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1 d regarding progression rates, distribution, end-stage aggregate levels, and histopathology.
2  metabolic function for acute liver failure, end-stage and congenital liver diseases, or for those pa
3 l gene expression in myocardial samples from end-stage CCC patients, compared to control samples from
4 umans is problematic because neutrophils are end-stage cells with a short half-life and minimal ongoi
5  the airway and parenchymal abnormalities in end-stage CF lungs.
6                                           In end-stage chronic kidney disease, the option of organ tr
7                             Complications of end-stage chronic liver disease signify a major cause of
8  biochemical changes, cholangiocarcinoma, or end-stage complications such as cirrhosis.
9 people receive organ transplants for various end-stage conditions.
10                                              End-stage COPD lungs showed markedly impaired immunoprot
11 clinical cases and was moderate to severe in end-stage corticobasal degeneration cases (P < 0.05).
12 basal degeneration cases and six age-matched end-stage corticobasal degeneration cases were included
13 l tau load (sum of all regional tau load) of end-stage corticobasal degeneration cases were nine time
14 reclinical cases was 12-fold greater than in end-stage corticobasal degeneration cases.
15 c arrest, metastatic cancer (requiring ICU), end-stage dementia (requiring ICU and transitioned to co
16 to TCR signaling, but rather than describing end-stage differentiation, such cells, whether isolated
17 nfected macaques during chronic infection or end stage disease and may not authentically recapitulate
18 PREVEND IT (Prevention of Renal and Vascular End-stage Disease Intervention Trial) study, a placebo-c
19    Neuropathologic analysis of the mice with end-stage disease revealed the accumulation of ubiquitin
20 DKN2A (INK4A/ARF) locus has been reported in end-stage disease, information is lacking on the status
21 the tumour and its spread, from diagnosis to end-stage disease, suggesting mutual need for tumorigene
22 ional motor units in EDL muscles and delayed end-stage disease.
23 asis and cholangitis, not for cholestasis in end-stage disease.
24 mesothelioma research is commonly focused on end-stage disease.
25 ogression rates were significantly slower at end-stage disease.
26 e not different between nonfailing donor and end-stage failing human hearts.
27                                              End stage glaucoma in patient 2 resulted in the enucleat
28 predictor of subsequent graft dysfunction or end-stage graft failure.
29                                Patients with end-stage HCC have advanced liver disease that is not su
30 able treatment option for patients with many end-stage heart and lung pathologies.
31 ransplantation is an excellent treatment for end-stage heart disease.
32 ardiomyocyte function of human myocardium in end-stage heart failure (HF).
33  follow-up period, 9 (12%) died, either from end-stage heart failure (n=7) or suddenly (n=2).
34            Skeletal muscle mass decreases in end-stage heart failure and is predictive of clinical ou
35 xamined tissue samples from AC patients with end-stage heart failure and tissue samples that were col
36 tained myocardial samples from patients with end-stage heart failure at time of transplant, with or w
37 vered a novel molecular basis for idiopathic end-stage heart failure in two sisters who underwent car
38 an cause dilated cardiomyopathy resulting in end-stage heart failure requiring advanced therapies.
39 anical circulatory support or transplant for end-stage heart failure, and 26% died.
40 ate of arrhythmia recurrence, progression to end-stage heart failure, and high mortality.
41 nd point (malignant ventricular arrhythmias, end-stage heart failure, or death) compared with carrier
42  were also seen in tissue from patients with end-stage heart failure.
43 of acetyl-CoA was significantly increased in end-stage heart failure.
44  transplantation is an effective therapy for end-stage heart failure.
45 er RNA levels in the hearts of patients with end-stage heart failure.
46 creased use of this therapy in patients with end-stage heart failure.
47 iomyocyte cellular activity in patients with end-stage HF after left ventricular assist device (LVAD)
48 stigated remodeling of the t-system in human end-stage HF and its role in cardiac recovery.
49                                              End-stage HF developed in 19% of patients, and 13% died.
50 pment of VA, whereas LVD was associated with end-stage HF or death (p < 0.001).
51                         Predictors of VA and end-stage HF or death were determined.
52 S AND Immunoblot analysis of myocardium from end-stage HF patients (n=12) and non-HF subjects undergo
53 ling human cardiac fibroblasts isolated from end-stage HF patients.
54 5 were significantly higher in patients with end-stage HF prior to LVAD placement and decreased signi
55 ched at the plasma membrane of patients with end-stage HF, but the functional consequences of this ar
56                                     In human end-stage HF, the complex formation between NDPK-C and G
57                              The t-system in end-stage human HF presents a characteristic novel pheno
58 nd mRNA levels of NDPK-C were upregulated in end-stage human HF, in rats after long-term isoprenaline
59                                           In end-stage, hypertrophic cardiomyopathy patients undergoi
60                                   At disease end-stage in a rat ALS model (SOD1(G93A) ), acute interm
61 entify common and specific signatures across end-stage interstitial lung disease (ILD) cases, (2) cha
62 ine estimated glomerular filtration rate and end stage kidney disease requiring renal replacement the
63 die prematurely than they are to progress to end stage kidney disease.
64 ation has become the preferred treatment for end stage kidney failure.
65 to 26]), total mortality (9% [-3 to 19]), or end-stage kidney disease (10% [-6 to 23]).
66 ary care perspective emphasizing the risk of end-stage kidney disease (ESKD) and need for renal repla
67                                The burden of end-stage kidney disease (ESKD) in sub-Saharan Africa is
68               Large numbers of patients with end-stage kidney disease caused by IgA nephropathy are t
69 Review describes the incidence and causes of end-stage kidney disease in children on long-term dialys
70 e patients has transformed the management of end-stage kidney disease in this population.
71                                Treatment for end-stage kidney disease is a major economic challenge a
72                                Children with end-stage kidney disease may have coexisting iatrogenic
73 (PBUTs) cause various deleterious effects in end-stage kidney disease patients, because their removal
74 and serious complication in individuals with end-stage kidney disease receiving peritoneal dialysis.
75  a heightened risk of developing chronic and end-stage kidney disease, an association that is largely
76 ), and non-vascular and all-cause mortality, end-stage kidney disease, and adverse events, as well as
77  outcomes were kidney events (a composite of end-stage kidney disease, renal death, development of an
78 eight (LMW) proteinuria that can progress to end-stage kidney disease.
79  of renal replacement therapy for those with end-stage kidney disease.
80 al brain activity in delirious patients with end stage liver disease (ESLD) is detected by fNIRS.
81  = 1.895, 95% CI: 1.081-3.323) and model for end stage liver disease (HR = 1.054, 95% CI: 1.020-1.090
82  (ALT), acute kidney injury (AKI), model for end stage liver disease (MELD) and septic shock are the
83 months, respectively) who received Model for End Stage Liver Disease exception listing for HCC from 2
84  shock, hepatic encephalopathy and model for end stage liver disease were significantly different amo
85 ermined along with the scores like model for end stage liver disease, child turcotte pugh were record
86 s of cirrhosis patients with higher Model of End-Stage Liver Disease (>15) showed significantly decre
87                                              End-stage liver disease (ESLD) caused by hepatitis C vir
88                                Patients with end-stage liver disease (ESLD) often have a high symptom
89 arting point, we analyzed the development of end-stage liver disease (ESLD), hepatocellular carcinoma
90  virus (HCV) is one of the leading causes of end-stage liver disease (ESLD), such as decompensated ci
91 and C (HCV) viruses are at increased risk of end-stage liver disease (ESLD).
92 er transplantation with laboratory Model for End-Stage Liver Disease (MELD) >/=12 at a single center
93 cs: total mortalities, DSA-average model for end-stage liver disease (MELD) at transplant, DSA-averag
94 ndication was defined as DC if the Model for End-Stage Liver Disease (MELD) at WL was >/=15 or hepato
95 nsplant for patients listed with a Model for End-Stage Liver Disease (MELD) between 22 and 27 will do
96 d the impact of this difference on Model for End-Stage Liver Disease (MELD) calculation.
97                            Current Model for End-Stage Liver Disease (MELD) exception points provided
98 llular carcinoma (HCC) can receive Model for End-Stage Liver Disease (MELD) exception points to incre
99 nsplantation Network policy grants Model for End-Stage Liver Disease (MELD) exception points to patie
100                                    Model for End-Stage Liver Disease (MELD) prioritization of liver r
101 re 35, of whom 4,599 (27.9%) had a Model for End-Stage Liver Disease (MELD) score >/=35.
102  at multivariate analysis included Model for End-Stage Liver Disease (MELD) score >10, and absence of
103                           Baseline Model for End-Stage Liver Disease (MELD) score alone (cut-off 18)
104 on in patients with cirrhosis with Model for End-Stage Liver Disease (MELD) score of 12 or less.
105 - 10 years, 63% men) with a median Model for End-Stage Liver Disease (MELD) score of 17 (interquartil
106 and recipients frequently attain a Model for End-Stage Liver Disease (MELD) score of 40 or higher bef
107                                The Model for End-Stage Liver Disease (MELD) score predicts higher tra
108                                    Model for End-Stage Liver Disease (MELD) score transiently worsene
109  adult patients with cirrhosis and Model for End-Stage Liver Disease (MELD) score within 3 months of
110 g HCV often improves our patients' model for end-stage liver disease (MELD) score, decreasing costs,
111 ered regionally to candidates with Model for End-Stage Liver Disease (MELD) scores >/=35 before being
112 sion patterns of 123 genes and the model for end-stage liver disease (MELD) scores to assign patients
113      Child-Turcotte-Pugh (CTP) and Model for End-stage Liver Disease (MELD) scores were calculated.
114 he effect of therapy on changes in model for end-stage liver disease (MELD) scores were derived from
115 om pre-LT treatment based on their Model for End-Stage Liver Disease (MELD) scores.
116 rtality not well quantified by the Model for End-Stage Liver Disease (MELD) Sodium (MELDNa) score.
117 k), but the Lille (P < 0.0001) and Model for End-Stage Liver Disease (P < 0.0001) scores were indepen
118 6 mg/dL); P < 0.001], and a higher pediatric end-stage liver disease (PELD) score [22 (14, 25) compar
119 ster of differentiation 34+HSCs and Model of End-Stage Liver Disease (rho = -0.582, P < 0.001) and Ch
120 nsplanting higher risk recipients (Model for End-Stage Liver Disease [MELD] score >/=35, inpatient or
121 seline prognostic scoring systems (Model for End-Stage Liver Disease and age, bilirubin, internationa
122       The admission model included Model for End-Stage Liver Disease and diabetes (c-statistic = 0.64
123 rsibility of renal failure for patients with end-stage liver disease and may be useful in the kidney
124 It is observed in up to 60% of patients with end-stage liver disease and portends a poor prognosis.
125 ednisolone therapy, independent of Model for End-Stage Liver Disease and white blood cell count (OR,
126 lity following recurrence included model for end-stage liver disease at LT >23, time to recurrence, >
127 olume, LOS, biliary complications, Model for End-Stage Liver Disease at transplant, and hepatitis C v
128 e North American Consortium for the Study of End-Stage Liver Disease consists of 16 tertiary-care hep
129 K transplants by 0.99 years in the Model for End-stage Liver Disease era and 1.71 years in the pre-Mo
130 es published between 2002 and 2016 (model of end-stage liver disease era).
131 ease era and 1.71 years in the pre-Model for End-stage Liver Disease era.
132 thin the Milan criteria for whom a Model for End-Stage Liver Disease exception was approved were retr
133 were found in patients with higher model for end-stage liver disease in the same disease group; and l
134       There were no differences in Model for End-Stage Liver Disease including serum sodium and Child
135               Changes in the epidemiology of end-stage liver disease may lead to increased risk of dr
136  with prednisolone, independent of model for end-stage liver disease or Lille score (OR, 2.46; 95% CI
137 enter study included a cohort of consecutive end-stage liver disease patients with indications for LT
138 ciated liver fibrosis is a critical step for end-stage liver disease progression.
139 onse rates, LT costs, and baseline Model for End-Stage Liver Disease score (DCC analysis only).
140 rage Child score 8.3 (+/-1.3), and Model for End-Stage Liver Disease score 11.7 (+/-3.9).
141 +/- 8 years) were analyzed (median Model for End-Stage Liver Disease score 20).
142 ed after the implementation of the model for end-stage liver disease score and a concomitant increase
143   The median age, body weight, and pediatric end-stage liver disease score at the time of transplant
144 n were acquisition of CRE post-LT, Model for End-Stage Liver Disease score greater than 32, combined
145 ikely to be used in recipients with model of end-stage liver disease score higher than 27 (13.2% vs.
146 , CDI was associated with having a model for end-stage liver disease score of 20 or greater (hazards
147 I was 50.16 +/- 11.7 years with a mean Model End-Stage Liver Disease score of 22.6 +/- 9.8.
148 ents with cirrhosis and with worse Model for End-Stage Liver Disease score or diabetes, those taking
149 s 50.2 +/- 8.5 years, and the mean model for end-stage liver disease score was 12.2 +/- 4.6.
150                           The mean Model for End-Stage Liver Disease score was 14.5 +/- 4.
151                                    Model for End-Stage Liver Disease score was 15 (IQR, 11-21); cold
152                       The baseline Model for End-Stage Liver Disease score was not predictive of long
153  used in Donor Risk Index with the model for end-stage liver disease score yields an AUC-ROC of 0.764
154 ence regarding cold ischemia time, model for end-stage liver disease score, and steatosis.
155  0.03) compared to those with lower Model of End-Stage Liver Disease scores (</=15).
156 fter LT was associated with higher model for end-stage liver disease scores and receiving a LT from a
157  maintained at 6 months; Child and Model for End-Stage Liver Disease scores did not change.
158 needed to calculate Child-Pugh and Model for End-Stage Liver Disease scores were recorded.
159 Cancer stage D ( P < .001), higher Model for End-Stage Liver Disease Sodium scores ( P < .001), highe
160 ollowing the implementation of the model for end-stage liver disease system for liver transplantation
161                    Four variables (Model for End-Stage Liver Disease, alpha-fetoprotein, Milan-Criter
162 reduce the untoward effects of sequelae from end-stage liver disease, and to minimize the requirement
163 bstructive cholangiopathy that progresses to end-stage liver disease, often requiring transplantation
164       The discharge model included Model for End-Stage Liver Disease, proton pump inhibitor use, and
165  to the severity of liver disease (Model for End-Stage Liver Disease, rho = 0.45, P < 0.001), the deg
166 usting for significant covariates (Model for End-Stage Liver Disease, vasopressor use).
167 gan transplantation (IFOT) for patients with end-stage liver disease.
168 sis does not resolve with FO may progress to end-stage liver disease.
169  in treating kidney failure in patients with end-stage liver disease.
170       Hepatic PP-IX accumulation may lead to end-stage liver disease.
171 py exists to halt disease progression toward end-stage liver disease.
172 cirrhosis, liver and kidney transplants, and end-stage liver disease.
173  challenges to using these cells in treating end-stage liver disease.
174 er disease, nonalcoholic steatohepatitis, or end-stage liver disease.
175 verage donor age and the advent of Model for End-stage Liver Diseases (MELD) score-based allocation c
176 onic carriers are at high risk of developing end-stage liver diseases and hepatocellular carcinoma.
177 ic liver transplantation in the treatment of end-stage liver diseases, its therapeutic utility is sev
178 lications to the development of fibrosis and end-stage liver diseases, such as cirrhosis and hepatoce
179 new therapeutic strategies for patients with end-stage liver diseases.
180 tes with EndMT in tissues from patients with end-stage liver fibrosis.
181 pectively reviewed consecutive patients with end-stage lung disease and a height of 65 inches or less
182                                           In end-stage male SOD1(G93A) rats and wild-type littermates
183 avitation (2.2%), patchy atrophy (0.9%), and end-stage MD (0.2%).
184                                           In end-stage mesothelioma, silencing of p16/Ink4a is sustai
185 HT2B/C receptors and abolished spasticity in end-stage mice.
186 s that may contribute towards progression to end-stage NAFLD.
187  Key recommendations were: (1) patients with end-stage nonrenal disease with estimated glomerular fil
188 ions in the use of TKR for the management of end-stage OA of the knee.
189 ve access to surgery for black patients with end-stage OA of the knee.
190 ssayed after HCC diagnosis, representing the end stage of progressive hepatic diseases.
191 pling is maintained by hypertrophy until the end stage of the disease, when progressive dilation begi
192 , thereby eliminating, presynaptic inputs at end stages of disease (>/=P56 Mecp2 null mice) concomita
193                                              End-stage organ diseases were associated with the greate
194 e further expounded toward the correction of end-stage organ dysfunction and composite tissue deficit
195  is now lifesaving therapy for patients with end-stage organ failure but requires lifelong immunosupp
196               Fibrosis is a common driver of end-stage organ failure in most organs.
197 y for hundreds of thousands of patients with end-stage organ failure.
198 hoice many patients have when suffering from end-stage organ failure.
199 is the preferred treatment for patients with end-stage organ failure.
200 fe-threatening symptoms, such as syncope and end-stage organ hypoperfusion.
201                 Total joint replacements for end-stage osteoarthritis of the hip and knee are cost-ef
202                      LRRK2 mutations produce end-stage Parkinson's disease (PD) with reduced nigrostr
203                     While progression to the end-stage phase occurs over several years for patients w
204 with the other groups (P = 0.06) and time to end stage renal disease (ESRD) was longer in this group
205   In conclusion, although many patients with end stage renal disease have received transplants throug
206 ors of Arrhythmic and Cardiovascular Risk in End Stage Renal Disease Study.
207 es leads to chronic kidney disease ending in end stage renal disease.
208 te phase and an increased risk of developing End Stage Renal Disease.
209 dly affects glomeruli and progresses towards end stage renal failure and multiple organ dysfunction.
210                                              End stage renal failure can be seen very rare.
211 g risk and accounting for the progression to end-stage renal disease (ESRD) after discharge.
212      We examined the association of incident end-stage renal disease (ESRD) after liver transplantati
213 familial Mediterranean fever (FMF) who reach end-stage renal disease (ESRD) due to reactive amyloidos
214  association between serum 1,5-AG levels and end-stage renal disease (ESRD) from baseline (1990-1992)
215  compared with dialysis, nearly one third of end-stage renal disease (ESRD) patients are not educated
216  protection of herpes zoster (HZ) vaccine in end-stage renal disease (ESRD) patients might be insuffi
217 etween hepatitis C virus (HCV) infection and end-stage renal disease (ESRD) remains controversial wit
218  of patients with CKD, especially those with end-stage renal disease (ESRD), are controversial.
219       ECR was associated with development of end-stage renal disease (ESRD).
220 es, have an increased risk of progression to end-stage renal disease (ESRD).
221 eficiency virus (HIV)-infected patients with end-stage renal disease (ESRD).
222 nsition from chronic kidney disease (CKD) to end-stage renal disease (ESRD).
223  PPI use also associated with development of end-stage renal disease (HR, 2.40; 95% CI, 0.76-7.58) an
224 exposure; adults with chronic liver disease, end-stage renal disease (including hemodialysis patients
225 ring immunosuppressive therapy, persons with end-stage renal disease (including hemodialysis patients
226                         Six (0.2%) developed end-stage renal disease 5 to 17 years after donation, (2
227 e endpoint, major cardiovascular outcome-and end-stage renal disease [ESRD], doubling of serum creati
228                      Secondary outcomes were end-stage renal disease and acute kidney injury.
229 nd are associated with an increased risk for end-stage renal disease and cardiovascular events.
230 ced chronic kidney disease, as patients with end-stage renal disease and kidney transplant recipients
231     Patients with chronic kidney disease and end-stage renal disease are at 5- to 10-fold higher risk
232 ystem, we identified all adult patients with end-stage renal disease attributed to 1 of 6 GN subtypes
233                  The number of patients with end-stage renal disease being relisted for a second kidn
234  than 0, public insurance or no insurance at end-stage renal disease diagnosis, more regional acute c
235  IgA deposition that leads to impairment and end-stage renal disease in 20-40% of patients within 10-
236 ases constitute the most important cause for end-stage renal disease in children and adolescents.
237 result of longer survival, the prevalence of end-stage renal disease in HIV is increasing.
238 itis, is the most common cause of hereditary end-stage renal disease in the first three decades of li
239 ase, chronic kidney disease progression, and end-stage renal disease is not clear.
240                     A 74-year-old woman with end-stage renal disease on maintenance hemodialysis pres
241 ta System Medicare-linked data on waitlisted end-stage renal disease patients between 2005 and 2009 w
242 is widely used in chronic kidney disease and end-stage renal disease patients with hyperphosphatemia.
243 mpatible living-donor kidney transplants for end-stage renal disease patients with willing but incomp
244                                   During the end-stage renal disease phase at the time of transplant,
245 enal transplant recipients with aHUS-related end-stage renal disease received eculizumab: 10 from day
246                     A 50-year-old woman with end-stage renal disease secondary to autosomal dominant
247 ection are at higher risk for progression to end-stage renal disease than those who have chronic kidn
248                                Patients with end-stage renal disease use the emergency department (ED
249                         An increased risk of end-stage renal disease was associated with an IQR incre
250 ta suggest that morbidly obese patients with end-stage renal disease who undergo LSG to improve trans
251 betic nephropathy (DN) is the major cause of end-stage renal disease worldwide.
252  urinary catheters, diabetes mellitus, AIDS, end-stage renal disease, and cirrhosis), need for intens
253 iabetic nephropathy (DN) is a major cause of end-stage renal disease, and therapeutic options for pre
254 splantation is the best treatment option for end-stage renal disease, but allograft loss remains a si
255 0.5% of live births and are a major cause of end-stage renal disease, but their genetic aetiology is
256 e used (recipients' age, cause and length of end-stage renal disease, hemoglobin, albumin, selected c
257 s (HCV) infection is common in patients with end-stage renal disease, highly efficacious, well-tolera
258 fect burden, especially its association with end-stage renal disease, may be less than many have surm
259 tent doubling of the serum creatinine level, end-stage renal disease, or death due to renal disease.
260 as a sustained doubling of serum creatinine, end-stage renal disease, or renal death.
261                  In HNF1B patients who reach end-stage renal disease, single kidney transplantation (
262    In patients with both type 1 diabetes and end-stage renal disease, SPK recipients had similar prog
263                             In patients with end-stage renal disease, the prevalence of acquired risk
264 .e., older than 65 years of age), such as in end-stage renal disease, this therapy has not been optim
265 n: mixed cryoglobulinemia, chronic kidney or end-stage renal disease, type 2 diabetes, B-cell lymphom
266 splantation is a lifesaving intervention for end-stage renal disease.
267 han 190 cm, obesity, and a family history of end-stage renal disease.
268 e of a reduced risk of future progression to end-stage renal disease.
269  epithelial cells will lead progressively to end-stage renal disease.
270 tic Nephropathy (DN) is the leading cause of end-stage renal disease.
271                      We enrolled adults with end-stage renal disease.
272 ng kidney donors are at an increased risk of end-stage renal disease.
273 fluid-filled kidney cysts and progression to end-stage renal disease.
274 eatment of choice for patients with terminal end-stage renal disease.
275 isease patients, including patients with non-end-stage renal disease.
276  discharge, ICU stay less than 24 hours, and end-stage renal disease.
277 is the preferred treatment for patients with end-stage renal disease.
278 ey disease, eGFR decline of 30% or more, and end-stage renal disease.
279 nt chronic kidney disease, eGFR decline, and end-stage renal disease.
280 rdiovascular events or mortality) and renal (end-stage renal disease: dialysis, transplantation, and/
281 s nephronophthisis, typically progressing to end-stage renal failure within the first two decades of
282 k factors of upper limb ischemia - diabetes, end-stage renal failure, hyperparathyroidism, or even sy
283 tion and is essential for the progression to end-stage renal failure.
284 ause of acute kidney injury that can lead to end-stage renal failure.
285 f most chronic kidney disease progression to end-stage renal failure.
286 able therapeutic option for the treatment of end-stage retinal degeneration in humans.
287     Following transplantation into mice with end-stage retinal degeneration, these cells differentiat
288 estore vision in patients who are blind from end-stage retinal degenerations aim to render remaining
289 ermany) for partial restoration of vision in end-stage retinitis pigmentosa (RP).
290 ) and diuresis with risk/injury/failure/loss/end stage (RIFLE), acute kidney injury network (AKIN), o
291  the worse-seeing eye of 6 participants with end-stage RP and no useful perception of light vision.
292 renic motor neuron numbers were decreased in end-stage SOD1(G93A) rats ( approximately 30% survival;
293                 Mechanisms enhancing pLTF in end-stage SOD1(G93A) rats are not known.
294  intermittent hypoxia is enhanced at disease end-stage, suggesting greater potential to preserve/rest
295            Heart failure represents a common end-stage syndrome for many adults with congenital heart
296 tified metabolites change with treatment for end-stage systolic HF.
297 tial influence on the time to development of end-stage TB.
298 rs, namely, CD8CD28, CD4CD57PD1, and CD8CD28 end-stage terminally differentiated memory T cells were
299  patients with greater than 35 cells CD8CD28 end-stage terminally differentiated memory T cells/muL r
300           Within the SC, slow MNs survive to end stage, whereas fast fatigable MNs are lost.

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