No abstract

The integration of frailty measures in clinical practice is crucial for the development of interventions against disabling conditions in older persons. The frailty phenotype (proposed and validated by Fried and colleagues in the Cardiovascular Health Study) and the Frailty Index (proposed and validated by Rockwood and colleagues in the Canadian Study of Health and Aging) represent the most known operational definitions of frailty in older persons. Unfortunately, they are often wrongly considered as alternatives and/or substitutables. These two instruments are indeed very different and should rather be considered as complementary. In the present paper, we discuss about the designs and rationals of the two instruments, proposing the correct ways for having them implemented in the clinical setting.

Objective: To evaluate the impact of a programme of integrated social and medical care among frail elderly people living in the community.

Chronic diuretic use was associated with increased long-term mortality and hospitalizations in a wide spectrum of ambulatory chronic systolic and diastolic HF patients. The findings of the current study challenge the wisdom of routine chronic use of diuretics in HF patients who are asymptomatic or minimally symptomatic without fluid retention, and are on complete neurohormonal blockade. These findings, based on a non-randomized design, need to be further studied in randomized trials.

The most important determinant of risk for ADR-related hospital admissions in older patients is number of drugs being taken. When considering only severe ADRs, risk is also related to age and frailty.

Daily nonmalignant pain is prevalent among nursing home residents and is often associated with impairments in ADL, mood, and decreased activity involvement. Even when pain was recognized, men, racial minorities, and cognitively impaired residents were at increased risk for undertreatment. More education and research is necessary to improve the recognition and management of pain in the nursing home, remembering that attention should be paid to populations at increased risk for underrecognition and undertreatment.

The gut is able to maintain tolerance to microbial and food antigens. The intestine minimizes the number of harmful bacteria by shaping the microbiota through a symbiotic relationship. In healthy human intestine, a constant homeostasis is maintained by the perfect regulation of microbial load and the immune response generated against it. Failure of this balance may result in various pathological conditions. Innate immune sensors, such as Toll-like receptors (TLRs), may be considered an interface among intestinal epithelial barrier, microbiota, and immune system. TLRs pathway, activated by pathogens, is involved in the pathogenesis of several infectious and inflammatory diseases. The alteration of the homeostasis between physiologic and pathogenic bacteria of intestinal flora causes a condition called dysbiosis. The breakdown of homeostasis by dysbiosis may increase susceptibility to inflammatory bowel diseases. It is evident that environment, genetics, and host immunity form a highly interactive regulatory triad that controls TLR function. Imbalanced relationships within this triad may promote aberrant TLR signaling, critically contributing to acute and chronic intestinal inflammatory processes, such as in IBD, colitis, and colorectal cancer. The study of interactions between different components of the immune systems and intestinal microbiota will open new horizons in the knowledge of gut inflammation.

1. The relation between mitochondrial membrane potential (AFm) and cell function was investigated in single adult rat cardiac myocytes during anoxia and reoxygenation. A9'm was studied by loading myocytes with JC-1 (5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide), a fluorescent probe characterized by two emission peaks (539 and 597 nm with excitation at 490 nm) corresponding to monomer and aggregate forms of the dye. 2. De-energizing conditions applied to mitochondria, cell suspensions or single cells decreased the aggregate emission and increased the monomer emission. This latter result cannot be explained by changes of JC-1 concentration in the aqueous mitochondrial matrix phase indicating that hydrophobic interaction of the probe with membranes has to be taken into account to explain JC-1 fluorescence properties in isolated mitochondria or intact cells.