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White blood cell population dynamics for risk stratification of acute coronary syndrome

Chaudhury, Anwesha ; Noiret, Lorette ; Higgins, John M.

Proceedings of the National Academy of Sciences ; 2017

In: Proceedings of the National Academy of Sciences Vol. 114, No. 46 ( 2017-11-14), p. 12344-12349

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In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 114, No. 46 ( 2017-11-14), p. 12344-12349

Abstract: The complete blood count (CBC) provides a high-level assessment of a patient’s immunologic state and guides the diagnosis and treatment of almost all diseases. Hematology analyzers evaluate CBCs by making high-dimensional single-cell measurements of size and cytoplasmic and nuclear morphology in high throughput, but only the final cell counts are commonly used for clinical decisions. Here, we utilize the underlying single-cell measurements from conventional clinical instruments to develop a mathematical model guided by cellular mechanisms that quantifies the population dynamics of neutrophil, lymphocyte, and monocyte characteristics. The dynamic model tracks the evolution of the morphology of WBC subpopulations as a patient transitions from a healthy to a diseased state. We show how healthy individuals and hospitalized patients with similar WBC counts can be robustly classified based on their WBC population dynamics. We combine the model with supervised learning techniques to risk-stratify patients under evaluation for acute coronary syndrome. In particular, the model can identify more than 70% of patients in our study population with initially negative screening tests who will be diagnosed with acute coronary syndrome in the subsequent 48 hours. More generally, our study shows how mechanistic modeling of existing clinical data can help realize the vision of precision medicine.

Type of Medium: Online Resource

ISSN: 0027-8424 , 1091-6490

URL: Article

DOI: 10.1073/pnas.1709228114

RVK:

TA 1000

RVK:

WA 15000

Language: English

Publisher: Proceedings of the National Academy of Sciences

Publication Date: 2017

detail.hit.zdb_id: 209104-5

detail.hit.zdb_id: 1461794-8

SSG: 11

SSG: 12

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Epithelial apoptotic pattern emerges from global and local regulation by cell apical area

Cachoux, Victoire M.L. ; Balakireva, Maria ; Gracia, Mélanie ; [et al.]

Elsevier BV ; 2023

In: Current Biology Vol. 33, No. 22 ( 2023-11), p. 4807-4826.e6

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In: Current Biology, Elsevier BV, Vol. 33, No. 22 ( 2023-11), p. 4807-4826.e6

Type of Medium: Online Resource

ISSN: 0960-9822

URL: Article

DOI: 10.1016/j.cub.2023.09.049

Language: English

Publisher: Elsevier BV

Publication Date: 2023

detail.hit.zdb_id: 2019214-9

SSG: 12

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Mathematical Model of Ammonia Handling in the Rat Renal Medulla

Noiret, Lorette ; Baigent, Stephen ; Jalan, Rajiv ; [et al.]

Public Library of Science (PLoS) ; 2015

In: PLOS ONE Vol. 10, No. 8 ( 2015-8-17), p. e0134477-

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In: PLOS ONE, Public Library of Science (PLoS), Vol. 10, No. 8 ( 2015-8-17), p. e0134477-

Type of Medium: Online Resource

ISSN: 1932-6203

URL: Article

DOI: 10.1371/journal.pone.0134477

DOI: 10.1371/journal.pone.0134477.g001

DOI: 10.1371/journal.pone.0134477.g002

DOI: 10.1371/journal.pone.0134477.g003

DOI: 10.1371/journal.pone.0134477.g004

DOI: 10.1371/journal.pone.0134477.g005

DOI: 10.1371/journal.pone.0134477.g006

DOI: 10.1371/journal.pone.0134477.g007

DOI: 10.1371/journal.pone.0134477.g008

DOI: 10.1371/journal.pone.0134477.g009

DOI: 10.1371/journal.pone.0134477.g010

DOI: 10.1371/journal.pone.0134477.t001

DOI: 10.1371/journal.pone.0134477.t002

DOI: 10.1371/journal.pone.0134477.t003

DOI: 10.1371/journal.pone.0134477.t004

DOI: 10.1371/journal.pone.0134477.t005

DOI: 10.1371/journal.pone.0134477.t006

DOI: 10.1371/journal.pone.0134477.t007

DOI: 10.1371/journal.pone.0134477.t008

DOI: 10.1371/journal.pone.0134477.t009

Language: English

Publisher: Public Library of Science (PLoS)

Publication Date: 2015

detail.hit.zdb_id: 2267670-3

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Albumin infusion improves renal blood flow autoregulation in patients with acute decompensation of cirrhosis and acute kidney injury

Garcia‐Martinez, Rita ; Noiret, Lorette ; Sen, Sambit ; [et al.]

Wiley ; 2015

In: Liver International Vol. 35, No. 2 ( 2015-02), p. 335-343

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In: Liver International, Wiley, Vol. 35, No. 2 ( 2015-02), p. 335-343

Abstract: In cirrhotic patients with renal failure, renal blood flow autoregulation curve is shifted to the right, which is consequent upon sympathetic nervous system activation and endothelial dysfunction. Albumin infusion improves renal function in cirrhosis by mechanisms that are incompletely understood. We aimed to determine the effect of albumin infusion on systemic haemodynamics, renal blood flow, renal function and endothelial function in patients with acute decompensation of cirrhosis and acute kidney injury. Methods Twelve patients with refractory ascites and 10 patients with acute decompensation of cirrhosis and acute kidney injury were studied. Both groups were treated with intravenous albumin infusion, 40–60 g/days over 3–4 days. Cardiac and renal haemodynamics were measured. Endothelial activation/dysfunction was assessed using von Willebrand factor and serum nitrite levels. F2α Isoprostanes, resting neutrophil burst and noradrenaline levels were quantified as markers of oxidative stress, endotoxemia and sympathetic activation respectively. Results Albumin infusion leads to a shift in the renal blood flow autoregulation curve towards normalization, which resulted in a significant increase in renal blood flow. Accordingly, improvement of renal function was observed. In parallel, a significant decrease in sympathetic activation, inflammation/oxidative stress and endothelial activation/dysfunction was documented. Improvement of renal blood flow correlated with improvement in endothelial activation ( r = 0.741, P 〈 0.001). Conclusions The data suggest that albumin infusion improves renal function in acutely decompensated cirrhotic patients with acute kidney injury by impacting on renal blood flow autoregulation. This is possibly achieved through endothelial stabilization and a reduction in the sympathetic tone, endotoxemia and oxidative stress.

Type of Medium: Online Resource

ISSN: 1478-3223 , 1478-3231

URL: Issue

URL: Article

DOI: 10.1111/liv.2015.35.issue-2

DOI: 10.1111/liv.12528

Language: English

Publisher: Wiley

Publication Date: 2015

detail.hit.zdb_id: 2124684-1

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Mathematical models and hepatology; oil and vinegar?

Noiret, Lorette ; Rose, Christopher F.

Elsevier BV ; 2016

In: Journal of Hepatology Vol. 64, No. 4 ( 2016-04), p. 768-769

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In: Journal of Hepatology, Elsevier BV, Vol. 64, No. 4 ( 2016-04), p. 768-769

Type of Medium: Online Resource

ISSN: 0168-8278

URL: Article

DOI: 10.1016/j.jhep.2016.01.021

Language: English

Publisher: Elsevier BV

Publication Date: 2016

detail.hit.zdb_id: 2027112-8

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Interleukin-3 amplifies acute inflammation and is a potential therapeutic target in sepsis

Weber, Georg F. ; Chousterman, Benjamin G. ; He, Shun ; [et al.]

American Association for the Advancement of Science (AAAS) ; 2015

In: Science Vol. 347, No. 6227 ( 2015-03-13), p. 1260-1265

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In: Science, American Association for the Advancement of Science (AAAS), Vol. 347, No. 6227 ( 2015-03-13), p. 1260-1265

Abstract: Sepsis is a frequently fatal condition characterized by an uncontrolled and harmful host reaction to microbial infection. Despite the prevalence and severity of sepsis, we lack a fundamental grasp of its pathophysiology. Here we report that the cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis. Using a mouse model of abdominal sepsis, we showed that innate response activator B cells produce IL-3, which induces myelopoiesis of Ly-6C high monocytes and neutrophils and fuels a cytokine storm. IL-3 deficiency protects mice against sepsis. In humans with sepsis, high plasma IL-3 levels are associated with high mortality even after adjusting for prognostic indicators. This study deepens our understanding of immune activation, identifies IL-3 as an orchestrator of emergency myelopoiesis, and reveals a new therapeutic target for treating sepsis.

Type of Medium: Online Resource

ISSN: 0036-8075 , 1095-9203

URL: Article

DOI: 10.1126/science.aaa4268

RVK:

TA 1000

RVK:

WA 15000

Language: English

Publisher: American Association for the Advancement of Science (AAAS)

Publication Date: 2015

detail.hit.zdb_id: 128410-1

detail.hit.zdb_id: 2066996-3

detail.hit.zdb_id: 2060783-0

SSG: 11

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Interorgan ammonia metabolism in liver failure: the basis of current and future therapies : Interorgan ammonia metabolism in liver failure

Wright, Gavin ; Noiret, Lorette ; Olde Damink, Steven W. M. ; [et al.]

Wiley ; 2011

In: Liver International Vol. 31, No. 2 ( 2011-02), p. 163-175

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In: Liver International, Wiley, Vol. 31, No. 2 ( 2011-02), p. 163-175

Type of Medium: Online Resource

ISSN: 1478-3223

URL: Issue

URL: Article

DOI: 10.1111/liv.2010.31.issue-2

DOI: 10.1111/j.1478-3231.2010.02302.x

Language: English

Publisher: Wiley

Publication Date: 2011

detail.hit.zdb_id: 2124684-1

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Arterial ammonia levels in cirrhosis are determined by systemic and hepatic hemodynamics, and by organ function : a quantitative modelling study

Noiret, Lorette ; Baigent, Stephen ; Jalan, Rajiv

Wiley ; 2014

In: Liver International Vol. 34, No. 6 ( 2014-07)

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In: Liver International, Wiley, Vol. 34, No. 6 ( 2014-07)

Abstract: Hyperammonaemia is a common complication of chronic liver failure. Two main factors are thought to underlie this complication: a loss of hepatic detoxification function and the development of portosystemic shunting. However, few studies have tried to quantify the importance of portosystemic shunting. Here, we used a theoretical approach to test the hypothesis that the development of portosystemic shunting is sufficient to cause hyperammonaemia in cirrhosis. Methods Two mathematical models are developed. The first one describes the main vascular resistances of the circulation and is used to provide scenarios for the distributions of organ blood flow in cirrhosis, which are necessary to run the second model. The second model predicts arterial ammonia levels resulting from ammonia metabolism in gut, liver, kidney, muscle and brain, and the distribution of organ blood flow. Results The fraction of gastrointestinal blood flow shunted through collaterals was estimated to be 41% in mild cirrhosis, 69% in moderate and 85% in severe cases. In the second model, the redistribution of organ blood flow associated with severe cirrhosis was sufficient to cause hyperammonaemia, even when the hepatic detoxification function and the ammonia production were set to normal. Conclusions The model indicates that the development of portosystemic shunting in cirrhosis is sufficient to cause hyperammonaemia. Interventions that reduce the fraction of shunting may be future targets of therapy to control severity of hyperammonaemia.

Type of Medium: Online Resource

ISSN: 1478-3223 , 1478-3231

URL: Issue

URL: Article

DOI: 10.1111/liv.2014.34.issue-6

DOI: 10.1111/liv.12361

Language: English

Publisher: Wiley

Publication Date: 2014

detail.hit.zdb_id: 2124684-1

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Ornithine phenylacetate revisited

Jover-Cobos, Maria ; Noiret, Lorette ; Sharifi, Yalda ; [et al.]

Springer Science and Business Media LLC ; 2013

In: Metabolic Brain Disease Vol. 28, No. 2 ( 2013-6), p. 327-331

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In: Metabolic Brain Disease, Springer Science and Business Media LLC, Vol. 28, No. 2 ( 2013-6), p. 327-331

Type of Medium: Online Resource

ISSN: 0885-7490 , 1573-7365

URL: Article

DOI: 10.1007/s11011-013-9391-5

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2013

detail.hit.zdb_id: 2018067-6

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Determinants of red blood cell alloantibody detection duration: analysis of multiply alloimmunized patients supports peritransfusion factors

Noiret, Lorette ; Slater, Amy ; Higgins, John M.

Wiley ; 2017

In: Transfusion Vol. 57, No. 8 ( 2017-08), p. 1930-1937

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In: Transfusion, Wiley, Vol. 57, No. 8 ( 2017-08), p. 1930-1937

Abstract: Alloimmunization to red blood cells (RBCs) can cause serious transfusion reactions and complicate the search for compatible blood products. Alloantibodies can be detected for periods ranging from a few days to several years, yet the mechanisms controlling the duration of detectability remain unknown. We studied the detection durations in patients forming multiple antibodies to investigate whether the duration is more strongly determined by conditions present at the time of each transfusion (peritransfusion factors) or by more stable patient‐specific factors likely to persist across transfusions. STUDY DESIGN AND METHODS We studied retrospective medical records for alloimmunized patients at Massachusetts General Hospital and Brigham and Women's Hospital (1461 patients; 2187 antibodies). RESULTS Antibodies discovered simultaneously in a patient shared similar fates: 76% persisted through the last screen or first became undetectable during the same screen. Simultaneously identified antibodies were also more persistent than sequentially identified antibodies (mean, 9.2 months vs. 4.9 months; p 〈 10 −3 ). Within a patient, antibodies discovered simultaneously tended to be detected for similar periods of time (mean difference, 25 days), compared to the detection period for sequentially discovered antibodies (107 days, p 〈 10 −3 ). CONCLUSIONS The similarity in detection duration of simultaneously identified antibodies suggests that peritransfusion factors are important determinants of alloantibody detectability and duration. We also find some evidence that detection durations for sequentially identified antibodies are also more highly correlated than those for randomly selected antibodies across all patients, suggesting that patient‐specific factors also play a role in determining alloantibody persistence.

Type of Medium: Online Resource

ISSN: 0041-1132 , 1537-2995

URL: Issue

URL: Article

DOI: 10.1111/trf.2017.57.issue-8

DOI: 10.1111/trf.14157

Language: English

Publisher: Wiley

Publication Date: 2017

detail.hit.zdb_id: 2018415-3

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