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1. |
Control strategies in physiological systems |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 97-107
James C. Houk,
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摘要:
In this paper, written for a general audience, I review and contrast various strategies that the body uses to control homeostasis and movement. Messages, signals, communication channels, and control systems are dealt with from both a cellular and an integrative perspective. The major global control strategies are feedback, feedforward, and adaptive control, and examples of each are presented to highlight advantageous and disadvantageous features. Many physiological systems use these three strategies in combination.— Houk, J. C. Control strategies in physiological systems.FASEB J.2: 97‐107; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.3277888
出版商:Wiley
年代:1988
数据来源: WILEY
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2. |
Biology of interleukin 1 |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 108-115
Charles A. Dinarello,
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摘要:
Interleukin 1 (IL 1) is a polypeptide that is produced after infection, injury, or antigenic challenge. Although the macrophage is a primary source of IL 1, epidermal, epithelial, lymphoid, and vascular tissues synthesize IL 1. When IL 1 gains access to the circulation, it acts like a hormone and induces a broad spectrum of systemic changes in neurological, metabolic, hematologic, and endocrinologic systems. Some of the IL 1 that is synthesized remains associated with the plasma membrane and induces changes in local tissues without producing systemic responses. IL 1 affects mesenchymal tissue remodeling where it contributes to both destructive and repair processes. IL 1 activates lymphocytes and plays an important role in the initiation of the immune response. Receptors for IL 1 have been identified, but receptors are scarce and their affinities often do not match the potency of the biological response. The most consistent property of IL 1 is up‐regulation of cellular metabolism and increased expression of several genes coding for biologically active molecules. IL 1 is a highly inflammatory molecule and stimulates the production of arachidonic acid metabolites. IL 1 also acts synergistically with other cytokines, particularly tumor necrosis factor. The multitude of biological responses to IL 1 is an example of the rapid adaptive changes that take place to increase the host's defensive mechanisms.—Dinarello, C. A. Biology of interleukin 1.FASEB J.2: 108‐115; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.3277884
出版商:Wiley
年代:1988
数据来源: WILEY
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3. |
Hemostatic properties of normal and perturbed vascular cells |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 116-123
George M. Rodgers,
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摘要:
Vascular endothelial and smooth muscle cells actively maintain vessel wall thromboresistance by expressing several antithrombotic properties. With perturbation or injury, vascular cells express thrombogenic properties. Loss of vessel wall thromboresistance may be associated with thrombosis and vascular disease.— Rodgers, G. M. Hemostatic properties of normal and perturbed vascular cells.FASEB J,2: 116‐123; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.3277885
出版商:Wiley
年代:1988
数据来源: WILEY
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4. |
Molecular basis of bacterial resistance to organomercurial and inorganic mercuric salts |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 124-130
Christopher T. Walsh,
Mark D. Distefano,
Melissa J. Moore,
Lisa M. Shewchuk,
Gregory L. Verdine,
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摘要:
Bacteria mediate resistance to organomercurial and inorganic mercuric salts by metabolic conversion to nontoxic elemental mercury, Hg(0). The genes responsible for mercury resistance are organized in themeroperon, and such operons are often found in plasmids that also bear drug resistance determinants. We have subcloned three of thesemergenes,merR, merB,andmerA,and have studied their protein products via protein overproduction and purification, and structural and functional characterization. MerR is a metallo‐regulatory DNA‐binding protein that acts as a repressor both its own and structural gene transcription in the absence of Hg(II); in addition it acts as a positive effector of structural gene transcription when Hg(II) is present. MerB, organomercury lyase, catalyzes the protonolytic fragmentation of organomercurials to the parent hydrocarbon and Hg(II) by an apparent SE2 mechanism. MerA, mercuric ion reductase, is an FAD‐containing and redox‐active disulfide‐containing enzyme with homology to glutathione reductase. It has evolved the unique catalytic capacity to reduce Hg(II) to Hg(0) and thereby complete the detoxification scheme.—Walsh, C. T.; Distefano, M. D.; Moore, M. J.; Shewchuk, L. M.; Verdine, G. L. Molecular basis of bacterial resistance to organomercurial and inorganic mercuric salts.FASEB J.2: 124‐130; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.3277886
出版商:Wiley
年代:1988
数据来源: WILEY
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5. |
Potential mechanisms mediating postprandial renal hyperemia and hyperfiltration |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 131-137
Andre J. Premen,
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摘要:
Although the existence of postprandial renal hyperemia and hyperfiltration has been established, the precise mechanism governing protein‐mediated increases in renal hemodynamics is not, as yet, clearly defined. Investigative effort over the past decade has provided at least two plausible mechanisms playing an important role in renal hyperemia and hyperfiltration associated with ingestion of a protein‐rich meal:1) blood‐borne vasoactive agents (e.g., pancreatic glucagon and/or hepatic glomerulopressin); and2) intrarenal mechanisms (e.g., the tubuloglomerular feedback system). Data supporting each of these two candidate mechanisms are reviewed as are data supporting the importance of other factors such as renal prostanoids, the renin‐angiotensin system, and renal cyclic nucleotides. It is anticipated that future investigative effort will be stimulated by our present knowledge of postprandial renal hemodynamics so that one day we not only will know the precise mechanisms governing postprandial renal hyperemia and hyperfiltration but, in addition, may gain valuable insight into the pathogenesis of chronic renal disease.— Premen, A. Potential mechanisms mediating postprandial renal hyperemia and hyperfiltration.FASEB J.2: 131‐137; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.3277887
出版商:Wiley
年代:1988
数据来源: WILEY
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6. |
Identification ofN‐(2‐propenal) serine as a urinary metabolite of malondialdehyde |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 138-140
Mary Hadley,
H. H. Draper,
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摘要:
N‐2‐(Propenal) serine (S‐MDA) was synthesized by reacting serine with malondialdehyde (MDA) and was shown to be a 1:1 adduct of the starting materials. The synthetic compound was found to be identical to a metabolite of MDA excreted in rat and human urine. The identity of the metabolite was confirmed by isolation and hydrolysis to yield equimolar quantities of serine and MDA. The presence of S‐MDA in urine constitutes direct evidence for oxidative decomposition of phospholipids by lipid peroxidation in vivo.— Hadley, M.; Draper, H. H. Identification ofN‐(2‐propenal) serine as a urinary metabolite of malondialdehyde.FASEB J.2: 138‐140; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.3125082
出版商:Wiley
年代:1988
数据来源: WILEY
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7. |
Induction of helper and suppressor T cells by nonoverlapping determinants on the large protein antigen, β‐galactosidase |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 141-145
Urszula Krzych,
Audree V. Fowler,
Alexander Miller,
Eli E. Sercarz,
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摘要:
The fine specificity of the T cell repertoire directed against T helper (Th)‐inducing and T suppressor (Ts)‐inducing determinants was examined with cyanogen bromide and tryptic peptides ofEscherichia coliβ‐galactosidase (GZ), a large tetrameric protein (monomer molecular weight = 116 kDa). Immunization with cyanogen bromide fragment 2 [CB‐2, amino acids (a.a.) 3‐92] induced both specific Th and Ts cells. Study of the induction of these functionally opposite T cell subpopulations with tryptic peptides of CB‐2 indicated that Th and Ts were activated by separate, nonoverlapping determinants. Th‐inducing activity resided in a nonapeptide, T6 (a.a. 44‐52), whereas T4 (a.a. 27‐37) induced Ts cells. The presence of distinct helper and suppressor determinants suggests that the specificity repertoire in these T cell sub‐populations may differ, perhaps owing to the expression of antigen‐recognizing receptors that are coded by unique gene families. Alternatively, antigen presentation structures may be physicochemically quite different, and bind to distinct parts of the peptide antigen.— Krzych, U.; Fowler, A. V.; Miller, A.; Sercarz, E. E. Induction of helper and suppressor T cells by nonoverlapping determinants on the large protein antigen, β‐galactosidase.FASEB J.2: 141‐145; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.2963778
出版商:Wiley
年代:1988
数据来源: WILEY
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8. |
Irreversible injury in anoxic hepatocytes precipitated by an abrupt increase in plasma membrane permeability |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 146-151
Brian Herman,
Anna‐Liisa Nieminen,
Gregory J. Gores,
John J. Lemasters,
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摘要:
Using low‐light digitized video microscopy, the onset, progression, and reversibility of anoxic injury were assessed in single hepatocytes isolated from fasted rats. Cell‐surface bleb formation occurred in three stages over 1‐3 h after anoxia. Stage I was characterized by formation of numerous small blebs. In stage II, small blebs enlarged by coalescence and fusion to form a few large terminal blebs. Near the end of stage II, cells began to swell rapidly, ending with the apparent breakdown of one of the terminal blebs. Breakdown of the bleb membrane initiated stage III of injury and was coincident with a rapid increase of nonspecific permeability to organic cationic and anionic molecules. On reoxygenation, stages I and II were fully reversible, and plasma membrane blebs were resorbed completely within 6 min of reoxygenation without loss of viability. Stage III, however, was not reversible, and no morphological changes occurred on reoxygenation. The results indicate that onset of cell death owing to anoxia is a rapid event initiated by a sudden increase of nonspecific plasma membrane permeability caused by rupture of a terminal bleb. Anoxic injury is reversible until this event occurs.— Herman, B.; Nieminen, A.‐L.; Gores, G. J.; Lemasters, J. J. Irreversible injury in anoxic hepatocytes precipitated by an abrupt increase in plasma membrane permeability.FASEB J.2: 146‐151; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.3342967
出版商:Wiley
年代:1988
数据来源: WILEY
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9. |
Bile acid synthesis: down‐regulation by monohydroxy bile acids1 |
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The FASEB Journal,
Volume 2,
Issue 2,
1988,
Page 152-156
Roberta Hall,
Engeline Kok,
Norman B. Javitt,
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摘要:
The regulation of bile acid synthesis was studied in rabbits after interruption of the enterohepatic circulation by choledochoureteral anastomosis. Total daily bile acid output was 772 ± 130 (SD) μmol/24 h, of which>95% was glycocholic acid. Administration of deoxycholic or cholic acid or their conjugates (300‐800 μmol) or gallbladder bile failed to down‐regulate endogenous bile acid synthesis. In contrast, chenodeoxycholic acid administration did down‐regulate bile acid synthesis, but this effect was related to the formation and excretion of lithocholic acid. This observation was confirmed by the finding that i.v. infusion of 10‐20 μmol of either lithocholic acid or 3β‐hydroxy‐5‐cholenoic acid significantly reduced cholic acid synthesis. Thus monohydroxy bile acids, derived from either hepatic or intestinal sources, participate in the down‐regulation of bile acid synthesis.— Hall, R.; Kok, E.; Javitt, N. B. Bile acid synthesis: down‐regulation by monohydroxy bile acids.FASEB J.2: 152‐156; 1988.
ISSN:0892-6638
DOI:10.1096/fasebj.2.2.3342968
出版商:Wiley
年代:1988
数据来源: WILEY
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