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G L Henry

Publications and source records attributed to G L Henry.

15 recordsLinked to original sources
PubMed1998

Mixer, a homeobox gene required for endoderm development.

An expression cloning strategy in Xenopus laevis was used to isolate a homeobox-containing gene, Mixer, that can cause embryonic cells to form endoderm. Mixer transcripts are found specifically in the prospective endoderm of gastrula, which coincides with the time and place that endodermal cells become histologically distinct and irreversibly determined. Loss-of-function studies with a dominant inhibitory mutant demonstrate that Mixer activity is required for endoderm development. In particular, the expression of Sox17alpha and Sox17beta, two previously identified endodermal determinants, require Mixer function. Together, these data suggest that Mixer is an embryonic transcription factor involved in specifying the endodermal germ layer.

Animals↗
PubMed1998

MR findings in Shone's complex of left heart obstructive lesions.

BACKGROUND: Shone's complex is a series of four obstructive or potentially obstructive left-sided cardiac lesions (supravalvular mitral ring, parachute deformity of the mitral value, subaortic stenosis, and coarctation of the aorta). Both the complete form (all four lesions) and incomplete forms (less than four lesions) have been described. OBJECTIVE: To determine which abnormalities of Shone's complex could be characterized by MR. MATERIALS AND METHODS: MR examinations in three patients (one complete, two incomplete) were retrospectively reviewed. RESULTS: A supravalvular mitral ring, found at surgery in one patient, was not identified. Regurgitant and stenotic flow across the mitral valve, abnormal motion of the valve leaflets and abnormalities of the papillary muscles were identified. Individual chordal attachments were difficult to resolve. Narrowing in the subaortic region and abnormal flow from the subaortic region through the valve plane were demonstrated. A discrete subaortic diaphragm in one patient was not resolved. Both focal and diffuse types of coarctation of the aorta were well characterized. CONCLUSION: MR imaging is suited to evaluation of patients with Shone's complex. Individual chordal attachments and thin diaphragms of the mitral and aortic valves were difficult to resolve.

Aortic Coarctation↗
PubMed1996

Mechanism of interferon action. Biochemical and genetic evidence for the intermolecular association of the RNA-dependent protein kinase PKR from human cells.

The interferon-inducible protein kinase (PKR) is activated by an RNA-dependent autophosphorylation. Structure-function studies of the 551 amino acid PKR kinase from human cells have revealed that catalytic-deficient PKR mutants such as PKR(1-551)K296R display a dominant negative behavior when expressed in transfected cells. The potential for PKR to form protein multimers has therefore been examined. Three types of studies, including both genetic and biochemical analyses, demonstrated that PKR from human cells undergoes an intermolecular association that is not dependent upon RNA. First, the intermolecular association of PKR in vitro was demonstrated in the context of an enzyme-substrate interaction. Purified recombinant histidine-tagged PKR(1-551)K296R mutant protein was phosphorylated by purified wild-type PKR; this intermolecular phosphorylation of PKR was dependent on double-stranded RNA. At a fixed RNA concentration, high concentrations of the HIS-PKR(1-551)K296R mutant both impaired the autophosphorylation of wild-type PKR and blocked the trans-phosphorylation of itself. Second, the yeast two-hybrid system was used to probe the intermolecular association of PKR in vivo. Coexpression of the full-length catalytic-deficient phosphotransfer mutant PKR(1-551)K296R as a fusion protein with the Gal4 activation domain and the Gal4 DNA binding domain resulted in the expression of two Gal4-responsive reporter genes, HIS3 and lacZ. The full-length RNA-binding deficient PKR(1-551)K64E/K296R double mutant also interacted with PKR(1-551)K296R sufficiently to activate Gal4-responsive reporter genes; however, other PKR mutants including PKR(1-280)wt and PKR(281-551)K296R as well as p53, RAS, and BCL2 did not. Third, both PKR(1-551)K296R and PKR(1-551)K64E/K296R enhanced the expression of the reovirus S1 gene and S1/S4 chimeric gene in cotransfected COS cells. By contrast, the expression of the reovirus S4 gene was not enhanced by cotransfection with either PKR(1-551)K296R or PKR(1-551)K64E/K296R. These results indicate that PKR interacts with itself in an intermolecular manner both in vivo and in vitro, and that RNA binding is neither necessary nor sufficient for PKR multimerization.

Animals↗
PubMed1996

TGF-beta signals and a pattern in Xenopus laevis endodermal development.

We have analyzed two gene products expressed in the early endoderm of Xenopus laevis: Xlhbox-8, a pancreas-specific transcription factor and intestinal fatty acid binding protein (IFABP), a marker of small intestinal epithelium. Expression of the pancreas marker relies on cell signaling mediated by both the TGF-beta and FGF classes of secreted peptide growth factors, whereas, expression of the more posterior small intestinal marker does not. Endodermal explants devoid of mesoderm express both markers in a regionalized manner. Cortical rotation is required for the expression of the more anterior marker, Xlhbox-8, but not for the small intestinal marker, IFABP. These findings suggest that endodermal patterning is dependent, in part, on the same events and signals known to play important roles in mesodermal development. Furthermore, inhibition of TGF-beta signaling in the endoderm leads to ectopic expression of both mesodermal and ectodermal markers, suggesting the TGF-beta signaling may play a general role in the segregation of the three embryonic germ layers.

Animals↗
PubMed1991

Common sense.

Explore the source record for details and available documents.

Adolescent↗
PubMed1989

Drug availability in Jamaica.

The availability of drugs and the supply system in Jamaica were examined. The Jamaica Commodity Trading Company imports all drugs through an international tendering system for the public health sector, and vital drugs for private distributors. For the 18-month period from January 1988, 652 awards were made, consisting of 426 (65%) brand and 226 (35%) generic drugs. There were several strengths and formulations for many drugs, including 19 preparations of 2 antibiotics. The University Hospital of the West Indies (UHWI) has been experiencing recurrent delays in the supply of several important drugs. In contrast, the private hospitals and pharmacies surveyed were adequately supplied. Many brands of several classes of drugs were available, including 51 antibiotics and 18 different anti-inflammatory analgesic and anti-hypertensive agents. However, several drugs used in special situations were only available at the UHWI. There is a need for the supply of drugs to be a priority in the public health sector and for the use of several drugs to be rationalized.

Delivery of Health Care↗
PubMedDate not supplied

Mechanism of interferon action. Translational control and the RNA-dependent protein kinase (PKR): antagonists of PKR enhance the translational activity of mRNAs that include a 161 nucleotide region from reovirus S1 mRNA.

The interferon-inducible, RNA-dependent protein kinase (PKR) is an important regulator of viral protein synthesis. Activated PKR inhibits protein synthesis by phosphorylating initiation factor eIF-2 alpha. The reovirus S4 gene, whose 1196 nucleotide mRNA transcript does not activate the PKR kinase, is efficiently expressed in vector-transfected monkey COS cells. By contrast, the 1463 nucleotide S1 gene of reovirus, which is a potent activator of PKR, is poorly expressed in COS cells. Virus genetic engineering was therefore used to examine the effect of the PKR activator sequence from the reovirus S1 gene on the expression of chimeric genes of reovirus in transfected COS cells. Chimeric S1/S4 and S4/S1/S4 reovirus constructions that included the PKR activator sequence from S1 in the sigma 3 ORF of S4 were expressed much less efficiently than wild-type S4. However, expression of sigma 3 from S4 (3'UTR/S1), which included the PKR activator sequence from S1 within the 3'-UTR of S4, was comparable to that from wild-type S4. Treatment of COS cells with 2-aminopurine, an inhibitor of PKR, increased the expression of the reovirus S1, S1/S4, and S4/S1/S4 chimeric genes but not the S4 gene or S4 (3'UTR/S1) chimera in transfected COS cells. Likewise, coexpression of the phosphotransfer-negative mutant PKR (K296R) increased the expression of reovirus S1, S1/S4 and S4/S1/S4 chimeric genes but not the S4 gene or S4 (3'UTR/S1) chimera in cotransfected COS cells. Truncated PKR(1-243) which includes the dsRNA binding domain but not the kinase catalytic subdomains was able to enhance the expression of reovirus S1, but did not affect S4 expression. The dsRNA binding protein E3L encoded by vaccinia virus also increased S1 expression similar to PKR (1-243) and PKR(K296R). These results suggest that the translational repression in vivo mediated by PKR is selective for mRNAs that possess the kinase activator region, and that the dominant negative effect of PKR on gene expression is likely mediated by the RNA binding activity of the PKR protein.

2-Aminopurine↗