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1 n imaging data were acquired at baseline and following therapy.
2 were measured at baseline and 6 and 9 months following therapy.
3 g indolent phases, and undergo rapid changes following therapy.
4 ome measure for recovery of binocular vision following therapy.
5 m, and Corynebacterium species were observed following therapy.
6 ons were carried out at baseline and 8 weeks following therapy.
7 els of adiponectin and adipsin that reversed following therapy.
8 mplete resolution of Guillain-Barre syndrome following therapy.
9 t high frequencies (42 to 50%) 70 to 90 days following therapy.
10 maging was performed at baseline and +4 days following therapy.
11 epeat liver biopsy were assessed at 24 weeks following therapy.
12 of Aa at baseline as well as 3 and 12 months following therapy.
13 se activity during the study or in the month following therapy.
14 oups and HGV was not associated with outcome following therapy.
15 mined during the course of HIV infection and following therapy.
16 ents at pre-treatment and 2, 6, and 12 weeks following therapy.
17 in and glucagon that increased significantly following therapy.
18 in lipid, nucleic acid, and collagen content following therapy.
19 asticity in the primary somatosensory cortex following therapy.
20 onal and synaptogenic pathways at recurrence following therapy.
21 s from individuals with persistent infection following therapy.
22 DCs and regulatory and proliferative T cells following therapy.
23 g tumors or the inevitability of progression following therapy.
24 , chemotherapy response, and tumor evolution following therapy.
25  patients under 60 years of age received the following therapy: 45 mg/m(2) daunorubicin on days 1-3,
26 s perceived their disease to be in remission following therapy, 78% of these patients required contin
27 atients who recovered from HCV infection (98 following therapy and 19 spontaneously).
28  pain and paraesthesia symptoms at baseline, following therapy and at 3-month follow-up.
29 from the end of the successful weaning trial following therapy and the previously failed one, were an
30 g how the extracellular matrix (ECM) evolves following therapy and whether it impacts treatment respo
31 ll clones, elimination of clonal populations following therapy, and subsequent appearance of a clone
32                                              Following therapy, aortic TBR fell to 1.90+/-0.29, P=0.0
33 t therapy, and patients with detectable DTCs following therapy are at substantially increased risk fo
34              Malignant carcinomas that recur following therapy are typically de-differentiated and mu
35 KLF4 at disease acceleration, which resolves following therapy, but reoccurs following relapse and de
36 ng period, the defects were treated with the following therapies: collagen membrane (GTR), human demi
37 vival and recurrence of residual tumor cells following therapy constitutes one of the biggest obstacl
38 ibute to the survival of breast cancer cells following therapy could aid in the development of more e
39  immunomodulators, and predictors of relapse following therapy discontinuation have become available.
40 rapies inducing delayed cardiac inflammation following therapy due to activation of cGAS- and STING-d
41 viral therapy era; however, data on outcomes following therapy for anal dysplasia (infrared coagulato
42 delines are commonly used to assess response following therapy for hepatocellular carcinoma (HCC).
43 to 12 days, 35 to 45 days, and 70 to 90 days following therapy for quantitative vaginal culture.
44 ion that gonococcal DNA is detectable by LCR following therapy for uncomplicated gonococcal infection
45 cted an increase in Ki-67+ PD-1+ CD8 T cells following therapy in approximately 70% of patients, and
46 t difference in alpha diversity was observed following therapy in both the omadacycline and vancomyci
47       GCF chemerin and IL-6 levels decreased following therapy in CP groups (P <0.02).
48 nd to analyze changes in cytokine expression following therapy in order to understand its primary mec
49 nt was numerically higher at all time points following therapy in the 500 mg rituximab group.
50  mice harbored abnormal lymphoproliferations following therapy--in these cases, comparison of the loc
51  the assessments of minimal residual disease following therapy, including for patients who have under
52 resentation levels are selectively augmented following therapy, including several epitopes present at
53 ed by diverse therapy-sensitive cancer cells following therapy-induced caspase cleavage of the tumor
54 mors is linked to the inflammatory processes following therapy-induced re-education of tumor-associat
55 g the persistence of disparities in survival following therapy initiation is mixed.
56 inations at baseline and within three months following therapy initiation were assessed.
57  mGPS predicted outcomes as early as 6 weeks following therapy initiation, thereby opening a window f
58 uppressor cells (MDSCs) at early time points following therapy initiation.
59 g- and vehicle-treated tumors within 5 hours following therapy initiation.
60  viral DNA level or to prevent virus rebound following therapy interruption in immune system-humanize
61  5 demonstrated an LVEF <50%, which reversed following therapy interruption.
62                             However, relapse following therapy is frequently observed, and mechanisms
63               The degree of residual disease following therapy is monotonically associated with pre-t
64 mycin-resistant anaerobic gram-negative rods following therapy is of concern.
65                           At 3 and 12 months following therapy mean PD at monitored sites in the test
66  the sensory scale of the SF-MPQ was reduced following therapy (P=0.02).
67 survival and proliferation of residual cells following therapy remains unexplored.
68 ssessment of restoration of retinal function following therapy renders achromatopsia a very attractiv
69  (IgE) and other Th2 responses in the months following therapy, responses that have been associated w
70 ividuals experiencing serious adverse events following therapy (see the related articles beginning on
71  the population of cancer cells that persist following therapy, serves as the critical reservoir for
72  showing a time-dependent response up to 3 h following therapy, suggesting a diffusion of soluble Fas
73 ared with T1DM patients and can be monitored following therapies targeted at improving inflammation a
74                                              Following therapy, Th17 cells were essentially lost, whe
75  eventual secondary decline of DP thymocytes following therapy was associated with renewed viral expr
76                     Sequencing of SARS-CoV-2 following therapy was successful in 16.
77        In contrast, initial tumor regression following therapy was unimpaired in CD1d(-/-) mice, whic
78                           Surgical specimens following therapy were assessed for the degree of pathol
79 lapse) and 10 patients with no response (NR) following therapy were identified through the Virahep-C
80 ite APBI developed peak distortion 21 months following therapy, which may be sooner than distortion f
81 lts with advanced renal cell carcinoma (RCC) following therapy with a programmed cell death protein 1
82 rinary storage symptoms (overactive bladder) following therapy with an alpha-blocker, the addition of
83  of these 6 proteins was significantly lower following therapy with AngII inhibitors (P < 0.05).
84 ssociated with DNA-damaging agents can occur following therapy with FND, with or without rituximab, a
85 cant reduction in plasma ADMA concentrations following therapy with hydrophilic statins.
86  myeloid leukemia (CML) SCs that is enriched following therapy with tyrosine kinase inhibitors (TKIs)
87 hat the reduction of DMN-insula connectivity following therapy would correlate with diminished pain.