戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 min, in parallel rodent and human studies of radiation injury.
2  multilineage in vivo repopulation following radiation injury.
3  of the host immune status on salivary gland radiation injury.
4 ive therapy to treat victims of severe acute radiation injury.
5 egulating the response of renal podocytes to radiation injury.
6 e of the endothelium in the manifestation of radiation injury.
7 c candidate for a medical countermeasure for radiation injury.
8 mucosa such as inflammatory bowel disease or radiation injury.
9 may improve mucosal healing in patients with radiation injury.
10 gic to treat inflammatory diseases including radiation injury.
11 ed injuries that may identify biomarkers for radiation injury.
12 ted that ISCs expressed IL-33 in response to radiation injury.
13 e-specific SMPDL3b-knock out (KO) mice after radiation injury.
14 l metabolism and cytoprotective responses to radiation injury.
15 ept under extreme conditions of depletion or radiation injury.
16 t development and in normal lens response to radiation injury.
17 r selective normal tissue protection against radiation injury.
18 arrow (BM), which did not increase following radiation injury.
19 lenished by bone marrow precursors following radiation injury.
20 t part of the adaptation of keratinocytes to radiation injury.
21 rgistic signalling protected ICPS cells from radiation injury.
22 lity to differentiate recurrent gliomas from radiation injury.
23 evels correlate with improved survival after radiation injury.
24 ization grade II-IV infiltrating gliomas and radiation injury.
25 regeneration, and are resistant to high-dose radiation injury.
26 is for distinguishing recurrent gliomas from radiation injury.
27 e eye is likely the most sensitive organ for radiation injury.
28 pendent compensatory proliferation following radiation injury.
29 tor of apoptosis) in apoptosis of HSCs after radiation injury.
30 nsible for long-term tissue damage following radiation injury.
31 ndin-1-null mice are remarkably resistant to radiation injury.
32 ased apoptosis alone and in combination with radiation injury.
33 equired for recovery of granulopoiesis after radiation injury.
34 vascular endothelium in the absence of acute radiation injury.
35 n(II) accumulation facilitates recovery from radiation injury.
36 l in tissue repair mechanisms resulting from radiation injury.
37 ructural, cellular, and molecular aspects of radiation injury.
38 ween bone marrow and brain in the setting of radiation injury.
39 aling pathways which is acutely sensitive to radiation injury.
40 e regeneration of hematopoietic tissue after radiation injury.
41 em cell survival and proliferation following radiation injury.
42 cal elements in the response of the brain to radiation injury.
43 dioresistant fungi that protect the gut from radiation injury.
44 ecialties to evaluate and manage large-scale radiation injuries.
45                              After sublethal radiation injury (500 rad), the infusion of purified CD4
46 ecurrent tumors (all K-ratios >/= 1.70) from radiation injury (all K-ratios < 1.50) (100% sensitivity
47 mice showed minimal histological evidence of radiation injury and near full retention of mitochondria
48 jury is a prominent feature of normal tissue radiation injury and plays a critical role in both acute
49 ch could be translated as biomarkers of both radiation injury and protection by countermeasures.
50 tion of rhIL-11 ameliorates early intestinal radiation injury and support further development of rhIL
51 fts that would provide an overall benefit to radiation injury and underscore the utility of metabolom
52 n of Wnt/beta-catenin signaling may mitigate radiation injury and/or speed recovery of taste cell ren
53 a offer new insight into the mechanism(s) of radiation-injury and suggest that CCR2 is a critical med
54 tors, such as dual oxidases, defense against radiation injuries, and novel proteins such as ZBP-89.
55 (e.g. bladder exstrophy, neurogenic bladder, radiation injury, and marked urethral dysfunction) or to
56 mors, the histologic changes associated with radiation injury, and the diagnostic and prognostic info
57          The vascular system is sensitive to radiation injury, and vascular damage is believed to pla
58 mal tissue or that facilitate the healing of radiation injury are being developed.
59  immune responses promote fibrosis following radiation injury, but the full spectrum of factors gover
60 ressed whether protection against intestinal radiation injury can be achieved by intraluminal adminis
61                                        Acute radiation injury can continue into a chronic phase or ch
62  fundamental understanding of the effects of radiation injury could further aid in the identification
63                                              Radiation injury depletes proliferative intestinal stem
64                                              Radiation injury, either from radiotherapy or a mass-cas
65 imals, animals that received G-CSF following radiation injury exhibited enhanced functional brain rep
66                           To protect against radiation injury from extravasation of therapeutic radio
67           PET has been used to differentiate radiation injury from malignancy on the basis of differe
68 vo utilizing an experimental rodent model of radiation injury, i.e., partial body irradiation (PBI).
69 crease) correctly differentiated tumors from radiation injury in all but 1 case (100% sensitivity and
70 arkedly decreases the deleterious effects of radiation injury in mesenchyme-derived tissues and prese
71 IL-17A as a hemopoietic response cytokine to radiation injury in mice and an inducible mechanism that
72 mediators has been proposed to contribute to radiation injury in normal tissues.
73   Expression of survivin correlated with the radiation injury in patients.
74 IL-11 to reduce manifestations of intestinal radiation injury in the clinic.
75                                              Radiation injury in the CNS has been linked to persisten
76 estinal morphology but are hypersensitive to radiation injury in the intestine compared with wild-typ
77                     The cellular response to radiation injury in the intestine or bone marrow can be
78 2 (PGE2) synthesis modulates the response to radiation injury in the mouse intestinal epithelium thro
79                                              Radiation injury induced a dose-dependent decrease in th
80 RIGS lethality in vivo after lethal ionizing radiation injury-induced intestinal epithelial damage.
81                 Our results demonstrate that radiation injury induces early cytoskeletal remodeling,
82 treatment resulted in a 36% reduction in the radiation injury intestinal mucosal damage score, corres
83                                   Intestinal radiation injury is associated with overexpression of al
84                                   Intestinal radiation injury is dose limiting during abdominal and p
85 brain metastases (RPBM) from late or delayed radiation injury (LDRI).
86 ost interactions before and after small bowl radiation injury may eventually allow prediction of dise
87  of small intestinal epithelial cells in the radiation injury model.
88 eters were higher in tumors (n = 12) than in radiation injury (n = 10) (P </= 0.012 in all comparison
89                                              Radiation injury occurs in 5% to 37% of cases and can be
90 tect individuals and mitigate the effects of radiation injury or Acute Radiation Syndrome (ARS) is st
91 nd the intestinal stem cell compartment upon radiation injury, promoting a fetal-like reprogramming a
92 r (TbetaR-II) protein ameliorates intestinal radiation injury (radiation enteropathy).
93 oting muscle regeneration, yet their role in radiation injury remains unclear.
94                             We conclude that radiation injury results in increased Cox-1 levels in cr
95 stations of radiation enteropathy, including radiation injury score (6.5 +/- 0.6 in the vehicle group
96                            Anterior thalamic radiation injury showed correlation with decreased proce
97                     The overt pathologies of radiation injury such as white matter necrosis or vascul
98             Chronic inflammation accompanies radiation injury, suggesting that inflammatory processes
99                                  In cases of radiation injury, the degree of severity, ranging from e
100 trategy may be limited by the possibility of radiation injury, the results are consistent with the pa
101  treating cancer comes the increased risk of radiation injury to bone marrow-both direct suppression
102                                    Utilizing radiation injury to model intestinal pathology, we repor
103 mor efficacy of radiation without increasing radiation injury to normal tissue.
104 early diagnosis, and management of potential radiation injury to the liver and to other organs.
105 ECT biomarkers have the potential to predict radiation injury to the lungs before substantial functio
106 time, in order to determine damage driven by radiation injury to the microvessels and to the inner re
107  is unlikely to result in acute or long-term radiation injury to the patient or to a measurable incre
108                           The acute phase of radiation injury to the rectum occurs during or up to 3
109 ies will be highly useful for characterizing radiation injury to the spinal cord and illuminate our u
110                    Understanding how initial radiation injury translates into long-term effects is an
111  Marrow Transplantation have established the Radiation Injury Treatment Network (RITN), a voluntary c
112                                        Acute radiation injury typically occurs 2 weeks to 3 months af
113 rovide comprehensive evaluation and care for radiation injury victims.
114                                              Radiation injury was assessed at 6 weeks using quantitat
115  computerized image analysis, and structural radiation injury was assessed by quantitative histopatho
116                            In the setting of radiation injury, we find dynamic fluctuations in marrow
117          Since RVCL pathology mimics that of radiation injury, we reasoned that nuclear TREX1 would c
118 ellular, and molecular aspects of intestinal radiation injury were assessed.
119 gnificantly improve patient care in cases of radiation injury, whether from radiotherapy or mass-casu
120 icacy of a single FSL-1 dose for alleviating radiation injury while protecting against adverse effect
121          Postn(-/-) mice recover faster from radiation injury with concomitant loss of primitive HSCs

 
Page Top