Mejorando la atención del paciente mayor ingresado por fractura de cadera. ¿Hemos de avanzar? / Improving the care of the elderly patient admitted for hip fracture. Should we move forward?

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Advantages of care for patients with hip fractures in the acute geriatric unit: Hip study Anoia.

AIM: Hip fracture as a result of bone fragility is characterized by poor health outcomes in the medium and long term. Our goal was to compare a new orthogeriatric model with the old trauma model and evaluate improvements in clinical management. METHODS: We carried out a comparative unicentric study, a historical sample (trauma model) collected from 1 June 2007 to 31 May 2010, versus a prospective sample (orthogeriatric model) collected from 1 June 2010 until 31 May 2013. We included all patients aged >69 years with hip fracture as a result of bone fragility. RESULTS: A total of 792 patients were evaluated (mean age 84.3 years). The surgical waiting period went from 2.70 days in the trauma model to 1.86 days in the orthogeriatric model (P < 0.001); the average stay was 15.76 days in the trauma model, and for the orthogeriatric model was reduced to 5.90 days (P < 0.001); mortality went from 4.5% to 1.3% (P ≤ 0.010); 1 month readmission for hip dislocation was reduced from 2.3% to 0.5% (P = 0.032). After a 6-month follow up, we had 302 trauma model patients and 287 orthogeriatric model patients. After 1 year, we had 288 patients in the trauma model and 264 patients in the orthogeriatric model. The main cause of abandonment was death, 108 patients (27.3%) in the trauma model and 100 patients (27.5%) in the orthogeriatric model (P = 0.951). CONCLUSIONS: When we compared the two models, we found statistically significant better results in the preoperative waiting period, average stay, hospital mortality and 1 month readmission as a result of hip prosthesis luxation in favor of the orthogeriatric model. Geriatr Gerontol Int 2018; 18: 407-414.

TGF-beta1 modulates matrix metalloproteinase-13 expression in hepatic stellate cells by complex mechanisms involving p38MAPK, PI3-kinase, AKT, and p70S6k.

Transforming growth factor-beta1 (TGF-beta1), the main cytokine involved in liver fibrogenesis, induces expression of the type I collagen genes in hepatic stellate cells by a transcriptional mechanism, which is hydrogen peroxide and de novo protein synthesis dependent. Our recent studies have revealed that expression of type I collagen and matrix metalloproteinase-13 (MMP-13) mRNAs in hepatic stellate cells is reciprocally modulated. Because TGF-beta1 induces a transient elevation of alpha1(I) collagen mRNA, we investigated whether this cytokine was able to induce the expression of MMP-13 mRNA during the downfall of the alpha1(I) collagen mRNA. In the present study, we report that TGF-beta1 induces a rapid decline in steady-state levels of MMP-13 mRNA at the time that it induces the expression of alpha1(I) collagen mRNA. This change in MMP-13 mRNA expression occurs within the first 6 h postcytokine administration and is accompanied by a twofold increase in gene transcription and a fivefold decrease in mRNA half-life. This is followed by increased expression of MMP-13 mRNA, which reaches maximal values by 48 h. Our results also show that this TGF-beta1-mediated effect is de novo protein synthesis-dependent and requires the activity of p38MAPK, phosphatidylinositol 3-kinase, AKT, and p70(S6k). Altogether, our data suggest that regulation of MMP-13 by TGF-beta1 is a complex process involving transcriptional and posttranscriptional mechanisms.