ライフサイエンスコーパス: endstage

1 phological features of esophagi resected for endstage achalasia showed marked depletion of myenteric

2 seases have a poor prognosis comparable with endstage cancer and are uncurable.

3 icipants in Prevention of Vascular and Renal Endstage Disease (mean age, 49 years; 50% men).

4 ed for age, gender, ethnicity, and model for endstage disease (MELD) score, donor risk index, and yea

5 Human lung tissue samples from patients with endstage emphysema have decreased levels of VEGF messeng

6 Here, we demonstrate that many endstage fibrotic diseases, including IPF; scleroderma;

7 l bronchiectasis, and a subset will go on to endstage fibrotic lung disease.

8 We studied 221 participants with non-endstage glaucoma or high-risk ocular hypertension and p

9 ion to become a reality for the treatment of endstage heart disease.

10 -related complications such as sudden death, endstage heart failure, and fatal stroke is roughly 1-2%

11 organ donors and transplant recipients with endstage ischemic cardiomyopathy or idiopathic dilated c

12 alent to or worse than that of patients with endstage kidney disease, congestive heart failure, or ce

13 INR (1.62 versus 1.33, P = 0.005), model for endstage liver (MELD) score (26 versus 20, P = 0.02), ME

14 perlipidemia, with their associated risks of endstage liver and cardiovascular diseases, is increasin

15 In children with concomitant endstage liver and kidney disease, LKT can be considered

16 e with the highest quartile of the Model for Endstage Liver Disease (MELD) (>40, survival 30% versus

17 warm ischemic time, pretransplant Model for Endstage Liver Disease (MELD) and viral load.

18 objective parameters including the Model for Endstage Liver Disease (MELD) as a gauge of liver dysfun

19 Model for Endstage Liver Disease (MELD) exception to facilitate LT

20 gh the proportion of patients with Model for Endstage Liver Disease (MELD) score over 20 points and w

21 The Model for Endstage Liver Disease (MELD) score serves as the basis

22 f ACLF were nosocomial infections, Model for Endstage Liver Disease (MELD) score, low mean arterial p

23 etiology, diabetes, history of HE, Model for Endstage Liver Disease (MELD) score, serum sodium, album

24 een questioned for candidates with Model for Endstage Liver Disease (MELD) scores <15, and the surviv

25 ollowing the implementation of the Model for Endstage Liver Disease (MELD) scoring system in 2002 (3.

26 dmission vitals, disease severity (model for endstage liver disease [MELD] and sequential organ failu

27 ge, weight/age) and serum albumin (pediatric endstage liver disease [PELD] formula) were not included

28 e procedure of choice for patients with both endstage liver disease and kidney failure.

29 Endstage liver disease caused by chronic hepatitis C vir

30 fat and fibrosis in the graft, patients with endstage liver disease due to NASH should be considered

31 atresia was the most common cause (50.4%) of endstage liver disease in this patient population.

32 Hepatitis C virus (HCV)-induced endstage liver disease is currently a major indication f

33 well to immunosuppression but progression to endstage liver disease occurs in 10%-20% of cases, leadi

34 with liver failure as assessed by model for endstage liver disease score (r = 0.41, P = 0.006) and M

35 (27 versus 22, P = 0.03) and United Kingdom endstage liver disease score (UKELD) score (59 versus 57

36 Based on this premise, two patients with HBV endstage liver disease underwent baboon liver xenotransp

37 In patients with endstage liver disease, liver CD34+ cells were comprised

38 itis C (CHC) infection is a leading cause of endstage liver disease.

39 splantation is the best treatment option for endstage liver disease.

40 2, 37 patients (Child A6-C13, MELD [Model of Endstage Liver Disease] 5-28) with refractory HE were di

41 s have revolutionized care for patients with endstage organ (kidney, liver, heart, lung, and pancreat

42 hippocampal atrophy might be a progressive "endstage" pathology resulting from years of spontaneous

43 stomy has been used successfully to palliate endstage primary pulmonary hypertension but has not been

44 coronary heart disease, cardiac failure, and endstage renal disease.

45 movement) were resistant to degeneration in endstage SMA mice, as well as in late symptomatic ALS mi

46 In endstage SOD-1 transgenic mice, there is marked loss of

47 weekly, beginning at postnatal day 50 until endstage, to G93A mutant SOD1 (G93A SOD1) mice.