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1 erihematoma regions (less than two cells per high power field).
2 as capillaries containing blue particles per high-power field).
3 d) than in the control group (7.92+/-.33 per high-power field).
4 0.999], P = .04; cutoff <=42 eosinophils per high-power field).
5 0%) had active disease (>=15 eosinophils per high-power field).
6 le adherence at baseline was uncommon (<2/50 high-power fields).
7 e and a peak eosinophil count <5 eosinophils/high power field.
8 ar the number of eosinophils must be >15 eos/high power field.
9 tom improvement and less than 15 eosinophils/high-power field.
10 ty and mast cell numbers were assessed in 20 high-power fields.
11 TAT3+, and CD4+/BNC2+ cells in 5 consecutive high-power fields.
12 single-cell resolution in a series of random high-power fields.
13 h-power fields, or (2) 30 eosinophils in 2-4 high-power fields.
16 (11 points), urine red blood cell count >10/high-power field (3 points), and urine white blood cell
17 hil count less than or equal to 32 cells per high power field (4.55, 1.62-12.78; p=0.0040), rectal bi
18 vs. 21%, P=0.03), contained >9.3 leukocytes/high power field (46.5 vs. 10.5%, P=0.006) or was both P
20 at later time points (mean+/-SEM capillaries/high-power field: 67.6+/-4.7 in control versus 44.1+/-4.
21 quartile range], 8 [8] vs 3 [4] cells per 10 high-power fields; 95% CI, 1-10 cells per 10 high-power
22 sy histology and remissions (<15 eosinophils/high-power field) after dietary therapy and food reintro
24 1.0 to 5.1; P = .04) and > 5 mitoses per 50 high-power fields (AHR, 2.5; 95% CI, 1.1 to 6.0; P = .03
26 no ganglion cells (0-0.30 ganglion cells per high-power field) and at least mild myenteric inflammati
27 n cell numbers (0.79-0.91 ganglion cells per high-power field) and at least mild myenteric inflammati
30 (P<0.05) in both the normal (1.70+/-0.15 per high-power field) and study groups (2.08+/-0.10 per high
31 re histologic remission (<=6 eosinophils per high-power field) and the change from baseline in the Dy
32 ere histologic response (<=6 eosinophils per high-power field) and the change from baseline in the sc
33 (380 +/- 21 polymorphonuclear leukocytes/50 high-power fields) and apoptosis (925% +/- 29% increase
34 ntermediate-level mitotic count (6-10 per 50 high-powered fields) and an intermediate tumor size (6-1
35 (6.4 +/- 1.0 vs 11.4 +/- 1.3 neutrophils per high power field), and less renal apoptosis, as assessed
36 ccurred in many viable hepatocytes (13 cells/high-power field), and nonviable hepatocytes increased s
37 ponds to approximately <5 eosinophils/median high-power field); and endoscopic remission as absence o
38 ochondria in quarter-size grafts were 15 per high power field, and dead cells were less than 1 per hi
39 classification, counting of lymphocytes per high-power field, and morphometry is important for diagn
40 30 Gardnerella or Prevotella morphotypes per high-power field, as detected by Gram staining of vagina
41 ith an elimination diet (<15 eosinophils per high power field at oesophageal biopsy), and who underwe
44 had an esophageal count of >= 15 eosinophils/high-power field at diagnosis, and were currently prescr
46 that demonstrates 3 or more erythrocytes per high-powered field before initiating further evaluation
47 trix of the hematoma (17.5 +/- 6.3 cells per high power field) but not in the perihematoma regions (l
49 ular density, as measured by capillaries per high-powered field (c/hpf), was significantly greater in
50 ng histologic remission (<15 eosinophils per high-power field); change in histologic features (histol
51 s a peak count of <20 eosinophils/mm(2) in a high-power field (corresponds to approximately <5 eosino
52 ageal biopsy depicts over 20 eosinophils per high-powered field despite the use of aggressive acid bl
53 gic responders, defined by </= 5 eosinophils/high-power field (eos/hpf) (n = 32), underwent systemati
54 d among patients with >/= 15 eosinophils per high-power field (eos/hpf) (OR, 0.79; 95% CI, 0.70-0.88)
55 post-treatment maximum eosinophil counts per high-power field (eos/hpf) and a validated dysphagia sco
56 ified based on the number of eosinophils per high-power field (eos/HPF) in esophageal biopsies into:
57 osis is considered if >or=15 eosinophils per high-powered field (eos/hpf) are detected in mucosal bio
58 stopathologic remission (<15 eosinophils per high-power field [eos/hpf]) and control (48 pediatric an
60 cantly, from 114.83 to 73.26 eosinophils per high-power field [(eos/hpf), P = 0.0256], whereas no red
62 an 10% but more than five tumor cells per 10 high power fields (focal) in a subset (7 of 26) of aggre
63 tion in sinusoids (515 +/- 30 neutrophils/50 high power fields) followed by transmigration at 7 h.
64 increased (P<0.05) to 9+/-5 and 5+/-4 per 50 high-power fields for albumin and anionic lipid microbub
65 ree tubules with tubulitis in 10 consecutive high-power fields from the most severely affected areas,
66 y was conducted and included eosinophils per high power field (from esophagogastroduodenoscopy biopsy
67 nophil density of 15 or more eosinophils per high-power field), from May 12, 2015, through November 9
68 of peri-nuclear lysosomes [4.1 x 10,000 per high power field (h.p.f.) +/- 1.9 vs. 2.0 x 10,000 per h
69 th greater than or equal to six CD138+ cells/high power field (hpf) had worse graft survival with a h
72 > or =30 polymorphonuclear cells (PMNL) per high-power field (hpf) on Gram stain (2050 vs. 320 ifu),
73 4), and >=20 macrophages per 0.3 mm-diameter high-power field (HPF) versus <20 macrophages per HPF (1
74 rmed on all biopsies; CD20+ cell density per high-power field (hpf) was determined for each core.
80 ial sarcoma with less than 10 mitoses per 10 high-power fields (hpf) had a 10-year cancer-specific su
81 oliferative threshold of five mitoses per 10 high-power fields (HPF) was of greater prognostic value
82 otic counts of three mitoses or fewer per 30 high-power fields (HPF), more than three to <or= 15 mito
83 of the difference between 0 to 2 mitoses/10 high-power fields (HPF; 5-year recurrence of 31%) and mo
84 valuated the mean number of Paneth cells per high-powered field (hpf) in 116 duodenal biopsies obtain
85 ur leukocyte, PMN) and macrophage counts per high-powered field (HPF) were performed on fixed section
86 hemotaxis from a baseline of 0.4+/-0.7 cells/high-powered field (hpf; mock-infected) to 21.8+/-2.3 ce
87 +/- 32 polymorphonuclear leukocytes [PMN]/50 high power fields [HPF]) and severe liver injury (plasma
88 h nontolerant grafts (n = 9; 15 vs. 23 cells/high-power field [hpf] [P < .01] and 16 vs. 26 cells/hpf
89 to anti-IL-5 (defined as <15 eosinophils per high-power field [hpf] after mepolizumab therapy), and 7
90 tatistically significant (30 ng/L and 1 cell/high-power field [hpf] in the no-pill group, 39 ng/L and
92 mnants were similar (laser, 1.87 +/- 1.05 NV/high-power field [hpf]; drill, 1.92 +/- 1.09 NV/hpf; P =
93 (low grade: no necrosis and < two mitoses/50 high-powered fields [HPF]; or intermediate grade: necros
94 in mean esophageal eosinophil count in the 5 high-power fields (hpfs) with the highest level of infla
95 , integrating Radscore, mitotic count per 50 high-power fields (HPFs), and current tumor distribution
96 sue neutrophils (20.3 versus 8.6 cells per 5 high-powered fields [HPFs]; P=0.02) and macrophages (6.1
97 gene; (3) pyuria (>=10 white blood cells per high powered field in the urine); and (4) dysuria and fe
98 he most effective, achieving <15 eosinophils/high-power field in 90.8% and 72.1% of patients, respect
99 IEE (defined as more than 20 eosinophils per high-power field in biopsy specimens) who had undergone
101 tients with EG and 11 +/- 9 eosinophils/x400 high-power field in control subjects (P = 6.1 x 10(-7)).
104 infiltration by immune cells <15 eosinophils/high-power field in esophageal biopsies) for pediatric a
105 ion, the presence of at least 15 eosinophils/high-power field in esophageal biopsy specimens, and exc
106 ophil count was 283 +/- 164 eosinophils/x400 high-power field in patients with EG and 11 +/- 9 eosino
107 sy demonstrating at least 15 eosinophils per high-power field in the absence of other conditions asso
109 d 84.6 +/- 19.7 vs 19.6 +/- 12.9 eosinophils/high-power field in the distal esophagus [P = .04]).
110 number of 30 IgG4-positive plasma cells per high-power field in the orbital tissue is compatible wit
111 ls (65.9 +/- 25.3 vs 1.4 +/- 1.1 eosinophils/high-power field in the proximal esophagus [P = .03] and
112 owed eosinophil infiltration of more than 40/high-power field in the stomach and duodenum, so he was
114 ation of polymorphonuclear leukocytes per 10 high-power fields in postischemic renal tissue (1111 +/-
115 er dystrophic tubular calcifications per ten high-power fields in the parenteral compared with the en
116 ically active EoG/EoGE (>=30 eosinophils per high-power field) in the stomach and/or duodenum and gas
117 r field, and dead cells were less than 1 per high power field, indicating that depolarization precede
118 cut-off of >=15 eosinophils in at least one high power field is the density threshold considered the
119 m-operated controls (< 10 neutrophils per 20 high-power fields), large numbers of neutrophils were pr
120 tained 180 and 300 IgG4 plasma cells/maximal high-power field, mainly in the deep lamina propria; the
122 was defined as more than 10 eosinophils per high-power field obtained from sinus mucosal biopsy and
123 , a histologic response (<=6 eosinophils per high-power field) occurred in significantly more patient
124 tly higher total positive area and intensity/high power field of VCAM-1 expression than did juvenile
125 ek-old mice, 38% (2.5 +/- 3.2 cells per 400x high-power field) of TAMs were GFP-positive, bone marrow
126 e of more than 10 IgG4-positive plasma cells/high power field on endoscopic biopsy of the bile duct w
127 nse, defined as less than 15 eosinophils per high-power field on endoscopic biopsy, in 41.7% of patie
129 ined as >=5 polymorphonuclear leukocytes per high-power field on urethral Gram stain plus either visi
131 resence of pyuria >=10 white blood cells per high-power field on urine microscopy offered negligible
132 ed a mean of (1) 20 eosinophils or more in 5 high-power fields, or (2) 30 eosinophils in 2-4 high-pow
133 duce esophageal eosinophil counts to <15 per high-power field over a short-term treatment period of 4
134 cing esophageal eosinophil counts to <15 per high-power field over a short-term treatment period, wit
135 d with hypoxia alone: 23.4 versus 35.0 cells/high-power field (p = 0.01), with no change in other mar
137 te analysis included < or = 2 mitoses per 50 high-power fields (P =.001, P =.002), vascular invasion
138 ignificantly fewer TUNEL-positive nuclei per high-powered field (P<0.01), less DNA fragmentation (ant
141 n chronically rejecting grafts (9+/-1 nuclei/high-powered field, P<0.0001), but the distribution betw
142 een in the lased (4.4 +/- 0.3 arterioles per high power field; p < 0.001 vs. both TMI and sham) compa
144 ed in the EPCM group (4.1 versus 6.2 vessels/high-powered field; P<0.001), and microvascular perfusio
145 positive cells were counted across 10 to 20 high-powered fields per patient by using an automated sy
146 unt were observed in all groups (neutrophils/high-power field): PLV-CVF (20 +/- 2, p = .009); PEEP-CV
147 rge or >/=5 polymorphonuclear leukocytes per high-power field [PMNs/HPF]) were eligible for this doub
148 inophil count by a mean 86.8 eosinophils per high-power field (reduction of 107.1%; P < .0001 vs plac
149 ctor only group (GV-CVF 47 +/- 2 neutrophils/high-power field), reductions in neutrophil count were o
152 wer field) and study groups (2.08+/-0.10 per high-power field) than in the control group (7.92+/-.33
153 end labeling-positive nuclei (53+/-3 nuclei/high-powered field) than chronically rejecting grafts (9
155 (defined as < 10 dysmorphic erythrocytes per high-power field, the absence of cellular casts, and exc
156 of >/= 2 leukocytes per epithelial cell per high-powered field, the positive predictive values for M
157 d by 1) varying polymorphonuclear leukocytes/high-powered field thresholds and placenta components in
158 was modest for polymorphonuclear leukocytes/high-powered field thresholds of greater than 10 and gre
160 he basis of mitotic rate (< 2 mitoses per 50 high-power fields v higher) and necrosis (present or abs
163 resence of 10 or more mitotic figures per 50 high power fields was an independent predictor of diseas
164 The number of stained blood vessels per high-power field was correlated with the sonographically
165 gment detected by histopathology in >=30% of high-powered fields was strongly associated with LBW (ad
166 rowth, acute inflammation (>/= 5 neutrophils/high-power field) was observed in only 40% of patients w
167 mitotic index (<5 or > or =5 mitoses per 50 high-power fields) was developed from 127 patients treat
169 ne 0.6-mm spot is equivalent to two to three high-power fields, we used TMAs to assess levels of hete
172 h 24 or more intraepithelial eosinophils per high-power field were randomly assigned to receive infus
174 large numbers of erythrocytes (> or =100 per high-power field), whereas it was 6.6% (98 of 1,486 spec
175 r-positive (i.e. , more than 100 bacilli per high-power field), while two patient's sputa contained 1
176 tients had 10 or more mitotic figures per 50 high power fields, while 11 had ulceration and/or necros
177 sceptibility, R2*, and R2' and the number of high-power fields with CD163-positive (r range, 0.64-0.7
178 easurements and number of 400x magnification high-power fields with iron-containing macrophages.