Advanced Search
Display options
Filter resources
Text Availability
Article type
Publication date
Species
Language
Sex
Age
Showing 1 to 12 of 58 entries
Sorted by: Best Match Show Resources per page
Gap Plasmon Resonance in a Suspended Plasmonic Nanowire Coupled to a Metallic Substrate.

Nano letters

Miyata M, Holsteen A, Nagasaki Y, Brongersma ML, Takahara J.
PMID: 26192214
Nano Lett. 2015 Aug 12;15(8):5609-16. doi: 10.1021/acs.nanolett.5b02307. Epub 2015 Jul 27.

We present an experimental demonstration of nanoscale gap plasmon resonators that consist of an individual suspended plasmonic nanowire (NW) over a metallic substrate. Our study demonstrates that the NW supports strong gap plasmon resonances of various gap sizes including...

Cite
Miyata M, Holsteen A, Nagasaki Y, et al. Gap Plasmon Resonance in a Suspended Plasmonic Nanowire Coupled to a Metallic Substrate. Nano Lett. 2015;15(8):5609-16doi: 10.1021/acs.nanolett.5b02307.
Miyata, M., Holsteen, A., Nagasaki, Y., Brongersma, M. L., & Takahara, J. (2015). Gap Plasmon Resonance in a Suspended Plasmonic Nanowire Coupled to a Metallic Substrate. Nano letters, 15(8), 5609-16. https://doi.org/10.1021/acs.nanolett.5b02307
Miyata, Masashi, et al. "Gap Plasmon Resonance in a Suspended Plasmonic Nanowire Coupled to a Metallic Substrate." Nano letters vol. 15,8 (2015): 5609-16. doi: https://doi.org/10.1021/acs.nanolett.5b02307
Miyata M, Holsteen A, Nagasaki Y, Brongersma ML, Takahara J. Gap Plasmon Resonance in a Suspended Plasmonic Nanowire Coupled to a Metallic Substrate. Nano Lett. 2015 Aug 12;15(8):5609-16. doi: 10.1021/acs.nanolett.5b02307. Epub 2015 Jul 27. PMID: 26192214.
Copy Download .nbib Format: NLM
PP035. Genome-wide expression profile of first and second trimester human uterine natural killer cells.

Pregnancy hypertension

Post Uiterweer ED, Eijkelkamp N, Groot Koerkamp MJ, Peeters LL, Holstege FC, Heijnen CJ, Franx A.
PMID: 26105890
Pregnancy Hypertens. 2013 Apr;3(2):79. doi: 10.1016/j.preghy.2013.04.062. Epub 2013 Jun 06.

INTRODUCTION: Uterine Natural Killer (uNK) cells are key regulators of the placental bed during early placental development and account for 40% of decidual cells. uNK cells have been suggested to play a role in pregnancy complications including maternal placental...

Cite
Post Uiterweer ED, Eijkelkamp N, Groot Koerkamp MJ, et al. PP035. Genome-wide expression profile of first and second trimester human uterine natural killer cells. Pregnancy Hypertens. 2013;3(2):79doi: 10.1016/j.preghy.2013.04.062.
Post Uiterweer, E. D., Eijkelkamp, N., Groot Koerkamp, M. J., Peeters, L. L., Holstege, F. C., Heijnen, C. J., & Franx, A. (2013). PP035. Genome-wide expression profile of first and second trimester human uterine natural killer cells. Pregnancy hypertension, 3(2), 79. https://doi.org/10.1016/j.preghy.2013.04.062
Post Uiterweer, Emiel D, et al. "PP035. Genome-wide expression profile of first and second trimester human uterine natural killer cells." Pregnancy hypertension vol. 3,2 (2013): 79. doi: https://doi.org/10.1016/j.preghy.2013.04.062
Post Uiterweer ED, Eijkelkamp N, Groot Koerkamp MJ, Peeters LL, Holstege FC, Heijnen CJ, Franx A. PP035. Genome-wide expression profile of first and second trimester human uterine natural killer cells. Pregnancy Hypertens. 2013 Apr;3(2):79. doi: 10.1016/j.preghy.2013.04.062. Epub 2013 Jun 06. PMID: 26105890.
Copy Download .nbib Format: NLM
Nerve Agent Toxicity and Treatment.

Current treatment options in neurology

Holstege CP, Dobmeier SG.
PMID: 15676112
Curr Treat Options Neurol. 2005 Mar;7(2):91-98. doi: 10.1007/s11940-005-0018-y.

The clinical syndrome of nerve agent toxicity varies widely, ranging from the classic cholinergic syndrome to flaccid paralysis and status epilepticus. All nerve agents are capable of producing marked neuropathology. Seizure control is strongly associated with protection against acute...

Cite
Holstege CP, Dobmeier SG. Nerve Agent Toxicity and Treatment. Curr Treat Options Neurol. 2005;7(2):91-98doi: 10.1007/s11940-005-0018-y.
Holstege, C. P., & Dobmeier, S. G. (2005). Nerve Agent Toxicity and Treatment. Current treatment options in neurology, 7(2), 91-98. https://doi.org/10.1007/s11940-005-0018-y
Holstege, Christopher P, and Dobmeier, Stephen G. "Nerve Agent Toxicity and Treatment." Current treatment options in neurology vol. 7,2 (2005): 91-98. doi: https://doi.org/10.1007/s11940-005-0018-y
Holstege CP, Dobmeier SG. Nerve Agent Toxicity and Treatment. Curr Treat Options Neurol. 2005 Mar;7(2):91-98. doi: 10.1007/s11940-005-0018-y. PMID: 15676112.
Copy Download .nbib Format: NLM
Oral antidiabetic agents: how much kidney disease can we tolerate?.

Expert review of endocrinology & metabolism

Mayer C, Holstein A, Stumvoll M.
PMID: 30290417
Expert Rev Endocrinol Metab. 2007 Jul;2(4):469-475. doi: 10.1586/17446651.2.4.469.

Type 2 diabetes mellitus and chronic kidney disease in mild and moderate stages is a common and underestimated comorbidity with relevant therapeutic consequences. Available oral antidiabetic agents are effectively used in keeping blood glucose levels within the guideline range...

Cite
Mayer C, Holstein A, Stumvoll M. Oral antidiabetic agents: how much kidney disease can we tolerate?. Expert Rev Endocrinol Metab. 2007;2(4):469-475doi: 10.1586/17446651.2.4.469.
Mayer, C., Holstein, A., & Stumvoll, M. (2007). Oral antidiabetic agents: how much kidney disease can we tolerate?. Expert review of endocrinology & metabolism, 2(4), 469-475. https://doi.org/10.1586/17446651.2.4.469
Mayer, Christof, et al. "Oral antidiabetic agents: how much kidney disease can we tolerate?." Expert review of endocrinology & metabolism vol. 2,4 (2007): 469-475. doi: https://doi.org/10.1586/17446651.2.4.469
Mayer C, Holstein A, Stumvoll M. Oral antidiabetic agents: how much kidney disease can we tolerate?. Expert Rev Endocrinol Metab. 2007 Jul;2(4):469-475. doi: 10.1586/17446651.2.4.469. PMID: 30290417.
Copy Download .nbib Format: NLM
[Updated S2k-Guideline "Complications of liver cirrhosis". German Society of Gastroenterology (DGVS)].

Zeitschrift fur Gastroenterologie

Gerbes AL, Labenz J, Appenrodt B, Dollinger M, Gundling F, Gülberg V, Holstege A, Lynen-Jansen P, Steib CJ, Trebicka J, Wiest R, Zipprich A.
PMID: 31127596
Z Gastroenterol. 2019 May;57(5):e168. doi: 10.1055/a-0928-2800. Epub 2019 May 24.

No abstract available.

Cite
Gerbes AL, Labenz J, Appenrodt B, et al. Aktualisierte S2k-Leitlinie der Deutschen Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS) „Komplikationen der Leberzirrhose“. [Updated S2k-Guideline "Complications of liver cirrhosis". German Society of Gastroenterology (DGVS)]. Z Gastroenterol. 2019;57(5):e168doi: 10.1055/a-0928-2800.
Gerbes, A. L., Labenz, J., Appenrodt, B., Dollinger, M., Gundling, F., Gülberg, V., Holstege, A., Lynen-Jansen, P., Steib, C. J., Trebicka, J., Wiest, R., Zipprich, A. (2019). Aktualisierte S2k-Leitlinie der Deutschen Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS) „Komplikationen der Leberzirrhose“. [Updated S2k-Guideline "Complications of liver cirrhosis". German Society of Gastroenterology (DGVS)]. Zeitschrift fur Gastroenterologie, 57(5), e168. https://doi.org/10.1055/a-0928-2800
Gerbes, Alexander L, et al. "Aktualisierte S2k-Leitlinie der Deutschen Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS) „Komplikationen der Leberzirrhose“." [Updated S2k-Guideline "Complications of liver cirrhosis". German Society of Gastroenterology (DGVS)]. Zeitschrift fur Gastroenterologie vol. 57,5 (2019): e168. doi: https://doi.org/10.1055/a-0928-2800
Gerbes AL, Labenz J, Appenrodt B, Dollinger M, Gundling F, Gülberg V, Holstege A, Lynen-Jansen P, Steib CJ, Trebicka J, Wiest R, Zipprich A. Aktualisierte S2k-Leitlinie der Deutschen Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS) „Komplikationen der Leberzirrhose“. [Updated S2k-Guideline "Complications of liver cirrhosis". German Society of Gastroenterology (DGVS)]. Z Gastroenterol. 2019 May;57(5):e168. doi: 10.1055/a-0928-2800. Epub 2019 May 24. German. PMID: 31127596.
Copy Download .nbib Format: NLM
SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network.

Cell reports

Hung C, Tuck E, Stubbs V, van der Lee SJ, Aalfs C, van Spaendonk R, Scheltens P, Hardy J, Holstege H, Livesey FJ.
PMID: 34133918
Cell Rep. 2021 Jun 15;35(11):109259. doi: 10.1016/j.celrep.2021.109259.

Dysfunction of the endolysosomal-autophagy network is emerging as an important pathogenic process in Alzheimer's disease. Mutations in the sorting receptor-encoding gene SORL1 cause autosomal-dominant Alzheimer's disease, and SORL1 variants increase risk for late-onset AD. To understand the contribution of...

Cite
Hung C, Tuck E, Stubbs V, et al. SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network. Cell Rep. 2021;35(11):109259doi: 10.1016/j.celrep.2021.109259.
Hung, C., Tuck, E., Stubbs, V., van der Lee, S. J., Aalfs, C., van Spaendonk, R., Scheltens, P., Hardy, J., Holstege, H., & Livesey, F. J. (2021). SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network. Cell reports, 35(11), 109259. https://doi.org/10.1016/j.celrep.2021.109259
Hung, Christy, et al. "SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network." Cell reports vol. 35,11 (2021): 109259. doi: https://doi.org/10.1016/j.celrep.2021.109259
Hung C, Tuck E, Stubbs V, van der Lee SJ, Aalfs C, van Spaendonk R, Scheltens P, Hardy J, Holstege H, Livesey FJ. SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network. Cell Rep. 2021 Jun 15;35(11):109259. doi: 10.1016/j.celrep.2021.109259. PMID: 34133918; PMCID: PMC8220253.
Copy Download .nbib Format: NLM
Neuron-Specific IMP2 Overexpression by Synapsin Promoter-Driven AAV9: A Tool to Study Its Role in Axon Regeneration.

Cells

Blizard S, Park D, O'Toole N, Norooz S, Dela Torre M, Son Y, Holstein A, Austin S, Harman J, Haraszti S, Fared D, Xu M.
PMID: 34685634
Cells. 2021 Oct 05;10(10). doi: 10.3390/cells10102654.

Insulin-like growth factor II mRNA-binding protein (IMP) 2 is one of the three homologues (IMP1-3) that belong to a conserved family of mRNA-binding proteins. Its alternative splice product is aberrantly expressed in human hepatocellular carcinoma, and it is therefore...

Cite
Blizard S, Park D, O'Toole N, et al. Neuron-Specific IMP2 Overexpression by Synapsin Promoter-Driven AAV9: A Tool to Study Its Role in Axon Regeneration. Cells. 2021;10(10)doi: 10.3390/cells10102654.
Blizard, S., Park, D., O'Toole, N., Norooz, S., Dela Torre, M., Son, Y., Holstein, A., Austin, S., Harman, J., Haraszti, S., Fared, D., & Xu, M. (2021). Neuron-Specific IMP2 Overexpression by Synapsin Promoter-Driven AAV9: A Tool to Study Its Role in Axon Regeneration. Cells, 10(10), . https://doi.org/10.3390/cells10102654
Blizard, Sarah, et al. "Neuron-Specific IMP2 Overexpression by Synapsin Promoter-Driven AAV9: A Tool to Study Its Role in Axon Regeneration." Cells vol. 10,10 (2021). doi: https://doi.org/10.3390/cells10102654
Blizard S, Park D, O'Toole N, Norooz S, Dela Torre M, Son Y, Holstein A, Austin S, Harman J, Haraszti S, Fared D, Xu M. Neuron-Specific IMP2 Overexpression by Synapsin Promoter-Driven AAV9: A Tool to Study Its Role in Axon Regeneration. Cells. 2021 Oct 05;10(10). doi: 10.3390/cells10102654. PMID: 34685634; PMCID: PMC8534607.
Copy Download .nbib Format: NLM
Conversations and Reactions Around Severe Hypoglycaemia (CRASH): Results from the German Cohort of a Global Survey of People with Type 1 Diabetes or Insulin-Treated Type 2 Diabetes and Caregivers.

Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association

Mönnig E, Spaepen E, Osumili B, Mitchell BD, Snoek F, Peyrot M, Kern W, Holstein A.
PMID: 33368091
Exp Clin Endocrinol Diabetes. 2020 Dec 23; doi: 10.1055/a-1310-7963. Epub 2020 Dec 23.

BACKGROUND: A global cross-sectional survey (CRASH) was designed to provide information about the experiences of people with diabetes (PWD) and their caregivers in relation to severe hypoglycaemic events.METHODS: Adults with type 1 diabetes or insulin-treated type 2 diabetes who...

Cite
Mönnig E, Spaepen E, Osumili B, et al. Conversations and Reactions Around Severe Hypoglycaemia (CRASH): Results from the German Cohort of a Global Survey of People with Type 1 Diabetes or Insulin-Treated Type 2 Diabetes and Caregivers. Exp Clin Endocrinol Diabetes. 2020;doi: 10.1055/a-1310-7963.
Mönnig, E., Spaepen, E., Osumili, B., Mitchell, B. D., Snoek, F., Peyrot, M., Kern, W., & Holstein, A. (2020). Conversations and Reactions Around Severe Hypoglycaemia (CRASH): Results from the German Cohort of a Global Survey of People with Type 1 Diabetes or Insulin-Treated Type 2 Diabetes and Caregivers. Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association, . https://doi.org/10.1055/a-1310-7963
Mönnig, Elisabeth, et al. "Conversations and Reactions Around Severe Hypoglycaemia (CRASH): Results from the German Cohort of a Global Survey of People with Type 1 Diabetes or Insulin-Treated Type 2 Diabetes and Caregivers." Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association vol. (2020). doi: https://doi.org/10.1055/a-1310-7963
Mönnig E, Spaepen E, Osumili B, Mitchell BD, Snoek F, Peyrot M, Kern W, Holstein A. Conversations and Reactions Around Severe Hypoglycaemia (CRASH): Results from the German Cohort of a Global Survey of People with Type 1 Diabetes or Insulin-Treated Type 2 Diabetes and Caregivers. Exp Clin Endocrinol Diabetes. 2020 Dec 23; doi: 10.1055/a-1310-7963. Epub 2020 Dec 23. PMID: 33368091.
Copy Download .nbib Format: NLM
Severe Diabetic Ketoacidosis Associated with Abdominal Lipohypertrophy.

Deutsches Arzteblatt international

Holstein A, Gehrig M, Holstein DJF.
PMID: 34935613
Dtsch Arztebl Int. 2021 Oct 08;118(40):682. doi: 10.3238/arztebl.m2021.0074.

No abstract available.

Cite
Holstein A, Gehrig M, Holstein DJF. Severe Diabetic Ketoacidosis Associated with Abdominal Lipohypertrophy. Dtsch Arztebl Int. 2021;118(40):682doi: 10.3238/arztebl.m2021.0074.
Holstein, A., Gehrig, M., & Holstein, D. J. F. (2021). Severe Diabetic Ketoacidosis Associated with Abdominal Lipohypertrophy. Deutsches Arzteblatt international, 118(40), 682. https://doi.org/10.3238/arztebl.m2021.0074
Holstein, Andreas, et al. "Severe Diabetic Ketoacidosis Associated with Abdominal Lipohypertrophy." Deutsches Arzteblatt international vol. 118,40 (2021): 682. doi: https://doi.org/10.3238/arztebl.m2021.0074
Holstein A, Gehrig M, Holstein DJF. Severe Diabetic Ketoacidosis Associated with Abdominal Lipohypertrophy. Dtsch Arztebl Int. 2021 Oct 08;118(40):682. doi: 10.3238/arztebl.m2021.0074. PMID: 34935613.
Copy Download .nbib Format: NLM
SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network.

Cell reports

Hung C, Tuck E, Stubbs V, van der Lee SJ, Aalfs C, van Spaendonk R, Scheltens P, Hardy J, Holstege H, Livesey FJ.
PMID: 34133918
Cell Rep. 2021 Jun 15;35(11):109259. doi: 10.1016/j.celrep.2021.109259.

Dysfunction of the endolysosomal-autophagy network is emerging as an important pathogenic process in Alzheimer's disease. Mutations in the sorting receptor-encoding gene SORL1 cause autosomal-dominant Alzheimer's disease, and SORL1 variants increase risk for late-onset AD. To understand the contribution of...

Cite
Hung C, Tuck E, Stubbs V, et al. SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network. Cell Rep. 2021;35(11):109259doi: 10.1016/j.celrep.2021.109259.
Hung, C., Tuck, E., Stubbs, V., van der Lee, S. J., Aalfs, C., van Spaendonk, R., Scheltens, P., Hardy, J., Holstege, H., & Livesey, F. J. (2021). SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network. Cell reports, 35(11), 109259. https://doi.org/10.1016/j.celrep.2021.109259
Hung, Christy, et al. "SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network." Cell reports vol. 35,11 (2021): 109259. doi: https://doi.org/10.1016/j.celrep.2021.109259
Hung C, Tuck E, Stubbs V, van der Lee SJ, Aalfs C, van Spaendonk R, Scheltens P, Hardy J, Holstege H, Livesey FJ. SORL1 deficiency in human excitatory neurons causes APP-dependent defects in the endolysosome-autophagy network. Cell Rep. 2021 Jun 15;35(11):109259. doi: 10.1016/j.celrep.2021.109259. PMID: 34133918; PMCID: PMC8220253.
Copy Download .nbib Format: NLM
Risk of dementia in .

Alzheimer's & dementia (Amsterdam, Netherlands)

Ebenau JL, van der Lee SJ, Hulsman M, Tesi N, Jansen IE, Verberk IMW, van Leeuwenstijn M, Teunissen CE, Barkhof F, Prins ND, Scheltens P, Holstege H, van Berckel BNM, van der Flier WM.
PMID: 34541285
Alzheimers Dement (Amst). 2021 Sep 14;13(1):e12229. doi: 10.1002/dad2.12229. eCollection 2021.

INTRODUCTION: We investigated relationships among genetic determinants of Alzheimer's disease (AD), amyloid/tau/neurodegenaration (ATN) biomarkers, and risk of dementia.METHODS: We studied cognitively normal individuals with subjective cognitive decline (SCD) from the Amsterdam Dementia Cohort and SCIENCe project. We examined associations...

Cite
Ebenau JL, van der Lee SJ, Hulsman M, et al. Risk of dementia in . Alzheimers Dement (Amst). 2021;13(1):e12229doi: 10.1002/dad2.12229.
Ebenau, J. L., van der Lee, S. J., Hulsman, M., Tesi, N., Jansen, I. E., Verberk, I. M. W., van Leeuwenstijn, M., Teunissen, C. E., Barkhof, F., Prins, N. D., Scheltens, P., Holstege, H., van Berckel, B. N. M., & van der Flier, W. M. (2021). Risk of dementia in . Alzheimer's & dementia (Amsterdam, Netherlands), 13(1), e12229. https://doi.org/10.1002/dad2.12229
Ebenau, Jarith L, et al. "Risk of dementia in ." Alzheimer's & dementia (Amsterdam, Netherlands) vol. 13,1 (2021): e12229. doi: https://doi.org/10.1002/dad2.12229
Ebenau JL, van der Lee SJ, Hulsman M, Tesi N, Jansen IE, Verberk IMW, van Leeuwenstijn M, Teunissen CE, Barkhof F, Prins ND, Scheltens P, Holstege H, van Berckel BNM, van der Flier WM. Risk of dementia in . Alzheimers Dement (Amst). 2021 Sep 14;13(1):e12229. doi: 10.1002/dad2.12229. eCollection 2021. PMID: 34541285; PMCID: PMC8438688.
Copy Download .nbib Format: NLM
Treatment patterns in pediatric patients with multiple sclerosis in Germany-a nationwide claim-based analysis.

Therapeutic advances in neurological disorders

Frahm N, Peters M, Bätzing J, Ellenberger D, Akmatov MK, Haas J, Rommer PS, Stahmann A, Zettl UK, Holstiege J.
PMID: 34646362
Ther Adv Neurol Disord. 2021 Oct 06;14:17562864211048336. doi: 10.1177/17562864211048336. eCollection 2021.

BACKGROUND: The manifestation of multiple sclerosis (MS) in childhood and adolescence occurs in 3%-5% of all MS cases. However, the immunomodulatory and symptomatic treatment options in this population group are still limited.OBJECTIVE: We aimed to elucidate the prescription frequency...

Cite
Frahm N, Peters M, Bätzing J, et al. Treatment patterns in pediatric patients with multiple sclerosis in Germany-a nationwide claim-based analysis. Ther Adv Neurol Disord. 2021;14:17562864211048336doi: 10.1177/17562864211048336.
Frahm, N., Peters, M., Bätzing, J., Ellenberger, D., Akmatov, M. K., Haas, J., Rommer, P. S., Stahmann, A., Zettl, U. K., & Holstiege, J. (2021). Treatment patterns in pediatric patients with multiple sclerosis in Germany-a nationwide claim-based analysis. Therapeutic advances in neurological disorders, 1417562864211048336. https://doi.org/10.1177/17562864211048336
Frahm, Niklas, et al. "Treatment patterns in pediatric patients with multiple sclerosis in Germany-a nationwide claim-based analysis." Therapeutic advances in neurological disorders vol. 14 (2021): 17562864211048336. doi: https://doi.org/10.1177/17562864211048336
Frahm N, Peters M, Bätzing J, Ellenberger D, Akmatov MK, Haas J, Rommer PS, Stahmann A, Zettl UK, Holstiege J. Treatment patterns in pediatric patients with multiple sclerosis in Germany-a nationwide claim-based analysis. Ther Adv Neurol Disord. 2021 Oct 06;14:17562864211048336. doi: 10.1177/17562864211048336. eCollection 2021. PMID: 34646362; PMCID: PMC8504210.
Copy Download .nbib Format: NLM
Showing 1 to 12 of 58 entries