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Biopsychosocial Factors Associated With Satisfaction and Sustained Use of Artificial Pancreas Technology and Its Components: a Call to the Technology Field

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6535227/

https://www.ncbi.nlm.nih.gov/pubmed/30259309?dopt=Abstract

TITLE:
Biopsychosocial Factors Associated With Satisfaction and Sustained Use of Artificial Pancreas Technology and Its Components: a Call to the Technology Field.

DESCRIPTION:
Related Articles

Biopsychosocial Factors Associated With Satisfaction and Sustained Use of Artificial Pancreas Technology and Its Components: a Call to the Technology Field.

Curr Diab Rep. 2018 09 26;18(11):114

Authors: Forlenza GP, Messer LH, Berget C, Wadwa RP, Driscoll KA

Abstract

PURPOSE OF REVIEW: Summarize biopsychosocial factors associated with using continuous glucose monitors (CGMs), insulin pumps, and artificial pancreas (AP) systems and provide a “call to the field” about their importance to technology uptake and maintained use.

RECENT FINDINGS: Insulin pumps and CGMs are becoming standard of care for individuals with type 1 diabetes (T1D). AP systems combining a CGM, insulin pump, and automated dosing algorithm are available for commercial use. Despite improved glycemic control with AP system use, numerous barriers exist which may limit their benefit. Studies on components of AP systems (pumps, CGMs) are limited and demonstrate mixed results of their impact on fear of hypoglycemia, adherence, quality of life, depression and anxiety, and diabetes distress. Studies examining biopsychological factors associated specifically with sustained use of AP systems are also sparse. Biological, psychological and social impacts of AP systems have been understudied and the information they provide has not been capitalized upon.

PMID: 30259309 [PubMed – indexed for MEDLINE]

PMID:
PubMed:30259309

DATE FOUND:
09/17/19 06:02AM

LINK / URL:
https://www.ncbi.nlm.nih.gov/pubmed/30259309?dopt=Abstract

Will Genetic Engineering Carry Xenotransplantation of Pig Islets to the Clinic?

https://link.springer.com/article/10.1007%2Fs11892-018-1074-5

https://www.ncbi.nlm.nih.gov/pubmed/30229378?dopt=Abstract

TITLE:
Will Genetic Engineering Carry Xenotransplantation of Pig Islets to the Clinic?

DESCRIPTION:
Related Articles

Will Genetic Engineering Carry Xenotransplantation of Pig Islets to the Clinic?

Curr Diab Rep. 2018 09 18;18(11):103

Authors: Kemter E, Denner J, Wolf E

Abstract

PURPOSE OF REVIEW: Porcine islets represent a potentially attractive beta-cell source for xenotransplantation into patients with type 1 diabetes, who are not eligible to islet allo-transplantation due to a lack of suitable human donor organs. Recent progress in genetic engineering/gene editing of donor pigs provides new opportunities to overcome rejection of xeno-islets, to improve their engraftment and insulin secretion capacity, and to reduce the risk for transmission of porcine endogenous retroviruses. This review summarizes the current issues and progress in islet xenotransplantation with special emphasis on genetically modified/gene edited donor pigs.

RECENT FINDINGS: Attempts to overcome acute rejection of xeno-islets, especially after intraportal transplantation into the liver, include the genetic elimination of specific carbohydrate antigens such as αGal, Neu5Gc, and Sd(a) for which humans and-in part-non-human primates have natural antibodies that bind to these targets leading to activation of complement and coagulation. A complementary approach is the expression of one or more human complement regulatory proteins (hCD46, hCD55, hCD59). Transgenic attempts to overcome cellular rejection of islet xenotransplants include the expression of proteins that inhibit co-stimulation of T cells. Expression of glucagon-like peptide-1 and M3 muscarinic receptors has been shown to increase the insulin secretion of virally transduced porcine islets in vitro and it will be interesting to see the effects of these modifications in transgenic pigs and islet products derived from them. Genome-wide inactivation of porcine endogenous retrovirus (PERV) integrants by mutating their pol genes using CRISPR/Cas9 is a recent approach to reduce the risk for PERV transmission by xeno-islets. Genetic engineering/gene editing of xeno-islet donor pigs facilitated major progress towards clinical islet xenotransplantation. The required set of genetic modifications will depend on the source of islets (fetal/neonatal vs. adult), the mode of delivery (encapsulated vs. free), and the transplantation site.

PMID: 30229378 [PubMed – indexed for MEDLINE]

PMID:
PubMed:30229378

DATE FOUND:
09/17/19 06:02AM

LINK / URL:
https://www.ncbi.nlm.nih.gov/pubmed/30229378?dopt=Abstract

Therapies to Suppress β Cell Autoimmunity in Type 1 Diabetes

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6105696/

https://www.ncbi.nlm.nih.gov/pubmed/30166987?dopt=Abstract

TITLE:
Therapies to Suppress β Cell Autoimmunity in Type 1 Diabetes.

DESCRIPTION:
Related Articles

Therapies to Suppress β Cell Autoimmunity in Type 1 Diabetes.

Front Immunol. 2018;9:1891

Authors: Kroger CJ, Clark M, Ke Q, Tisch RM

Abstract

Type 1 diabetes (T1D) is an autoimmune disease that is generally considered to be T cell-driven. Accordingly, most strategies of immunotherapy for T1D prevention and treatment in the clinic have targeted the T cell compartment. To date, however, immunotherapy has had only limited clinical success. Although certain immunotherapies have promoted a protective effect, efficacy is often short-term and acquired immunity may be impacted. This has led to the consideration of combining different approaches with the goal of achieving a synergistic therapeutic response. In this review, we will discuss the status of various T1D therapeutic strategies tested in the clinic, as well as possible combinatorial approaches to restore β cell tolerance.

PMID: 30166987 [PubMed – indexed for MEDLINE]

PMID:
PubMed:30166987

DATE FOUND:
10/01/19 06:02AM

LINK / URL:
https://www.ncbi.nlm.nih.gov/pubmed/30166987?dopt=Abstract

Carbamazepine, a beta-cell protecting drug, reduces type 1 diabetes incidence in NOD mice

https://www.nature.com/articles/s41598-018-23026-w

https://www.ncbi.nlm.nih.gov/pubmed/29545618?dopt=Abstract

TITLE:
Carbamazepine, a beta-cell protecting drug, reduces type 1 diabetes incidence in NOD mice.

DESCRIPTION:
Related Articles

Carbamazepine, a beta-cell protecting drug, reduces type 1 diabetes incidence in NOD mice.

Sci Rep. 2018 03 15;8(1):4588

Authors: Lee JTC, Shanina I, Chu YN, Horwitz MS, Johnson JD

Abstract

Pancreatic beta-cells are selectively destroyed by the host immune system in type 1 diabetes. Thus, drugs that preserve beta-cell mass and/or function have the potential to prevent or slow the progression of this disease. We recently reported that the use-dependent sodium channel blocker, carbamazepine, protects beta-cells from inflammatory cytokines in vitro. Here, we tested the effects of carbamazepine treatment in female non-obese diabetic (NOD) mice by supplementing LabDiet 5053 with 0.5% w/w carbamazepine to achieve serum carbamazepine levels of 14.98 ± 3.19 µM. Remarkably, diabetes incidence over 25 weeks, as determined by fasting blood glucose, was ~50% lower in carbamazepine treated animals. Partial protection from diabetes in carbamazepine-fed NOD mice was also associated with improved glucose tolerance at 6 weeks of age, prior to the onset of diabetes in our colony. Less insulitis was detected in carbamazepine treated NOD mice at 6 weeks of age, but we did not observe differences in CD4+ and CD8+ T cell composition in the pancreatic lymph node, as well as circulating markers of inflammation. Taken together, our results demonstrate that carbamazepine reduces the development of type 1 diabetes in NOD mice by maintaining functional beta-cell mass.

PMID: 29545618 [PubMed – indexed for MEDLINE]

PMID:
PubMed:29545618

DATE FOUND:
09/26/19 06:00AM

LINK / URL:
https://www.ncbi.nlm.nih.gov/pubmed/29545618?dopt=Abstract

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