Older adults are about four to seven times more likely than younger persons to experience adverse drug events (ADEs) that cause hospitalization, especially if they are women and take multiple medications. The prevalence of drug-related hospitalizations has been reported to be as high as 31%, with large heterogeneity between different studies, depending on study setting (all hospital admissions or only acute hospital admissions), study population (entire hospital, specific wards, selected population and/or age groups), type of drug-related problem measured (adverse drug reaction or ADE), method of data collection (chart review, spontaneous reporting or database research) and method and definition used to detect ADEs. The higher risk of drug-related hospitalizations in older adults is mainly caused by age-related pharmacokinetic and pharmacodynamic changes, a higher number of chronic conditions and polypharmacy, which is often associated with the use of potentially inappropriate drugs. Other factors that have been involved are errors related to prescription or administration of drugs, medication non-adherence and inadequate monitoring of pharmacological therapies. A few commonly used drugs are responsible for the majority of emergency hospitalizations in older subjects, i.e. warfarin, oral antiplatelet agents, insulin and oral hypoglycaemic agents, central nervous system agents. The aims of the present review are to summarize recent evidence concerning drug-related hospitalization in older adults, to assess the contribution of specific medications, and to identify potential interventions able to reduce the occurrence of these drug-related events, as they are, at least partly, potentially preventable.

Summary A total of 80 primary human breast carcinoma DNAs were analysed for loss of heterozygosity (LOH) on the long arm of chromosome 6, using microsatellite markers whose location has been defined physically and by linkage analysis. Loss of heterozygosity was observed in 38 of 80 (48%) tumours that were informative for at least one locus. The analysis revealed partial or interstitial deletions of chromosome 6q. Detailed mapping of chromosome 6q in these tumour DNAs identified two and perhaps three commonly deleted regions. One of these is located between markers D6S251 and D6S252 (6q14 -q16.2), another between D6S268 and D6S261 (6q 16.3 -q23) and a third between D6S287 and D6S270 (6q22.3 -q23. 1).Keywords: breast cancer; deletion; chromsome 6q; tumour-suppressor gene Cytogenetic (Dutrillaux et al., 1990;Lu et al., 1993;Thompson et al., 1993; Trent et al., 1985Trent et al., , 1993 and molecular analyses (reviewed in Callahan et al., 1993) of primary human breast carcinomas have documented frequently occurring genetic alterations that take place during the evolution of tumour development. It is thought that these mutations either inactivate normal growth controls or give the tumour some selective advantage. At the molecular level, loss of heterozygosity (LOH) is the most frequent type of genetic alteration in primary human breast tumours . LOH at specific chromosomal loci has been taken as evidence for the presence of putative tumour-suppressor genes within the affected regions (Knudson, 1989). In sporadic primary human breast carcinomas LOH has been detected on at least 12 different chromosome arms . However only in the case of chromosome l7pl3 has the target gene for LOH (TP53) been identified (Hollstein et al., 1991). Generally one allele of the target gene is lost and the remaining allele contains a nonsense or missense mutation. The involvement of chromosome 6q in breast carcinomas has been noted in cytogenetic analysis of primary tumours (Dutrillaux et al., 1990;Lu et al., 1993;Thompson et al., 1993; Trent et al., 1985Trent et al., , 1993. Similarly, molecular analysis of primary breast tumour DNAs has shown that chromosome 6q is frequently affected by LOH (Devilee et al., 1991). In this report, we describe studies aimed at defining the location of putative tumour-suppressor gene(s) on Table I. The PCR products were diluted with loading buffer (95% formamide, 20 mM EDTA, 0.05% bromophenol blue and 0.05% xylene cyanol), heat denatured and rapidly cooled. Samples were run in pairs (tumour and lymphocyte PCR product from the same patient) on a denaturing gel (7% acrylamide, 32% formamide, 6 M urea, 1 x TBE) at a constant 30-35 W. After electrophoresis the gel was transferred to 3MM Whatman paper and autoradiography performed with Kodak X-Omat AR film at -70'C. When the signal of an allele in tumour DNA was less than 50% of intensity observed in matching normal DNA from a heterozygous patient, LOH was considered to have occurred (Bieche et al., 1993). ResultsPreliminary results obtained at 6 loci (D6S254,...

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During wound healing, bacterial infections may prolong skin regeneration and tissue repair, causing delayed or incomplete healing. The therapeutic strategies currently used include general therapeutic modes, growth factors, skin substitutes, matrices and/or cell therapy. Among recent technologies, wound dressing materials comprising silver nitrate or silver sulfadiazine as the antimicrobial agent are widespread, despite their known cytotoxicity. The aim of this work was to develop and evaluate the efficacy of gelatinous injectable biomaterials composed of collagen and alginates, enriched with silver against bacterial pathogens commonly involved in wound infections. To reduce cytotoxicity, silver was used as lactate and saccharinated salts. Results show that silver-enriched beads were effective against both Gram-positive and Gram-negative strains in a concentration-dependent manner. Silver addition was more active against Staphylococcus epidermidis than against Pseudomonas aeruginosa. The antibacterial activity was localized only in the area of contact with the beads at concentrations lower than 0.3 mM, whereas at higher concentrations a larger inhibition halo was observed. No cytotoxic effect on eukaryotic cells was seen both testing the materials’ extracts or the Ag-doped beads in contact tests. These results, although preliminary, suggest that these scaffolds are a promising approach for realizing injectable or spreadable functional biomaterials with antibacterial activity for applications in wound management.

The long-term consequences of COVID-19 in those who recover from acute infection requiring hospitalization have not been defined yet. In this study, we aim to describe the long-term symptoms and respiratory outcomes over 12 months in patients hospitalized for severe COVID-19. In this prospective cohort study, patients admitted to hospital for severe COVID-19 were prospectively followed up at 6 and 12 months after discharge from the Hospital of Fermo, Italy. Patients were interviewed for persisting symptoms and underwent physical examination, routine blood test, pulmonary function tests, chest high-resolution CT (HRCT), and 6 min walking test. A total of 64 patients were evaluated and participated in this study. The mean age of participants was 68 years, 41 (64%) were males, and the median body mass index (BMI) was 26 kg/m2. After 6 months, 36% of patients reported persistent dyspnea, 37.5% persistent fatigue, 30.6% hair loss, 14% arthralgia and 11% memory and attention deficits. The rate of these symptoms reduced at the 12 month follow-up. At least 50% of the patients reported anxiety and depression symptoms. At 6 months 57.4% of patients showed reduced DLCO and 21.3% reduced FVC% and improvement at 12 months was noted for FVC but not for DLCO and TLC. Persistent radiographic abnormalities, most commonly ground-glass opacities and interstitial changes, were observed at both timepoints in many patients. Long-term symptoms and pulmonary deficits are common in patients admitted for severe COVID-19. Further studies are needed to assess the clinical significance of long-term consequences of severe COVID-19.