Effects of early mobilisation in patients after cardiac surgery: a systematic review.

BACKGROUND: Early mobilisation is prescribed after cardiac surgery to prevent postoperative complications, decrease length of hospital stay, and augment return to daily activities. OBJECTIVE: To evaluate the evidence for the effects of early mobilisation in patients after cardiac surgery on length of hospital stay, functional capacity and postoperative complications. DATA SOURCES: The data sources used were Medline, Embase, CINAHL, PEDro, Web of Science and Cochrane Central Register of Controlled Trials. STUDY SELECTION: Randomised controlled trials of early mobilisation after cardiac surgery. Study selection was not restricted by language or publication time. STUDY APPRAISAL AND SYNTHESIS METHODS: The methodological quality of each article was appraised with the PEDro scale. All review phases (selection, data extraction and appraisal) were conducted by two investigators, and a third investigator provided consensus. RESULTS: Nine trials were selected. The PEDro scale showed that the studies had a low risk of bias (range 5 to 9 points). The trials revealed diversity in techniques used for mobilisation, as well as periods considered early for the start of the intervention. Early mobilisation groups had improved outcomes compared with control groups without treatment. Generally, these advantages did not differ when groups of interventions were compared. LIMITATIONS: It was not possible to perform a meta-analysis due to the variability of the interventions proposed as early mobilisation. CONCLUSIONS: Regardless of the techniques used as mobilisation, the essential point is to avoid bed rest. Early mobilisation seems to be important to prevent postoperative complications, improve functional capacity and reduce length of hospital stay in patients after cardiac surgery.

Molecularly organized Langmuir-Blodgett films from a ruthenium biphosphine complex.

Langmuir-Blodgett (LB) films from a ruthenium complex mer-[RuCl3 (dppb)(4-Mepy)] (dppb = PPh2 (CH2)4PPh2; 4-Mepy = 4-methylpyridine), termed Ru-Pic, display a distinct color, which is different from the coloration exhibited by cast films or chloroform solutions. The solution and cast films are red, while the LB films are green-bluish. The manifestation of the blue color in the LB film finds its explanation in a unique absorption band at 690 nm, which is associated with the oxidation of the phosphine moieties. Fluorescence emission and absorption-reflection infrared spectroscopy measurements revealed the molecular organization in the LB films. In contrast, cast films showed a random distribution of complexes. Surface-enhanced Raman scattering was also used in an attempt to identify the main interactions in Ru-Pic.

Studies of adenovirus-induced eye disease in the rabbit model.

PURPOSE: To achieve a better understanding of the pathogenic processes associated with human adenovirus (Ad)-induced ocular disease. METHODS: Growth curves of Ad5 and Ad14 were performed in cell cultures derived from rabbit and human corneal epithelium (CE) and corneal keratocytes (CK). For in vivo studies, rabbit eyes were inoculated intrastromally and topically with 10(6) plaque-forming units per eye of Ad5 and ultraviolet light-inactivated (UV-1) Ad5 or Ad14, and the clinical features of the eyes were evaluated by biomicroscopic slit lamp examinations. Duration and quantitation of virus in tear samples were monitored. Humoral response was evaluated by enzyme-linked immunosorbent assay and serum neutralization titrations. Histopathologic and immunocytochemical staining of frozen corneal tissues was performed to determine the expression of major histocompatibility complex (MHC) class I and II and the presence of CD4+ and CD8+ T lymphocytes and CD18+ cells after the immunopathologic response elicited by virus inoculation. RESULTS: Both Ad5 and Ad14 replicated in all human cell cultures studied. In cells of rabbit origin, Ad5 replicated in cultured CE and CK cells, whereas Ad14 replication appeared restricted. Virus titers in ocular samples from Ad5-inoculated eyes peaked on postinoculation days 3 through 4, with approximately a 100-fold increase in infectious virus in comparison to initial titers. The duration of Ad5 shedding was 8.9 +/- 2.4 days. Ad5, Ad5 UV-I, and Ad14 induced seroconversion and subepithelial opacities. CD4+ and CD8+ T lymphocytes and CD18+ cells were present in these intrastromal immune cell infiltrates. Expression of MHC class I and II was observed in keratocytes and immune cells; MHC class I also was expressed on CE cells in inflamed areas. CONCLUSIONS: Ad5 is capable of replicating in both CE and CK cells of the rabbit eye. The presence of Ad antigens within the corneal stroma originating from infectious virus (Ad5), UV-inactivated virus (Ad5), or nonreplicating infectious virus (Ad14) can elicit indistinguishable immunopathologic responses in the stroma composed of CD4+, CD8+, and CD18+ cells.

Role of adenovirus type 5 early region 3 in the pathogenesis of ocular disease and cell culture infection.

Experimental animal virus replication models make it possible to study the role of viral gene products in adenovirus (Ad)-induced ocular disease. This study tested the hypothesis that the early region 3 (E3) of the human Ad genome plays an important role in the pathogenesis of Ad-induced ocular disease. Both Ad5 wt300, a genetically defined E3+ parent, and Ad5 dl327, a deletion mutant without E3 (E3-), replicated in ocular-derived cell cultures. Ad5 E3+ and Ad8 replicated more efficiently than did Ad5 E3- in cornea and conjunctival cell cultures. Lacrimal gland-derived cell cultures supported human Ad8 replication significantly more efficiently than did either Ad5 E3+ or Ad5 E3-. After intrastromal and topical inoculation of rabbits with either Ad wt300 or Ad dl327, a specific immune response was elicited that coincided with the appearance of subepithelial opacities that mimicked human disease both clinically and histologically. The clinical features (i.e., conjunctivitis, iritis, and corneal edema) were not significantly different for Ad5 E3(+)- and Ad5 E3(-)-induced ocular infection. Ad5 E3(+)- and Ad5 E3(-)-inoculated eyes shed virus for up to 7 and 5 days, respectively, and occasionally established persistent and/or latent infections in corneal, conjunctival, and, infrequently, lacrimal gland cells. Both Ad5 E3+ and Ad5 E3- spread from virus-inoculated animals to the cornea and conjunctiva of normal animals. Under current experimental conditions, expression of the E3 gene does not appear to affect the degree of virulence in ocular disease induced by Ad5 in the rabbit eye model. Deletion of the E3 gene from Ad5 does not make the model more like human disease.