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Mechanisms that hinder ischemia-induced neovascularization in diabetes remain poorly understood. We hypothesized that endogenous bone marrow mononuclear cell (BM-MNC) dysfunction may contribute to the abrogated postischemic revascularization reaction associated with diabetes. We first analyzed the effect of diabetes (streptozotocin, 40 mg/kg) on BM-MNC pro-angiogenic potential in a model of surgically induced hindlimb ischemia. In nondiabetic animals, transplantation of BM-MNCs isolated from nondiabetic animals raised the ischemic/nonischemic angiographic score, capillary number, and blood flow recovery by 1.8-, 2.7-, and 2.2-fold, respectively, over that of PBS-injected nondiabetic animals (P < 0.05). Administration of diabetic BM-MNCs also improved the neovascularization reaction in ischemic hindlimbs of nondiabetic mice but to a lesser extent from that observed with nondiabetic BM-MNC transplantation. In diabetic mice, injection of nondiabetic BM-MNCs was still more efficient than that of diabetic BM-MNCs. Such BM-MNC dysfunction was associated with the impairment of diabetic BM-MNC capacity to differentiate into endothelial progenitor cells (EPCs) in vitro and to participate in vascular-like structure formation in a subcutaneous Matrigel plug. Placenta growth factor (PlGF) administration improved by sixfold the number of EPCs differentiated from diabetic BM-MNCs in vitro and enhanced ischemic/nonischemic angiographic score, capillary number and blood flow recovery by 1.9-, 1.5- and 1.6-fold, respectively, over that of untreated diabetic animals (P < 0.01). Endogenous BM-MNC pro-angiogenic potential was affected in diabetes. Therapeutic strategy based on PlGF administration restored such defects and improved postischemic neovascularization in diabetic mice.

Background— Bone marrow–derived mononuclear cells (BM-MNCs) enhance postischemic neovascularization, and their therapeutic use is currently under clinical investigation. We evaluated the safety of BM-MNC–based therapy in the setting of atherosclerosis. Methods and Results— Apolipoprotein E (apoE)–knockout (KO) mice were divided into 4 groups: 20 nonischemic mice receiving intravenous injection of either saline (n=10) or 10 6 BM-MNCs from wild-type animals (n=10) and 20 mice with arterial femoral ligature receiving intravenous injection of either saline (n=10) or 10 6 BM-MNCs from wild-type animals (n=10) at the time of ischemia induction. Animals were monitored for 4 additional weeks. Atherosclerosis was evaluated in the aortic sinus. BM-MNC transplantation improved tissue neovascularization in ischemic hind limbs, as revealed by the 210% increase in angiography score ( P P =0.01), and the 65% increase in tissue Doppler perfusion score ( P =0.0002). Hindlimb ischemia without BM-MNC transplantation or BM-MNC transplantation without ischemia did not affect atherosclerotic plaque size. However, transplantation of 10 6 BM-MNCs into apoE-KO mice with hindlimb ischemia induced a significant 48% to 72% increase in lesion size compared with the other 3 groups ( P =0.0025), despite similar total cholesterol levels. Transplantation of 10 5 BM-MNCs produced similar results, whereas transplantation of 10 6 apoE-KO–derived BM-MNCs had neither proangiogenic nor proatherogenic effects. There was no difference in plaque composition between groups. Conclusions— BM-MNC therapy is unlikely to affect atherosclerotic plaque stability in the short term. However, it may promote further atherosclerotic plaque progression in an ischemic setting.

The purpose of this study was to assess the effect of nutritional supplementation on dietary intake and on pressure ulcer development in critically ill older patients. The multi-center trial involved 19 wards stratified according to specialty and recruitment for critically ill older patients; 9 wards were randomly selected for nutritional intervention (nutritional intervention group), consisting of the daily distribution of two oral supplements, with each supplement containg 200 kcal, for 15 d. Pressure ulcer incidence was prospectively recorded for grades I (erythema), II (superficial broken skin), and III (subcutaneous lesion) for 15 d. Nutritional intake was monitored by using estimates in units of quarters validated by comparison with weight measurement. There were 672 subjects older than 65 y, and 295 were in the nutritional intervention group versus 377 in the control group. The patients were similar for age, sex ratio, and C-reactive protein. In comparison with the control group, the nutritional intervention group included more patients with stroke, heart failure, and dyspnea and fewer with antecedent falls, delirium, lower limb fractures, and digestive disease. The nutritional intervention group had a lower risk of pressure ulcers according to the Norton score but was less dependent (Kuntzman score) and had a lower serum albumin level. During the trial, energy and protein intakes were higher in the nutritional intervention group (day 2: 1081 +/- 595 kcal versus 957 +/- 530 kcal, P = 0.006; 45.9 +/- 27.8 g protein versus 38.3 +/- 23.8 g protein in the control group, P0.001). At 15 d, the cumulative incidence of pressure ulcers was 40.6% in the nutritional intervention group versus 47.2% in the control group. The proportion of grade I cases relative to the total number of cases was 90%. Multivariate analysis, taking into account all diagnoses, potential risk factors, and the intra-ward correlation, indicated that the independent risk factors of developing a pressure ulcer during this period were: serum albumin level at baseline, for 1 g/L decrease: 1.05 (95% confidence interval: 1.02 to 1.07, P0.001); Kuntzmann score at baseline, for 1-point increase: 1.22 (0.32 to 4.58, P = 0.003); lower limb fracture: 2.68 (1.75 to 4.11, P0.001); Norton score10 versus14: 1.28 (1.01 to 1.62, P = 0.04); and belonging to the control group: 1.57 (1.03 to 2.38, P = 0.04). In conclusion, it was possible to increase the dietary intake of critically ill elderly subjects by systematic use of oral supplements. This intervention was associated with a decreased risk of pressure ulcer incidence.

Bedsores prevention is part of the specific role of the nurse, as defined namely in the order 84-869 of the 17. July 1984. The analysis of the risk factors for the appearance of bedsores shows that immobilization, reduction of mobility linked to vigilance disorders and the urinary and faecal incontinence are major elements which justify protocols of well defined local cares. More recently, the role of undernutrition was highlighted but the recommendations lack accuracy. The proteino-energizing undernutrition is frequent among the elderly patients in hospital, reaching 60% of all the patients in the department of acute affections. The association of a constituted bedsore and of clinical and/or biological scars of protein-energizing undernutrition is demonstrated and justifies a re-feeding of the patients suffering from bedsores. On the other hand, although a bad nutrition state seems to favour the appearance of a bedsore, it is not proved that the nutrition intensification associating the diagnosis of an under-nutrition and the starting of an adapted re-feeding (with enriched food or assistance) decreases the actual incidence of the bedsores. A prospective, multicentered, randomized survey was therefore proposed. Its aim was to study the Influence of Nutrition in the Bedsores Prevention among the Elderly Patients in hospitals, suffering from acute affections. This research follows upon the preventions audits of bedsores and the nutrition protocol started up in a department of geriatrics intern medicine in the Regional Center of Geriatrics of Bordeaux.Two results must be retained in this nursing survey. It gave the possibility of calling into question the professional experience of the nursing teams which participated to the research and to update their knowledge in the field of the bedsores prevention. They could thus be acquainted with the existence of the grids which evaluate the risk of bedsore, the dependence or even the nutrition supply and to assess the interest for improving the cares quality. On the other hand, we highlighted the possibility of increasing the energy and protein supply by a distribution of enriched food supplements. Moreover, this action has had a beneficial influence in the bedsores prevention among the old people.

Undereating is a frequent concern in acute care geriatric settings and is supposed to worsen the outcomes of the underlying diseases, while the quality of nutritional support could be improved.Two consecutive and prospective audits (A and B) with team training over a 1 year period investigated the quality of malnutrition recognition and nutritional support and outcomes in immobilized, critically ill elderly subjects.Audit A included 170 patients (86.3+/-6.1 years old) and audit B, 232 patients (86.3+/-6.3), respectively 20.6% and 31.4% of the hospitalized population. Misclassifications occurred in A in 54.0% compared to 34.05% in B (P0.001). 32.6% in A versus 86.9% in B adequately received oral supplements (P = 0.02). Significant risk factors for the adverse outcomes in the combined two audits were: dementia (RR: 1.8, 95%CI: 1.0 to 3.0, P= 0.04) and dehydration (RR: 2.0, 95%CI:1.0 to 4.1, P= 0.05) for pressure ulcer incidence; stroke (RR: 8.8, 95%CI: 4.8 to 16.0, P0.001) for pressure ulcer prevalence at discharge; neoplasms (RR: 1.1, 95%CI: 1.0 to 1.2, P = 0.02) for nosocomial infections; bladder indwelling for urinary tract infections (RR: 4.8, 95%CI: 2.9 to 7.7, P0.001); swallowing problems for pulmonary infections (RR: 5.4, 95%CI: 2.8 to 10.5, P0.001); venous indwelling for septicaemia (RR: 5.4, 95%CI: 1.3 to 23. 3, P= 0.02). However, after adjustment on significant risk factors, the outcome rate was similar in audit B: death rate: A (15.6%), B (14.2%); length of stay: A (17.3+/-10.4 days), B (17.4+/-10.0); pressure ulcer incidence: A (26.4%), B (20.2%), (83% were erythema); pressure ulcer prevalence at discharge: A (14.7%), B (10.3%), (40% were erythema); nosocomial infections: A (26.4%), B (19.0%).The improvement of malnutrition recognition and nutritional support was not followed by a perceptible decrease in adverse outcome rate, this latter being mainly related to the underlying conditions of these critically ill elderly patients.

Results.– A total of 17 articles met the inclusion criteria. Nine studies used sensor monitoring solely as a method to measure and to recognize ADL and detect changes in ADL. These studies focus on the technical investigation of the sensor monitoring method used. Theother studies investigated clinical applications indaily practice. The sensor data could enable healthcare professionals to detect alert conditions, start and periods of decline and enabling earlier intervention. However for these studies we found limited evidence because of a lack of methodological high quality studies. Conclusions.– Studies on effectiveness of sensor monitoring to supportpeople inADLare still scarce.Weproposea roadmap for further development.