ライフサイエンスコーパス: diabetic

1 used for special groups of consumers (obese, diabetic).

2 rotocol, is a promising treatment for type I diabetics.

3 the impact of LTBI screening programs among diabetics.

4 rinary sTyro3 and sMer than normoalbuminuric diabetics.

5 n provide lifesaving benefits to millions of diabetics.

6 Wild type, diabetic Akita mice as well as mouse glomerular endothel

7 Diabetic Akita mice, which carry a heterozygous C96Y Ins

8 reated counterparts, ReninAAV-treated type 1 diabetic Akita/129 mice exhibited a substantial increase

9 rom small resistance adipose arteries of non-diabetic and clinically diagnosed type 2 diabetic patien

10 ive GLP-1 vs glucagon production in both non-diabetic and diabetic islets, suggesting a positive role

11 th Indian TB patients with and without DM to diabetic and non-diabetic controls without TB.

12 omposition of RSSC components between type-1 diabetic and non-diabetic individuals.

13 trols, whereas no difference was observed in diabetic and nondiabetic REDD1-deficient mice.

14 m is implicated in abnormal wound healing in diabetic and older adults.

15 rs the range of tear glucose levels for both diabetics and healthy subjects.

16 algia, weakness, loss of vitality, and being diabetic) and major decreases in quality-of-life scores.

17 f those randomized, 42% were women, 25% were diabetic, and 91% were hypertensive; 104 started interve

18 > 600 nmol/mg mito prot, in both control and diabetic animals.

19 action of orally administered CrP in type 1 diabetic apolipoprotein E-deficient (ApoE(-/-)) mice and

20 Diabetics are at increased risk for eye infections inclu

21 To confirm a direct role of TSP-1 in diabetic atherosclerosis, hyperglycemic TSP-1(-/-)/ApoE(

22 The impaired diabetic BMPC angiogenic function was rescued by adenovi

23 R is a promising target for the treatment of diabetic bone marrow mobilopathy and vascular disease.

24 C57BL/6J mice were rendered obese and pre-diabetic by feeding a high-fat diet for 15 weeks and the

25 and cathepsin K knockout mice were rendered diabetic by streptozotocin (STZ) injections.

26 Non-diabetic (C) db/m mice were followed concurrently.

27 Diabetic cardiomyopathy (DCM) has been increasingly cons

28 nto the mechanism driving the development of diabetic cardiomyopathy, we studied a unique model of T2

29 art and contribute to the pathophysiology of diabetic cardiomyopathy.

30 e molecular mechanisms of this regulation in diabetic cataract still need to be investigated.

31 d that miR-30a was markedly downregulated in diabetic cataract tissues.

32 BKCa channels in diabetic cells exhibited reduced Ca(2+) sensitivity, sin

33 racellular reduction of alphaKG synthesis in diabetic CMSCs and in the whole heart of HFD mice.

34 ion reactions, which are the major causes of diabetic complications.

35 adical activity underlie the pathogenesis of diabetic complications.

36 nificant biomarker towards the prediction of diabetic complications.

37 of hyperglycemic excursions associated with diabetic complications.

38 eostasis; however, how MAM is affected under diabetic condition remains elusive.

39 role in maintaining BMPC function under the diabetic condition.

40 in liver-related hypothalamic neurons in the diabetic condition.

41 vity of liver-related neurons in control and diabetic conditions is not known.

42 ents with and without DM to diabetic and non-diabetic controls without TB.

43 clearance in the scaffold groups compared to diabetic controls.

44 tients with equivalent neuropathy and 11 non-diabetic controls.

45 Diabetic D2 mice manifested increased mitochondrial DNA

46 Diabetic dogs demonstrated significant upregulation of g

47 To test the hypothesis that diabetic dogs have similar metabolomic perturbations to

48 n the KFTS were more likely to be from older diabetic donors, had a higher frequency of poor ex vivo

49 Metformin, an anti-diabetic drug commonly used for type 2 diabetes therapy,

50 can serve as a promising candidate for anti-diabetic drug discovery; and b) provide a rational basis

51 zolidinediones (TZD) function as potent anti-diabetic drugs through their direct action on the nuclea

52 analogues represent a new generation of anti-diabetic drugs, which have also demonstrated propensity

53 onsecutive patients attending routine annual diabetic eye screening between June 1, 2012, and Novembe

54 Mean FAZ area was greater in diabetic eyes compared with control eyes both in the sup

55 Mean VLD was also lower in diabetic eyes compared with control eyes in both the sup

56 Mean VAD was lower in diabetic eyes compared with control eyes in both the sup

57 Doppler OCT can measure TRBF in healthy and diabetic eyes.

58 Male Zucker diabetic fatty (ZDF) and Male Zucker lean (ZL) control r

59 Diabetic foot ulcer microbiota were found to exist in on

60 nopathy, nephropathy, peripheral neuropathy, diabetic foot, and ischemic heart disease were 21.9%, 17

61 erstitial cells of Cajal (ICCs) is common in diabetic gastroparesis.

62 ovel role for miR-146a in protecting against diabetic glomerulopathy and podocyte injury.

63 om biopsies performed from 1995 to 2011 with diabetic glomerulosclerosis as the only glomerular disea

64 plasmid DNA (pDNA) encoding GLP-1 decreased diabetic glucose levels to the normoglycemic range with

65 interval, 1.28-1.91; P<0.001) than in non-IT diabetics (hazard ratio, 1.17; 95% confidence interval,

66 showed stronger mortality association in IT diabetics (hazard ratio, 1.57; 95% confidence interval,

67 th and eye-care practitioners need to expand diabetic health education and promotion among diabetic p

68 lation of Akt and ERK phosphorylation in the diabetic heart.

69 rmed that cardiac DHA levels are elevated in diabetic humans relative to controls.

70 increased diacylglycerol (DG) production in diabetic hyperglycaemia.

71 In NUGENOB, diabetic individuals lost a mean of 2.04 kg (95% CI: -0.

72 roEL (BPSL2697) was specifically impaired in diabetic individuals.

73 C components between type-1 diabetic and non-diabetic individuals.

74 differentially methylated regions (DMRs) in diabetic islets, and to investigate the function of DMRs

75 mmune system in obesity; inflammation within diabetic islets, brain, liver, gut, and muscle; the role

76 glucagon production in both non-diabetic and diabetic islets, suggesting a positive role of linaglipt

77 96]; p<0.0001), and were more likely to have diabetic ketoacidosis (11% [61/537] vs 0.3% [30/11 696];

78 4.42 [95% CI, -6.15 to -2.69]; P < .001) and diabetic ketoacidosis (3.64 vs 4.26 per 100 patient-year

79 requency of AKI in children hospitalized for diabetic ketoacidosis (DKA) has not been previously exam

80 ine whether rates of severe hypoglycemia and diabetic ketoacidosis are lower with insulin pump therap

81 tcomes were rates of severe hypoglycemia and diabetic ketoacidosis during the most recent treatment y

82 Severe hypoglycemia and diabetic ketoacidosis were absent in patients with funct

83 ed a significant increase in C1-Ten level in diabetic kidney and in high glucose-induced damaged podo

84 is a spectrum of biological processes in the diabetic kidney and that assessing protein networks may

85 Pathogenetic markers of diabetic kidney disease (DKD) progression to ESRD are la

86 with type 1 had significantly higher odds of diabetic kidney disease (odds ratio [OR], 2.58; 95% CI,

87 However, no T2D mouse model of combined diabetic kidney disease and atherosclerosis exists.

88 Diabetic kidney disease is among the most frequent compl

89 terized for a wider range of cross-sectional diabetic kidney disease phenotypes.

90 rates of the development and progression of diabetic kidney disease than placebo.

91 Diabetic kidney disease, retinopathy, peripheral neuropa

92 s (P=6.1x10(-4)) associated with the risk of diabetic kidney disease.

93 BTBR Lep(ob) mice exhibited diabetic kidney disease.

94 onversions (P=3.0x10(-6)) in pathogenesis of diabetic kidney disease.

95 s of lower frequency influencing the risk of diabetic kidney disease.

96 e sought to provide a set of gene profile in diabetic kidneys.

97 dothelial growth factor therapy in eyes with diabetic macular edema (DME) with vision loss after macu

98 Diabetic retinopathy, diabetic macular edema (DME), vision-threatening diabeti

99 (PDR), with or without concomitant baseline diabetic macular edema (DME).

100 Total of 456 patients with center-involved diabetic macular edema (DME).

101 Diabetic macular edema is one of the leading causes of v

102 CF photographs of 30 eyes (20 patients) with diabetic macular edema were obtained.

103 treal Aflibercept Injection in Patients With Diabetic Macular Edema) and VIVID (Intravitreal Afliberc

104 Of 124 eyes analyzed, 60 (48.4%) had diabetic macular edema, 32 (25.8%) had neovascular age-r

105 vascular age-related macular degeneration or diabetic macular edema.

106 lar age-related macular degeneration (nAMD), diabetic macular oedema (DME) or branch/central retinal

107 5% of total hemoglobin, self-reported use of diabetic medication, or history of physician-diagnosed d

108 Current anti-diabetic medications often result in adverse weight gain

109 rvations indicate that a commonly prescribed diabetic medicine can restrain mitochondrial metabolism

110 0.75-0.87; P<0.001), irrespective of sex and diabetic mellitus status.

111 pulation studies have shown that compared to diabetic men, diabetic women are at a higher risk of car

112 STZ-induced diabetic mice exhibited distinct cardiac dysfunction, da

113 eeks starting from 3 weeks of age, and to HF diabetic mice induced by high fat diet (HFD) plus strept

114 germ-free mice, that the oral microbiota of diabetic mice is more pathogenic.

115 After diabetic mice were wounded in the right eye and treated

116 Treating diabetic mice with a specific sEH inhibitor prevented th

117 Furthermore, treatment of non-obese diabetic mice with a Y1 receptor antagonist delays the o

118 -alpha was not detected in Muller cells from diabetic mice with CD40(+) Muller cells.

119 In the embryos of diabetic mice, OGT is highly activated in association wi

120 In diabetic mice, plasma H2S levels were decreased while RO

121 In the retinas of streptozotocin-induced diabetic mice, retinal apoptosis was dramatically elevat

122 uminuria in streptozotocin-induced and Akita diabetic mice.

123 terone were investigated using male nonobese diabetic mice.

124 is significantly downregulated in embryos of diabetic mice.

125 ed angiogenesis and arteriogenesis in type 2 diabetic mice.

126 ntitatively assessed at stages of increasing diabetic microvasculopathy based on diabetic retinopathy

127 can potentially be useful for evaluation of diabetic microvasculopathy.

128 stive of the potential of WSS as a marker of diabetic microvasculopathy.

129 e anti-oxidative effects in podocytes in the diabetic milieu.

130 t reduction in a high-fat diet (HFD) induced diabetic mouse model and a genetically engineered T2DM r

131 vival and number in a streptozotocin-induced diabetic mouse model.

132 and associated metabolic dysfunction in two diabetic mouse models.

133 profiles of breed- and body weight-matched, diabetic (n = 6) and healthy (n = 6) dogs by liquid chro

134 Patients with diabetic nephropathy (DN) and autosomal-dominant polycys

135 Diabetic nephropathy (DN) is one of vascular complicatio

136 e severity of kidney injury in patients with diabetic nephropathy (DN).

137 cation, has been used to treat patients with diabetic nephropathy (DN).

138 ranscription (STAT) signaling contributes to diabetic nephropathy by inducing genes involved in leuko

139 In univariate analyses, diabetic nephropathy class was not statistically signifi

140 loss of tubular Tyro3 and Mer expression in diabetic nephropathy tissue and glomerular depositions o

141 rotein-protein interactions at each stage of diabetic nephropathy to provide an overview of the event

142 mL/min per 1.73m(2), or development of overt diabetic nephropathy), eye events (a composite of requir

143 a is a major pathogenic factor that promotes diabetic nephropathy, but the underlying mechanism remai

144 In diabetic nephropathy, the gene expression of claudins, i

145 he endothelial glycocalyx is also reduced in diabetic nephropathy, we hypothesized that MCP-1 inhibit

146 t among children who are already at risk for diabetic nephropathy.

147 Risk of death was higher among patients with diabetic nephropathy.

148 n implicated as a major pathogenic factor in diabetic nephropathy.

149 d in renal biopsies from human subjects with diabetic nephropathy.

150 elated sporadic patient with type 1 painless diabetic neuropathy and chronic itch.

151 the development of therapies for peripheral diabetic neuropathy.

152 inal inhibitory dysfunction in human painful diabetic neuropathy.

153 preclinical experiments using the non-obese diabetic (NOD) mouse model reported mucosal administrati

154 patients with T1D and mice of the non-obese diabetic (NOD) strain, we detected alterations in MAIT c

155 e islets of Langerhans of 3-wk-old non-obese diabetic (NOD), NOD.Rag1(-/-), and B6.g7 mice.

156 B and RPE permeability by vasoinhibins under diabetic or hyperglycemic-mimicking conditions, but that

157 resistance in mammalian models to elucidate diabetic pathogenesis and evaluate therapeutics.

158 Two families and the diabetic patient carried the nonsense c.6814G>T (p.Glu22

159 Sequential NAION occurred in 36.8% of diabetic patients and 20.9% of nondiabetic patients.

160 d to screen fundus photographs obtained from diabetic patients and to identify, with high reliability

161 scatheter aortic valve replacement (TAVR) in diabetic patients are limited by small sample size and c

162 delivery systems in protecting the health of diabetic patients during times of economic stress.

163 Diabetic patients experience functional deficits in dark

164 Diabetic patients have a greater risk of nonarteritic an

165 mmended period, however less than 75% of pre-diabetic patients have repeated tests within the suggest

166 orming retinal screening examinations on all diabetic patients is an unmet need, and there are many u

167 In the diabetic patients the level of glucose must be determine

168 Overall, 6600 of the diabetic patients were insulin treated (IT).

169 A total of 180 diabetic patients were recruited (90 patients with no di

170 upillary light reflex (PLR) abnormalities in diabetic patients who have non-proliferative diabetic re

171 Results Between diabetic patients with and diabetic patients without DPN

172 reas transplant is a potential treatment for diabetic patients with end-organ complications.

173 er healing and address MRSA into the care of diabetic patients with foot ulcers.

174 rcise or increased fibre-intake alone in pre-diabetic patients with NAFLD.

175 f DN patients (macroalbuminuric, n = 121) to diabetic patients with no evidence of DN (normoalbuminur

176 n rate and the composition of RSSC in type-1 diabetic patients with those in matched controls in orde

177 dal thickness (CT) and all retinal layers of diabetic patients without diabetic retinopathy (DR) afte

178 Results Between diabetic patients with and diabetic patients without DPN, mean age (60 years [range

179 Diabetic patients without DR showed a thicker choroid an

180 2016, which analyzed 41 eyes with DR from 31 diabetic patients, 20 eyes without DR from 11 diabetic p

181 iabetic patients, 20 eyes without DR from 11 diabetic patients, and 16 eyes from 12 healthy age-match

182 s a main cause of heart failure and death in diabetic patients.

183 non-diabetic and clinically diagnosed type 2 diabetic patients.

184 ction and grading of coronary lesions in non-diabetic patients.

185 bese/T2D mice that was comparable to that of diabetic patients.

186 ioside, making this formulation suitable for diabetic patients.

187 f acute chest pain of coronary origin in non-diabetic patients.

188 on of a GABAA-R PAM reducing HbA1c levels in diabetic patients.

189 with RNFL and macular thickness among type 2 diabetic patients.

190 t not Ca(2+) sparks were lower in cells from diabetic patients.

191 iabetic health education and promotion among diabetic patients.

192 eric-Coated and Immediate Release Aspirin in Diabetic Patients; NCT01515657).

193 e considered as a proper food ingredient for diabetic people and patients in weight gain control.

194 CML) found to be predominantly higher in the diabetic population.

195 Amelioration of ophthalmologic education in diabetic programs might take up patients' propensity for

196 ere transplanted in the PDLLCL scaffold in a diabetic rat model.

197 Streptozotocin-induced diabetic rats (STZ-rats) were treated with 15 mug/kg GHR

198 was identified after calorie restriction in diabetic rats (ZDF-CR).

199 of action on intravenous bolus injection in diabetic rats are indistinguishable from wild-type (WT)

200 allodynia were present in type 1 and type 2 diabetic rats but not in rats with type 1 diabetes recei

201 Diabetic rats of both sexes exhibit a reduction in cardi

202 Streptozotocin-induced diabetic rats showed decreased a- and b-wave amplitudes

203 protein showed significantly lower levels in diabetic rats than those in nondiabetic controls.

204 Impaired RDD in diabetic rats was rapidly normalized by spinal delivery

205 4 and retinoids were significantly lower in diabetic rats.

206 thelial cells, thus mediating progression of diabetic related diseases.

207 ts of SGLT2 inhibition in the progression of diabetic renal disease.

208 Bevacizumab use increased each year for diabetic retinal disease (2.4 injections/1000 patients w

209 l disease (2.4 injections/1000 patients with diabetic retinal disease in 2009 to 13.6 per 1000 in 201

210 visual pigments, were significantly lower in diabetic retinas compared to those in controls, suggesti

211 retinal layers of diabetic patients without diabetic retinopathy (DR) after 1 year of follow-up.

212 of four ocular diseases; cataract, glaucoma, diabetic retinopathy (DR) and dry eye disease (DED) was

213 nd clinical stages leading to vision loss in diabetic retinopathy (DR) are highlighted.

214 : 210 normal (NL), 183 glaucoma (GL), and 18 diabetic retinopathy (DR) at Tilganga Institute of Ophth

215 prevalence of diabetes, annual screening for diabetic retinopathy (DR) by expert human grading of ret

216 Ophthalmic screening to check for diabetic retinopathy (DR) is important to prevent vision

217 The presence and severity of diabetic retinopathy (DR) may contribute to the risk of

218 , their results regarding the progression of diabetic retinopathy (DR) were neutral with liraglutide

219 ous forms of exudative maculopathy including diabetic retinopathy (DR), retinal vein occlusion (RVO),

220 eir mechanism of action were investigated in diabetic retinopathy (DR).

221 have not identified any robust risk loci for diabetic retinopathy (DR).

222 creasing diabetic microvasculopathy based on diabetic retinopathy (DR).

223 ), moderate (27.2%), severe nonproliferative diabetic retinopathy (NPDR) (45.5%).

224 diabetic patients who have non-proliferative diabetic retinopathy (NPDR).

225 nd risk factors for developing proliferative diabetic retinopathy (PDR) and vitreous hemorrhage (VH).

226 ts that represent worsening of proliferative diabetic retinopathy (PDR) in eyes treated with panretin

227 oagulation (PRP) when managing proliferative diabetic retinopathy (PDR), with or without concomitant

228 s hemorrhage (VH) secondary to proliferative diabetic retinopathy (PDR).

229 evere manifestations of active proliferative diabetic retinopathy (PDR).

230 in the incidence of PME among patients with diabetic retinopathy (RR 1.06, 95% 0.81-1.38).

231 etic macular edema (DME), vision-threatening diabetic retinopathy (VTDR), defined as the presence of

232 patients were recruited (90 patients with no diabetic retinopathy and 90 patients with NPDR) into the

233 posterior (age-related macular degeneration, diabetic retinopathy and glaucoma) segments of the eye.

234 ty of human diseases including proliferative diabetic retinopathy and wet age-related macular degener

235 Diabetic Retinopathy Clinical Research Network (DRCR.net

236 The Diabetic Retinopathy Clinical Research Network Protocol

237 Diabetic retinopathy is a common complication of diabete

238 billing claim codes used during the care of diabetic retinopathy is a necessary precursor to fully u

239 probability of progression to proliferative diabetic retinopathy or clinically significant macular e

240 ression from no retinopathy to proliferative diabetic retinopathy or clinically significant macular e

241 e likelihood of progression to proliferative diabetic retinopathy or clinically significant macular e

242 To evaluate self-reported adherence to diabetic retinopathy screening examinations among diabet

243 ng as compared with standard Early Treatment Diabetic Retinopathy Study (ETDRS) 7-field photographs (

244 of patients with 15 or more Early Treatment Diabetic Retinopathy Study (ETDRS) letter score change,

245 as lower in patients with Early Treatment of Diabetic Retinopathy Study (ETDRS) level 20-35 than in p

246 cuity was measured using the Early Treatment Diabetic Retinopathy Study (ETDRS) protocol.

247 sual acuity (VA) measured on Early Treatment Diabetic Retinopathy Study charts, injection episodes, a

248 es into categories of no DR (Early Treatment Diabetic Retinopathy Study levels 10-15; n = 154), mild

249 with the drusen area in the Early Treatment Diabetic Retinopathy Study Report (ETDRS) grid (P = 2.29

250 was classified according to Early Treatment Diabetic Retinopathy Study Research Group - report no.

251 hotograph grading, using the Early Treatment Diabetic Retinopathy Study severity scale.

252 oundary Segmentation at 9 Early Treatment of Diabetic Retinopathy Study subfields.

253 he best-corrected electronic Early Treatment Diabetic Retinopathy Study VALS (scores range from 0-100

254 eir distribution around the 5 North Carolina Diabetic Retinopathy Telemedicine Network sites by zip c

255 patients participating in the North Carolina Diabetic Retinopathy Telemedicine Network, (2) the locat

256 ophthalmology referral in the North Carolina Diabetic Retinopathy Telemedicine Network.

257 Diabetic retinopathy was based on fundus photograph grad

258 Diabetic retinopathy was graded from 2-field retinal ima

259 proliferative retinopathy, or progression of diabetic retinopathy), and nerve events (a composite of

260 r mild, moderate, or severe nonproliferative diabetic retinopathy).

261 eases, including retinopathy of prematurity, diabetic retinopathy, and age-related macular degenerati

262 Diabetic retinopathy, diabetic macular edema (DME), visi

263 age-related macular degeneration, cataracts, diabetic retinopathy, glaucoma, and intraocular cancers.

264 allmark of CADASIL and other SVDs, including diabetic retinopathy, resulting in vascular instability.

265 BCVA after cataract surgery in patients with diabetic retinopathy, with no unanticipated safety event

266 ths among those with severe nonproliferative diabetic retinopathy.

267 such as age-related macular degeneration and diabetic retinopathy.

268 on to determine the presence and severity of diabetic retinopathy.

269 development of PDR and slows progression of diabetic retinopathy.

270 that are characteristic of non-proliferative diabetic retinopathy.

271 reflect the medical record for patients with diabetic retinopathy.

272 deficiency impairs this process and prevents diabetic retinopathy.

273 stigated the pathogenesis of impaired RDD in diabetic rodents exhibiting features of painful neuropat

274 In diabetic rodents, inhibition of MGO prevents cardiovascu

275 e 2 diabetes, and in the beta cells of obese diabetic rodents.

276 beneficial role on the integrity of BSCB in diabetic SCI rats, leading to improved prognosis.

277 pidomics reveal a proinflammatory profile in diabetic serum.

278 Humanized nonobese diabetic severe combined immunodeficient common gamma ch

279 Nonobese diabetic severe combined immunodeficient gammac(-/-) (NS

280 In contrast to nonobese diabetic severe combined immunodeficient Il2rg(-/-) (NSG

281 primary ALL cells transplanted onto nonobese diabetic/severe combined immunodeficiency mice faithfull

282 cs and tubular functions in anesthetized non-diabetic Sprague Dawley (SD) rats and 5/6 nephrectomized

283 avitreal bevacizumab (IVB) administration in diabetic subjects undergoing pars plana vitrectomy (PPV)

284 tic retinopathy screening examinations among diabetic subjects.

285 This pathway is engaged by the anti-diabetic sulfonylurea drugs to exert their full glucose-

286 Similarly, adrenalectomized type 1 diabetic (T1D) rats exhibited decreased rates of lipolys

287 In addition, in diabetics, the relationship between FFR and angiographic

288 rs for cardiovascular disease even below the diabetic threshold, and their study can additionally yie

289 (ERM) (n = 121), vitreous floaters (n = 69), diabetic tractional retinal detachment (n = 49), vitreou

290 ic regulation of MIOX in the pathogenesis of diabetic tubulopathy.

291 Analyzing data from 113 203 non-diabetic UK Biobank participants, we observed three (nea

292 RAGE impairs inflammation and progression of diabetic vascular complications, cardiovascular disease

293 target for an anti-inflammatory approach in diabetic vascular disease.

294 have important atheroprotective potential in diabetic vascular disease.

295 acetylation in vascular oxidative stress and diabetic vascular pathophysiology.

296 f glucose concentration of type 1 and type 2 diabetics were acquired at the Department of Endocrinolo

297 CASE PRESENTATION: A 52 year-old diabetic woman collapsed at her home in front of an acqu

298 es have shown that compared to diabetic men, diabetic women are at a higher risk of cardiovascular di

299 to VEGF-induced angiogenesis, especially in diabetic wound healing.

300 for the treatment of chronic inflammation in diabetic wounds.