Hepatocyte Growth Factor Is a Better Indicator of Therapeutic Response than C-Reactive Protein within the First Day of Treatment in Pneumonia

Chemotherapy ◽  
2006 ◽  
Vol 52 (5) ◽  
pp. 260-263 ◽  
Author(s):  
Hossein Abednazari ◽  
Junyang Xu ◽  
Eva Millinger ◽  
Lars Brudin ◽  
Pia Forsberg ◽  
...  
2019 ◽  
Author(s):  
T Robinson ◽  
RM Martin ◽  
J Yarmolinsky

AbstractAdipokines and C-reactive protein (CRP) have been proposed as molecular mediators linking adiposity to breast cancer (BCa). Mendelian randomization (MR) uses genetic variants as proxies for risk factors to strengthen causal inference in observational studies. We performed a MR analysis to evaluate the causal relevance of six circulating adipokines (adiponectin, hepatocyte growth factor, interleukin-6, leptin receptor, plasminogen activator inhibitor-1, resistin) and CRP in risk of overall and oestrogen receptor-stratified BCa in up to 122,977 cases and 105,974 controls. Genetic instruments were constructed from single-nucleotide polymorphisms robustly (P<5×10−8) associated with risk factors in genome-wide association studies. In MR analyses, there was evidence for a causal effect of hepatocyte growth factor on ER- BCa (OR per SD increase:1.17, 95% CI: 1.01-1.35; P=0.035) but little evidence for effects of other adipokines or CRP on overall or oestrogen receptor-stratified BCa. Collectively, these findings do not support an important etiological role of various adipokines or CRP in BCa risk.


1997 ◽  
Vol 32 (1) ◽  
pp. 63-70 ◽  
Author(s):  
Takashi Ueda ◽  
Yoshifumi Takeyama ◽  
Yuichi Hori ◽  
Junsuke Nishikawa ◽  
Masahiro Yamamoto ◽  
...  

2003 ◽  
Vol 12 (4) ◽  
pp. 229-235 ◽  
Author(s):  
Halina Urbańska-Ryś ◽  
Tadeusz Robak

We investigated the serum concentration of endostatin in 84 patients with multiple myeloma (MM) and in 13 healthy controls. The level of measured anti-angiogenic agent was correlated with the phase and stage of the disease, and most importantly with clinical and laboratory parameters depicting the disease activity (haemoglobin, creatinine, albumins, calcium, M-component, C-reactive protein, β2-microglobulin, lactate dehydrogenase, stage of bone disease) as well as serum levels of pro-angiogenic cytokines such as vascular endothelial growth factor, hepatocyte growth factor, fibroblast growth factor and transforming growth factor-β. The median serum level of endostatin in MM patients was 58 ng/ml and was statistically significantly higher than in the control group (median, 40 ng/ml; P=0.015). MM patients in phase I (at diagnosis) had higher levels of endostatin (median, 69 ng/ml) than those in phase II (plateau phase after treatment) (median, 49 pg/ml; P=0.044). We did not find any statistical correlation between the level of endostatin and stage of MM according to the Durie and Salmon system. The serum concentration of endostatin in MM patients with a normal level of albumins was significantly higher than in others with hypoalbuminaemia (median, 62 ng/ml versus 39 ng/ml; P=0.033). Also, patients with a normal value of lactate dehydrogenase had a higher concentration of endostatin than those with values >425 U/l (median, 70 ng/ml versus 39 ng/ml; P=0.019). We did not show any statistical correlation between the concentration of endostatin and level of haemoglobin, creatinine, calcium, C-reactive protein, β2-microglobulin and stage of bone disease. We failed to find positive or negative correlations between the level of endostatin and vascular endothelial growth factor, hepatocyte growth factor, fibroblast growth factor and transforming growth factor-β. The concentration of endostatin did not influence the probability of survival in MM patients in our study.In conclusion, our data indicate that endostatin has a higher level in MM patients than in healthy controls. Highest values were stated in active phases of the disease (at presentation and in progression). Different clinical and laboratory parameters generally do not influence the concentration of endostatin (except albumins and lactate dehydrogenase).


Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
S Skwarna ◽  
I Henneke ◽  
W Seeger ◽  
T Geiser ◽  
A Günther ◽  
...  

Diabetes ◽  
1997 ◽  
Vol 46 (1) ◽  
pp. 138-142 ◽  
Author(s):  
R. Morishita ◽  
S. Nakamura ◽  
Y. Nakamura ◽  
M. Aoki ◽  
A. Moriguchi ◽  
...  

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