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Book: Catalogue of rapid microbiological methods

Baylis, Chris / Mitchell, C.

(Review / Campden BRI ; 1)

2008

Author's details	C. Baylis and C. Mitchell
Series title	Review / Campden BRI ; 1
Collection
Language	English
Size	119 S.
Edition	6. ed.
Publisher	Campden BRI
Publishing place	Chipping Campden
Publishing country	Great Britain
Document type	Book
HBZ-ID	HT015927977
ISBN	978-0-907503-53-8 ; 0-907503-53-5
Database	Catalogue ZB MED Nutrition, Environment, Agriculture

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Shelf mark	Loan status	Location
094/77	available for loan (reading room)	Freihandmagazin (U1)

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Article ; Online: Sexual dimorphism: the aging kidney, involvement of nitric oxide deficiency, and angiotensin II overactivity.

Baylis, Chris

The journals of gerontology. Series A, Biological sciences and medical sciences

2012 Volume 67, Issue 12, Page(s) 1365–1372

Abstract: Females develop less age-dependent loss of renal function, which may be in part due to cardiorenal protective effects of estrogens. The impact of androgen level on cardiovascular-renal health is controversial. Estrogen acts through multiple mechanisms, ... ...

Abstract	Females develop less age-dependent loss of renal function, which may be in part due to cardiorenal protective effects of estrogens. The impact of androgen level on cardiovascular-renal health is controversial. Estrogen acts through multiple mechanisms, sometimes beneficial, sometimes damaging, which makes it difficult to predict the effect of hormone replacement therapy (HRT) in an aging population. Nitric oxide (NO) deficiency occurs in aging and contributes to age-dependent cardiovascular risk and kidney damage. The increased oxidative stress of aging has effects at multiple sites in the NO biosynthetic pathway to lower NO production/action. Loss of NO together with activated angiotensin promotes some of the decrements in cardiovascular-renal function seen with age, which may be related to actions of the sex steroids.
MeSH term(s)	Aged ; Aging/physiology ; Androgens/physiology ; Angiotensin II/physiology ; Animals ; Female ; Glomerular Filtration Rate/physiology ; Humans ; Kidney Glomerulus/physiology ; Male ; Nitric Oxide/deficiency ; Oxidative Stress/physiology ; Sex Characteristics
Chemical Substances	Androgens ; Angiotensin II (11128-99-7) ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2012-09-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/gls171
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Article ; Online: Nitric oxide synthase derangements and hypertension in kidney disease.

Baylis, Chris

Current opinion in nephrology and hypertension

2011 Volume 21, Issue 1, Page(s) 1–6

Abstract: Purpose of review: Nitric oxide deficiency occurs by multiple mechanisms and contributes to the pathogenesis of progression of chronic kidney disease (CKD) and its cardiovascular complications. This article concentrates on recent developments on the ... ...

Abstract	Purpose of review: Nitric oxide deficiency occurs by multiple mechanisms and contributes to the pathogenesis of progression of chronic kidney disease (CKD) and its cardiovascular complications. This article concentrates on recent developments on the regulation of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA) in CKD and on the importance of the nitric oxide synthases in kidney disease progression, particularly in diabetic nephropathy. Recent findings: The increased plasma ADMA seen in renal disease is generally predictive of severity of CKD progression and cardiovascular risk. However, some assumptions about the control of ADMA have been challenged: the primacy of the kidney as a metabolic organ for plasma ADMA regulation has come under scrutiny and the relative importance of the two isoforms of the ADMA-metabolizing enzymes dimethylarginine dimethylaminohydrolases (DDAHs) is being re-evaluated. Alterations in NOS also contribute to CKD progression with the endothelial isoform playing a major role in diabetic nephropathy. Summary: Improving our understanding of ADMA regulation is important since pharmacologic targeting of DDAH is underway. The major role of endothelial NOS-derived nitric oxide in diabetic nephropathy should lead to novel therapies. The beneficial actions of dietary nitrate supplementation on blood pressure and kidney disease are of considerable clinical relevance.
MeSH term(s)	Amidohydrolases/metabolism ; Animals ; Arginine/analogs & derivatives ; Arginine/metabolism ; Chronic Disease ; Disease Progression ; Humans ; Hypertension/drug therapy ; Hypertension/enzymology ; Hypertension/etiology ; Kidney/enzymology ; Kidney Diseases/complications ; Kidney Diseases/drug therapy ; Kidney Diseases/enzymology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Amidohydrolases (EC 3.5.-) ; dimethylargininase (EC 3.5.3.18)
Language	English
Publishing date	2011-11-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0b013e32834d54ca
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Article ; Online: Sexual dimorphism in the aging kidney: differences in the nitric oxide system.

Baylis, Chris

Nature reviews. Nephrology

2009 Volume 5, Issue 7, Page(s) 384–396

Abstract: Females-both rats and women-are substantially protected against the age-dependent decrease in renal function that occurs in males of the species. In part, this finding reflects the cardioprotective and renoprotective effects of estrogens, but estrogen ... ...

Abstract	Females-both rats and women-are substantially protected against the age-dependent decrease in renal function that occurs in males of the species. In part, this finding reflects the cardioprotective and renoprotective effects of estrogens, but estrogen has multiple actions, not all of which are beneficial. In addition, the low androgen level in women might be protective against a decline in renal function, but animal and clinical data on possible adverse effects of androgens are controversial. Androgens also have multiple actions, one of which-aromatization to estrogen-is likely to be protective. Sex steroids clearly have many complex actions, which explains the conflicting information on their relative benefits and dangers. Endothelial nitric oxide (NO) deficiency contributes importantly to cardiovascular risk and intrarenal NO deficiency is clearly linked to chronic kidney disease progression in animal models. Endothelial dysfunction develops with increasing age but is delayed in females, correlating with a delayed rise in asymmetric dimethylarginine level. There is no clear link between aging and arginine (the NO synthase substrate) deficiency. Animal data suggest that the aging kidney develops NO deficiency as a result of changes in neuronal NO synthase. The increased oxidative stress that occurs with aging affects multiple stages of the NO biosynthetic pathway and results in decreased production and/or action of NO. NO production is better preserved in females than in males, partly as a result of the actions of estrogens.
MeSH term(s)	Aging/physiology ; Animals ; Female ; Gonadal Steroid Hormones/physiology ; Humans ; Kidney/physiology ; Kidney Diseases/epidemiology ; Kidney Diseases/physiopathology ; Male ; Nitric Oxide/deficiency ; Risk Factors ; Sex Characteristics
Chemical Substances	Gonadal Steroid Hormones ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2009-06-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/nrneph.2009.90
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Article ; Online: Sexual dimorphism, the aging kidney, and involvement of nitric oxide deficiency.

Baylis, Chris

Seminars in nephrology

2009 Volume 29, Issue 6, Page(s) 569–578

Abstract: Females develop less age-dependent loss of renal function, in part because of cardiorenal protective effects of estrogens. The low androgen level in women also may be protective, although the animal and clinical data are controversial. Both estrogen and ... ...

Abstract	Females develop less age-dependent loss of renal function, in part because of cardiorenal protective effects of estrogens. The low androgen level in women also may be protective, although the animal and clinical data are controversial. Both estrogen and androgens act through multiple mechanisms, sometimes beneficial, sometimes damaging, which makes it difficult to predict the impact of hormone replacement therapy in an aging population. Nitric oxide (NO) deficiency contributes to age-dependent cardiovascular risk and kidney damage in animal models. The increased oxidative stress of aging impacts at multiple sites in the NO biosynthetic pathway to decrease NO production/action. Endothelial dysfunction develops with aging and is delayed in women, in association with a delayed increase in asymmetric dimethylarginine. Animal data suggest that the aging kidney develops NO deficiency because of changes in the neuronal NO synthase. Relative preservation of NO production in females contributes to the better cardiovascular and renal responses to aging.
MeSH term(s)	Aging/physiology ; Androgens/physiology ; Animals ; Estrogens/physiology ; Female ; Glomerular Filtration Rate/physiology ; Humans ; Kidney Diseases/physiopathology ; Kidney Glomerulus/physiopathology ; Male ; Nitric Oxide/deficiency ; Nitric Oxide Synthase/physiology ; Rats ; Sex Characteristics ; Sex Factors
Chemical Substances	Androgens ; Estrogens ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39)
Language	English
Publishing date	2009-12-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2009.07.003
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Article: Sexual dimorphism of the aging kidney: role of nitric oxide deficiency.

Baylis, Chris

Physiology (Bethesda, Md.)

2008 Volume 23, Page(s) 142–150

Abstract: GFR falls with aging in humans and rats due to renal vasoconstriction and structural damage. The rate of deterioration is influenced by race/genetic background, environment, and sex, with females protected. Part of the female advantage relates to ... ...

Abstract	GFR falls with aging in humans and rats due to renal vasoconstriction and structural damage. The rate of deterioration is influenced by race/genetic background, environment, and sex, with females protected. Part of the female advantage relates to protective effects of estrogens. There is little information on impact of aging on the distribution/cardiovascular actions of the estrogen receptor subtypes. In rats, androgens may contribute to injury, but in men, high testosterone levels predict cardiovascular health. In women, the association is controversial. Nitric oxide deficiency contributes to the hypertension and renal dysfunction of aging, which may be delayed in the female.
MeSH term(s)	Aging/metabolism ; Animals ; Cardiovascular Diseases/metabolism ; Female ; Gonadal Steroid Hormones/metabolism ; Humans ; Kidney/metabolism ; Kidney Diseases/metabolism ; Male ; Nitric Oxide/deficiency ; Rats ; Sex Characteristics
Chemical Substances	Gonadal Steroid Hormones ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2008-06
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Review
ZDB-ID	2158667-6
ISSN	1548-9221 ; 1548-9213
ISSN (online)	1548-9221
ISSN	1548-9213
DOI	10.1152/physiol.00001.2008
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Article: Nitric oxide deficiency in chronic kidney disease.

Baylis, Chris

American journal of physiology. Renal physiology

2008 Volume 294, Issue 1, Page(s) F1–9

Abstract: The overall production of nitric oxide (NO) is decreased in chronic kidney disease (CKD) which contributes to cardiovascular events and further progression of kidney damage. There are many likely causes of NO deficiency in CKD and the areas surveyed in ... ...

Abstract	The overall production of nitric oxide (NO) is decreased in chronic kidney disease (CKD) which contributes to cardiovascular events and further progression of kidney damage. There are many likely causes of NO deficiency in CKD and the areas surveyed in this review are: 1. Limitations on substrate (l-Arginine) availability, probably due to impaired renal l-Arginine biosynthesis, decreased transport of l-Arginine into endothelial cells and possible competition between NOS and competing metabolic pathways, such as arginase. 2. Increased circulating levels of endogenous NO synthase (NOS) inhibitors, in particular asymmetric dimethylarginine (ADMA). Increased methylation of proteins and their subsequent breakdown to release free ADMA may contribute but the major culprit is probably reduced ADMA catabolism by the enzymes dimethylarginine dimethylaminohydrolases. 3. Reduced renal cortex abundance of the neuronal NOS (nNOS)alpha protein correlates with injury while increasing nNOSbeta abundance may provide a compensatory, protective response. Interventions that can restore NO production by targeting these various pathways are likely to reduce the cardiovascular complications of CKD as well as slowing the rate of progression.
MeSH term(s)	Arginine/analogs & derivatives ; Arginine/metabolism ; Chronic Disease ; Humans ; Kidney Diseases/metabolism ; Nitric Oxide/deficiency ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; Nitric Oxide Synthase (EC 1.14.13.39)
Language	English
Publishing date	2008-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	603837-2
ISSN	1522-1466 ; 1931-857X ; 0363-6127
ISSN (online)	1522-1466
ISSN	1931-857X ; 0363-6127
DOI	10.1152/ajprenal.00424.2007
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Article ; Online: Relaxin-mediated renal vasodilation in the rat is associated with falls in glomerular blood pressure.

Deng, Aihua / Conrad, Kirk / Baylis, Chris

American journal of physiology. Regulatory, integrative and comparative physiology

2017 Volume 314, Issue 2, Page(s) R147–R152

Abstract: Relaxin (RLX) is a pleiotropic peptide hormone with marked renal vasodilatory actions that are physiologically important during pregnancy. RLX also has potent antifibrotic actions and is being tested therapeutically in various fibrotic diseases, ... ...

Abstract	Relaxin (RLX) is a pleiotropic peptide hormone with marked renal vasodilatory actions that are physiologically important during pregnancy. RLX also has potent antifibrotic actions and is being tested therapeutically in various fibrotic diseases, including chronic kidney disease (CKD). Since renal vasodilation may expose the glomerulus to increased blood pressure [glomerular capillary pressure (P
MeSH term(s)	Animals ; Arterial Pressure/drug effects ; Arterioles/drug effects ; Arterioles/physiopathology ; Glomerular Filtration Rate/drug effects ; Infusions, Intravenous ; Kidney Glomerulus/blood supply ; Male ; Rats, Sprague-Dawley ; Relaxin/administration & dosage ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/physiopathology ; Renal Plasma Flow/drug effects ; Time Factors ; Vascular Resistance/drug effects ; Vasodilation/drug effects ; Vasodilator Agents/administration & dosage
Chemical Substances	Vasodilator Agents ; Relaxin (9002-69-1)
Language	English
Publishing date	2017-10-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00148.2017
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Article: Arginine, arginine analogs and nitric oxide production in chronic kidney disease.

Baylis, Chris

Nature clinical practice. Nephrology

2006 Volume 2, Issue 4, Page(s) 209–220

Abstract: Nitric oxide (NO) production is reduced in renal disease, partially due to decreased endothelial NO production. Evidence indicates that NO deficiency contributes to cardiovascular events and progression of kidney damage. Two possible causes of NO ... ...

Abstract	Nitric oxide (NO) production is reduced in renal disease, partially due to decreased endothelial NO production. Evidence indicates that NO deficiency contributes to cardiovascular events and progression of kidney damage. Two possible causes of NO deficiency are substrate (L-arginine) limitation and increased levels of circulating endogenous inhibitors of NO synthase (particularly asymmetric dimethylarginine [ADMA]). Decreased L-arginine availability in chronic kidney disease (CKD) is due to perturbed renal biosynthesis of this amino acid. In addition, inhibition of transport of L-arginine into endothelial cells and shunting of L-arginine into other metabolic pathways (e.g. those involving arginase) might also decrease availability. Elevated plasma and tissue levels of ADMA in CKD are functions of both reduced renal excretion and reduced catabolism by dimethylarginine dimethylaminohydrolase (DDAH). The latter might be associated with loss-of-function polymorphisms of a DDAH gene, functional inhibition of the enzyme by oxidative stress in CKD and end-stage renal disease, or both. These findings provide the rationale for novel therapies, including supplementation of dietary L-arginine or its precursor L-citrulline, inhibition of non-NO-producing pathways of L-arginine utilization, or both. Because an increase in ADMA has emerged as a major independent risk factor in end-stage renal disease (and probably also in CKD), lowering ADMA concentration is a major therapeutic goal; interventions that enhance the activity of the ADMA-hydrolyzing enzyme DDAH are under investigation.
MeSH term(s)	Absorption ; Amidohydrolases/genetics ; Arginine/analogs & derivatives ; Arginine/metabolism ; Biological Availability ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/physiopathology ; Chronic Disease ; Comorbidity ; Enzyme Inhibitors/metabolism ; Humans ; Kidney/metabolism ; Kidney Diseases/metabolism ; Kidney Diseases/physiopathology ; Kidney Failure, Chronic/epidemiology ; Kidney Failure, Chronic/metabolism ; Kidney Failure, Chronic/physiopathology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/antagonists & inhibitors ; Nitric Oxide Synthase/metabolism ; Polymorphism, Genetic
Chemical Substances	Enzyme Inhibitors ; Nitric Oxide (31C4KY9ESH) ; N,N-dimethylarginine (63CV1GEK3Y) ; Arginine (94ZLA3W45F) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Amidohydrolases (EC 3.5.-) ; dimethylargininase (EC 3.5.3.18)
Language	English
Publishing date	2006-08-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2228557-X
ISSN	1745-8331 ; 1745-8323
ISSN (online)	1745-8331
ISSN	1745-8323
DOI	10.1038/ncpneph0143
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Article: Acute and long-term effects of modified hemoglobin (HBOC-201) in a rat model of hypertension and chronic kidney disease.

Baylis, Chris

Transfusion

2006 Volume 46, Issue 7, Page(s) 1104–1111

Abstract: Background: The goal was to determine whether administration of the oxygen-therapeutic blood substitute HBOC-201 had any deleterious effect on renal function and/or structure in a rat model of chronic kidney disease (CKD).: Study design and methods: ... ...

Abstract	Background: The goal was to determine whether administration of the oxygen-therapeutic blood substitute HBOC-201 had any deleterious effect on renal function and/or structure in a rat model of chronic kidney disease (CKD). Study design and methods: Longitudinal studies were conducted in the conscious chronically catheterized male Sprague-Dawley rat with rapidly progressing CKD produced by ablation-infarction of 5/6th of the functional renal mass. Experimental rats received a loading dose (after acute removal of 10% blood volume) and six subsequent daily maintenance doses of HBOC-201 at Weeks 4 to 5 after induction of CKD and were studied again at 6 weeks. Controls received isoosmotic human serum albumin (HSA, 13%) over the same period. Blood pressure (BP) and renal function were measured in acute experiments at Weeks 4, 5, and 6. Proteinuria and 24-hour creatinine clearance was measured longitudinally and renal pathology was assessed at killing. Results: There were differences in the acute response to the infusions, with rats given HBOC-201 exhibiting an increase in BP and renal vascular resistance, whereas rats given HSA showed a decrease in BP. These changes did not persist, however, because mean BP, glomerular filtration rate, level of proteinuria, and glomerular pathology were all similar at the end of the study (6 weeks after induction of CKD) in rats given HBOC-201 and HSA. Conclusion: In this model of CKD, daily doses of HBOC-201 had no long-term damaging effects on renal function or structure, compared to rats given the osmotic control agent, 13 percent HSA.
MeSH term(s)	Acute Disease ; Animals ; Blood Pressure/drug effects ; Blood Substitutes/adverse effects ; Blood Substitutes/therapeutic use ; Chronic Disease ; Creatine/urine ; Disease Models, Animal ; Hemoglobins/administration & dosage ; Hemoglobins/adverse effects ; Hypertension/complications ; Hypertension/drug therapy ; Kidney Diseases/complications ; Kidney Diseases/drug therapy ; Kidney Function Tests ; Longitudinal Studies ; Male ; Proteinuria ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Blood Substitutes ; HBOC 201 ; Hemoglobins ; Creatine (MU72812GK0)
Language	English
Publishing date	2006-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	208417-x
ISSN	1537-2995 ; 0041-1132
ISSN (online)	1537-2995
ISSN	0041-1132
DOI	10.1111/j.1537-2995.2006.00858.x
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