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Article ; Online: Renal Hypokalemia: An Endocrine Perspective.

Culver, Silas A / Suleman, Nawar / Kavuru, Varun / Siragy, Helmy M

The Journal of clinical endocrinology and metabolism

2024

Abstract: The majority of disorders which cause renal potassium wasting present with abnormalities in adrenal hormone secretion. While these findings frequently lead patients to seek endocrine evaluation, clinicians often struggle to accurately diagnose these ... ...

Abstract	The majority of disorders which cause renal potassium wasting present with abnormalities in adrenal hormone secretion. While these findings frequently lead patients to seek endocrine evaluation, clinicians often struggle to accurately diagnose these conditions, delaying treatment and adversely impacting patient care. At the same time, growing insight into the genetic and molecular basis of these disorders continues to improve their diagnosis and management. In this review we outline a practical integrated approach to the evaluation of renal hypokalemia syndromes that are seen in endocrine practice while highlighting recent advances in understanding of the genetics and pathophysiology behind them.
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgae201
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Article ; Online: Adrenal Insufficiency in Cirrhosis.

Wentworth, Brian J / Siragy, Helmy M

Journal of the Endocrine Society

2022 Volume 6, Issue 10, Page(s) bvac115

Abstract: Hypothalamus-pituitary-adrenal axis assessment in patients with cirrhosis is challenging. The phenotype of fatigue, hypotension, electrolyte disarray, and abdominal pain characterizing primary adrenal insufficiency (AI) overlaps significantly with ... ...

Abstract	Hypothalamus-pituitary-adrenal axis assessment in patients with cirrhosis is challenging. The phenotype of fatigue, hypotension, electrolyte disarray, and abdominal pain characterizing primary adrenal insufficiency (AI) overlaps significantly with decompensated liver disease. Reliance on total cortisol assays in hypoproteinemic states is problematic, yet abnormal stimulated levels in cirrhosis are associated with poor clinical outcomes. Alternative measures including free plasma or salivary cortisol levels have theoretical merit but are limited by unclear prognostic significance and undefined cirrhosis-specific reference ranges. Further complicating matters is that AI in cirrhosis represents a spectrum of impairment. Although absolute cortisol deficiency can occur, this represents a minority of cases. Instead, there is an emerging concept that cirrhosis, with or without critical illness, may induce a "relative" cortisol deficiency during times of stress. In addition, the limitations posed by decreased synthesis of binding globulins in cirrhosis necessitate re-evaluation of traditional AI diagnostic thresholds.
Language	English
Publishing date	2022-07-29
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2472-1972
ISSN (online)	2472-1972
DOI	10.1210/jendso/bvac115
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Article ; Online: Author's reply: Plasma corticosteroid-binding globulin levels in cirrhosis.

Wentworth, Brian J / Schliep, Matthew / Siragy, Helmy M / Henry, Zachary H

Liver international : official journal of the International Association for the Study of the Liver

2023 Volume 43, Issue 3, Page(s) 742–743

MeSH term(s)	Humans ; Transcortin/metabolism ; Liver Cirrhosis ; Plasma/metabolism
Chemical Substances	Transcortin (9010-38-2)
Language	English
Publishing date	2023-01-24
Publishing country	United States
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2102783-3
ISSN	1478-3231 ; 1478-3223
ISSN (online)	1478-3231
ISSN	1478-3223
DOI	10.1111/liv.15525
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Article ; Online: How I Approach It: Adrenal Insufficiency in Cirrhosis.

Wentworth, Brian J / Henry, Zachary H / Siragy, Helmy M

The American journal of gastroenterology

2022 Volume 117, Issue 12, Page(s) 1889–1893

MeSH term(s)	Humans ; Adrenal Insufficiency/complications ; Adrenal Insufficiency/diagnosis ; Liver Cirrhosis/complications ; Hydrocortisone
Chemical Substances	Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2022-08-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	390122-1
ISSN	1572-0241 ; 0002-9270
ISSN (online)	1572-0241
ISSN	0002-9270
DOI	10.14309/ajg.0000000000001939
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Article ; Online: Angiotensin Type-2 Receptors: Transducers of Natriuresis in the Renal Proximal Tubule.

Carey, Robert M / Siragy, Helmy M / Gildea, John J / Keller, Susanna R

International journal of molecular sciences

2022 Volume 23, Issue 4

Abstract: Angiotensin II (Ang II) type-2 receptors ( ... ...

Abstract	Angiotensin II (Ang II) type-2 receptors (AT
MeSH term(s)	Animals ; Humans ; Hypertension/metabolism ; Kidney Tubules, Proximal/metabolism ; Natriuresis/physiology ; Receptor, Angiotensin, Type 2/metabolism ; Transducers
Chemical Substances	Receptor, Angiotensin, Type 2
Language	English
Publishing date	2022-02-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23042317
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Article ; Online: Basal cortisol levels do not predict adrenal responsiveness in acute decompensated cirrhosis.

Wentworth, Brian J / Schliep, Matthew / Novicoff, Wendy M / Henry, Zachary H / Siragy, Helmy M

European journal of gastroenterology & hepatology

2023 Volume 36, Issue 2, Page(s) 238–244

Abstract: Objective: Morning total cortisol (TC) levels have been shown to predict adrenal dysfunction (AD) in the general population, but their utility in cirrhosis is unknown.: Methods: A retrospective cohort study was performed including all noncritically ... ...

Abstract	Objective: Morning total cortisol (TC) levels have been shown to predict adrenal dysfunction (AD) in the general population, but their utility in cirrhosis is unknown. Methods: A retrospective cohort study was performed including all noncritically ill patients at our institution between 2011 and 2022 admitted with acute decompensated cirrhosis who underwent standard-dose adrenocorticotropic hormone (ACTH) stimulation testing. Adrenal dysfunction was defined as an increase in TC (delta TC) level <9 µg/dl 60 minutes after ACTH dosing. Spearman correlation was utilized to assess the relationship between binding globulins and cortisol levels. Multivariate regression analysis was performed to determine if basal TC level or common clinical parameters were predictive of AD. Results: One hundred and nineteen patients were included, with a median model for end-stage liver disease score of 18. Albumin levels did not correlate with basal TC levels (ρ = 0.127; P = 0.169); basal TC did not correlate with delta TC (ρ = 0.050; P = 0.591). The degree of hypoalbuminemia did not alter these relationships. On multivariate regression, only albumin level [odds ratio (OR) = 0.418; 95% confidence interval (CI), 0.196-0.890; P = 0.024] and MELD score (OR, 1.094; 95% CI, 1.019-1.174; P = 0.014) were predictive of AD. Basal TC levels were not predictive of AD (OR = 0.991; 95% CI, 0.903-1.088; P = 0.855) or delta TC (β = 0.000; 95% CI -0.147 to 0.147; P = 0.999). Conclusion: Baseline TC levels do not predict ACTH stimulation testing response in patients with acute decompensated cirrhosis. Clinicians should avoid utilizing an isolated morning cortisol result as a screening method for AD in this population.
MeSH term(s)	Humans ; Hydrocortisone ; Adrenal Insufficiency/diagnosis ; Adrenal Insufficiency/etiology ; Retrospective Studies ; End Stage Liver Disease ; Severity of Illness Index ; Adrenocorticotropic Hormone ; Liver Cirrhosis/complications ; Liver Cirrhosis/diagnosis ; Albumins
Chemical Substances	Hydrocortisone (WI4X0X7BPJ) ; Adrenocorticotropic Hormone (9002-60-2) ; Albumins
Language	English
Publishing date	2023-12-10
Publishing country	England
Document type	Journal Article
ZDB-ID	1034239-4
ISSN	1473-5687 ; 0954-691X
ISSN (online)	1473-5687
ISSN	0954-691X
DOI	10.1097/MEG.0000000000002694
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Article ; Online: Novel regulation of renal gluconeogenesis by Atp6ap2 in response to high fat diet via PGC1-α/AKT-1 pathway.

Akhtar, Safia / Culver, Silas A / Siragy, Helmy M

Scientific reports

2021 Volume 11, Issue 1, Page(s) 11367

Abstract: Recent studies suggested that renal gluconeogenesis is substantially stimulated in the kidney in presence of obesity. However, the mechanisms responsible for such stimulation are not well understood. Recently, our laboratory demonstrated that mice fed ... ...

Abstract	Recent studies suggested that renal gluconeogenesis is substantially stimulated in the kidney in presence of obesity. However, the mechanisms responsible for such stimulation are not well understood. Recently, our laboratory demonstrated that mice fed high fat diet (HFD) exhibited increase in renal Atp6ap2 [also known as (Pro)renin receptor] expression. We hypothesized that HFD upregulates renal gluconeogenesis via Atp6ap2-PGC-1α and AKT pathway. Using real-time polymerase chain reaction, western blot analysis and immunostaining, we evaluated renal expression of the Atp6ap2 and renal gluconeogenic enzymes, PEPCK and G6Pase, in wild type and inducible nephron specific Atp6ap2 knockout mice fed normal diet (ND, 12 kcal% fat) or a high-fat diet (HFD, 45 kcal% fat) for 8 weeks. Compared with ND, HFD mice had significantly higher body weight (23%) (P < 0.05), renal mRNA and protein expression of Atp6ap2 (39 and 35%), PEPCK (44 and 125%) and G6Pase (39 and 44%) respectively. In addition, compared to ND, HFD mice had increased renal protein expression of PGC-1α by 32% (P < 0.05) and downregulated AKT by 33% (P < 0.05) respectively in renal cortex. Atp6ap2-KO abrogated these changes in the mice fed HFD. In conclusion, we identified novel regulation of renal gluconeogenesis by Atp6ap2 in response to high fat diet via PGC1-α/AKT-1 pathway.
MeSH term(s)	Animals ; Blood Glucose/analysis ; Body Weight ; Diet, High-Fat ; Fructose-Bisphosphatase/metabolism ; Gluconeogenesis/physiology ; Glucose-6-Phosphatase/metabolism ; Kidney/enzymology ; Kidney/metabolism ; Mice ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Phosphoenolpyruvate Carboxykinase (ATP)/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Proton-Translocating ATPases/genetics ; Proton-Translocating ATPases/physiology ; Pyruvate Kinase/metabolism ; RNA, Messenger/genetics ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/physiology
Chemical Substances	ATP6AP2 protein, mouse ; Blood Glucose ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Ppargc1a protein, mouse ; RNA, Messenger ; Receptors, Cell Surface ; Pyruvate Kinase (EC 2.7.1.40) ; Akt1 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Fructose-Bisphosphatase (EC 3.1.3.11) ; Glucose-6-Phosphatase (EC 3.1.3.9) ; Proton-Translocating ATPases (EC 3.6.3.14) ; Phosphoenolpyruvate Carboxykinase (ATP) (EC 4.1.1.49)
Language	English
Publishing date	2021-05-31
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-90952-7
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Article ; Online: Pro-renin receptor suppresses mitochondrial biogenesis and function via AMPK/SIRT-1/ PGC-1α pathway in diabetic kidney.

Akhtar, Safia / Siragy, Helmy M

PloS one

2019 Volume 14, Issue 12, Page(s) e0225728

Abstract: Abnormal mitochondrial biogenesis and function has been linked to multiple diseases including diabetes. Recently, we demonstrated the role of renal (Pro)renin receptor (PRR) in the dysregulation of mitochondria. We hypothesized that PRR contributes to ... ...

Abstract	Abnormal mitochondrial biogenesis and function has been linked to multiple diseases including diabetes. Recently, we demonstrated the role of renal (Pro)renin receptor (PRR) in the dysregulation of mitochondria. We hypothesized that PRR contributes to the reduction of mitochondrial biogenesis and function in diabetic kidney via PGC-1α/AMPK/SIRT-1 signaling pathway. In vivo and in vitro studies were conducted in C57BL/6 mouse and mouse renal mesangial cells (mRMCs). Control and streptozotocin-induced diabetic mice were injected with scramble or PRR shRNA and followed for a period of eight weeks. PRR mRNA and protein expression increased by 44% and 39% respectively (P<0.05) in kidneys of diabetic mice, and in mRMCs exposed to high glucose by 43 and 61% respectively compared to their respective controls. These results were accompanied by reduced mRNA and protein expressions of PGC-1α (67% and 75%), nuclear respiratory factors (NRF-1, 48% and 53%), mitochondrial transcriptional factor A (mtTFA, 56% and 40%), mitochondrial DNA copy number by 75% (all, P<0.05), and ATP production by 54%, respectively in diabetic kidneys and in mRMCs exposed to high glucose. Compared to non-diabetic control mice, PRR knockdown in diabetic mice and in mRMCs, not only attenuated the PRR mRNA and protein expression but also normalized mRNA and protein expressions of PGC-1α, NRF-1, mtTFA, mitochondrial DNA copy number, and ATP production. Treatment with AMPK inhibitor, Compound C, or SIRT-1 inhibitor, EX-527, alone, or combined with PRR siRNA caused marked reduction of mRNA expression of PGC-1α, NRF-1 and mtTFA, and ATP production in mRMCs exposed to high glucose. In conclusion, our study demonstrated the contribution of the PRR to the reduction of mitochondrial biogenesis and function in diabetic kidney disease via decreasing AMPK/SIRT-1/ PGC-1α signaling pathway.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Biomarkers ; Biopsy ; Cell Line ; DNA Copy Number Variations ; Diabetes Mellitus, Experimental ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/pathology ; Disease Models, Animal ; Gene Expression ; Immunohistochemistry ; Male ; Mesangial Cells/metabolism ; Mesangial Cells/pathology ; Mice ; Mitochondria/genetics ; Mitochondria/metabolism ; NF-E2-Related Factor 1/genetics ; NF-E2-Related Factor 1/metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; RNA Interference ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Signal Transduction ; Sirtuin 1/metabolism
Chemical Substances	Biomarkers ; NF-E2-Related Factor 1 ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Ppargc1a protein, mouse ; Receptors, Cell Surface ; prorenin receptor ; Adenosine Triphosphate (8L70Q75FXE) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2019-12-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0225728
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Article ; Online: Novel regulation of renal gluconeogenesis by Atp6ap2 in response to high fat diet via PGC1-α/AKT-1 pathway

Safia Akhtar / Silas A. Culver / Helmy M. Siragy

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 10

Abstract: Abstract Recent studies suggested that renal gluconeogenesis is substantially stimulated in the kidney in presence of obesity. However, the mechanisms responsible for such stimulation are not well understood. Recently, our laboratory demonstrated that ... ...

Abstract	Abstract Recent studies suggested that renal gluconeogenesis is substantially stimulated in the kidney in presence of obesity. However, the mechanisms responsible for such stimulation are not well understood. Recently, our laboratory demonstrated that mice fed high fat diet (HFD) exhibited increase in renal Atp6ap2 [also known as (Pro)renin receptor] expression. We hypothesized that HFD upregulates renal gluconeogenesis via Atp6ap2-PGC-1α and AKT pathway. Using real-time polymerase chain reaction, western blot analysis and immunostaining, we evaluated renal expression of the Atp6ap2 and renal gluconeogenic enzymes, PEPCK and G6Pase, in wild type and inducible nephron specific Atp6ap2 knockout mice fed normal diet (ND, 12 kcal% fat) or a high-fat diet (HFD, 45 kcal% fat) for 8 weeks. Compared with ND, HFD mice had significantly higher body weight (23%) (P < 0.05), renal mRNA and protein expression of Atp6ap2 (39 and 35%), PEPCK (44 and 125%) and G6Pase (39 and 44%) respectively. In addition, compared to ND, HFD mice had increased renal protein expression of PGC-1α by 32% (P < 0.05) and downregulated AKT by 33% (P < 0.05) respectively in renal cortex. Atp6ap2-KO abrogated these changes in the mice fed HFD. In conclusion, we identified novel regulation of renal gluconeogenesis by Atp6ap2 in response to high fat diet via PGC1-α/AKT-1 pathway.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2021-05-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Pro-renin receptor suppresses mitochondrial biogenesis and function via AMPK/SIRT-1/ PGC-1α pathway in diabetic kidney.

Safia Akhtar / Helmy M Siragy

PLoS ONE, Vol 14, Iss 12, p e

2019 Volume 0225728

Abstract	Abnormal mitochondrial biogenesis and function has been linked to multiple diseases including diabetes. Recently, we demonstrated the role of renal (Pro)renin receptor (PRR) in the dysregulation of mitochondria. We hypothesized that PRR contributes to the reduction of mitochondrial biogenesis and function in diabetic kidney via PGC-1α/AMPK/SIRT-1 signaling pathway. In vivo and in vitro studies were conducted in C57BL/6 mouse and mouse renal mesangial cells (mRMCs). Control and streptozotocin-induced diabetic mice were injected with scramble or PRR shRNA and followed for a period of eight weeks. PRR mRNA and protein expression increased by 44% and 39% respectively (P<0.05) in kidneys of diabetic mice, and in mRMCs exposed to high glucose by 43 and 61% respectively compared to their respective controls. These results were accompanied by reduced mRNA and protein expressions of PGC-1α (67% and 75%), nuclear respiratory factors (NRF-1, 48% and 53%), mitochondrial transcriptional factor A (mtTFA, 56% and 40%), mitochondrial DNA copy number by 75% (all, P<0.05), and ATP production by 54%, respectively in diabetic kidneys and in mRMCs exposed to high glucose. Compared to non-diabetic control mice, PRR knockdown in diabetic mice and in mRMCs, not only attenuated the PRR mRNA and protein expression but also normalized mRNA and protein expressions of PGC-1α, NRF-1, mtTFA, mitochondrial DNA copy number, and ATP production. Treatment with AMPK inhibitor, Compound C, or SIRT-1 inhibitor, EX-527, alone, or combined with PRR siRNA caused marked reduction of mRNA expression of PGC-1α, NRF-1 and mtTFA, and ATP production in mRMCs exposed to high glucose. In conclusion, our study demonstrated the contribution of the PRR to the reduction of mitochondrial biogenesis and function in diabetic kidney disease via decreasing AMPK/SIRT-1/ PGC-1α signaling pathway.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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