ライフサイエンスコーパス: gastrointestinal

1 5% CI 1.12-2.31, p=0.0089), which was mainly gastrointestinal.

2 epresented in the patient cohort were mainly gastrointestinal (31.8%), brain (22.7%), or lung (20.7%)

3 Fever (73%), neurological (72%), gastrointestinal (41%), and cardiac (40%) symptoms were

4 AEs associated with methotrexate, primarily gastrointestinal (67 [24.8%]).

5 on, controlling blood pressure, and enabling gastrointestinal activity.

6 s likely to discontinue sorafenib because of gastrointestinal adverse effects (8.7% v 10.8%; P = .047

7 ent; the main reason for discontinuation was gastrointestinal adverse events such as nausea.

8 Having 1 or more AEs related to medication, gastrointestinal AE, laboratory abnormality, or AE leadi

9 protected more against methotrexate-induced gastrointestinal AEs than did weekly administration.

10 litis syndrome (FPIES) is a non-IgE-mediated gastrointestinal allergic disorder.

11 GBS commonly colonizes the lower gastrointestinal and genital tracts and, during pregnanc

12 duced by specialized epithelial cells of the gastrointestinal and genito-urinary tracts.

13 Gastrointestinal and gynecological malignancies dissemin

14 Bortezomib, however, associated with gastrointestinal and hematologic toxicity.

15 However, there are many gastrointestinal and hepatic diseases for which obesity

16 Gastrointestinal and liver-related adverse events were t

17 cystectomy are associated with occurrence of gastrointestinal and nongastrointestinal cancers.

18 general population is associated with pooled gastrointestinal and right-side colon cancers.

19 eye conditions; cardiovascular, neurologic, gastrointestinal, and endocrine disease; cognitive funct

20 this autopsy study was to determine whether gastrointestinal angiodysplasia develops during continuo

21 between LVAD support, abnormal angiogenesis, gastrointestinal angiodysplasia, and bleeding.

22 rst direct evidence that LVAD support causes gastrointestinal angiodysplasia.

23 action and speciation (DNAS) and an in vitro gastrointestinal assay to provide an upper bound and bio

24 ssue drug penetration to account for delayed gastrointestinal-associated lymphoid tissue immune recov

25 chemical changes that impair function of the gastrointestinal barrier.

26 flood-like disturbances that eliminate most gastrointestinal biomass can be induced using a clinical

27 use to prevent one disabling or fatal upper gastrointestinal bleed over 5 years fell from 338 for in

28 to study devices occurred during the study (gastrointestinal bleed).

29 Upper gastrointestinal bleeding (UGIB) is a common gastrointes

30 ing severe enough to result in massive upper gastrointestinal bleeding and death.

31 of major gastrointestinal bleeding, with all gastrointestinal bleeding as a secondary outcome.

32 ted with a reduced risk of all severities of gastrointestinal bleeding compared with warfarin (0.25 [

33 Upper gastrointestinal bleeding developed in 6.1% of patients

34 terectomy included systemic infection in 11, gastrointestinal bleeding in 1, and severe electrolyte i

35 Acute lower gastrointestinal bleeding is a common reason for emergen

36 Acute upper gastrointestinal bleeding is a leading indication for re

37 nts and those with kidney disease had higher gastrointestinal bleeding rates with dabigatran.

38 e-variant confounders, the incidence rate of gastrointestinal bleeding was similar during dabigatran

39 performance to identify patients with lower gastrointestinal bleeding who are suitable for safe outp

40 e risk score to identify patients with lower gastrointestinal bleeding who could safely avoid hospita

41 r findings show no increase in risk of major gastrointestinal bleeding with direct oral anticoagulant

42 In patients with overt gastrointestinal bleeding, and negative findings on esop

43 idered a complementary test in patients with gastrointestinal bleeding, Crohn's disease, or celiac di

44 CT) has also gained importance in diagnosing gastrointestinal bleeding, particularly in hemodynamical

45 Age, sex, previous admission for lower gastrointestinal bleeding, rectal examination findings,

46 tect both the source and the cause of active gastrointestinal bleeding, thereby expediting treatment

47 e primary outcome was the incidence of major gastrointestinal bleeding, with all gastrointestinal ble

48 ble tool for detecting the location of acute gastrointestinal bleeding.

49 as no alarming increase in the risk of upper gastrointestinal bleeding; the effect of proton pump inh

50 proton-pump inhibitors (PPIs) reduces upper gastrointestinal bleeds by 70-90%, uptake is low and gui

51 ovement of insulin resistance/diabetes after gastrointestinal bypass surgery.

52 e tubal fibrosis; this may be induced by the gastrointestinal C. muridarum, as a second hit, to trans

53 associated with family history (FH) of upper gastrointestinal cancer (UGI) cancer in cases with ESCC.

54 sing bioelectrical impedance analysis in 128 gastrointestinal cancer patients provided with or withou

55 Cognizance of these disparities in gastrointestinal cancer risk, as well as approaches that

56 to the mutations found in p53 gene of human gastrointestinal cancers.

57 st exclusively to treat colorectal and other gastrointestinal cancers.

58 ex and gut microbiota, bile acids (BAs), and gastrointestinal cancers.

59 Colorectal cancer is the commonest gastrointestinal carcinoma.

60 Detection of patients with gastrointestinal carriage of CPO is necessary to interru

61 development of persistent and non-persistent gastrointestinal carriage states in genetically identica

62 Many nosocomial infections arise from gastrointestinal colonization.

63 with implications for the pathophysiology of gastrointestinal comorbidities of ASD.

64 ssion before surgery and major postoperative gastrointestinal complications after bariatric surgery a

65 sed odds ratios or relative risks of several gastrointestinal complications of obesity: gastroesophag

66 fier structure and emulsion stability during gastrointestinal conditions in modulating lipolysis kine

67 roplet sizes and were submitted to simulated gastrointestinal conditions using a kinetic digestion pr

68 ndividuals not experiencing these functional gastrointestinal conditions.

69 In all cases, upper gastrointestinal contrast swallow with the use of a wate

70 eview is to examine current knowledge of the gastrointestinal contributions to metabolic control.

71 We review the mechanisms of gastrointestinal damage induction by NSAIDs via COX-medi

72 Often the origin of antibiotic-associated gastrointestinal deterioration remains elusive and no sp

73 The effect of simulated gastrointestinal digestion (GID) on phenolic content, co

74 olysis of protein concentrate under in vitro gastrointestinal digestion (pepsin-trypsin system) great

75 dy was to evaluate the influence of in vitro gastrointestinal digestion and colonic fermentation on t

76 te purified TCMPs retained the resistance to gastrointestinal digestion and the inhibitory activity t

77 These results highlighted that gastrointestinal digestion may substantially affect the

78 According to the results of an in vitro gastrointestinal digestion model, industrial processing

79 ute; the acrylamide content evolution during gastrointestinal digestion of French fries and chips; an

80 es a good approximation to the physiological gastrointestinal digestion of milk proteins.

81 Gastrointestinal digestion of peptides improved their du

82 s and oxidation taking place during in vitro gastrointestinal digestion of slightly oxidized sunflowe

83 The influence of gastrointestinal digestion on peptide bioactivity was al

84 ptides may be further hydrolysed through the gastrointestinal digestion resulting in a pool of peptid

85 Simulated gastrointestinal digestion was used for determination of

86 An in vitro method involving simulated gastrointestinal digestion was used to assess the bioacc

87 of industrial and home processing, in vitro gastrointestinal digestion, individual phenolic content,

88 nd air-frying on acrylamide mitigation after gastrointestinal digestion.

89 bres taking into account their changes along gastrointestinal digestion.

90 function, at the organ level, in a dysmotile gastrointestinal disease model.

91 Non-typhoidal Salmonella are associated with gastrointestinal disease worldwide and invasive disease

92 l therapeutic strategies in the treatment of gastrointestinal diseases associated with altered IESC f

93 ronic constipation is a prevalent functional gastrointestinal disorder accompanied with intestinal dy

94 reflux disease (GERD) is the most prevalent gastrointestinal disorder in the United States, and lead

95 ncreasingly used for treatment of functional gastrointestinal disorders (FGIDs), now recognized as di

96 ficacy for abdominal pain-related functional gastrointestinal disorders in adolescents.

97 arly robust clinical evidence for other rare gastrointestinal disorders is needed.

98 Gastrointestinal disorders were the most common adverse

99 Gastrointestinal disorders were the most common adverse

100 is an enteropathogenic bacterium that causes gastrointestinal disorders, as well as extraintestinal m

101 e (IBS) is one of the most common functional gastrointestinal disorders.

102 imal performance included these factors plus gastrointestinal disturbance, severe neutropenia, and pr

103 As gastrointestinal disturbances are common in children wit

104 Ensuring reliable gastrointestinal drug absorption of orally administered

105 c could improve adherence and reduce adverse gastrointestinal effects.

106 gastrointestinal bleeding (UGIB) is a common gastrointestinal emergency, which is potentially fatal.

107 ulticentre, cohort study using routine lower gastrointestinal endoscopy and pathology data from patie

108 : Use of monitored anesthesia care (MAC) for gastrointestinal endoscopy has increased in the Veterans

109 Intriguingly, mice with gastrointestinal epithelial cell-specific Egfr deletion

110 hyme and find that, although dispensable for gastrointestinal epithelial development and homeostasis,

111 hat glia are required for maintenance of the gastrointestinal epithelium.

112 olorectal cancer liver metastases and murine gastrointestinal experimental liver metastases are infil

113 ofile from crosslinked nanogels in simulated gastrointestinal fluids.

114 tion about host-gut microbiome interactions, gastrointestinal functionality, and dietary patterns.

115 ing sympathetic nerve activity, respiration, gastrointestinal functions, hormonal release, and behavi

116 eric nervous system (ENS) regulates numerous gastrointestinal functions, including epithelial barrier

117 gnificant degree of independent control over gastrointestinal functions, the central nervous system p

118 e enteric glia and their regulatory roles in gastrointestinal (GI) (patho)physiology; from GI motilit

119 llosteric modulator (PAM) contributes to the gastrointestinal (GI) and cardiovascular (CV) cholinergi

120 n studies exploring the correlations between gastrointestinal (GI) bacterial biota and diseases.

121 Gastrointestinal (GI) bleeding is one of the most common

122 : In most patients with Parkinson's disease, gastrointestinal (GI) dysfunctions, such as gastroparesi

123 ug release kinetics and interaction with the gastrointestinal (GI) membrane.

124 hysiological roles that maintain and restore gastrointestinal (GI) mucosal homeostasis.

125 The FilmArray gastrointestinal (GI) panel (BioFire Diagnostics, Salt L

126 Furthermore, respondents with overlapping gastrointestinal (GI) symptom complexes have significant

127 Lower gastrointestinal (GI) tract graft-versus-host disease (G

128 evolved as a commensal organism of the human gastrointestinal (GI) tract primarily transmissible via

129 estradiol (EE2) sorbed onto SWCNTs in a fish gastrointestinal (GI) tract.

130 d variable conditions encountered throughout gastrointestinal (GI) transit, leading to degradation of

131 erse events were anaemia (eight [4%]), upper gastrointestinal haemorrhage (eight [4%]), pneumonia (se

132 n [3%]), gastric haemorrhage (six [3%]), and gastrointestinal haemorrhage (five [2%]) in the trastuzu

133 yed worm expulsion during infection with the gastrointestinal helminth Nippostrongylus brasiliensis O

134 Gastrointestinal helminth parasites share their habitat

135 tachycardia (3%), thoracic pain (3%), upper gastrointestinal hemorrhage (3%), and vomiting (3%).

136 es in patients with severe nonvariceal upper gastrointestinal hemorrhage.

137 QMRA) to estimate risk [probability of acute gastrointestinal illness (AGI)] for individuals exposed

138 Our estimates suggest gastrointestinal illness attributed to surface water rec

139 borne pathogenic bacterium that causes acute gastrointestinal illness, but its mechanisms of infectio

140 daily surf activities and illness symptoms (gastrointestinal illness, sinus infections, ear infectio

141 sense single-stranded RNA viruses that cause gastrointestinal illness.

142 h exerts pleiotropic and dominant effects on gastrointestinal immunity.

143 verse events in both semaglutide groups were gastrointestinal in nature: nausea was reported in 26 (2

144 piratory infections and HBoV2 to HBoV4 cause gastrointestinal infections in young children.

145 These findings indicate that early gastrointestinal infections may be relevant for CD devel

146 Necrotising enterocolitis is a neonatal gastrointestinal inflammatory disease with high mortalit

147 Inflammatory bowel diseases are chronic gastrointestinal inflammatory disorders that affect mill

148 epetitive behavior, immune dysregulation and gastrointestinal issues are common comorbidities.

149 cutaneous and internal venous malformations; gastrointestinal lesions are pathognomonic.

150 We describe an aberrant gastrointestinal-lineage transcriptome expressed in appr

151 a and bile acids), the transformation of the gastrointestinal lining, increases in postprandial gut h

152 the maintenance of tissue fluid homeostasis, gastrointestinal lipid absorption, and immune traffickin

153 rdiovascular, neuronal, immune, respiratory, gastrointestinal, liver, and endocrine systems, by influ

154 ne of the terpenes, after having experienced gastrointestinal malaise.

155 and lipid in the intestine could account for gastrointestinal manifestations of Wilson disease.

156 alth effects on the cardiovascular, nervous, gastrointestinal, metabolic, respiratory, and reproducti

157 ollectively, these finding indicate that the gastrointestinal microbiome is an important modulator of

158 luences the composition and diversity of the gastrointestinal microbiome.

159 ogenic forces can dramatically reshape equid gastrointestinal microbiomes, which has broader implicat

160 ration.These results indicate that the human gastrointestinal microbiota composition and function var

161 Here we show that secretory products from gastrointestinal microbiota derived from a human donor s

162 Preclinical research has shown that the gastrointestinal microbiota exhibits circadian rhythms a

163 letion, and reestablishment of a physiologic gastrointestinal microbiota might be beneficial for this

164 iceptive influences; the contribution by the gastrointestinal microbiota to this balance has received

165 Prebiotics are selectively fermented by the gastrointestinal microflora, resulting in benefits to hu

166 agastrically to assess its effect on fasting gastrointestinal motility and hunger ratings, motilin an

167 We measured epithelial barrier function and gastrointestinal motility in these mice and littermate c

168 les that act on enteric neurons to influence gastrointestinal motility, and metabolites that stimulat

169 cells compromises epithelial maintenance or gastrointestinal motility.

170 Whether gastrointestinal motor and sensory function is primary c

171 ABSTRACT: Membrane potentials of gastrointestinal muscles are important because voltage-d

172 years) had 405 first bleeding events (n=218 gastrointestinal, n=45 intracranial, and n=142 other) du

173 associated with accelerated expulsion of the gastrointestinal nematode Nippostrongylus brasiliensis o

174 en these periods were noted in distant-stage gastrointestinal NETs (HR, 0.71; 95% CI, 0.62-0.81) and

175 oved over time, especially for distant-stage gastrointestinal NETs and pancreatic NETs in particular,

176 nd symptoms, e.g., fever (n = 281; 13%), and gastrointestinal or genitourinary conditions (n = 268; 1

177 These results extend our understanding of gastrointestinal organogenesis and of how Wnt and BMP mi

178 ifferentiated (grade 1 or 2) NETs of lung or gastrointestinal origin.

179 Cancer incidence, gastrointestinal outcomes, psychological outcomes, child

180 Early satiety (P = 0.043), gastrointestinal pain and discomfort (P = 0.01), altered

181 ing evidence of benefit for treating chronic gastrointestinal pain and painful FGIDs and serotonin no

182 of data for FGIDs, we included data for non-gastrointestinal painful disorders and specific symptoms

183 ted with the multianalyte assay Luminex xTAG Gastrointestinal Pathogen Panel, an in-house five-virus

184 nventional methods for the identification of gastrointestinal pathogens are time-consuming and expens

185 of bacteria and reveals a mechanism by which gastrointestinal pathogens directly target RHIM-dependen

186 and assessed inter-observer agreement among gastrointestinal pathologists from 5 tertiary centers in

187 The gastrointestinal peptide hormone, secretin (SCT) that bi

188 t changes in the gut microbiota can modulate gastrointestinal physiology, immune function, and even b

189 onal results indicate that interactions with gastrointestinal proteins may decrease the level of adso

190 erative changes in satiety, body weight, and gastrointestinal quality of life.

191 was 1.67 days, and the average duration for gastrointestinal reactors was 2.29 days.

192 The most common adverse events were gastrointestinal-related disorders, primarily nausea (65

193 nd myasthenia gravis (76 cases) and, rarely, gastrointestinal-related illness (5 cases), multiple scl

194 gies being utilized or developed to leverage gastrointestinal signals in order to treat obesity.

195 We show that three gastrointestinal signals-serotonin, CCK, and PYY-are nec

196 inimide (EDC/NHS) was adopted to improve the gastrointestinal stability of nanogels.

197 Gastrointestinal stromal tumor (GIST) is the most common

198 urrence-free survival (RFS) in patients with gastrointestinal stromal tumors (GISTs) treated with sur

199 escent and young adult (AYA) population with gastrointestinal stromal tumors (GISTs).

200 initiating events, fostering hyperplasia in gastrointestinal stromal tumours (GISTs), and additional

201 s included 5556 patients undergoing elective gastrointestinal surgery and 1523 patients undergoing em

202 d using data from 17,114 patients undergoing gastrointestinal surgery between 2010 and 2013.

203 Recent developments in paediatric gastrointestinal surgery have focused on minimally invas

204 n this observational cohort study, inpatient gastrointestinal surgical procedures performed at 117 Ve

205 Therefore, this study aimed to translate the Gastrointestinal Symptom Rating Scale for Irritable Bowe

206 Symptoms were measured by Gastrointestinal Symptom Rating Scale Irritable Bowel Sy

207 parameters, and tolerability as rated by the Gastrointestinal Symptom Rating Scale.

208 s the change in symptoms using the validated Gastrointestinal Symptom Score (GIS(c)).

209 neuromodulators in the treatment of chronic gastrointestinal symptoms and FGIDs.

210 The incidence and severity of 15 gastrointestinal symptoms and overall symptoms were meas

211 tives included patients' assessment of their gastrointestinal symptoms as well as treatment safety an

212 ee diet associated with small improvement in gastrointestinal symptoms compared with no gluten-free d

213 are not involved in the pathogenesis or the gastrointestinal symptoms of PD.

214 Injection site reactions and gastrointestinal symptoms were common adverse events in

215 The patient had worsened gastrointestinal symptoms with mycophenolate mofetil or

216 e and included respiratory tract infections, gastrointestinal symptoms, and hypertension.

217 ing to absence of gut innervation and severe gastrointestinal symptoms.

218 (10% of the overall group) due to persistent gastrointestinal symptoms.

219 ars or diagnosed with CMA with predominantly gastrointestinal symptoms.

220 tely 70% of these tumours are located in the gastrointestinal system (GI), followed by the bronchi, e

221 and secretion, and rhythmic movements of the gastrointestinal system.

222 mide was safe and well tolerated with better gastrointestinal tolerability than dolutegravir, abacavi

223 ring pelvic radiotherapy resulted in reduced gastrointestinal toxicity both acutely and at 1 y compar

224 estinal membrane integrity and contribute to gastrointestinal toxicity.

225 Development of the dairy calf gastrointestinal tract (GIT) and its associated microbio

226 her to their antioxidant activity within the gastrointestinal tract (GIT) or to bioactivity of their

227 otic microorganisms inhabiting the mammalian gastrointestinal tract (i.e., the microbiota) influence

228 .The pharmacologic inhibition of STRs in the gastrointestinal tract alters insulin responses during a

229 The mammalian gastrointestinal tract and associated mucosal immune sys

230 sitional zone in the epithelium of the upper gastrointestinal tract and provide evidence that the p63

231 l antimicrobial activity of adenosine in the gastrointestinal tract and unveil an important role for

232 e patients and in cases with suspected lower gastrointestinal tract bleeding.

233 rived organ malformations in liver, lung and gastrointestinal tract by whole exome sequencing.

234 been recently identified as a risk factor of gastrointestinal tract cancers, especially hepatocellula

235 Here we demonstrate that ILC2s in the mouse gastrointestinal tract co-localize with cholinergic neur

236 Although the gastrointestinal tract contains intrinsic neural plexuse

237 The enteric nervous system (ENS) of the gastrointestinal tract controls many diverse functions,

238 degradation under alkaline conditions in the gastrointestinal tract dominates.

239 o and establishes stable colonization of the gastrointestinal tract following intravaginal inoculatio

240 A prophylactic treatment that protects the gastrointestinal tract from deleterious effects of radio

241 ing.The use of drug delivery systems for the gastrointestinal tract has been faced with a number of d

242 The gastrointestinal tract is a highly complex organ in whic

243 We show that the gastrointestinal tract is deficient in de novo generatio

244 re hypothesized that other polyamines in the gastrointestinal tract may control V. cholerae biofilm f

245 , promoting C. muridarum colonization of the gastrointestinal tract may represent a primary function

246 Overall, patients with gastrointestinal tract metastases undergoing complete, c

247 reus found to be persistently colonising the gastrointestinal tract of BALB/c mice.

248 to detect and quantify microplastics in the gastrointestinal tract of fishes.

249 C. jejuni's adaptation to the oxygen-limited gastrointestinal tract of the host.

250 from rice bran might also be produced in the gastrointestinal tract of the human body.

251 erestingly, C. muridarum colonization of the gastrointestinal tract positively correlated with pathog

252 ted with enterovirus infections of the human gastrointestinal tract remain largely unknown.

253 The gastrointestinal tract represents the largest interface

254 mplex chronic inflammatory conditions of the gastrointestinal tract that are driven by perturbed cyto

255 pose a model for NSAID-induced damage to the gastrointestinal tract that includes these complex, inte

256 genes required for infection of the porcine gastrointestinal tract utilising a transposon (Tn) mutan

257 of multifocal GIST-like tumors in the mouse gastrointestinal tract with 100% penetrance.

258 nal characteristics of the microbiota in the gastrointestinal tract, along with fundamental and emerg

259 ht the immune communication between skin and gastrointestinal tract, and identifies novel mechanisms

260 bacterial pathogen that invades cells of the gastrointestinal tract, causing severe dysentery.

261 i-inflammatory drugs (NSAIDs) can damage the gastrointestinal tract, causing widespread morbidity and

262 ndigested starch are transported through the gastrointestinal tract, contributing to fewer calories e

263 Human DAO is abundant only in the gastrointestinal tract, kidney, and placenta, and glycos

264 attern, with the highest levels in the upper gastrointestinal tract, particularly in the squamous epi

265 It is known to infect the host gastrointestinal tract, specifically, in locations assoc

266 f CD40 in DCs results in inflammation of the gastrointestinal tract, thereby impairing lipid uptake,

267 ke other barrier sites, such as the skin and gastrointestinal tract, we found that Th17 cells can dev

268 cture of survivin expression patterns in the gastrointestinal tract, we used an immunohistochemical a

269 n host diet for metabolic substrates and the gastrointestinal tract, which is influenced by enteral n

270 itioned to regulate distinct portions of the gastrointestinal tract, with implications for the pathop

271 ase is a chronic inflammatory disease of the gastrointestinal tract, with increasing incidence worldw

272 events with liraglutide affected mainly the gastrointestinal tract.

273 ime to obtain the desired release profile in gastrointestinal tract.

274 mon with barrier macrophages of the lung and gastrointestinal tract.

275 al distension as the meal passes through the gastrointestinal tract.

276 ollows the natural route of infection in the gastrointestinal tract.

277 (MET+) neurons in the DMV and nAmb, and the gastrointestinal tract.

278 that are expressed on the tongue and in the gastrointestinal tract.

279 (II) is essential for iron absorption in the gastrointestinal tract.

280 hat Clec2e transcripts are restricted to the gastrointestinal tract.

281 ritical for C. muridarum colonization of the gastrointestinal tract.

282 pe the bacterial communities residing in the gastrointestinal tract.

283 om the nasal cavity, lungs, and possibly the gastrointestinal tract.

284 pGP4, also consistently colonized the mouse gastrointestinal tract.

285 sed to study motility disorders of the human gastrointestinal tract.

286 y which ExPEC strains colonize the mammalian gastrointestinal tract.

287 eria contribute to immune homeostasis in the gastrointestinal tract; however, the underlying mechanis

288 ce identified Fibrobacter populations in the gastrointestinal tracts of numerous hindgut-fermenting h

289 NF4G at physiologic levels recapitulates the gastrointestinal transcriptome, chromatin landscape, and

290 creased which negatively correlated with the gastrointestinal transit time.

291 diated induction of JAK/STAT3 is critical in gastrointestinal tumorigenesis following Lkb1 mutations

292 ncoding tumor suppressor kinase LKB1 lead to gastrointestinal tumorigenesis in Peutz-Jeghers syndrome

293 rization of a large series of SBAs and other gastrointestinal tumors to draw comparisons and identify

294 ation is an important treatment modality for gastrointestinal tumors, but intestinal injury is a comm

295 omplications include radiation gastritis and gastrointestinal ulcers, cholecystitis, radiation pneumo

296 sis, hypertension, obesity, type 2 diabetes, gastrointestinal ulcers/bleeds, fractures, and cataracts

297 technique facilitating ocular, oral mucosal, gastrointestinal, ungual and vaginal drug administration

298 g pancreatic uptake, focal liver uptake, and gastrointestinal uptake in the treated mice, whereas the

299 mary diagnosis of intracranial hemorrhage or gastrointestinal, urogenital, or other bleeding.

300 tinuations were due to adverse events-mostly gastrointestinal with semaglutide, and others such as sk