A general defect relation and height inequality for divisors in subgeneral position

2018 ◽  
Vol 22 (3) ◽  
pp. 477-492
Author(s):  
Saud Hussein ◽  
Min Ru
Keyword(s):  
Defect Relation ◽  
General Defect

scholarly journals Effect of Transcription Factor GATA-2 on Phagocytic Activity of Alveolar Macrophages from Pneumocystis carinii-Infected Hosts

2003 ◽  
Vol 71 (9) ◽  
pp. 4943-4952 ◽  
Author(s):  
Mark E. Lasbury ◽  
Xing Tang ◽  
Pamela J. Durant ◽  
Chao-Hung Lee
Keyword(s):  
Transcription Factor ◽  
Alveolar Macrophages ◽  
Phagocytic Activity ◽  
Pneumocystis Carinii ◽  
Fluorescein Isothiocyanate ◽  
Cmv Promoter ◽  
Latex Beads ◽  
Expression Construct ◽  
Sense Orientation ◽  
General Defect

ABSTRACT Alveolar macrophages from Pneumocystis carinii-infected hosts are defective in phagocytosis (W. Chen, J. W. Mills, and A. G. Harmsen, Int. J. Exp. Pathol. 73:709-720, 1992; H. Koziel et al., J. Clin. Investig. 102:1332-1344, 1998). Experiments were performed to determine whether this defect is specific for P. carinii organisms. The results showed that these macrophages were unable to phagocytose both P. carinii organisms and fluorescein isothiocyanate (FITC)-conjugated latex beads, indicating that alveolar macrophages from P. carinii-infected hosts have a general defect in phagocytosis. To determine whether this defect correlates with the recently discovered down-regulation of the GATA-2 transcription factor gene during P. carinii infection, alveolar macrophages from dexamethasone-suppressed or healthy rats were treated with anti-GATA-2 oligonucleotides and then assayed for phagocytosis. Aliquots of the alveolar macrophages were also treated with the sense oligonucleotides as the control. Cells treated with the antisense oligonucleotides were found to have a 46% reduction in phagocytosis of P. carinii organisms and a 65% reduction in phagocytosis of FITC-latex beads compared to those treated with the sense oligonucleotides. To determine whether the defect in phagocytosis in alveolar macrophages from P. carinii-infected hosts can be corrected by overexpression of GATA-2, a plasmid containing the rat GATA-2 gene in the sense orientation driven by the cytomegalovirus (CMV) promoter was introduced into alveolar macrophages from P. carinii-infected rats. Aliquots of the same cells transfected with a plasmid containing GATA-2 in the antisense orientation relative to the CMV promoter served as the control. Alveolar macrophages treated with the sense GATA-2 expression construct were found to increase their phagocytic activity by 66% in phagocytosis of P. carinii organisms and by 280% in phagocytosis of FITC-latex beads compared to those that received the antisense GATA-2 construct. The results of this study indicate that GATA-2 plays an important role in the regulation of phagocytosis in alveolar macrophages during P. carinii infection.

Experimental studies on a mutant gene (p) causing premature death of Ambystoma mexicanum embryos

Development ◽  
1977 ◽  
Vol 39 (1) ◽  
pp. 139-149
Author(s):  
Thomas M. Trottier ◽  
John B. Armstrong
Keyword(s):  
Muscle Development ◽  
Experimental Studies ◽  
Circulatory System ◽  
Premature Death ◽  
Mutant Gene ◽  
Ambystoma Mexicanum ◽  
Recessive Lethal ◽  
Homozygous Condition ◽  
General Defect ◽  
Superficial Tissue

The premature death (p) mutation is a recessive lethal, which, in the homozygous condition, gives rise to a complex of abnormalities. The mutant embryos develop only to stage 37, at which time disintegration of superficial tissue begins. Many of the abnormalities observed in sections of the stage-37 mutant embryo are related to its failure to establish a functioning circulatory system, or to the resulting edema and/or ascites that distend the abdomen and flanks. There are, however, abnormalities of heart, liver, gill and muscle development which cannot be attributed to lack of circulation and edema. All of these abnormalities can be indirectly related to the endoderm, particularly the anterior and dorsal endoderm. The findings, therefore, suggest that the mutation leads to a fairly general defect of the endoderm.

scholarly journals Defects on carbons for electrocatalytic oxygen reduction

2018 ◽  
Vol 47 (20) ◽  
pp. 7628-7658 ◽  
Author(s):  
Xuecheng Yan ◽  
Yi Jia ◽  
Xiangdong Yao
Keyword(s):  
Oxygen Reduction ◽  
Active Sites ◽  
Catalysis Mechanism ◽  
Electrocatalytic Oxygen Reduction ◽  
General Defect ◽  
Carbon Based

A general defect promoted catalysis mechanism is established to reveal the active sites of various defective carbon based ORR electrocatalysts.

scholarly journals Unusual late presentation of X-linked chronic granulomatous disease in an adult female with a somatic mosaic for a novel mutation in CYBB

Blood ◽  
2005 ◽  
Vol 105 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Baruch Wolach ◽  
Yitshak Scharf ◽  
Ronit Gavrieli ◽  
Martin de Boer ◽  
Dirk Roos
Keyword(s):  
Nadph Oxidase ◽  
Chronic Granulomatous Disease ◽  
X Chromosome ◽  
Clinical Symptoms ◽  
Novel Mutation ◽  
Late Presentation ◽  
Granulomatous Disease ◽  
Phagocyte Nadph Oxidase ◽  
Mucosal Cells ◽  
General Defect

Abstract Most patients with chronic granulomatous disease (CGD) have mutations in the X-linked CYBB gene that encodes gp91phox, a component of the phagocyte NADPH oxidase. The resulting X-linked form of CGD is usually manifested in boys. Rarely, X-CGD is encountered in female carriers with extreme expression of the mutated gene. Here, we report on a woman with a novel mutation in CYBB (CCG[90-92] → GGT), predicting Tyr30Arg31 → stop, Val in gp91phox, who presented with clinical symptoms at the age of 66. The mutation was present in heterozygous form in genomic DNA from her leukocytes but was fully expressed in mRNA from these cells, indicating that in her leukocytes the X chromosome carrying the nonmutated CYBB allele had been inactivated. Indeed, only 0.4% to 2% of her neutrophils showed NADPH oxidase activity. This extreme skewing of her X-chromosome inactivation was not found in her cheek mucosal cells and is thus not due to a general defect in gene methylation on one X chromosome. Moreover, the CYBB mutation was not present in the DNA from her cheek cells and was barely detectable in the DNA from her memory T lymphocytes. Thus, this patient shows a somatic mosaic for the CYBB mutation, which probably originated during her lifetime in her bone marrow.

scholarly journals Elevating PI3P drives select downstream membrane trafficking pathways

2020 ◽  
pp. mbc.E20-03-0191
Author(s):  
Noah Steinfeld ◽  
Vikramjit Lahiri ◽  
Anna Morrison ◽  
Shree Padma Metur ◽  
Daniel J. Klionsky ◽  
...  
Keyword(s):  
Membrane Trafficking ◽  
Retrograde Transport ◽  
Lipid Kinase ◽  
Phosphoinositide Signaling ◽  
Cellular Processes ◽  
Vacuole Fusion ◽  
General Defect ◽  
Downstream Processes ◽  
The Impact ◽  
Phosphatidylinositol 3

Phosphoinositide signaling lipids are essential for several cellular processes. The requirement for a phosphoinositide is conventionally studied by depleting the corresponding lipid kinase. However, there are very few reports on the impact of elevating phosphoinositides. That phosphoinositides are dynamically elevated in response to stimuli suggests that, in addition to being required, phosphoinositides drive downstream pathways. To test this hypothesis, we elevated the levels of phosphatidylinositol-3-phosphate (PI3P) by generating hyperactive alleles of the yeast phosphatidylinositol 3-kinase, Vps34. We find that hyperactive Vps34 drives certain pathways, including PI(3,5)P2 synthesis and retrograde transport from the vacuole. This demonstrates that PI3P is rate limiting in some pathways. Interestingly, hyperactive Vps34 does not affect ESCRT function. Thus, elevating PI3P does not always increase the rate of PI3P-dependent pathways. Elevating PI3P can also delay a pathway. Elevating PI3P slowed late steps in autophagy, in part by delaying the disassembly of autophagy proteins from mature autophagosomes as well as delaying fusion of autophagosomes with the vacuole. This latter defect is likely due to a more general defect in vacuole fusion, as assessed by changes in vacuole morphology. These studies suggest that stimulus-induced elevation of phosphoinositides provides a way for these stimuli to selectively regulate downstream processes.

Sign in / Sign up

Export Citation Format

Share Document