was reported. A review of the literature with the clinical presentations, bacteriology, diagnosis and treatment was presented. The key to successful management is early recognition, broad-spectrum antibiotics and prompt aggressive surgical intervention with medical support and hyperbaric oxygen therapy.

Fasciitis, Necrotizing↗

PubMed1998

[Effect of neurotoxin on spinal cord injury in rats].

OBJECTIVE: To elucidate the effect of neurotoxin, excitatory amino acid and neuropeptide on spinal cord injury post trauma. METHODS: We detected the changes of concentration of EAA, glutamate(Glu) and aspartate(Asp) at injured segment tissue after spinal cord injury. Changes in dynorphin DynA1-13, an endogenous opioid, immnoreactivity following traumatic spinal cord injury in the rat were examined. We observed the effects of Glu and dynorphin DynA1-13 administered intrathecally on function of spinal cord in rats and the effects of 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP), an antagonist of EAA receptor, and antisera against dynorphin administered intrathecally on secondary spinal cord injury. RESULTS: The concentrations of EAA and dynorphin DynA1-13 increased progressively along with the severity of injury, and were related to injury time. Glu exacerbated the extent of spinal cord injury. Dynorphin DynA1-13 administered intrathecally caused dose-related hindlimb paraplysis in rats, whereas CPP and antisera against dynorphin DynA1-13 were found to have protective effect on spinal cord injury. CONCLUSION: These findings further support the potential pathophysiological role of EAA and dynorphin DynA1-13 as neurotoxin in spinal cord injury.

Animals↗

PubMed1998

[The development of computer-assisted gastric function testing system].

This paper introduces a system consisting of the PC computer, sensing device, the card for electro-gastric signals amplifier and analog-digital converter. By using only one piece of 1.2 M 3" diskette, the system can realize the dialogue between human and the computer to sample, process, store and display the electro-gastric signals, and print the auxiliary analysis and diagnostic results for doctors to refer to. When the computer is more and more popular today, it is one of the convenient, painless and effective method to check up the gastric functional disease.

Adult↗

PubMed1998

[Determination of polyamines in pyronaridine-sensitive and -resistant Plasmodium berghei-infected erythrocytes].

AIM: To understand the relationship between polyamine metabolism and pyronaridine resistance of malaria parasites. METHODS: Kunming strain mice weighing 18 g-22 g were inoculated intraperitoneally with Plasmodium berghei ANKA strain (pyronaridine-sensitive, PS), and P. berghei ANKA strain low and high pyronaridine resistant lines (PRA and PRB), respectively. Seven days after inoculation, blood samples were collected and WBC in the blood were removed by the method of chromatography using SE-cellulose and Sephadex G25 (1:2). After thin layer chromatography, the contents of three polyamines, i.e. putrescine(PTC), spermidine (SPD), and spermine(SPM) in normal and infected erythrocytes were determined with fluorescence spectrometer. The changes of polyamine level in PS and PRB infected erythrocytes of mice treated by a single oral dose of PND 5 and 10 mg/kg respectively were also observed. RESULTS: The contents of PTC, SPD and SPM in PS infected erythrocytes were 47.5 +/- 28.6, 97.7 +/- 34.0 and 81.7 +/- 23.8 nmol/10(9) RBC (n = 9), respectively, being 1.5, 3.5, and 6.6 times of those appeared in the normal RBC (32.0 +/- 9.9, 28.2 +/- 12.3, and 12.4 +/- 15.0 nmol/10(9) RBC, n = 9), respectively. The differences between two groups were significant. Interestingly, when mice infected with pyronaridine resistant line PRA and PRB, the contents of PTC, SPD and SPM in the infected erythrocytes increased to 187.7 +/- 139.9, 258.3 +/- 137.9 and 142.8 +/- 143.8 nmol/10(9) RBC (n = 18), and 345.5 +/- 223.0, 435.8 +/- 265.4 and 189.4 +/- 171.7 noml/10(9) RBC, respectively. Except for SPM, PTC and SPD in the PRA and PRB infected erythrocytes were significantly higher than those in the PS and PRA infected erythrocytes, respectively, being 3.9, 2.6 and 1.8, 1.7 times of those appeared in PS and PRA infected erythrocytes. In PND treated group, SPD and SPM contents of PS infected erythrocytes were decreased by 31.6% and 47.3% compared with non-treated group, but the polyamine level of PRB infected erythrocytes did not significantly change after PND administration. CONCLUSION: The resistance of P. berghei to PND is related to the alteration of polyamine metabolism in the malarial parasites.

Animals↗

PubMed1998

Expression of apoptosis regulatory genes by retinal pericytes after rapid glucose reduction.

PURPOSE: Retinal capillary pericytes underwent apoptosis in vitro after they had been exposed long-term to high levels of glucose followed by a rapid glucose reduction. The present work was designed to study the expression of bcl-2 family members and apoptosis regulatory genes and to determine the status of oxidative stress induced by high concentrations of glucose in this in vitro apoptosis model. METHODS: Pericytes were grown in normal or high glucose concentrations (5, 20, 30, and 40 mM) for 10 days and then exposed to a rapid reduction of glucose to 0.5 mM or 5 mM. Pericyte cell death was evaluated by determining the loss of cell viability and the fragmentation of DNA using agarose gel electrophoresis. In parallel, the quantitative reverse transcription-polymerase chain reaction technique was used to determine the expression of bcl-2, bax, p53, and glutathione peroxidase (GSH-Px) genes. The intracellular level of glutathione (GSH) and the DNA fragmentation were determined simultaneously for pericytes treated with or without exogenous GSH monoethylester. Retinal capillary endothelial cells, experiencing the same glucose variation, were studied as a comparison. RESULTS: For pericytes, downregulation of bcl-2 was observed as early as 24 hours after rapid glucose reduction, whereas DNA fragmentation was not detectable at that time. After 72 hours, a decreased protein ratio of Bcl-2 to Bax was concomitant to evident loss of pericyte viability. During the period of high glucose and the following glucose reduction, p53 expression essentially was unchanged. Decreased levels of GSH induced by high concentrations of glucose (>30 mM) became further depleted when the glucose levels were rapidly reduced. Addition of GSH monoethylester to the medium restored the level of GSH in pericytes and prevented pericyte apoptosis induced by glucose variation. Moreover, the mRNA levels of GSH-Px were significantly elevated. By contrast, with the same glucose reduction endothelial cells did not undergo apoptosis. Their mRNA levels of bcl-2, bax, and GSH-Px essentially were unchanged. CONCLUSIONS: High levels of glucose and rapid reduction of glucose modulate the expression of bcl-2 family genes in retinal pericytes. Upregulation of GSH-Px and depletion of GSH indicate a reparative process of accelerated elimination of reactive oxygen species following rapid glucose reduction. These findings indicate that the aggravated oxidative stress and the weakened antioxidant defense induced by the combined effects of high levels of glucose and subsequent rapid glucose reduction cause pericyte apoptosis. Prevention of DNA fragmentation of pericytes by exogenous GSH further supports this notion. Because endothelial cells did not show similar pathologic changes, this proposed mechanism seems to be specific to pericytes.

Animals↗

PubMed1998

Parallel comparative trial of amlodipine and nitrendipine monotherapy in patients with essential hypertension.

OBJECTIVES: To compare the blood pressure effects of two dihydropyridine calcium channel blockers, amlodipine and nitrendipine, in 488 patients with essential hypertension. METHODS: The study used a randomized, single-blind design of 4 weeks' duration conducted at four medical centres in China. Patients were randomized to receive either amlodipine monotherapy (5-10 mg once daily; n = 334) or nitrendipine (10 mg twice or three times daily; n = 1 54). Blood pressure was evaluated by standard blood pressure measurements before and after treatment, and by 24 h ambulatory blood pressure monitoring in a subgroup of patients (n = 18). RESULTS: Both systolic and diastolic blood pressures were reduced from baseline after 4 weeks of amlodipine and nitrendipine monotherapy. Diastolic blood pressure was reduced by 14.4% in the amlodipine group, which was significantly better than the 13.0% reduction in the nitrendipine group (P< 0.05). In addition, blood pressure response rates were significantly better with amlodipine monotherapy than with nitrendipine monotherapy. In the subgroup of patients undergoing 24 h ambulatory blood pressure monitoring, both systolic and diastolic blood pressure were reduced from baseline in the amlodipine and nitrendipine groups. Adverse effects were generally mild, with dizziness, flushing, palpitation, headache, drowsiness and ankle oedema being the most common. Rushing and headache were more frequent in the nitrendipine group than in the amlodipine group (P< 0.05 for flushing and P<0.01 for headache). CONCLUSIONS: Amlodipine monotherapy reduced blood pressure more effectively than nitrendipine monotherapy in patients with essential hypertension and was associated with fewer adverse events.

Adult↗

PubMed1997

Suppression of cytochrome P450 Cyp2f2 mRNA levels in mice by the peroxisome proliferator diethylhexylphthalate.

Exposure to peroxisome proliferators, which are extensively used, causes a number of pleiotrophic effects. Prolonged exposure to the peroxisome proliferator, DEHP, causes hepatic hyperplasia and liver tumors in rats and mice. This exposure can also induce a number of enzymes. To identify additional genes that are regulated by DEHP, mRNA differential display was used. One of the genes affected is cytochrome 450 Cyp2f2, a naphthalene hydroxylase. Using northern analysis, RNase protection assay, and RT-PCR, we show that the Cyp2f2 mRNA levels are decreased in mouse liver following DEHP treatment. A smaller Cyp2f2 mRNA transcript was also detected in kidney and these transcript levels were also suppressed but to a lesser extent than that in the liver. The response to DEHP in mouse liver is both dose and time dependent.

Animals↗

PubMed1997

Excitotoxic mechanisms of neurodegeneration in transmissible spongiform encephalopathies.

Endogenous excitatory amino acids (EAAs) such as glutamic or aspartic acids have been proposed to mediate the brain damage to EAA receptor-rich brain sites that is caused by a variety of external toxic agents (glutamic acid, domoic acid, kainic acid, ibogaine, trimethyltin (TMT), 3-nitropropionic acid (3-NPA)), as well as from such naturally-occurring age-related neurodegenerative diseases as Alzheimer's disease, Huntington's chorea, and Parkinson's disease. Sites often damaged include the hypothalamus (glutamate), the hippocampal and neocortical pyramidal neurons (domoic acid), the cerebellar Purkinje neurons (ibogaine) and the corpus striatum (3-NPA, amphetamine). The excitotoxic damage occurs to neuronal cell bodies and their dendrites, resulting in a characteristics appearance of pyknotic neurons surrounded by their vacuolated, swollen dendrites. Axons passing through the region that lack EAA receptors are completely spared. However, astrocytes with swollen perikarya and nuclei (Alzheimer's type II "reactive" astrocytes) are often observed in the vicinity of the lesions. Animal and human "Prion Diseases" or "Transmissible Spongiform Encephalopathies" (TSEs) result (after a period of months to years) in a neurodegenerative picture characterized by pyknotic neurons surrounded by vacuoles with numerous reactive astrocytes in the vicinity of the damage. In addition, amyloid deposits composed of a protease-resistant protein (PrPSc) characteristic of the particular host species with the disease are found near the degenerating neurons. By using different strains of the scrapies TSE agent to inoculate hamsters and mice, reproducible models of hypothalamic, hippocampal, or cerebellar damage resulting in the appropriate functional deficits may be obtained. Because of the close similarity in the appearance, localization, and functional consequences from TSE neuropathology compared to some of the well-known EAA syndromes, we propose that excitotoxic mechanisms may play a role in the pathogenesis of TSE neurodegenerative diseases. The similarity in pathogenesis of the neurodegenerative processes in excitotoxicity compared to TSE diseases also implies that neuroprotective strategies against excitotoxicity may also be effective against TSEs.

Animals↗

PubMed1997

In vivo inhibition of nuclear factor-kappa B activation prevents inducible nitric oxide synthase expression and systemic hypotension in a rat model of septic shock.

We determined the in vivo function of LPS-induced nuclear factor-kappa B (NF-kappa B) activation in mediating inducible nitric oxide synthase (iNOS) mRNA and protein expression, and systemic arterial hypotension in a rat model of septic shock. LPS (8 mg/kg i.v.) challenge of rats activated NF-kappa B within 15 min in lung tissue, and the response persisted up to 4 h. NF-kappa B activation preceded the induction of iNOS mRNA. Pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kappa B effective in cellular studies, prevented NF-kappa B activation in vivo and reduced iNOS mRNA expression and the increase in iNOS activity activated by LPS. At PDTC concentrations of 50, 100, and 200 mg/kg, the reductions of iNOS mRNA were 20, 46, and 48%, and the reductions in iNOS activity were 59, 66, and 75%, respectively. The PDTC concentration-dependent reductions in iNOS activity produced similar decreases in plasma nitrite/nitrate concentrations. PDTC also prevented the decrease in arterial blood pressure induced by LPS. These results demonstrate that activation of NF-kappa B is a critical in vivo regulatory mechanism mediating LPS-induced iNOS expression and the resultant systemic hypotension.

Animals↗

PubMed1997

Cloning and gene mapping of the chromosome 13q14 region deleted in chronic lymphocytic leukemia.

Frequent deletions and loss of heterozygosity in a segment of chromosome 13 (13q14) in cases of B-cell chronic lymphocytic leukemia (CLL) have suggested that this malignancy is caused by inactivation of an unknown tumor suppressor gene located in this region. Toward the identification of the putative CLL tumor suppressor, we have constructed a high-resolution physical map of YAC, PAC, and cosmid contigs covering 600 kb of the 13q14 genomic region. In addition to densely positioned genetic markers and STSs, this map was further annotated by localization of 32 transcribed sequences (ESTs) using a combination of exon trapping, direct cDNA selection, sample sequencing of cosmids and PACs, and homology searches. On the basis of these mapping data, allelic loss analyses at 13q14 using CLL tumor samples allowed narrowing of the genomic segment encompassing the putative CLL gene to <300 kb. Twenty-three ESTs located within this minimally deleted region are candidate exons for the CLL-associated tumor suppressor gene.

Alleles↗

PubMed1997

Molecular characterization of p62, a mitotic apparatus protein required for mitotic progression.

A 62-kDa (p62) mitotic apparatus-associated protein is important for the proper progression of mitosis in sea urchin embryos (Dinsmore, J. H., and Sloboda, R. D. (1989) Cell 53, 769-780). We have isolated and characterized a full-length p62 cDNA of 3374 base pairs which encodes an extremely acidic polypeptide of 411 amino acids having a calculated Mr of 46,388 and a pI of 4.01; p62 is a unique protein with no significant identity to any known proteins. Southern and Northern blot analyses demonstrate that the gene for p62 is present once in the sea urchin genome and the corresponding mRNA is present in unfertilized eggs and in early embryos through and up to the gastrula stage. Sequence analysis suggests certain regions may participate in chromatin association and microtubule binding, an observation that is consistent with previous immunological data (Ye, X., and Sloboda, R. D. (1995) Cell Motil. Cytoskeleton 30, 310-323) as well as data reported herein. Confocal microscopy reveals that during interphase the protein binds to chromatin in the nuclei of sea urchin eggs. In the germinal vesicles of clam oocytes at prophase of meiosis I, p62 binds to the condensed chromosomes. Currently, truncated clones of p62 are being used to identify the tubulin and chromatin binding domains.

Amino Acid Sequence↗

PubMed1997

Extracellular matrix of retinal pigment epithelium regulates choriocapillaris endothelial survival in vitro.

The role of extracellular matrix of retinal pigment epithelial cells (RPE-ECM) in the regulation of the survival of choriocapillaris endothelial cells (CCE) was investigated in vitro. The CCE survival was evaluated by trypan blue staining, neutral red uptake, and the counting of viable cells. Results showed that CCE cells survived on RPE-ECM. Pre-treatment of RPE-ECM individually with neutralizing antibodies to acidic fibroblast growth factor, vascular endothelial growth factor, platelet-derived growth factor, or transforming growth factor beta(pan specific to TGFbeta1, TGFbeta1.2, TGFbeta2 and TGFbeta5), did not alter the survival rate of CCE cells on RPE-ECM, as compared to that of the control (CCE survival rates on RPE-ECM pretreated with normal rabbit IgG). However, the treatment of RPE-ECM with neutralizing antibody to basic fibroblast growth factor (bFGF) caused CCE death by 77.1+/-15.7%. The CCE death was defined as apoptosis based on the morphological markers (shrinkage in cell size with blebbing of plasma membranes, condensation and fragmentation of nuclei, and DNA fragmentation in multiples of approximately 200 bp). The addition of phorbol 12-myristate 13-acetate (PMA) (2 nM) to the culture medium was effective for complete prevention of CCE apoptosis; the protecting effect of PMA on CCE apoptosis can be abolished by H7 (25 microM), but not HA1004 (50 microM), suggesting the involvement of PKC in protecting CCE from apoptosis. The inhibition of protein synthesis of CCE cells by cycloheximide (0.1 microM) did not affect the apoptotic process of the cells. In a separate experiment, when CCE cells were cultured in a medium saturated with bFGF (5 ng ml-1) without RPE-ECM, the cells also died by apoptosis. However, this apoptotic process was not affected by PMA. Cycloheximide also failed to affect the apoptotic process. These results suggest that both RPE-ECM insoluble molecules and RPE-ECM-bound bFGF modulate choriocapillaris survival by suppressing CCE apoptosis.

Animals↗

PubMed1997

TWH regulates the development of subsets of spinal cord neurons.

Thymocyte winged helix (TWH) is a putative transcription factor expressed in the developing neural tube. At midgestation, TWH expression identifies subsets of spinal cord motor neurons and interneurons. TWH-expressing motor neurons were restricted to specific spinal cord levels, distinguishing motor neurons at lumbar from those at cervical levels. To understand the developmental role of TWH, we replaced the TWH gene with the lacZ reporter gene and generated mice with a homozygous disruption of the TWH gene. TWH(-/-) mutant mice had increased perinatal mortality, retarded postnatal growth, and motor weakness. The TWH(-/-) mutation resulted in alterations in the sizes and position of different neuronal populations. Our results demonstrate that TWH plays a critical role in neuronal development and suggest that TWH regulates the early differentiation of neural progenitors.

Animals↗

PubMed1997

Influence of crossing a line selected for increased shank width and a commercial sire line on performance and walking ability of turkeys.

The present study was initiated to determine whether walking ability (WA) could be markedly improved without seriously compromising growth rate and body conformation by crossing a relatively unimproved commercial sire line (UC) with a line (FL) selected for increased shank width and backcrossing F1 females to UC line males. Body weights at 8, 16, and 20 wk of age were generally similar for both lines at the time of the initial cross. The UC line had inferior WA, shorter and narrower shanks, and wider breasts compared with the FL line. The F1 birds exhibited overdominance for BW at all ages. Heterosis in BW ranged from 3.2 to 7.8%. At 16 wk of age, the WA scores decreased (indicating improved WA) in the F1 relative to the average of the parental lines. Heterosis of WA scores was -10.5% (P > or = 0.05) for males and -23.5% (P < or = 0.05) for females. Heterosis was observed in the F1 for shank length but not for other shank measurements (width and depth). No heterosis was observed for breast width. Mortality from 8 through 20 wk of age was reduced in the F1 relative to the parental lines. The backcross of the F1 females to UC males still exhibited heterosis for male BW at 16 and 20 wk of age and for WA scores, although the magnitude was reduced 50% or more. Mortality from 8 to 20 wk of age decreased in the backcross compared with the parental lines. The results suggest that a line exhibiting improved leg structure and WA, and poor conformation, such as FL, can be used to greatly improve the WA of a cross involving a sire line with poor WA but excellent conformation. A portion of the gains in BW and breast width obtained in the F1 was retained in a backcross to the sire line, making such a crossing scheme commercially feasible.

Animals↗

PubMed1997

Ultrabithorax and Antennapedia 5' untranslated regions promote developmentally regulated internal translation initiation.

The 5' untranslated regions (UTRs) of the Drosophila Ubx and Antp genes were tested for their ability to promote cap-independent translation initiation. The Ubx and the Antp 5' UTR were inserted between the CAT and lacZ coding sequences in a dicistronic gene and tested for IRES activity in transgenic Drosophila. Northern analysis of the mRNAs showed the presence of the predicted full-length dicistronic mRNAs. High CAT activity was expressed from the first cistron from all of the dicistronic constructs introduced into the fly genome. The dicistronic transgenic strains bearing the Ubx and Antp IRES elements expressed significant levels of beta-galactosidase (betaGAL) from the second cistron whereas little or no betaGAL was expressed in the controls lacking the IRESs. In situ analysis of betaGAL expression in the transgenic strains indicates that expression of the second cistron is spatially and temporally regulated. Although the developmental patterns of expression directed by the Antp and Ubx IRESs overlap, they exhibit several differences indicating that these IRESs are not functionally equivalent.

Animals↗