ライフサイエンスコーパス: lymphedema

1 ome increasingly popular in the treatment of lymphedema.

2 ctor FOXC2 are predominately associated with lymphedema.

3 ent to limit the development of postsurgical lymphedema.

4 ing lymph nodes for the purpose of relieving lymphedema.

5 atalogue of human GATA2 mutations results in lymphedema.

6 es of bilateral lower extremity inflammatory lymphedema.

7 se of bilateral lower extremity inflammatory lymphedema.

8 h both cancer-related and non-cancer-related lymphedema.

9 that VLNT may help alleviate the severity of lymphedema.

10 ecessary axillary lymph node dissections and lymphedema.

11 stases, but is associated with a 14% risk of lymphedema.

12 comes after use of these techniques to treat lymphedema.

13 ene cause Hennekam syndrome, a primary human lymphedema.

14 n promising results in preclinical models of lymphedema.

15 ting their possible involvement in secondary lymphedema.

16 of VEGFR3 has been reported to cause primary lymphedema.

17 ique provided a fresh hope for patients with lymphedema.

18 s immediately applicable to reduce secondary lymphedema.

19 oma formation was increased in patients with lymphedema.

20 with a frameshift mutation also have primary lymphedema.

21 atic vessel function in 5 of 6 patients with lymphedema.

22 th symptomatic pathologic conditions such as lymphedema.

23 and normal limbs of patients with secondary lymphedema.

24 lymphatic function that result in inherited lymphedema.

25 l that manifested lymphatic hyperplasia with lymphedema.

26 ions in the transcription factor GATA2 cause lymphedema.

27 ng lymphatic development result in inherited lymphedema.

28 gents as potential therapy for some forms of lymphedema.

29 ise did not result in increased incidence of lymphedema.

30 ngs, such as radiation or associated chronic lymphedema.

31 as used to ascertain factors associated with lymphedema.

32 patients had claims indicating treatment of lymphedema.

33 d symptoms can be early signs of progressing lymphedema.

34 e presence of measured and patient-perceived lymphedema.

35 there remains a clinically relevant risk of lymphedema.

36 recautions if they had measured or perceived lymphedema.

37 and 2% reported chronically moderate/severe lymphedema.

38 ients reporting no arm swelling had measured lymphedema.

39 are significant risk factors for developing lymphedema.

40 are significant risk factors for perceiving lymphedema.

41 e mechanism through which obesity may worsen lymphedema.

42 can be utilized for effective management of lymphedema.

43 e B4 (LTB4) in the molecular pathogenesis of lymphedema.

44 reatment for patients with chronic extremity lymphedema.

45 ed lymphatic maps in patients with secondary lymphedema.

46 ics within the axilla and its use may reduce lymphedema.

47 phedema development and treating established lymphedema.

48 sm that becomes compromised in some forms of lymphedema.

49 She did not develop postsurgical lymphedema.

50 lay a key role in mediating the pathology of lymphedema.

51 yed hypoplastic facial lymphatics and severe lymphedema.

52 institution were screened prospectively for lymphedema.

53 reatment risk, prevention, and management of lymphedema.

54 al manifestation of lymphatic malfunction is lymphedema.

55 breast reconstruction impacts development of lymphedema.

56 phangiogenesis in clinical settings, such as lymphedema.

57 tic endothelial cells at the early stages of lymphedema.

58 9-cis RA significantly prevents postsurgical lymphedema.

59 s treated for breast cancer and screened for lymphedema.

60 , vascular/lymphatic (venous thrombosis 25%, lymphedema 11%), sensorineural hearing loss 76%, miscarr

61 for 3 years, 23% reported no more than mild lymphedema, 12% reported moderate/severe lymphedema, and

62 274 patients with secondary lymphedema (197 upper, 77 lower) were included in the st

63 one results in a significantly lower rate of lymphedema 5 years postoperatively.

64 cute pneumonitis (1.2% vs. 0.2%, P=0.01) and lymphedema (8.4% vs. 4.5%, P=0.001).

65 Secondary lymphedema, a life-long complication of cancer treatment

66 In breast cancer survivors at risk for lymphedema, a program of slowly progressive weight lifti

67 ctive formation of lymphatic valves leads to lymphedema, a progressive and debilitating condition for

68 idelines for breast cancer survivors without lymphedema advise against upper body exercise, preventin

69 Lymphedema affects up to 1 in 6 patients who undergo tre

70 Lymphedema after breast cancer is common but mostly mild

71 Postoperative lymphedema after breast cancer surgery is a challenging

72 2.5-fold greater fluid retention and severe lymphedema after inflammation.

73 es may represent a novel means of preventing lymphedema after lymph node resection.

74 an ideal option for patients who suffer from lymphedema after mastectomy and axillary dissection.

75 was to determine the long-term prevalence of lymphedema after SLN biopsy (SLNB) alone and after SLNB

76 ional analyses to describe the prevalence of lymphedema and arm symptoms and multivariate-adjusted ge

77 or lymphatic related diseases, which include lymphedema and cancer.

78 Two larger families cosegregate lymphedema and GJC2 mutation (LOD score = 6.5).

79 ped a highly reproducible model of secondary lymphedema and have demonstrated that 9-cis RA significa

80 ng tissue fibrosis, we used a mouse model of lymphedema and inhibited TGF-beta function either system

81 consecutive patients with uni- or bilateral lymphedema and lymph vessel transplants of the lower ext

82 iated with several human diseases, including lymphedema and metastatic spread of cancer.

83 aploinsufficiency of GATA2 underlies primary lymphedema and predisposes to acute myeloid leukemia in

84 berger syndrome, a disorder characterized by lymphedema and predisposition to myelodysplastic syndrom

85 deficient in lymphovenous hemostasis exhibit lymphedema and sometimes chylothorax phenotypes indicati

86 tations to include predisposition to primary lymphedema and suggest that complete haploinsufficiency

87 tissue fibrosis and lymphatic dysfunction in lymphedema and that inhibition of Th2 differentiation ma

88 thogenesis of many human diseases, including lymphedema and tumor metastasis.

89 undertaken to examine patient perceptions of lymphedema and use of precautionary behaviors several ye

90 her 15 unrelated microcephalic probands with lymphedema and/or chorioretinopathy identified additiona

91 osomal-dominant microcephaly associated with lymphedema and/or chorioretinopathy.

92 s correlated positively with the severity of lymphedema (and presumed inflammation) in filarial-disea

93 ild lymphedema, 12% reported moderate/severe lymphedema, and 2% reported chronically moderate/severe

94 BrCa survivors, 8.1% self-reported diagnosed lymphedema, and 37.2% self-reported arm symptoms.

95 patients reporting arm swelling had measured lymphedema, and 5% of patients reporting no arm swelling

96 L) among working-age women, the incidence of lymphedema, and associated risk factors.

97 e recently identified to cause microcephaly, lymphedema, and chorioretinal dysplasia (MLCRD) as well

98 e formation in lymphatic collecting vessels, lymphedema, and chylothorax.

99 ts molecular regulation during inflammation, lymphedema, and lymphatic metastasis.

100 utation is associated with immunodeficiency, lymphedema, and myelodysplastic syndrome.

101 incidence of long-term side effects, notably lymphedema, and the procedure is of no therapeutic benef

102 ymphatic development, the pathophysiology of lymphedema, and the role of leukotrienes in lymphedema p

103 nt of various human diseases such as cancer, lymphedema, and tissue allograft rejection.

104 disease, obesity, cancer, and cancer-related lymphedema are highlighted.

105 Animal models of lymphedema are used to test pharmacologic and microsurgi

106 ue node metastases, axillary recurrence, and lymphedema as measured by volume displacement.

107 surgery were prospectively screened for arm lymphedema as quantified by the weight-adjusted volume c

108 Using mouse models of lymphedema, as well as clinical lymphedema specimens, we

109 rger syndrome, an autosomal dominant primary lymphedema associated with a predisposition to acute mye

110 We sought to determine the risk of lymphedema associated with immediate breast reconstructi

111 pression of several molecules, including the lymphedema-associated transcription factor FOXC2.

112 There was no difference in lymphedema at any time point.

113 005 and 2013 were prospectively screened for lymphedema at our institution, with 22.2 months' median

114 ated in a number of chronic diseases such as lymphedema, atherosclerosis, and cancer.

115 into therapies for conditions as diverse as lymphedema, autoimmunity, and cancer.

116 the economic burden of breast cancer-related lymphedema (BCRL) among working-age women, the incidence

117 nd rate of infections likely associated with lymphedema between a woman with BCRL and a matched contr

118 postoperative recovery between the 2 groups (lymphedema breast reconstruction and breast reconstructi

119 verage operation time was 426 minutes in the lymphedema breast reconstruction group and 391 minutes i

120 ckade prevents initiation and progression of lymphedema by decreasing tissue fibrosis and significant

121 cacy in ameliorating experimental mouse tail lymphedema by enhancing lymphatic vessel regeneration.

122 T cells play a key role in the pathology of lymphedema by promoting tissue fibrosis and inhibiting l

123 iopsy use and 5-year cumulative incidence of lymphedema by race.

124 y account for about one third of all primary lymphedema cases, underscoring the existence of addition

125 implicate it as a candidate gene for primary lymphedema caused by valve defects.

126 dred inheriting a unique autosomal-recessive lymphedema-choanal atresia syndrome.

127 clerosing cholangitis and was diagnosed with lymphedema cholestasis syndrome (LCS).

128 es characterized by variable combinations of lymphedema, chorioretinal dysplasia, microcephaly and/or

129 rocephaly and lymphedema from a microcephaly-lymphedema-chorioretinal-dysplasia cohort.

130 ilial forms of primary lymphedema, secondary lymphedema, chylothorax and chylous ascites, lymphatic m

131 resided in the West were more likely to have lymphedema claims than those in the Northeast (OR = 2.05

132 ted as cancer-related and non-cancer-related lymphedema cohorts.

133 reconstruction does not increase the risk of lymphedema compared to mastectomy alone.

134 ociated with a significantly reduced risk of lymphedema compared to no reconstruction.

135 ostsurgical edema and significantly less paw lymphedema compared with vehicle-treated animals at all

136 bility that restoring HIF-2alpha pathways in lymphedema could mitigate long-term pathology and disabi

137 Of the 654 arms, 83 developed lymphedema, defined as a WAC >/= 10% relative to baselin

138 sive drug, is highly effective in preventing lymphedema development and treating established lymphede

139 g this model to study the role of obesity in lymphedema development, we show that obesity exacerbates

140 tigating the molecular mechanisms leading to lymphedema development.

141 e that debilitating and persistent preputial lymphedema develops after a prepuce-sparing penile deglo

142 s, or lymphatic vessel obstruction can cause lymphedema, disfiguring tissue swelling often associated

143 genital fibrosis of the extraocular muscles, lymphedema-distichiasis syndrome, neurofibromatosis type

144 As FOXC2 is mutated in lymphedema-distichiasis syndrome, our data also undersco

145 econd row of eyelashes is a feature of human lymphedema-distichiasis syndrome, which is associated wi

146 ranscription factor that is mutated in human lymphedema-distichiasis syndrome.

147 causes congenital lymphatic dysfunction and lymphedema due to defective lymphatic vessel patterning

148 ssociated with a higher probability of later lymphedema (eg, hazard ratio for jewelry too tight = 7.3

149 en genes have already been linked to primary lymphedema, either isolated, or as part of a syndrome.

150 undation for clinical investigations whereby lymphedema etiogenesis and therapies may be interrogated

151 Pathologic lymphatic remodeling in lymphedema evolves during periods of tissue inflammation

152 r both comparisons) and a lower incidence of lymphedema exacerbations as assessed by a certified lymp

153 ility in the study of diseases as diverse as lymphedema, filariasis, transplant rejection, obesity, a

154 Among the 238 affected women, lymphedema first occurred within 2 years of diagnosis in

155 Patients who presented with chronic lymphedema followed a systematic multi-disciplinary work

156 entative technique for breast cancer-related lymphedema from a cost-utility standpoint.

157 duals with a combination of microcephaly and lymphedema from a microcephaly-lymphedema-chorioretinal-

158 esults with the use of VLNT for treatment of lymphedema have been largely positive, further explorati

159 Patients who suffer from lymphedema have impaired immunity and, as a result, are

160 echanisms by which GATA2 mutations result in lymphedema have not been characterized.

161 Head and neck lymphedema (HNL) is a disfiguring disease affecting over

162 C2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a clo

163 recent report presented new cases of primary lymphedema in 22q11.2DS patients.

164 the lifestyle and clinical risk factors for lymphedema in a cohort of patients who underwent bilater

165 been suggested that many forms of secondary lymphedema in humans are driven by a progressive loss of

166 sed as a preventative agent for postsurgical lymphedema in humans.

167 egulation of GATA2, which has been linked to lymphedema in patients with Emberger syndrome.

168 assumption that it would reduce the risk of lymphedema in women with breast cancer.

169 assumption that it would reduce the risk of lymphedema in women with breast cancer.

170 quivalence margin was defined as doubling of lymphedema incidence.

171 s expressed in tissue components affected by lymphedema, including epidermis, lymphatics, and blood v

172 is necessary for the pathological changes of lymphedema, including fibrosis, adipose deposition, and

173 system in edema, genetic aspects of primary lymphedema, infection (cellulitis/erysipelas), Crohn's d

174 olved in many pathological processes such as lymphedema, inflammatory diseases, and tumor metastasis.

175 s that although cellulitis increases risk of lymphedema, ipsilateral blood draws, injections, blood p

176 Lymphedema is a common complication that occurs after br

177 Lymphedema is a complication of cancer treatment occurri

178 Lymphedema is a debilitating condition that often result

179 Secondary lymphedema is a debilitating condition, and genetic fact

180 Lymphedema is a dreaded complication of cancer treatment

181 Breast cancer-related lymphedema is a well-documented complication of breast c

182 Primary lymphedema is due to developmental and/or functional def

183 The prevalence and clinical burden of lymphedema is known to be increasing.

184 Lymphedema is the clinical manifestation of defects in l

185 uman analog is mutated in some families with lymphedema, is also highly enriched in a subset of endot

186 to determine whether improvement of filarial lymphedema (LE) by doxycycline is restricted to patients

187 and access to surgical treatment for chronic lymphedema (LE) in the United States have increased in r

188 PURPOSE Cancer-related lymphedema (LE) is an incurable condition associated wit

189 l details, subjective reported improvements, Lymphedema Life Impact Scale (LLIS) scores, and postoper

190 uineous family with two children affected by lymphedema, lymphangiectasia and distinct facial feature

191 of pathological tissue changes that occur in lymphedema may be a viable treatment strategy for this d

192 the time of surgery, or have upper extremity lymphedema may be less likely to undergo repeated mammog

193 phatic drainage after injection of MSCs in a lymphedema model indicates that MSCs play a role in lymp

194 We used an experimental murine tail lymphedema model where sustained fluid stasis was genera

195 ological hallmarks of the typical mouse tail lymphedema model while leaving an intact collecting vess

196 In a murine lymphedema model, galectin-1(-/-) animals had increased

197 es lymphatic regeneration in an experimental lymphedema model, presenting it as a promising novel the

198 GATA2 mutation is associated with deafness, lymphedema, mononuclear cytopenias, infection, myelodysp

199 e than a quarter of the incidence of primary lymphedema, mostly of inherited forms.

200 ma was low among survivors without diagnosed lymphedema (n = 1,183).

201 following three survivor groups: women with lymphedema (n = 104), women with arm symptoms without di

202 curred in 32 patients (13%) in the CLND arm; lymphedema (n = 20) and delayed wound healing (n = 5) we

203 ), women with arm symptoms without diagnosed lymphedema (n = 475), and women without lymphedema or ar

204 we assigned a score indicating the degree of lymphedema (none, mild, or moderate/severe) to each mont

205 s included the incidence of exacerbations of lymphedema, number and severity of lymphedema symptoms,

206 %) of bilateral lower extremity inflammatory lymphedema occurred during the first 120 hours of traini

207 Primary lymphedema occurs as a result of aberrations in the deve

208 ving 141 breast-cancer survivors with stable lymphedema of the arm.

209 ous bypass (LVB), on patients with secondary lymphedema of the upper or lower extremity (UEL/LEL).

210 ould like to know what she can do to prevent lymphedema on her upcoming flight to Vienna.

211 Lymphedema onset was associated with pronounced infiltra

212 utations, is the key predisposing factor for lymphedema onset.

213 osed lymphedema (n = 475), and women without lymphedema or arm symptoms (n = 708).

214 e impaired immune responses in patients with lymphedema or following lymphatic injury remain unknown.

215 s that involve the lymphatic system, such as lymphedema or lymphatic metastasis.

216 ing lymphadenectomy poses risks, such as leg lymphedema or lymphocyst formation.

217 by mycobacterial infection, myelodysplasia, lymphedema, or aplastic anemia that progress to myeloid

218 quent long-term effects (eg, second cancers, lymphedema, osteoporosis).

219 physiologic surgical treatment of secondary lymphedema over a 5.5-year period was performed.

220 nd, potentially, tumor lymphangiogenesis and lymphedema (pages 993-994).

221 r endogenous AM as a key factor in secondary lymphedema pathogenesis and provided experimental in viv

222 lymphedema, and the role of leukotrienes in lymphedema pathogenesis.

223 ermine the role of inflammatory responses in lymphedema pathology.

224 C-specific deletion of Hif2alpha exacerbated lymphedema pathology.

225 Lymphedema patients have decreased quality of life and r

226 ovides a basis for future clinical trials in lymphedema patients.

227 ising novel therapeutic agent to treat human lymphedema patients.

228 we have provided a molecular explanation for lymphedema predisposition in a subset of patients with g

229 scribed for women with breast-cancer-related lymphedema, preventing them from obtaining the well-esta

230 e lymphatic vasculature during the course of lymphedema progression.

231 A 52-year old patient presented with lymphedema, protein loosing enteropathy, and sclerosing

232 tion of GJC2 mutations as a cause of primary lymphedema raises the possibility of novel gap-junction-

233 Lymphedema rates after each of the following surgical op

234 ression analyses were performed to determine lymphedema rates and risk factors.

235 Lymphedema rates are dramatically reduced using ARM when

236 Objective lymphedema rates for SLNB and ALND were 0.8% and 6.5% re

237 We hypothesized that disconcerting lymphedema rates in both sentinel lymph node biopsy (SLN

238 in a decreased incidence of exacerbations of lymphedema, reduced symptoms, and increased strength.

239 Among the cancer cohort, total lymphedema-related costs per patient, excluding medical

240 Lymphedema-related direct costs were measured for home h

241 in the noncancer cohort; P < .001 for both), lymphedema-related manual therapy (from 35.6% to 24.9%in

242 Rates of cellulitis, use of lymphedema-related manual therapy, outpatient hospital v

243 Because of its morbidity and chronicity, arm lymphedema remains a concerning complication of breast c

244 is limited by the fact that the pathology of lymphedema remains unknown.

245 oportions of women with increasing degree of lymphedema reported symptoms (eg, jewelry too tight, tir

246 Podoconiosis is a tropical lymphedema resulting from long-term barefoot exposure to

247 ompletely characterized, and their effect on lymphedema risk is not known.

248 gs may help to guide patient education about lymphedema risk reduction strategies for those who under

249 ratified by type of axillary surgery, 5-year lymphedema risk was 6.8% in whites undergoing SLNB (HR,

250 Overall, the 5-year cumulative lymphedema risk was 8.2% in whites and 12.3% in blacks (

251 LNB use contributed to racial disparities in lymphedema risk.

252 (P = 0.0324) were associated with increased lymphedema risk.

253 th invasive breast cancer were enrolled in a lymphedema screening trial.

254 sels: sporadic and familial forms of primary lymphedema, secondary lymphedema, chylothorax and chylou

255 In breast-cancer survivors with lymphedema, slowly progressive weight lifting had no sig

256 ema exacerbations as assessed by a certified lymphedema specialist (14% vs. 29%, P=0.04).

257 se models of lymphedema, as well as clinical lymphedema specimens, we show that lymphatic stasis resu

258 tions in patients with chorioretinopathy and lymphedema suggests that EG5 is involved in the developm

259 ean (+/- SE) time between BrCa diagnosis and lymphedema survey was 8.1 +/- 0.2 years.

260 For all patients with lymphedema symptoms (n = 9), we used a modified lower ab

261 er improvements in self-reported severity of lymphedema symptoms (P=0.03) and upper- and lower-body s

262 ations of lymphedema, number and severity of lymphedema symptoms, and muscle strength.

263 Hennekam lymphangiectasia-lymphedema syndrome (Online Mendelian Inheritance in Man

264 ons that cause the Hennekam lymphangiectasia-lymphedema syndrome syndrome type1.

265 of lymphatic vessels and valves causes human lymphedema syndromes.

266 othelial markers and the study of congenital lymphedema syndromes.

267 propranolol in a patient with Hypotrichosis-Lymphedema-Telangiectasia and Renal (HLTRS) syndrome, ca

268 loped bilateral lower extremity inflammatory lymphedema that occurred during the 8(1/2)-week basic tr

269 Although RLNR adds to the risk of lymphedema, the main risk factor is the type of axillary

270 Lymphedema, the most common lymphatic anomaly, involves

271 sed comparative effectiveness data regarding lymphedema therapeutic interventions have been poor.

272 In human and mouse lymphedema, there is a significant increase of hypoxia i

273 lity was evaluated in patients with stage II lymphedema (three women; age range, 43-64 years) and in

274 These results have profound implications for lymphedema treatment as topical tacrolimus is FDA-approv

275 led equivalence trial (Physical Activity and Lymphedema trial) in the Philadelphia metropolitan area

276 lysis of data from the Physical Activity and Lymphedema Trial, we examined incident deterioration of

277 Five-year cumulative incidence of lymphedema was 42 (42%) per 100 women.

278 The two-year cumulative incidence of lymphedema was as follows: 4.08% [95% confidence interva

279 Lymphedema was defined as 10% or more arm volume increas

280 Lymphedema was defined as a >= 10% relative increase in

281 Lymphedema was induced in the right hind limb after a si

282 Knowledge of lymphedema was low among survivors without diagnosed lym

283 Postsurgical lymphedema was observed 100% of the time.

284 g our combined injury protocol, postsurgical lymphedema was observed 89% of the time.

285 Lymphedema was observed in 24.1% of the patients in the

286 Secondary lymphedema was prevented when circulating AM levels in A

287 group of families with dominantly inherited lymphedema, we identified six probands with unique misse

288 ether AM deficiency predisposes to secondary lymphedema, we used heterozygous adult mice with Adm gen

289 ptoms present before the first occurrence of lymphedema were associated with a higher probability of

290 me since surgery, and having upper extremity lymphedema were associated with lower mammography adhere

291 en previously treated for breast cancer with lymphedema were enrolled from six institutions.

292 Risk factors associated with measured lymphedema were greater body weight (P < .0001), higher

293 Viral infections and lymphedema were more common in individuals with null mut

294 Toxic effects, including lymphedema, were increased in the cohorts receiving comp

295 e characteristic swelling of tissues, called lymphedema, which arises as a consequence of insufficien

296 Patients with lymphedema who received an APCD who were commercially in

297 to demonstrate a significant improvement in lymphedema with decongestive therapy compared with a mor

298 ukemia (AML); and Emberger syndrome (primary lymphedema with MDS).

299 data may underestimate the true incidence of lymphedema, women with BCRL had a greater risk of infect

300 function of lymphatic valves underlies human lymphedema, yet the process of valve morphogenesis is po