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Article ; Online: Long-Term Activity and Safety of a Low-Dose Hydrocortisone Tear Substitute in Patients with Dry Eye Disease.

Rolando, Maurizio / Villella, Elena / Loreggian, Lara / Marini, Sara / Loretelli, Cristian / Fiorina, Paolo / Barabino, Stefano

Current eye research

2023 Volume 48, Issue 9, Page(s) 799–804

Abstract: Purpose: A clinical trial was conducted to evaluate the activity of a new artificial tear containing hyaluronic acid (HA) and low-dose hydrocortisone to control dry-eye disease (DED) symptoms.: Methods: a randomized, controlled, double-masked study ... ...

Abstract	Purpose: A clinical trial was conducted to evaluate the activity of a new artificial tear containing hyaluronic acid (HA) and low-dose hydrocortisone to control dry-eye disease (DED) symptoms. Methods: a randomized, controlled, double-masked study was carried out at the Ocular Surface and Dry Eye Center, "Luigi Sacco" University Hospital (Milan, Italy), between June 2020 and June 2021. The study involved patients with DED for at least 6 months. After an initial 7-day treatment with corticosteroid, the treatment with the new artificial tear (four-times a day for 6 months) was compared with a control HA solution. Results: A total of 40 patients were considered. We observed a significant improvement in the frequency and intensity of DED symptoms in both groups. After corticosteroid discontinuation, the maintenance of the therapeutic advantage was observed only in the treatment group, which also showed a significant improvement of the tear film break-up time ( Conclusions: Our findings support the prolonged use of the new eye drop with low-dose hydrocortisone, also in the DED initial stages, to prevent the degenerating towards a chronic condition (http://www.isrctn.com/ISRCTN16288419).
MeSH term(s)	Humans ; Lubricant Eye Drops ; Hydrocortisone ; Dry Eye Syndromes/drug therapy ; Dry Eye Syndromes/diagnosis ; Hyaluronic Acid ; Tears
Chemical Substances	Lubricant Eye Drops ; Hydrocortisone (WI4X0X7BPJ) ; Hyaluronic Acid (9004-61-9)
Language	English
Publishing date	2023-06-19
Publishing country	England
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	82079-9
ISSN	1460-2202 ; 0271-3683
ISSN (online)	1460-2202
ISSN	0271-3683
DOI	10.1080/02713683.2023.2214948
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Zs.A 1775: Show issues

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Article: TMEM219 regulates the transcription factor expression and proliferation of beta cells.

D'Addio, Francesca / Assi, Emma / Maestroni, Anna / Rossi, Giada / Usuelli, Vera / Petrazzuolo, Adriana / Nardini, Marta / Loretelli, Cristian / Ben Nasr, Moufida / Fiorina, Paolo

Frontiers in endocrinology

2024 Volume 15, Page(s) 1306127

Abstract: Pancreatic beta cells replenishment is considered the next therapeutic option for type 1 diabetes; while stimulating endogenous beta cells proliferation is the "holy grail" for those patients with exhausted beta cell mass. Here we are demonstrating that ... ...

Abstract	Pancreatic beta cells replenishment is considered the next therapeutic option for type 1 diabetes; while stimulating endogenous beta cells proliferation is the "holy grail" for those patients with exhausted beta cell mass. Here we are demonstrating that the pro-apoptotic receptor TMEM219 is expressed in fetal pancreas, in beta cell precursors and in
MeSH term(s)	Humans ; Cell Proliferation ; Diabetes Mellitus, Type 1/metabolism ; Insulin-Secreting Cells/metabolism ; Insulinoma/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Pancreatic Neoplasms/metabolism ; Transcription Factors/metabolism
Chemical Substances	MicroRNAs ; Mirn129 microRNA, human ; Transcription Factors ; TMEM219 protein, human
Language	English
Publishing date	2024-01-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2024.1306127
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Article ; Online: Idebenone and T2D: A new insulin-sensitizing drug for personalized therapy.

Dassano, Alice / Loretelli, Cristian / Fiorina, Paolo

Pharmacological research

2018 Volume 139, Page(s) 469–470

MeSH term(s)	Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Humans ; Hypoglycemic Agents/therapeutic use ; Insulin Resistance ; Precision Medicine ; Src Homology 2 Domain-Containing, Transforming Protein 1/metabolism ; Ubiquinone/analogs & derivatives ; Ubiquinone/therapeutic use
Chemical Substances	Hypoglycemic Agents ; Src Homology 2 Domain-Containing, Transforming Protein 1 ; Ubiquinone (1339-63-5) ; idebenone (HB6PN45W4J)
Language	English
Publishing date	2018-12-12
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2018.12.008
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Zs.A 721: Show issues

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Article ; Online: Cell therapy for type 1 diabetes.

Loretelli, Cristian / Assi, Emma / Seelam, Andy Joe / Ben Nasr, Moufida / Fiorina, Paolo

Expert opinion on biological therapy

2020 Volume 20, Issue 8, Page(s) 887–897

Abstract: Introduction: Type 1 diabetes (T1D) is a lifelong condition resulting from autoimmune destruction of insulin-producing β-cells. Islet or whole-pancreas transplantation is limited by the shortage of donors and need for chronic immune suppression. Novel ... ...

Abstract	Introduction: Type 1 diabetes (T1D) is a lifelong condition resulting from autoimmune destruction of insulin-producing β-cells. Islet or whole-pancreas transplantation is limited by the shortage of donors and need for chronic immune suppression. Novel strategies are needed to prevent β-cell loss and to rescue production of endogenous insulin. Areas covered: This review covers the latest advances in cell-based therapies for the treatment and prevention of T1D. Topics include adoptive transfer of cells with increased immunoregulatory potential for β-cell protection, and β-cell replacement strategies such as generation of insulin-producing β-like cells from unlimited sources. Expert opinion: Cell therapy provides an opportunity to prevent or reverse T1D. Adoptive transfer of autologous cells having enhanced immunomodulatory properties can suppress autoimmunity and preserve β-cells. Such therapies have been made possible by a combination of genome-editing techniques and transplantation of tolerogenic cells.
MeSH term(s)	Animals ; Cell Differentiation ; Cell- and Tissue-Based Therapy/methods ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 1/therapy ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Human Embryonic Stem Cells/cytology ; Human Embryonic Stem Cells/metabolism ; Humans ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/transplantation ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/metabolism ; T-Lymphocytes, Regulatory/transplantation
Language	English
Publishing date	2020-04-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052501-1
ISSN	1744-7682 ; 1471-2598
ISSN (online)	1744-7682
ISSN	1471-2598
DOI	10.1080/14712598.2020.1748596
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 6094: Show issues

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Article ; Online: Next-gen therapeutics to spare and expand beta-cell mass.

Bolla, Andrea Mario / Usuelli, Vera / Ben Nasr, Moufida / Frigerio, Sofia / Loretelli, Cristian / D'Addio, Francesca / Fiorina, Paolo

Current opinion in pharmacology

2021 Volume 61, Page(s) 77–82

Abstract: The most effective and physiological way to treat hyperglycemia is to restore beta-cell function and to rescue production of endogenous insulin. Increasing evidence suggests that both type 1 and type 2 diabetes are characterized by a significant defect ... ...

Abstract	The most effective and physiological way to treat hyperglycemia is to restore beta-cell function and to rescue production of endogenous insulin. Increasing evidence suggests that both type 1 and type 2 diabetes are characterized by a significant defect in beta-cell mass, leading to the manifestation of the disease. Novel alternative approaches are needed to spare and expand beta-cell mass in patients with diabetes. This review sets out to describe the latest findings on how to restore the beta-cell mass and function in both forms of diabetes to modulate their progression.
MeSH term(s)	Diabetes Mellitus, Type 2/drug therapy ; Humans ; Hyperglycemia ; Insulin ; Insulin-Secreting Cells
Chemical Substances	Insulin
Language	English
Publishing date	2021-10-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2021.09.001
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Zs.A 5608: Show issues

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Article ; Online: Novel Soluble Mediators of Innate Immune System Activation in Solid Allograft Rejection.

Usuelli, Vera / Loretelli, Cristian / Seelam, Andy Joe / Pastore, Ida / D'Addio, Francesca / Ben Nasr, Moufida / Fiorina, Paolo

Transplantation

2021 Volume 106, Issue 3, Page(s) 500–509

Abstract: During the past years, solid allograft rejection has been considered the consequence of either cellular- or antibody-mediated reaction both being part of the adaptive immune response, whereas the role of innate immunity has been mostly considered less ... ...

Abstract	During the past years, solid allograft rejection has been considered the consequence of either cellular- or antibody-mediated reaction both being part of the adaptive immune response, whereas the role of innate immunity has been mostly considered less relevant. Recently, a large body of evidence suggested that the innate immune response and its soluble mediators may play a more important role during solid allograft rejection than originally thought. This review will highlight the role of novel soluble mediators that are involved in the activation of innate immunity during alloimmune response and solid allograft rejection. We will also discuss emerging strategies to alleviate the aforementioned events. Hence, novel, feasible, and safe clinical therapies are needed to prevent allograft loss in solid organ transplantation. Fully understanding the role of soluble mediators of innate immune system activation may help to mitigate solid allograft rejection and improve transplanted recipients' outcomes.
MeSH term(s)	Allografts ; Graft Rejection/prevention & control ; Immune System ; Immunity, Innate ; Organ Transplantation/adverse effects ; Transplantation, Homologous
Language	English
Publishing date	2021-05-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/TP.0000000000003834
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Zs.A 488: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 509: Show issues

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Article ; Online: Daytime hypoglycemic episodes during the use of an advanced hybrid closed loop system.

Rossi, Antonio / Montefusco, Laura / Reseghetti, Elia / Pastore, Ida Fabrizia / Rossi, Giada / Usuelli, Vera / Loretelli, Cristian / Boci, Denisa / Ben Nasr, Moufida / D'Addio, Francesca / Bucciarelli, Loredana / Argenti, Sabrina / Morpurgo, Paola / Lunati, Maria Elena / Fiorina, Paolo

Diabetes research and clinical practice

2023 Volume 206, Page(s) 111011

Abstract: Aims: The use of advanced hybrid closed loop systems is spreading due to the beneficial effects on glycometabolic control obtained in patients with type 1 diabetes. However, hypoglycemic episodes can be sometimes a matter of concern. We aim to compare ... ...

Abstract	Aims: The use of advanced hybrid closed loop systems is spreading due to the beneficial effects on glycometabolic control obtained in patients with type 1 diabetes. However, hypoglycemic episodes can be sometimes a matter of concern. We aim to compare the hypoglycemic risk of an advanced hybrid closed loop system and a predictive low glucose suspend sensor augmented pump. Methods: In this retrospective three months observational study, we included 30 patients using Medtronic Minimed™ 780G advanced hybrid closed loop system and 30 patients using a Medtronic Minimed™ predictive low glucose suspend sensor augmented pump. Results: The advanced hybrid closed loop system reduced the time spent above 180 mg/dL threshold and increased the time in range as compared to the predictive low glucose suspend. No severe hypoglycemia occurred in both groups and no differences were observed in the percentage of time spent below 70 mg/dl and 54 mg/dl glucose threshold. Nevertheless, more hypoglycemic episodes were recorded during daytime, but not in nighttime, with the use of the advanced hybrid closed loop system. Conclusions: Our results confirmed the general improvement of glycemic outcomes obtained with the advanced hybrid closed loop system; however more hypoglycemic episodes during daytime were evident.
MeSH term(s)	Humans ; Blood Glucose ; Retrospective Studies ; Insulin/therapeutic use ; Insulin Infusion Systems ; Hypoglycemia/prevention & control ; Hypoglycemia/chemically induced ; Hypoglycemic Agents/therapeutic use ; Diabetes Mellitus, Type 1/drug therapy ; Glucose/therapeutic use ; Blood Glucose Self-Monitoring
Chemical Substances	Blood Glucose ; Insulin ; Hypoglycemic Agents ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-11-11
Publishing country	Ireland
Document type	Observational Study ; Journal Article
ZDB-ID	632523-3
ISSN	1872-8227 ; 0168-8227
ISSN (online)	1872-8227
ISSN	0168-8227
DOI	10.1016/j.diabres.2023.111011
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Zs.A 2047: Show issues

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Article ; Online: Broadening horizons in mechanisms, management, and treatment of diabetic kidney disease.

Petrazzuolo, Adriana / Sabiu, Gianmarco / Assi, Emma / Maestroni, Anna / Pastore, Ida / Lunati, Maria Elena / Montefusco, Laura / Loretelli, Cristian / Rossi, Giada / Ben Nasr, Moufida / Usuelli, Vera / Xie, Yanan / Balasubramanian, Hari Baskar / Zocchi, Monica / El Essawy, Basset / Yang, Jun / D'Addio, Francesca / Fiorina, Paolo

Pharmacological research

2023 Volume 190, Page(s) 106710

Abstract: Diabetic kidney disease (DKD) is the first cause of end-stage kidney disease in patients with diabetes and its prevalence is increasing worldwide. It encompasses histological alterations that mainly affect the glomerular filtration unit, which include ... ...

Abstract	Diabetic kidney disease (DKD) is the first cause of end-stage kidney disease in patients with diabetes and its prevalence is increasing worldwide. It encompasses histological alterations that mainly affect the glomerular filtration unit, which include thickening of the basement membrane, mesangial cell proliferation, endothelial alteration, and podocyte injury. These morphological abnormalities further result in a persistent increase of urinary albumin-to-creatinine ratio and in a reduction of the estimated glomerular filtration rate. Several molecular and cellular mechanisms have been recognized, up to date, as major players in mediating such clinical and histological features and many more are being under investigation. This review summarizes the most recent advances in understanding cell death mechanisms, intracellular signaling pathways and molecular effectors that play a role in the onset and progression of diabetic kidney damage. Some of those molecular and cellular mechanisms have been already successfully targeted in preclinical models of DKD and, in some cases, strategies have been tested in clinical trials. Finally, this report sheds light on the relevance of novel pathways that may become therapeutic targets for future applications in DKD.
MeSH term(s)	Humans ; Diabetic Nephropathies/metabolism ; Podocytes/pathology ; Signal Transduction ; Glomerular Filtration Rate ; Diabetes Mellitus/metabolism
Language	English
Publishing date	2023-03-04
Publishing country	Netherlands
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2023.106710
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Zs.A 721: Show issues

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Article ; Online: eATP and autoimmune diabetes.

Loretelli, Cristian / Pastore, Ida / Lunati, Maria Elena / Abdelsalam, Ahmed / Usuelli, Vera / Assi, Emma / Fiorina, Emma / Loreggian, Lara / Balasubramanian, Hari Baskar / Xie, Yanan / Yang, Jun / El Essawy, Basset / Montefusco, Laura / D'Addio, Francesca / Ben Nasr, Moufida / Fiorina, Paolo

Pharmacological research

2023 Volume 190, Page(s) 106709

Abstract: Purpose of review: The purine nucleotide adenosine triphosphate (ATP) is released into extracellular spaces as extracellular ATP (eATP) as a consequence of cell injury or death and activates the purinergic receptors. Once released, eATP may facilitate T- ...

Abstract	Purpose of review: The purine nucleotide adenosine triphosphate (ATP) is released into extracellular spaces as extracellular ATP (eATP) as a consequence of cell injury or death and activates the purinergic receptors. Once released, eATP may facilitate T-lymphocyte activation and differentiation. The purpose of this review is to elucidate the role of ATP-mediated signaling in the immunological events related to type 1 diabetes (T1D). Recent findings: T lymphocytes mediate immune response during the onset of T1D and promote pancreatic islet or whole pancreas rejection in transplantation. Recent data suggest a potential role for eATP in early steps of T1D onset and of allograft rejection. In different preclinical experimental models and clinical trials, several drugs targeting purinergic signaling have been employed to abrogate lymphocyte activation and differentiation, thus representing an achievable treatment to prevent/revert T1D or to induce long-term islet allograft function. Summary: In preclinical and clinical settings, eATP-signaling inhibition induces immune tolerance in autoimmune disease and in allotransplantation. In this view, the purinergic system may represent a novel therapeutic target for auto- and allo-immunity.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 1/drug therapy ; Autoimmune Diseases/drug therapy ; Transplantation, Homologous ; T-Lymphocytes/metabolism ; Adenosine Triphosphate/metabolism
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2023-02-25
Publishing country	Netherlands
Document type	Review ; Journal Article
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2023.106709
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Zs.A 721: Show issues

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Article ; Online: Sitagliptin favorably modulates immune-relevant pathways in human beta cells.

Malvandi, Amir Mohammad / Loretelli, Cristian / Ben Nasr, Moufida / Zuccotti, Gian Vincenzo / Fiorina, Paolo

Pharmacological research

2019 Volume 148, Page(s) 104405

Abstract: Type 2 diabetes (T2D) is a condition characterized by hyperglycemia and chronic complications. Antidiabetic drugs and lifestyle interventions are the current gold standard therapy for T2D; current therapies, however, can only delay long-term diabetic ... ...

Abstract	Type 2 diabetes (T2D) is a condition characterized by hyperglycemia and chronic complications. Antidiabetic drugs and lifestyle interventions are the current gold standard therapy for T2D; current therapies, however, can only delay long-term diabetic complications and can additionally be associated with beta cell failure. While the mechanism of beta cell failure is well-studied, little is known about the immunological and inflammatory events associated with antidiabetic agents. Here we studied the effects of three antidiabetic drugs (Metformin, Sitagliptin, and Liraglutide) on immune-relevant pathways in a human beta cell line. Costimulatory molecule expression, cytokine secretion, and gene expression profiles were evaluated at different time points following challenge with the aforementioned antidiabetic agents. Our results showed that these three antidiabetic agents, particularly Sitagliptin, downregulate HLA Class I and II expression and upregulate the immune-regulatory molecules PD-L1 and CTLA4. Metformin and Liraglutide were shown to elicit significantly greater release of TNFa, IL-6, and GM-CSF, while Sitagliptin had a lesser effect on pro-inflammatory cytokine production. Gene expression analysis confirmed the aforementioned observations and also demonstrated upregulation of NOS2, SIRT1, SITR3, POLRMT, MRPL43 and NFkB with antidiabetic agents. We conclude that Sitagliptin most effectively modulates beneficial immune-relevant pathways in a human beta cell line.
MeSH term(s)	Cell Line ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/immunology ; Diabetes Mellitus, Type 2/metabolism ; Gene Expression/drug effects ; Glucagon-Like Peptide 1/metabolism ; Glycated Hemoglobin A/metabolism ; Humans ; Hypoglycemic Agents/pharmacology ; Immunologic Factors/metabolism ; Inflammation/drug therapy ; Inflammation/immunology ; Inflammation/metabolism ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/immunology ; Insulin-Secreting Cells/metabolism ; Interleukin-6/metabolism ; Liraglutide/pharmacology ; Metformin/pharmacology ; Signal Transduction/drug effects ; Signal Transduction/immunology ; Sitagliptin Phosphate/pharmacology ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation/drug effects
Chemical Substances	Glycated Hemoglobin A ; Hypoglycemic Agents ; Immunologic Factors ; Interleukin-6 ; Tumor Necrosis Factor-alpha ; Liraglutide (839I73S42A) ; Glucagon-Like Peptide 1 (89750-14-1) ; Metformin (9100L32L2N) ; Sitagliptin Phosphate (TS63EW8X6F)
Language	English
Publishing date	2019-08-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2019.104405
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