Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0027947 (
neutropenia
)
17,527
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The effects of lisofylline [(R)-1-(5-hydroxyhexyl)-3,7-dimethylxanthine] (
LSF
), an inhibitor of de novo phosphatidic acid (PA) generation, on sepsis-induced acute lung injury was studied using Hanford minipigs weighing 18 to 25 kg. Sepsis was induced by an intravenous infusion of Pseudomonas aeruginosa (1 x 10(6)/colony-forming units/kg/min over 2 h). Saline was used as the control vehicle. Six groups were studied: saline control group (SALINE: n = 5); sepsis control group (SEPSIS: n = 5);
LSF
control group (
LSF
: n = 5), which received a 25-mg/kgbolus of
LSF
30 min before time zero followed by continuous infusion of 10 mg/kg/h throughout the study;
LSF
-treated septic groups, which were treated with
LSF
30 min prior to sepsis (Pre: n = 5), 1 h postonset (Post-1 h: n = 8) or h postonset (Post-2 h: n = 8) of the bacterial infusion. Hemodynamics PaO2, neutrophil counts, and plasma porcine tumor necrosis factor-alpha concentrations were monitored for 6 h. After the minipigs were killed, lung tissue was sampled to measured wet-to-dry weight ratio (W/D), tissue albumin index (TAI), thiobarbituric acid-reactive material content (TBARM), and myeloperoxidase (MPO) activity. Compared with the SALINE group, the SEPSIS group showed significant systemic hypotension, pulmonary hypertension, arterial hypoxemia,
neutropenia
, and increase in TNF-alpha, MPO activity, W/D, TBARM, and TAI.
LSF
treatment attenuated sepsis-induced pulmonary hypertension,
neutropenia
, and hypoxemia, and increased MPO activity and lung injury measurements in the Pre and Post-1 h groups, but its efficacy was blunted in the Post-2 h group. Plasma TNF-alpha was decreased only in the Pre group. Thus, inhibition of intracellular PA generation through de novo pathways attenuates sepsis-induced acute lung injury.
...
PMID:The effects of post-treatment with lisofylline, a phosphatidic acid generation inhibitor, on sepsis-induced acute lung injury in pigs. 911 28
This retrospective case-matched study evaluated the efficacy of reduced intensity conditioning (RIC) regimen on early and late allogeneic transplant outcome in chronic myeloid leukemia (CML) patients. Twenty-eight patients conditioned with RIC regimen were matched to 56 patients who received a myeloablative conditioning (MAC) regimen. The main criteria for case matching among our CML allotransplant cohort were the Gratwohl scoring system. The median score was 2 (1-4) in each group. The pretransplant disease status was first chronic phase (CP1, n = 20),
CP2
(n = 2), and advanced phase (n = 6) in RIC, and CP1 (n = 46),
CP2
(n = 3), and advanced phase (n = 7) in MAC. The duration of
neutropenia
and thrombocytopenia was shorter in RIC than MAC. The grade and duration of mucositis were less in RIC. The need for total parenteral nutrition (21% vs. 77%, p < 0.0001) and febrile neutropenic episodes (50% vs. 95%, p < 0.0001) were observed less frequently in RIC compared with MAC-given patients. Acute or chronic graft versus host diseases (GvHD) were not affected by the intensity of conditioning regimen. The incidence of transplant-related mortality was higher in MAC (7% vs. 14%, p = 0.01). Although more relapse/progression was observed in the RIC group, the probability of 5- and 10-year leukemia-free- and overall survival were similar regardless of conditioning regimen intensity (p > 0.05). In early first CP, the pair of female donor-male recipient and the development of chronic GvHD prolonged both leukemia-free survival and overall survival in multivariate analysis. According to our single-center matched-pair analysis, the use of RIC regimens in patients with low-risk CML results with toxicities less, responses later, and relapses more frequent than the MAC regimens.
...
PMID:Case-matched comparison with standard versus reduced intensity conditioning regimen in chronic myeloid leukemia patients. 2197 69