Cox regression models for prediction of mortality 6 months after hip fracture.

<p>MMP: matrix metalloproteinase; NGAL: neutrophil gelatinase-associated lipocalin</p>*<p>Adjusted by age, gender, length of hospital stay and C-reactive protein.</p

Logistic regression for prediction of gait status recovery 6 months after hip fracture.

<p>MMP: matrix metalloproteinase; NGAL: neutrophil gelatinase-associated lipocalin</p>*<p>Adjusted by age, gender, length of hospital stay and C-reactive protein.</p

Gelatin zymograms of serum samples with all forms of MMPs usually found in human: the homodimer of the pro-MMP-9 form (225 kDa), the pro-MMP-9 complexed with neutrophil gelatinase-associated lipocalin form (130 kDa), the pro-MMP-9 form (92 kDa) and the pro-MMP-2 (72 kDa) form.

<p>Gelatin zymograms of serum samples with all forms of MMPs usually found in human: the homodimer of the pro-MMP-9 form (225 kDa), the pro-MMP-9 complexed with neutrophil gelatinase-associated lipocalin form (130 kDa), the pro-MMP-9 form (92 kDa) and the pro-MMP-2 (72 kDa) form.</p

Demographic and clinical data of 82 patients with hip fracture.

<p>LOS: length of hospital stay; A-S time: admission to surgery time. Data are expressed as median (including the lower and upper quartiles).</p

Baseline biochemical and zymography results of 82 patients with hip fracture.

<p>CRP: C-reactive protein, MMP: matrix metalloproteinase; NGAL: neutrophil gelatinase-associated lipocalin. Data are expressed as the mean ± standard deviation or median (including the lower and upper quartiles).</p

Logistic regression for prediction of pressure ulcer 6 months after hip fracture.

<p>MMP: matrix metalloproteinase; NGAL: neutrophil gelatinase-associated lipocalin</p>*<p>Adjusted by age, gender, length of hospital stay and C-reactive protein.</p

Demographic and clinical data of 82 patients with hip fracture.

<p>LOS: length of hospital stay; A-S time: admission to surgery time. Data are expressed as the mean ± standard deviation or median (including the lower and upper quartiles).</p

Baseline biochemical and zymography results of 82 patients with hip fracture.

<p>CRP: C-reactive protein, MMP: matrix metalloproteinase; NGAL: neutrophil gelatinase-associated lipocalin. Data are expressed as the mean ± standard deviation or median (including the lower and upper quartiles).</p

The Role of Lipotoxicity in Smoke Cardiomyopathy

<div><p>Background/Aims</p><p>Experimental and clinical studies have shown the direct toxic effects of cigarette smoke (CS) on the myocardium, independent of vascular effects. However, the underlying mechanisms are not well known.</p><p>Methods</p><p>Wistar rats were allocated to control (C) and cigarette smoke (CS) groups. CS rats were exposed to cigarette smoke for 2 months.</p><p>Results</p><p>After that morphometric, functional and biochemical parameters were measured. The echocardiographic study showed enlargement of the left atria, increase in the left ventricular systolic volume and reduced systolic function. Within the cardiac metabolism, exposure to CS decreased beta hydroxy acyl coenzyme A dehydrogenases and citrate synthases and increased lactate dehydrogenases. Peroxisome proliferator-activated receptor alpha (PPARα) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) were expressed similarly in both groups. CS increased serum lipids and myocardial triacylglycerols (TGs). These data suggest that impairment in fatty acid oxidation and the accumulation of cardiac lipids characterize lipotoxicity. CS group exhibited increased oxidative stress and decreased antioxidant defense. Finally, the myocyte cross-sectional area and active Caspase 3 were increased in the CS group.</p><p>Conclusion</p><p>The cardiac remodeling that was observed in the CS exposure model may be explained by abnormalities in energy metabolism, including lipotoxicity and oxidative stress.</p></div

Energy Metabolism.

<p>C: control group; CS: cigarette smoke group; LDH: lactate dehydrogenases C vs. CS <i>p</i><0.001; 3-hydroxyacyl-CoA: 3-hydroxy acyl coenzyme A dehydrogenases C vs. CS <i>p</i> = 0.004; citrate synthase C vs. CS <i>p</i> = 0.008; cardiac TG: cardiac triacylglycerol C vs. CS <i>p</i> = 0.004.</p