الثلاثاء، 29 مارس 2016

Matrix metalloproteinases in the wound microenvironment

Krejner A, Litwiniuk M, Grzela T

Source Chronic Wound Care Management and Research http://ift.tt/1MRurys

Your Rights, One Voice: Ashlynn’s Story

SAS_ 2016_3-29

SAS_ 2016_3-29

Education about diabetes and its care can sometimes make a big difference.

The CREST program, run by the city of Santa Monica, California, adds learning adventures to the lives of children who attend the program. This city-funded program provides enrichment classes, including music, art, theater and sports to children in grades K-5. Nine-year-old Ashlynn had been participating in the program since she was five, playing volleyball and participating in track and field.

The program feared liability after Ashlynn’s type 1 diabetes diagnosis.

But in April 2015, Ashlynn was diagnosed with type 1 diabetes and her access to CREST activities became more limited. Ashlynn’s mother, Audrey, learned that the program would not train its staff to administer glucagon. Glucagon is sometimes necessary when a person with diabetes experiences extremely low blood glucose, also known as hypoglycemia. Without trained staff around, Ashlynn would not be fully protected during program activities, unless her mother could also be there to provide it. Audrey was told the City of Santa Monica feared a lawsuit if its staff did not administer glucagon correctly—and that was the reason for this policy.

Ashlynn loved being part of the CREST program. 

Audrey, a single mother who could not always be there the entire time, worried that if the CREST staff was not able to provide glucagon when it was needed, Ashlynn could not attend. This was not acceptable. So Audrey contacted the program directors and tried to educate them about diabetes care. She also stressed that it would not endanger Ashlynn’s life if someone gave her glucagon, even if she didn’t need it.

But the program’s policy still did not change. Ashlynn was only able to attend CREST when Audrey could also be there. That meant that Ashlynn had to miss out on many activities she loved.

Audrey contacted the American Diabetes Association® for help.

She confirmed that Ashlynn had the legal right to fully participate in the program. A legal advocate at the Association gave Audrey some information and guidance. Audrey then wrote a letter to the program that outlined Ashlynn’s rights and addressed the program’s concerns about its legal responsibility.

Things turned around.

The directors of CREST program changed the policy and agreed to train their staff about type 1 diabetes, diabetes care (including glucagon administration) and the signs and symptoms of hypoglycemia. Ashlynn would be able to fully attend the program once again.

Audrey’s experience working on this issue was a positive one. She says that the program’s directors were nothing but gracious through the whole process. And the result was what she wanted for Ashlynn.

Audrey’s advice

The Association is here to help. You can fight discrimination when you understand the laws that protect people with diabetes and can educate others about diabetes care. Sometimes information and negotiation go a long way.

“Thank you to the American Diabetes Association’s legal advocate for her time, effort and expertise,” says Audrey Berry. “When you see your child triumph through the daily struggles of managing type 1 diabetes, you will go to great lengths to ensure his or her well-being. For every parent out there who feels defeated by the weight of advocating for your child, remind yourself that there are people out there who will help. When you feel like you are going through a rough journey all by yourself, stay true to yourself and true to your cause. The city of Santa Monica, the American Diabetes Association and I worked positively together to achieve the best outcome for my daughter Ashlynn. For this I am grateful.”


 

The American Diabetes Association leads the effort to prevent and eliminate discrimination against people with diabetes at school, at work and in other parts of daily life. If you need help, call 1-800-DIABETES or visit http://ift.tt/1zCIiW2.

Through our nationwide Safe at School program, the Association is dedicated to making sure that all children with diabetes are medically safe at school and have the same educational opportunities as their peers. Visit our Safe at School website for information and resources.

Give the gift of fairness — donate now to help people with diabetes facing discrimination, just like Ashlynn.

donate now



Source Diabetes Stops Here http://ift.tt/1pHsrne

الجمعة، 25 مارس 2016

الخميس، 24 مارس 2016

Health Tip: Setting Goals for a Healthier Lifestyle

Title: Health Tip: Setting Goals for a Healthier Lifestyle
Category: Health News
Created: 3/24/2016 12:00:00 AM
Last Editorial Review: 3/24/2016 12:00:00 AM

Source MedicineNet Diabetes General http://ift.tt/1VLTJWh

Euglycemia Restoration by Central Leptin in Type 1 Diabetes Requires STAT3 Signaling but Not Fast-Acting Neurotransmitter Release

Central leptin action is sufficient to restore euglycemia in insulinopenic type 1 diabetes (T1D); however, the underlying mechanism remains poorly understood. To examine the role of intracellular signal transducer and activator of transcription 3 (STAT3) pathways, we used LepRs/s mice with disrupted leptin-phosphorylated STAT3 signaling to test the effect of central leptin on euglycemia restoration. These mice developed streptozocin-induced T1D, which was surprisingly not associated with hyperglucagonemia, a typical manifestation in T1D. Further, leptin action on euglycemia restoration was abrogated in these mice, which was associated with refractory hypercorticosteronemia. To examine the role of fast-acting neurotransmitters glutamate and -aminobutyric acid (GABA), two major neurotransmitters in the brain, from leptin receptor (LepR) neurons, we used mice with disrupted release of glutamate, GABA, or both from LepR neurons. Surprisingly, all mice responded normally to leptin-mediated euglycemia restoration, which was associated with expected correction from hyperglucagonemia and hyperphagia. In contrast, mice with loss of glutamate and GABA appeared to develop an additive obesity effect over those with loss of single neurotransmitter release. Thus, our study reveals that STAT3 signaling, but not fast-acting neurotransmitter release, is required for leptin action on euglycemia restoration and that hyperglucagonemia is not required for T1D.



Source Diabetes Pathophysiology http://ift.tt/1VHQBuv

Disulfide Mispairing During Proinsulin Folding in the Endoplasmic Reticulum

Proinsulin folding within the endoplasmic reticulum (ER) remains incompletely understood, but it is clear that in mutant INS gene–induced diabetes of youth (MIDY), progression of the (three) native disulfide bonds of proinsulin becomes derailed, causing insulin deficiency, β-cell ER stress, and onset of diabetes. Herein, we have undertaken a molecular dissection of proinsulin disulfide bond formation, using bioengineered proinsulins that can form only two (or even only one) of the native proinsulin disulfide bonds. In the absence of preexisting proinsulin disulfide pairing, Cys(B19)-Cys(A20) (a major determinant of ER stress response activation and proinsulin stability) preferentially initiates B-A chain disulfide bond formation, whereas Cys(B7)-Cys(A7) can initiate only under oxidizing conditions beyond that existing within the ER of β-cells. Interestingly, formation of these two "interchain" disulfide bonds demonstrates cooperativity, and together, they are sufficient to confer intracellular transport competence to proinsulin. The three most common proinsulin disulfide mispairings in the ER appear to involve Cys(A11)-Cys(A20), Cys(A7)-Cys(A20), and Cys(B19)-Cys(A11), each disrupting the critical Cys(B19)-Cys(A20) pairing. MIDY mutations inhibit Cys(B19)-Cys(A20) formation, but treatment to force oxidation of this disulfide bond improves folding and results in a small but detectable increase of proinsulin export. These data suggest possible therapeutic avenues to ameliorate ER stress and diabetes.



Source Diabetes Pathophysiology http://ift.tt/1XP8GFt

الثلاثاء، 22 مارس 2016