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1 nist of NK1R, in patients with idiopathic or diabetic gastroparesis.
2 with placebo, in patients with idiopathic or diabetic gastroparesis.
3 expression in ICC may directly contribute to diabetic gastroparesis.
4 is and compare findings in idiopathic versus diabetic gastroparesis.
5 strointestinal motility disorders, including diabetic gastroparesis.
6 ht be a therapeutic option for patients with diabetic gastroparesis.
7 ing studies on the morbidity associated with diabetic gastroparesis.
8 changes in the gastric wall in patients with diabetic gastroparesis.
9 erstitial cells of Cajal (ICCs) is common in diabetic gastroparesis.
10  a loss of Kit expression and development of diabetic gastroparesis.
11 has shown to be beneficial in idiopathic and diabetic gastroparesis.
12 cells could contribute to the development of diabetic gastroparesis.
13 resent to a lesser extent in idiopathic than diabetic gastroparesis.
14  in patients with diabetes) in patients with diabetic gastroparesis.
15 cterized clinical profiles in idiopathic and diabetic gastroparesis and are defining roles of gastric
16          We identified a correlation between diabetic gastroparesis and cardiovascular disease, hyper
17 no1 gene in gastric muscles of patients with diabetic gastroparesis and nondiabetic control tissues.
18 , 46.7 [13.2] years), of whom 31 (81.6%) had diabetic gastroparesis, and 7 (18.4%) had idiopathic gas
19     Peripheral neuropathy (PN) is present in diabetic gastroparesis but is not described in idiopathi
20 vomiting and also improved other symptoms of diabetic gastroparesis compared with placebo.
21                                              Diabetic gastroparesis (delayed gastric emptying) is a w
22  proposed that Kit expression is lost during diabetic gastroparesis due to increased levels of oxidat
23                   Furthermore, patients with diabetic gastroparesis express mRNA for a previously unk
24                                              Diabetic gastroparesis involves neuropathy, myopathy, an
25        The importance of glycemic control in diabetic gastroparesis is a focus of current investigati
26 e) intended to reduce the aspiration risk of diabetic gastroparesis is likely over-utilized and may o
27              The pathophysiological basis of diabetic gastroparesis is poorly understood, in large pa
28         In a clinical trial of patients with diabetic gastroparesis, relamorelin (10 mug twice daily)
29 ession and splicing of Ano1 in patients with diabetic gastroparesis that alter the electrophysiologic
30 an age, 55 y; 88% with type 2 diabetes) with diabetic gastroparesis with moderate to severe symptoms