ライフサイエンスコーパス: diabetic

1 women and 41.0% of men were hyperglycemic or diabetic.

2 high glycemic index makes it unsuitable for diabetics.

3 sults, we found that in contrast to WT mice, diabetic 4E-BP1/2-deficient mice did not exhibit enhance

4 ion could be a key strategy to prevent these diabetic abnormalities.

5 , antimicrobial, anti-inflammation, and anti-diabetic activities, as well as antioxidant and antinitr

6 Charantin has anti-diabetic activity comparable to insulin.

7 dies have shown no beneficial effect of anti-diabetic agents and statins on outcomes in heart failure

8 ls are constitutively up-regulated in type 1 diabetic Akita mice; CAR spontaneously accumulates in th

9 atients were divided into two groups; 33 non-diabetic and 34 with T2D.

10 n, 19.4% had no formal education, 28.1% were diabetic and 56.9% were hypertensive.

11 Non-diabetic and Akita/+ male mice with different duration o

12 ivity and reduces inflammasome activation in diabetic and insulin resistance-induced human cells, as

13 blastocyst stage in vitro or transferred to diabetic and non-diabetic recipients.

14 ency of fundus abnormalities were similar in diabetic and non-diabetic thalassemia patients indicatin

15 insulin-producing cells in HPS from both non-diabetic and type 2 diabetic donors.

16 PNS) disorders such as chemotherapy-induced, diabetic, and inherited neuropathies, and ocular disorde

17 Hearts from type 2 diabetic animals display perturbations in excitation-con

18 olinesterase and -butylcholinesterase), anti-diabetic (anti-alpha-amylase, -alpha-glucosidase, -pancr

19 The results for non-diabetics are also reported.

20 ging of autoimmune diabetes and reveals that diabetic autoimmunity is driven by transcriptionally dis

21 ticles were injected into 12-week-old female diabetic Balb/c mice via pancreatic duct.

22 hich advances our etiologic understanding of diabetic bone deterioration and increased fragility from

23 crocracks increased within 10-day loading in diabetic bone, whereas peaked at Day 7 in non-diabetic b

24 iabetic bone, whereas peaked at Day 7 in non-diabetic bone.

25 Early pathogenesis of diabetic cardiomyopathy (DMCM) may involve lipotoxicity

26 ith a cardiac or renal stressor, would mimic diabetic cardiomyopathy and nephropathy, respectively.

27 The clinical features of diabetic cardiomyopathy are cardiac hypertrophy and dias

28 The term diabetic cardiomyopathy is defined as the presence of ab

29 Diabetic cardiomyopathy occurs as a result of the dysreg

30 ately produced clinical endpoints related to diabetic cardiomyopathy, the combination of the two did

31 re, we summarize the molecular mechanisms of diabetic cardiomyopathy, with a special emphasis on card

32 lying mechanisms and early interventions for diabetic cardiomyopathy.

33 ocytes, thereby worsening the progression of diabetic cardiomyopathy.

34 reas SINE-catabolizing DICER1 is reduced, in diabetic cells and mice.

35 /transitional B cells increase remarkably in diabetic CHCpatients and might have a role in liver dise

36 re good potential predictors of LC and HCCin diabetic CHCpatients, respectively.

37 ng (odds ratio, 1.35; 95% CI, 1.23-1.47) and diabetic complications (odds ratio, 1.35; 95% CI, 1.2-1.

38 Monocytes are rapidly recruited to sites of diabetic complications and differentiate into macrophage

39 for controlling protein glycation associated diabetic complications.

40 t endothelial function from dyslipidemia and diabetic complications.

41 open new avenues for targeting human FN3K in diabetic complications.

42 might contribute to CaMKII-dependent retinal diabetic complications.

43 m of diabetes but not the sole cause of late diabetic complications; instead, other diabetes-related

44 odel treatments that mimic type-1 and type-2 diabetic conditions and discovered striking shifts in ca

45 ts into gluconeogenesis under euglycemic and diabetic conditions.

46 ury, and interstitial fibrosis compared with diabetic controls fed normal chow or a zero-fiber diet.

47 the retinal vessels and protect vessels from diabetic damage.

48 tors reduced hepatic triglyceride content in diabetic (db/db) mice.

49 lls in HPS from both non-diabetic and type 2 diabetic donors.

50 d that SC-Exos promoted neurite outgrowth of diabetic DRG neurons and migration of Schwann cells chal

51 Metformin, the world's most prescribed anti-diabetic drug, is also effective in preventing type 2 di

52 Diabetic dyslipidemia, characterized by increased plasma

53 ne of the underlying mechanisms for the anti-diabetic effect of metformin is mediated by the stimulat

54 d CDK4 inhibition, suggesting that the obese/diabetic environment confers cancer-selective dependenci

55 of the 180 study participants had referable diabetic eye disease, 13.3% had vision-threatening disea

56 ), and optical coherence tomography (OCT) in diabetic eyes and compare the CCT values in patients wit

57 EAAs detected by OCTA in diabetic eyes are significantly associated with baseline

58 Diabetic eyes without DR (n = 138) and eyes with mild/mo

59 Moreover, diabetic fatigued ulnae had more severe disruptions of o

60 However, diabetic females displayed impaired responsiveness to su

61 ber 2019, we recruited 305 patients from two diabetic foot clinics.

62 nfectious Diseases Society of America (IDSA) diabetic foot infection classification by adding a separ

63 In patients with diabetic foot osteomyelitis (DFO) who underwent surgical

64 PAD is a major risk factor for diabetic foot ulceration and amputation.

65 Diabetic foot ulcers (DFUs) are a life-threatening disea

66 and the "role of pressure in pathogenesis of diabetic foot ulcers".

67 Only well-controlled type-2 diabetics, free of pre-proliferative retinopathy, were i

68 ion of stable TWIST1 rEC into a type 1 and 2 diabetic full-thickness splinted wound healing murine mo

69 nist of NK1R, in patients with idiopathic or diabetic gastroparesis.

70 lators are potential strategies to treat non-diabetic glomerular disease.

71 d tubular mRNA markers were increased in all diabetic groups in cross-sectional analysis.

72 structural impairments that characterize the diabetic heart are considered in light of the clinical c

73 nisms of the complex phenotype, that is, the diabetic heart, form the basis of this review.

74 oves the outcome of the chronically stressed diabetic heart.

75 ound that glucose increases lipolysis in non-diabetic human islets, but not in type 2 diabetic (T2D)

76 In this study, we established a diabetic humanized NOD-scidIL2Rgamma(null) (NSG) mouse m

77 fic Prmt1 deficiency drastically ameliorated diabetic hyperglycemia.

78 contribute to vascular complications during diabetic hyperglycemia.

79 ncreatic alpha-cells strongly contributes to diabetic hyperglycemia.

80 The diabetic, hypertensive heart failure rat (mRen27/tetO-sh

81 ntrolled conditions in healthy controls, pre-diabetic individuals and patients with type-2 diabetes m

82 Patients with type-2 DM and CP; group-2: Non-diabetic individuals with CP; group-3: Non-diabetic indi

83 n-diabetic individuals with CP; group-3: Non-diabetic individuals without periodontal diseases.

84 rferon, is expressed in the islets of type 1 diabetic individuals, and its expression and signaling a

85 r blood concentrations reported in obese and diabetic individuals.

86 o prevent the development and progression of diabetic interstitial fibrogenesis.

87 racrine mechanisms play an important role in diabetic interstitial fibrogenesis; therefore, targeting

88 Diabetic keratopathy occurs in ~70% of all people with d

89 psis (41.1%), cardiogenic shock (20.9%), and diabetic ketoacidosis (16%).

90 nt in CGM group and 4 in the BGM group), and diabetic ketoacidosis (3 participants with an event in t

91 Diabetic ketoacidosis (DKA), a severe complication of di

92 , gastritis, pancreatitis and arthritis, and diabetic ketoacidosis each occurring in one (2%) patient

93 co-transporter-2 inhibitors and the risk of diabetic ketoacidosis in patients with type 2 diabetes:

94 tment-limiting and life-threatening, such as diabetic ketoacidosis, which appears to be more frequent

95 Two children had diabetic ketoacidosis.

96 cotransporter-2 inhibitors and the risk for diabetic ketoacidosis: a multicenter cohort study.

97 host genetic predisposition are critical for diabetic kidney disease (DKD) development.

98 Diabetic kidney disease (DKD) is a major complication of

99 s can lead to development and progression of diabetic kidney disease (DKD).

100 evated in glomerular tissue of patients with diabetic kidney disease compared with control glomerular

101 Although diabetic kidney disease is the leading cause of ESKD in

102 ciated with a greater risk of progression of diabetic kidney disease, even after adjustment for estab

103 ney disease of varied aetiologies, including diabetic kidney disease, focal segmental glomerulosclero

104 GFR is a risk factor for the development of diabetic kidney disease.

105 nts and they may serve as new biomarkers for diabetic kidney disease.

106 s with type 1 diabetes and early-to-moderate diabetic kidney disease.

107 L-40 remained associated with progression of diabetic kidney disease; TNFR-2 had the highest risk (ad

108 revealed abnormal cardiolipin remodeling in diabetic kidneys, a cardinal sign of disrupted mitochond

109 pstream of proximal tubule YAP activation in diabetic kidneys.

110 We crossed diabetic leptin receptor-mutant mice to mice lacking CaM

111 s (IDI) in naive and previously treated (PT) diabetic macular edema (DME) eyes in a real-life setting

112 and decreased macular thickness in eyes with diabetic macular edema (DME) in clinical trials.

113 ry VA, age <75 years, absence of preexisting diabetic macular edema (DME) or postvitrectomy persisten

114 ith aflibercept monotherapy for treatment of diabetic macular edema (DME).

115 angiography (OCTA) and treatment response in diabetic macular edema (DME).

116 agnosis of exudative macular degeneration or diabetic macular edema requiring bilateral anti-vascular

117 c (H) ethnicity aged 18 years and older with diabetic macular edema who received intravitreal injecti

118 n occlusion (RVO), diabetic retinopathy (DR; diabetic macular edema, DME), or noninfectious uveitis (

119 in DR severity scale score or development of diabetic macular edema.

120 s for RLT were diabetic retinopathy (DR) and diabetic macular oedema (DMO) (542 cases, 66.0%), follow

121 The first was a 53-year old diabetic male farmer who presented with 2 nontender righ

122 lta), which is known to be activated through diabetic metabolism.

123 regulated blood glucose in insulin-deficient diabetic mice and minipigs (for minipigs >25 kg, glucose

124 When hindlimb ischemia is induced in diabetic mice and QKI-7 is knocked-down in vivo in ECs,

125 xpression is highly increased in islets from diabetic mice as well as in plasma of diabetic patients.

126 Diabetic mice fed a high-fiber diet were significantly l

127 s restore normal glycemia in immunocompetent diabetic mice for at least 6 weeks, can be visualized us

128 from the pancreatic infiltrates of nonobese diabetic mice have been shown to recognize epitopes form

129 studied lung and kidney ACE2 and TMPRSS2 in diabetic mice mimicking host factors linked to severe CO

130 Administration of AFSE to diabetic mice reduced total cholesterol, triglycerides,

131 encapsulated in the device and implanted in diabetic mice restored normoglycaemia in the mice for ov

132 ed insulin levels were measured in recipient diabetic mice upon implantation of the islet-seeded biom

133 as able to identify unique differences among diabetic mice with different duration of diabetes.

134 e and less frequent injections, in non-obese diabetic mice with insulin resistance symptoms.

135 Treatment of diabetic mice with the NFAT blocker A-285222 reduced NFA

136 ors, CCL2 levels were increased in wounds of diabetic mice, and subsequent experiments showed that lo

137 ft ventricle (LV) dysfunction in hearts from diabetic mice, improving contractility and relaxation wh

138 hich resulted in improved visual function in diabetic mice, suggesting that chromophore deficiency pl

139 In alloxan-induced diabetic mice, the AFS methanol extract (AFSE) rich in c

140 l sensitivity was significantly decreased in diabetic mice, which was prevented by fenofibrate.

141 prevented oxidative stress in the retina of diabetic mice.

142 pithelial wound healing and nerve density in diabetic mice.

143 ress in the retina of streptozotocin-induced diabetic mice.

144 synthase expression and plasma NO levels of diabetic mice.

145 ein expression is elevated in Muller glia of diabetic mice; however, the mechanisms responsible for t

146 Exosomes from macrophages exposed to diabetic milieu (high glucose or db/db mice) significant

147 ant recipients evaluating cardiac effects of diabetic milieu (hyperglycemia and insulin resistance) o

148 vity is impaired by insults, which mimic the diabetic milieu, including high glucose and/or fatty lev

149 Here, Akita mice, type 1 diabetic model, were treated with the visual pigment chr

150 rapeutic efficacy over wildtype hMSCs in the diabetic mouse model without replacing resident cells lo

151 s derived from three different hyperglycemic diabetic mouse models: streptozotocin-treated, high-fat

152 re transplanted into the peritoneal pouch of diabetic mouse recipients.

153 s during autoimmune diabetes in the nonobese diabetic mouse.

154 ranoproliferative glomerulonephritis (MPGN), diabetic nephropathy (DN) and obesity-related glomerulop

155 renal proximal tubule is a site of injury in diabetic nephropathy (DN), and progressive renal tubuloi

156 min-to-creatinine ratio (ACR) is a marker of diabetic nephropathy and microvascular damage.

157 in kidney disease, including podocytopathy, diabetic nephropathy, albuminuria, autosomal dominant po

158 et were significantly less likely to develop diabetic nephropathy, exhibiting less albuminuria, glome

159 and the damaged rat mesangial cells leads to diabetic nephropathy, fibrosis, and proteinurea, which a

160 iber's effect on development of experimental diabetic nephropathy, we used streptozotocin to induce d

161 igation as a novel renoprotective therapy in diabetic nephropathy.

162 factors and phenotypes of participants with diabetic neuropathy that can be used in the design of ne

163 step polyol pathway previously implicated in diabetic neuropathy.

164 In nonobese diabetic (NOD) mice, a model of T1D, diabetes developmen

165 ive T cells in newly hyperglycemic non-obese diabetic (NOD) mice, protecting the insulin-producing be

166 across training levels were able to identify diabetic NV with equal accuracy using SS-OCTA and FA.

167 and non-hypertensive cardiomyopathy, termed diabetic or lipotoxic cardiomyopathy.

168 The plasmas of diabetic or uremic patients and of those receiving perit

169 en comparing nondiabetic participants versus diabetic participants without retinopathy.

170 opulation consisted of 194 metformin-treated diabetic patients (median age: 68.6; males: 113 [58.2%])

171 cross-sectional retrospective study of 3120 diabetic patients aged >= 60 years, those taking metform

172 tionnaire was used to collect data among 230 diabetic patients aged 18 years and above.

173 negatively correlated with renal function in diabetic patients and they may serve as new biomarkers f

174 d knowledge about diabetic retinopathy among diabetic patients at Debark hospital was fair (47.4%) an

175 factors of diabetic retinopathy among adult diabetic patients at Debark hospital, Northwest Ethiopia

176 Diabetic patients attained the screening level of CRC ri

177 Diabetic patients often experience functional deficits i

178 /or their products in the lungs of obese and diabetic patients promotes interactions between viral an

179 rols in each year, but no more than 40.4% of diabetic patients received an examination in any given y

180 Diabetic patients received more eye examinations than co

181 Diabetic patients treated with adjunctive MTZ+AMX were b

182 Retinopathy continues to progress even when diabetic patients try to control their blood sugar, but

183 yes (156 right eyes, 148 left eyes) from 178 diabetic patients were analyzed in the study.

184 d a reduction in corneal nerve parameters in diabetic patients with and without DSPN.

185 ome associations of relative hypoglycemia in diabetic patients with critical illness.

186 tients, 170 diabetic patients without DR, 57 diabetic patients with mild to moderate nonproliferative

187 moderate nonproliferative DR (NPDR), and 12 diabetic patients with severe NPDR to proliferative DR.

188 in this study: 90 nondiabetic patients, 170 diabetic patients without DR, 57 diabetic patients with

189 shock, lung injuries, insulin resistance in diabetic patients, and cancer.

190 The hazard ratio for 28-day mortality of diabetic patients, censored at hospital discharge, for p

191 ents in the inpatient or outpatient setting, diabetic patients, patients with an indwelling urethral

192 lets of rodent diabetes models and of type 2 diabetic patients, possibly explaining their impaired se

193 In diabetic patients, while CD19(+)CD24(+)CD38(-) primarily

194 pathy should be evaluated more cautiously in diabetic patients.

195 approaches to prevent cardiac dysfunction in diabetic patients.

196 s important for healthy subjects and crucial diabetic patients.

197 le with interstitial fluid glucose levels of diabetic patients.

198 s from diabetic mice as well as in plasma of diabetic patients.

199 istics of dysfunctional endothelial cells in diabetic patients.

200 tion offers a potential cure for a subset of diabetic patients.

201 regadenoson was less pronounced in obese and diabetic patients.

202 Diabetic Peripheral Neuropathy (DPN) typically is accomp

203 unctional level, collectively referred to as diabetic peripheral neuropathy (DPN).

204 s on magnetic resonance neurography (MRN) in diabetic polyneuropathy (DPN) have found proximal sciati

205 of polyneuropathy and to detect the onset of diabetic polyneuropathy.

206 ion as functional food ingredients with anti-diabetic properties because strong alpha-amylase inhibit

207 cantly altered neurotrophic factor levels in diabetic rat corneas, which were partially restored by f

208 mpared with age- and duration-matched type 1 diabetic rats (T1D) (60 mg/kg streptozotocin).

209 otocin-induced T1DM rats and age-matched non-diabetic rats were subjected to daily uniaxial ulnar loa

210 urea, which are inhibited in heparin-treated diabetic rats.

211 ings was evaluated in streptozotocin-induced diabetic rats.

212 d in the corneas of humans with diabetes and diabetic rats.

213 n the absence of systemic immunosuppression, diabetic recipients containing PVPON/TA-encapsulated isl

214 However, fetuses carried by diabetic recipients were smaller compared to those carri

215 ere smaller compared to those carried by non-diabetic recipients, regardless hyperglycemia status of

216 e observed only among the fetuses carried by diabetic recipients.

217 eeded in a bioscaffold for implantation into diabetic recipients.

218 in vitro or transferred to diabetic and non-diabetic recipients.

219 tic defects or age-related diseases, such as diabetic retinopathies, glaucoma, and macular degenerati

220 32-1.82), as did patients with proliferative diabetic retinopathy (CVA: HR, 2.53; 95% CI, 1.84-3.48;

221 The most common indications for RLT were diabetic retinopathy (DR) and diabetic macular oedema (D

222 Diabetic retinopathy (DR) is a common complication of di

223 Diabetic retinopathy (DR), the most common cause of visi

224 d with ME from retinal vein occlusion (RVO), diabetic retinopathy (DR; diabetic macular edema, DME),

225 tivity, and specificity for nonproliferative diabetic retinopathy (NPDR) and proliferative diabetic r

226 nopathy, those with minimal nonproliferative diabetic retinopathy (NPDR) had a higher risk of CVA (ha

227 -world outcomes of people with proliferative diabetic retinopathy (PDR) in India and highlight opport

228 iabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR) were excellent (>90%).

229 VR) (n = 30), PVR (n = 16) and proliferative diabetic retinopathy (PDR) with tractional RD (n = 8).

230 ) in treatment-naive eyes with proliferative diabetic retinopathy (PDR).

231 check-up practice and associated factors of diabetic retinopathy among adult diabetic patients at De

232 The proportion of good knowledge about diabetic retinopathy among diabetic patients at Debark h

233 coherence tomography (OCT) mainly focused on diabetic retinopathy and age-related macular degeneratio

234 errant retinal angiogenesis in proliferative diabetic retinopathy and its modulation has proven to be

235 Diabetes associated complications, including diabetic retinopathy and loss of vision, are major healt

236 which underlies diseases like proliferative diabetic retinopathy and retinopathy of prematurity.

237 dge about the nature and the consequences of diabetic retinopathy and routine eye checkup helps for t

238 ation of DNA methylation can prevent/reverse diabetic retinopathy by maintaining mitochondrial dynami

239 The total caseload of diabetic retinopathy in adults age 40 and older is expec

240 examination plays a vital role in detecting diabetic retinopathy in its earliest stage before the on

241 rogression of retinal vascular diseases like diabetic retinopathy in small animal models is often com

242 Diabetic retinopathy is significantly associated with fu

243 Implementation of an automated diabetic retinopathy screening system in a primary care

244 icantly associated with adherence to initial diabetic retinopathy screening.

245 f referral and best-corrected visual acuity, diabetic retinopathy status in both eyes.

246 t DR gained a median of 11.0 Early Treatment Diabetic Retinopathy Study (ETDRS) letters (interquartil

247 l acuity (BCVA) of 5 or more Early Treatment Diabetic Retinopathy Study (ETDRS) letters (Snellen equi

248 tients gaining 15 or more Early Treatment of Diabetic Retinopathy Study (ETDRS) letters from baseline

249 hange from baseline was -4.6 Early Treatment Diabetic Retinopathy Study (ETDRS) letters, -2.3 ETDRS l

250 an+/-standard deviation [SD] Early Treatment Diabetic Retinopathy Study [ETDRS] letters) were similar

251 , vision loss of more than 5 Early Treatment Diabetic Retinopathy Study letters from baseline, as wel

252 ed vision gain of 15 or more Early Treatment Diabetic Retinopathy Study letters, vision loss of more

253 defined as improvement in 3 Early Treatment Diabetic Retinopathy Study lines (doubling of the visual

254 Diabetic retinopathy was significantly associated with a

255 rimary vitrectomy for TRD from proliferative diabetic retinopathy were studied.

256 ue to vitreous hemorrhage from proliferative diabetic retinopathy who were enrolled from November 201

257 .4 for cataract, glaucoma, near-sightedness, diabetic retinopathy, and macular degeneration, respecti

258 of cataract, macular degeneration, glaucoma, diabetic retinopathy, and near-sightedness using the Goo

259 into two groups according to the presence of diabetic retinopathy, as Group I with retinopathy and Gr

260 glaucoma, age-related macular degeneration, diabetic retinopathy, cataract, glaucoma surgery, catara

261 of this study was to assess knowledge about diabetic retinopathy, eye check-up practice and associat

262 od vessels, which is an essential element of diabetic retinopathy, is driven by chronic elevation of

263 risk of early onset and rapid progression of diabetic retinopathy, the leading cause of blindness and

264 oxidative damage and to prevent or slow down diabetic retinopathy.

265 sfunction before the clinical development of diabetic retinopathy.

266 the CCT values in patients with and without diabetic retinopathy.

267 e to glucose was greater in individuals with diabetic retinopathy.

268 glaucoma, pediatric neuro-ophthalmology, and diabetic retinopathy.

269 ponse genes were tested for association with diabetic retinopathy.

270 es in neural and retinal diseases, including diabetic retinopathy.

271 hyperlipidemia is also closely related with diabetic retinopathy.

272 However, the microdamage accumulation in diabetic skeleton and the corresponding bone remodeling

273 on and abnormal remodeling mechanisms in the diabetic skeleton, which advances our etiologic understa

274 ells were identified at both prediabetic and diabetic stages comprising two distinct high- and low-af

275 In obese and diabetic states, macrophage expression of purinergic rec

276 alteration in the extracellular matrix with diabetic status and its implications on incident heart f

277 The findings support that the diabetic status during pregnancy, and not the preconcept

278 ntly, irrespective of blood glucose level or diabetic status.

279 rane discs were implanted under the scalp in diabetic (streptozotocin-induced) and control rats, whic

280 ile of FLI), 1.45; 95% CI, 1.07-1.96 for non-diabetic subgroup).

281 uartile of FLI), 2.89; 95% CI, 1.01-8.27 for diabetic subgroup; OR (highest vs. lowest quartile of FL

282 and the delay in P1-implicit time in type 2 diabetic subjects were statistically significant in most

283 rbidly obese nondiabetic subjects but not in diabetic subjects, suggesting continued inflammation.

284 Using type 1 diabetic (T1DM) mouse models together with cultured Schw

285 on but downregulated in dysfunctional type 2 diabetic (T2D) human beta cells.

286 non-diabetic human islets, but not in type 2 diabetic (T2D) islets, indicating dysregulation of lipol

287 normalities were similar in diabetic and non-diabetic thalassemia patients indicating close monitorin

288 Most patients needing diabetic tractional retinal detachment (TRD) surgery are

289 visual acuity are seen after vitrectomy for diabetic TRD that can result in functional improvement i

290 ulation of linear and diffuse microdamage in diabetic ulnae than non-diabetic ulnae.

291 ffuse microdamage in diabetic ulnae than non-diabetic ulnae.

292 and its potential as a therapeutic target in diabetic vascular complications.

293 ts a promising strategy for the treatment of diabetic vascular complications.

294 randomized study that included 34 eyes with diabetic VH.

295 In type 2 diabetics with micro- or macro-albuminuria UPPod:CR and

296 P with KDR/SFRP4 and CD31 in the regenerated diabetic wound bed with TWIST1 overexpression or silenci

297 4 (Tlr4(f/f)Lyz2(Cre+)) resulted in improved diabetic wound healing.

298 alpha-2-glycoprotein 1 (LRG1) in normal and diabetic wound healing.

299 herapy to induce neovascularization-mediated diabetic wound tissue regeneration.

300 omotes angiogenesis and expedites healing in diabetic wounds.