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1 tween participants in strata of baseline CD4 cell count.
2 IV-1) RNA <50 copies/mL and change in CD4+ T-cell count.
3 on gender distribution, viral load, and CD4 cell count.
4 ecreased appetite, and decreased white blood cell count.
5 ecurrent viral infections and reduced CD8+ T cell count.
6 at the time of infection and baseline CD4+ T-cell count.
7 etroviral therapy (cART) irrespective of CD4 cell count.
8 Prevalences were adjusted for age and CD4 cell count.
9 ut differed in terms of myeloid and lymphoid cell counts.
10 asing platelet counts, and lower white blood cell counts.
11 n antiretroviral therapy (cART), at high CD4 cell counts.
12 likely to normalize in those with low CD4+ T cell counts.
13 troviral therapy (ART) with high pre-ART CD4 cell counts.
14 symptoms and increased myeloid and CD4(+) T-cell counts.
15 eolin, dose-dependently increased osteoblast cell counts.
16 le LGCs numbers and decreased dead/apoptotic cell counts.
17 ning (p=5.9e-3), after adjusting for age and cell counts.
18 ell signatures as well as activated CD4(+) T cell counts.
19 s normal CD4(+) but lower than normal CD8(+) cell counts.
20 ubunit C storage, astrogliosis, and neuronal cell counts.
21 g HIV co-infected individuals with low CD4 T-cell counts.
22 linical outcomes of body weight and CD4(+) T cell counts.
23 All three regimens improved patients' CD4 cell counts.
24 and investigated the aetiology of low CD4 T-cell counts.
25 nts regarding preservation injury and goblet cells count.
26 diagnostic platform technology for CD4(+) T cell counting.
27 les, but not to zygotic genome activation or cell counting.
28 muL, 1.61 to 2.39; p<0.0001), decreased CD4 cell count (0.53 per 5 square-root cells per muL, 0.35 t
29 unit, 0.56 to 0.92; p=0.0078), increased CD8 cell count (1.51 per 5 square-root cells, 1.11 to 2.06;
32 severe COVID-19 had higher peak white blood cell counts (15.8 vs 7 x 10(3) /uL, P = .019), C-reactiv
34 , 551-1210] cells/mm; P < 0.0001) and CD4+ T cell count (29 cells/mm [IQR, 1.3-116.0] vs 325.5 cells/
37 98.3% on antiretroviral therapy, median CD4+ cell count 527 cells/mm 3, 86.6% with HIV-1 RNA < 50 cop
39 31 [42%] vs 28 [39%]), decreased white blood cell count (8 [11%] vs 5 [7%]), and hypophosphataemia (3
40 ciated with a 29% lower baseline white blood cell count (95% confidence interval [CI], -7% to -46%; P
41 Cerebrospinal fluid testing showed normal cell counts, a negative result on reverse-transcription
43 er levels of C-reactive protein, white blood cell count, absolute neutrophil count, and procalcitonin
44 er levels of C-reactive protein, white blood cell count, absolute neutrophil count, and procalcitonin
45 or demographic factors, baseline HIV RNA/CD4 cell counts, AIDS defining events and the type of InSTI.
50 levels were inversely associated with CD4 T-cell count and CD4:CD8 ratio, while positively correlate
58 low-cost, label-free, and real-time on-chip cell counting and quantifying method for sorted/separate
59 BA pool increases colonic RORgamma(+ )T(reg) cell counts and ameliorates host susceptibility to infla
63 toma and is characterized by decreased CD4 T-cell counts and downregulation of major histocompatibili
64 s consistently associated with reduced CD4 T cell counts and elevated levels of T cell activation and
66 ociations between higher relative FOXP3(+) T-cell counts and increased risks of colorectal and breast
67 lysis of the humoral system shows that blood cell counts and inflammatory markers are differentially
68 ity of patients who maintain normal CD4(+) T-cell counts and low or undetectable viral loads for deca
69 pha exhibited a more pronounced elevation of cell counts and protein content in bronchoalveolar lavag
70 ncology to psychiatry, can lower white blood cell counts and thus access to these treatments can be r
71 of monocytes to lymphocytes, activated CD4 T cell count, and a blood RNA signature could be correlate
72 es were assessed for HIV RNA viral load, CD4 cell count, and antiretroviral drug-resistant mutations.
73 rate, virus clearance, viral load, CD4(+) T cell count, and CD4(+) T cell loss in SIV-infected macaq
75 and phenotype, early thymic progenitor (ETP) cell count, and expression of FOXN1 target genes (Ccl25,
76 r changes, contrast sensitivity, endothelial cell count, and possible adverse events were assessed at
77 viral therapy (ART) at a higher vs lower CD4 cell count, and the longer-term harms associated with cu
78 nterior chamber depth and angle, endothelial cell count, and visual acuity did not change in this coh
79 against viremia, fever, elevated white blood cell counts, and CHIKF-associated cytokine changes after
80 was associated with older ages, lower white cell counts, and earlier stages of illness at presentati
83 up plasma viremia, peripheral blood CD4(+) T cell counts, and lymph node and rectal tissue viral load
84 ation, complete and differential white blood cell counts, and lymphocyte subsets for 301 infants, wit
85 We examined hemoglobin, red and white blood cell counts, and platelet counts and volume in regular m
86 thymic involution, declines in peripheral T-cell counts, and reduced major histocompatibility comple
87 copies per mL, changes from baseline in CD4 cell counts, and the frequency of adverse events, advers
88 individuals, those with higher nadir CD4+ T-cell counts, and those who had received lopinavir/ritona
89 estimated glomerular filtration rate, CD4+ T-cell count, antiretroviral drug class and duration of th
90 nfection (aOR 1.14), recent high white blood cell count (aOR 1.08), and genitourinary disorder (aOR 1
91 od function with respect to a time series of cell counts, approximated by the Central Limit Theorem f
92 onor cornea age and higher donor endothelial cell count are associated with better long-term graft su
93 ng of low-abundance cells, particularly when cell counts are sample-limited and operationally difficu
95 gevity, neurobehavioral parameters, neuronal cell counts, astrogliosis, and diminution in brain and s
96 s (IQR 30-43), 45.4% were female, median CD4 cell count at admission was 76 cells/mul (IQR 23-206), a
97 ime with NVL, and WHO clinical stage and CD4 cell count at ART initiation, rates of excess all-cause
100 ling defined a minimal model including white cell count at diagnosis, pretreatment cytogenetics, and
101 ethod, with balancing for circulating tumour cell count at screening, to receive 400 mg or 300 mg ola
102 ls were characterized by flow cytometry, and cell counts at different time-points were compared with
105 f the year, whereas results from microscopic cell counts, biovolume analysis and metatranscriptomics
106 use serum and significantly increasing blood cell counts, BM hematopoietic cellularity and stem and p
107 wed accelerated recovery in peripheral blood cell counts, bone marrow colony forming units, sternal c
112 cent, past, cumulative, or nadir/peak CD4+ T-cell count (CD4) and/or HIV-1 RNA level (HIV RNA) best p
113 ntry regimen, duration of ART, and nadir CD4 cell count; CD4 and CD8 cell counts were also associated
114 to placebo-treated subjects, in mean CD4+ T-cell count change (278 vs 250 cells/muL, P = .474) or CD
116 ors on the causal pathway (most notably, CD4 cell count, clinical signs of advanced HIV, and poor fun
117 2%; 17.2-46.1) of 43; and circulating tumour cell count conversion was achieved in 15 (53.6%; 33.9-72
118 ut robustly-correlated with anterior chamber cell count (correlation coefficient range 0.41-0.81).
119 gth increased red blood cell and white blood cell counts, decreased mean corpuscular hemoglobinand me
120 iciency virus (HIV)-positive adults, low CD4 cell counts despite fully suppressed HIV-1 RNA on antire
122 T cells and B cells, and normalization of NK-cell counts during a median follow-up of 16 months.
124 mes measured were visual acuity, endothelial cell count (ECC), rates of secondary graft failure (SGF)
125 controls, had significantly increased immune cell counts, especially neutrophils, CD4(+) T cells, and
126 logical cancer requires complete white blood cell count, followed by flow cytometry with multiple mar
127 see text]=1.47, 95% CI 0.26, 2.67) and CD4 + cell count ([Formula: see text]= - 0.68, 95% CI - 1.10,
128 mains inherently challenging, with a limited cell count from tumor samples, to achieve potent persona
129 aseline, or conversion of circulating tumour cell count (from >=5 cells per 7.5 mL blood at baseline
131 of ART to asymptomatic individuals with CD4 cell counts greater than 500/mm3 and shows sustained red
132 ng stable antiretroviral therapy with CD4+ T-cell count >100 cells/mm3, and with low to moderate card
134 ious anterior uveitis (anterior chamber [AC] cell count >=11 cells) were randomized to EGP-437 delive
135 ature >=39 degrees C, peripheral white blood cell count >=20 000/mm3, C-reactive protein >=70.0 mg/L,
136 >=40 years old with treated HIV, with CD4+ T-cell count >=400 cells/muL and with/at increased risk fo
137 d/or recent HIV infection (patients with CD4 cell count >=500/mm3 at HIV diagnosis; (PRHI) between 20
138 nosis soon after HIV infection (ie, with CD4 cell count >=500/muL or with acute HIV infection) and us
139 9% vs 36.6%; P < .0001), and had white blood cell counts >=15 000 cells/uL (31.4% vs 21.4%; P < .0001
140 ified 333 HIV-infected patients with CD4 + T-cell-counts >= 500/ul, among them 178 met the inclusion
141 opportunistic infections, and minimum CD4 T-cell counts (>100 cells per muL for liver and >200 cells
142 up among WLHIV with higher contemporary CD4+ cell counts (>=200 cells/uL vs <200 cells/uL [cOR = 0.36
143 ociated with weight gain including lower CD4 cell count, higher HIV type 1 RNA, no injection drug use
145 cies occur in different contexts of age, CD4 cell count, HIV control, viral co-infections, or chronic
146 eatment history, plasma HIV RNA, nadir CD4+T-cell count, HIV subtype, and country were investigated.
147 rved between microbiome diversity and CD4+ T-cell count, HIV viral load, or HIV-associated chronic lu
148 r all coinfected patients, regardless of CD4 cell count.HIV/human T-cell lymphotrophic virus type 1 c
149 on was measured based on sputum differential cell counts, IL-1beta protein levels (ELISA), and sputum
151 stics, plasma HIV RNA, nadir and current CD4 cell count in blood, current CD8 cell count in blood, es
152 current CD4 cell count in blood, current CD8 cell count in blood, estimated duration of HIV infection
155 res were negatively associated with the CD4+ cell count in male children (beta: -0.13, 95% confidence
157 tly reduced viral loads and increased CD4+ T cell counts in blood and bronchoalveolar lavage (BAL) sa
158 d high peripheral T follicular helper (pTfh) cell counts in blood but low Tfh cell counts in lymph no
159 hanges were associated with reduced CD4(+) T cell counts in both the mesenteric lymph nodes and colon
160 UFP-exposed offspring had lower white blood cell counts in bronchoalveolar lavage fluid and less pro
163 n of L. rhamnosus were assessed by bacterial cell counts in nasal mucosa, fecal samples, cervical lym
164 with CD4+CD38+ cell numbers and total CD4+ T cell counts in patients with a suppressed viral load.
165 of M2 macrophages, correlate with low CD4+ T cell counts in patients with suppressed viral load, rais
167 nergic cell distribution, density, and total cell counts in the different cell-type-specific KO lines
171 hromatin accessibility (MACC) assay with low-cell count input, we profile both small-scale (kilobase)
172 onth BSCVA; 3-, 6-, and 12-month endothelial cell counts; intraoperative and postoperative complicati
174 tes, survival time, baseline and current CD4 cell count, last HIV-1 RNA plasma viral load (pVL), and
175 performance status of 3 or less, white blood cell count less than 10 x 10(9) per L, and adequate end-
177 ase and had significantly higher white blood cell counts, lower lymphocyte counts, and increased C-re
178 Before ART initiation, PTCs had higher CD4 T cell counts, lower plasma viremia, and SIV-DNA content i
179 tive serology, 22 (22.5%) had an endothelial cell count < 2000 cells/mm(2) and 6 (6.1%) are at time o
180 HIV-1 RNA >=100 000 copies/mL, 21% had CD4+ cell count <200 cells/uL, and 31% enrolled <=48 hours fr
182 ry post-ART initiation in patients with CD4+ cell counts <200 cells/mm3 and >=200 cells/ mm3 was 27.4
184 lass B or C at SVR (10.71 [1.32-87.01]), CD4 cell counts <200/uL at SVR time-point (4.42 [1.49-13.15]
185 lass B or C at SVR (10.71 [1.32-87.01]), CD4 cell counts <200/uL at SVR time-point (4.42 [1.49-13.15]
187 viduals having detectable HIV RNA and CD4+ T-cell counts <500 cells/uL with HIV-negative individuals.
188 HIV and having detectable HIV RNA and CD4+ T-cell counts <500 cells/uL with individuals living withou
189 ia (ICL) is defined by persistently low CD4+ cell counts (<300 cells/muL) in the absence of a causal
190 prospective cohort of patients with AHD (CD4 cell count, <=200/mul) receiving CD4 count testing, whol
191 erum antibody levels, bronchoalveolar lavage cell counts, lung histology, lung cytokine levels, and a
192 mmon processing pipelines to produce gene-by-cell count matrices from droplet-bases scRNA-seq data, d
193 between normalization of CSF WBCs and CD4+ T cell count may indicate continued imprecision in neurosy
194 e normalization of CSF WBC counts and CD4+ T cell counts may indicate continued imprecision in neuros
195 types according to their sputum granulocytic cell count.Measurements and Main Results: In the discove
196 ing of HBECs, without influencing epithelial cell count, metabolic activity, or barrier function.
197 tive protein (n = 2), albumin (n = 2), white cell count (n = 3), neutrophils (n = 2), and platelets (
198 Despite ART-associated improvement in CD4+ T cell counts (nadir CD4 <200 cells/mm3 with >350 cells/mm
199 ral therapy-associated improvement in CD4+ T-cell counts (nadir, <200/muL; >350/muL after antiretrovi
200 usting for sex, ethnicity, hypertension, CD4 cell count, nadir CD4 <200u/L, and time since HIV diagno
201 cluded initial respiratory rate, white blood cell count, neutrophil/lymphocyte ratio, and lactate deh
202 tion raises inflammatory-related white blood cell counts (neutrophils and monocytes), thereby increas
203 rs and for high vs lower initial white blood cell count, no significant differences between TDT group
204 k of circadian rhythmicity in GR-deficient B cell counts normally associated with diurnal patterns of
206 d group, followed by the group with a CD4+ T-cell count of >=200 cells/muL and the group with a CD4+
207 g antiretroviral therapy (ART) with a CD4+ T-cell count of <100 cells/muL were enrolled and followed
210 tures (age >= 1 and < 10 years), white blood cell count of <50 x109/L, lack of extramedullary leukemi
211 (normal range, 0.2-0.9 mg/L), a white blood cell count of 11.69 x10(9)/L (normal range, 4-10 x10(9)/
212 test results showed an increased white blood cell count of 13 000/muL (13 x10(9)/L) (normal range, 37
213 test results showed an increased white blood cell count of 13,000/uL (13 x 109/L) (normal range, 3700
214 es revealed leukocytosis, with a white blood cell count of 15.1 x 10(3)/uL (15.1 x 10(9)/L) (normal r
215 es revealed leukocytosis, with a white blood cell count of 15.1 x 103/muL (15.1 x 109/L) (normal rang
216 g/L (normal range, 0-10 mg/L), a white blood cell count of 24.5 x 10(9)/L (normal range, [4.0-11.0] x
217 al range, [4.0-11.0] x 10(9)/L), a red blood cell count of 3.39 x 10(12)/L (normal range, [4.5-5.5] x
219 value, <8.0 mg/L [76.2 nmol/L]), and a white cell count of 7 x 10(9)/L (normal range, [4-11] x 10(9)/
220 ts who were HIV positive with a baseline CD4 cell count of less than 100 cells per uL were excluded.
221 normalized hepcidin expression and the total cell count of the bone marrow and spleen, but it had no
222 nd 32 of 97 PA 1% subjects (33.0%) had an AC cell count of zero (difference, 0.34; 95% CI, -12.94 to
224 , p=0.94) and for each increase in nadir CD4 cell counts of 100 cells per muL, there was a 40% decrea
225 in ART group during the first 6 months, CD4 cell counts of patients in CHM group and CHM combined wi
226 interaction between PM(2.5) and white blood cell count only in the model of lung function (p=0.0003)
227 r an investigator to correctly model the CD4 cell count or disease biomarkers of a patient in the pre
228 d placebo participants were observed in CD4+ cell counts or plasma HIV-1 RNA over the first year afte
229 ting for probe correlations, data structure (cell-count or relatedness), and single-nucleotide polymo
230 ss index (BMI; P = .003), higher white blood cell count (P = .005), and higher D-dimer levels (P = .0
231 The lowest EFA group had lower median CD4 T-cell counts (P < .01) and lower proportion of patients w
232 IV-infected individuals who had lower CD4+ T-cell counts (P = .01), had higher viral loads (P < .01),
233 bacterium animalis subsp lactis BB-12 (total cell count per capsule, 1.3 x 1010 to 1.6 x 1010) (n = 1
234 nfectant byproducts) and microbiology (total cell counts, plate counts, and opportunistic pathogen ge
236 croscopy, root growth kinematics, G2/M phase cell count, ploidy levels and ribosome polysome profiles
238 after controlling for the most recent CD4+ T-cell count, pregnancy incidence rates in HIV-positive wo
239 ratio, BAL protein levels, BAL inflammatory cell counts, pro-inflammatory cytokines, and pulmonary f
240 te the monthly probabilities of on-ART CD4 T-cell count progression, mortality, ART dropout, and ART
241 tation-positive non-MPNs with elevated blood cell counts raise concerns of MPN underdiagnosis in the
242 (HR), 95% confidence interval (CI)] only red cell count (RCC) (p = 0.004), red cell distribution widt
248 an be predicted using blood biochemistry and cell count results andthe recent advances in artificial
250 Galactosylceramide also increased neuronal cell counts significantly in male and female mice and te
251 city, baseline BMI, nadir and current CD4+ T-cell count, smoking, diabetes and follow-up time with su
252 r muL (Jan 1, 2016-Sept 30, 2016) to any CD4 cell count (test and treat, Oct 1, 2016-March 31, 2017).
253 advocate continued provision of baseline CD4 cell count testing in HIV care in low- and middle-income
255 ence for associations between mLOY and blood cell counts that should stimulate investigation of the u
256 y with suppressed HIV viremia and high CD4 T cell counts, the efficacy of conventional chemotherapies
257 taking into consideration immune status, CD4 cell counts, the presence of systemic disease, and the r
258 o 2 subgroups by forced binary clustering of cell counts: the inflamed depression subgroup (n = 81 ou
260 or less or a decline in absolute neutrophil cell count to 1.0 x 109/L or less leading to a dose redu
261 defined as a decline in absolute white blood cell count to 2.5 x 109/L or less or a decline in absolu
262 ral replication and decays in their CD4(+) T-cell counts to identify potential immune and virological
263 evels of albumin and sodium, and white blood cell count, to identify metabolites that differed betwee
264 After adjustment for age, BMI, sex, CD4 cell count, triglycerides, and separately adding sCD163,
265 After adjustment for age, BMI, sex, CD4 cell count, triglycerides, and separately adding sCD163,
266 es of each CpG site, adjusting for estimated cell count using a cord blood reference, sample plate, m
269 to explore the influence of baseline CD4+ T-cell count, viral load, study type, previous time on com
270 ationship of mtDNA CN to HIV markers (CD4+ T-cell counts, viral load, antiretroviral therapy [ART] us
271 tive protein, plasma fibrinogen, white blood cell count, vitamin D, high-density lipoprotein choleste
272 ized cohort; the mean increase in the CD4+ T-cell count was 139 cells per cubic millimeter and 64 cel
277 Median age was 40 years (IQR 35-48), CD4 cell count was 683 cells per muL (447-935), and body-mas
284 h culture-negative meningitis with CSF white cell count (WCC) above 20 cells per muL were included in
285 tion monitoring (QCM-D) and microscopy-based cell counting were used to quantify DC field effects on
287 f ART, and nadir CD4 cell count; CD4 and CD8 cell counts were also associated with body mass index an
288 OY, detected by genotyping arrays, and blood cell counts were assessed by multivariable linear models
291 on, allergen-driven IL-35 levels and iT(R)35 cell counts were increased in patients receiving SLIT (a
294 er or presented earlier and with lower white cell counts were more likely to have poor platelet recov
296 stological signs of damage and higher goblet cells count when compared with samples without LP, regar
299 a viral load [PVL], and nadir or current CD4 cell count) with outcomes of anal high-risk HPV prevalen
300 resonance imaging (CMR) and a complete blood cell count within 24 hours before and after PCI were enr