The FRAIL-NH Scale: Systematic Review of the Use, Validity and Adaptations for Frailty Screening in Nursing Homes.

OBJECTIVES: To investigate frailty prevalence, cross-sectional associations, predictive validity, concurrent validity, and cross-cultural adaptations of the FRAIL-NH scale. DESIGN: Systematic review. SETTING AND PARTICIPANTS: Frail residents living in nursing homes. METHODS: MEDLINE, EMBASE, CINAHL, and Cochrane Library were searched from January 2015 to June 2021 for primary studies that used the FRAIL-NH scale, irrespective of study designs and publication language. RESULTS: Overall, 40 studies conducted across 20 countries utilized the FRAIL-NH scale; majority in Australia (n=14), followed by China (n=6), United States (n=3), and Spain (n=3). The scale has been translated and back-translated into Brazilian Portuguese, Chinese, and Japanese. Various cut-offs have been used, with ≥2 and ≥6 being the most common cut-offs for frail and most frail, respectively. When defined using these cut-offs, frailty prevalence varied from 15.1-79.5% (frail) to 28.5-75.0% (most frail). FRAIL-NH predicted falls (n=2), hospitalization or length of stay (n=4), functional or cognitive decline (n=4), and mortality (n=9) over a median follow-up of 12 months. FRAIL-NH has been compared to 16 other scales, and was correlated with Fried's phenotype (FP), Frailty Index (FI), and FI-Lab. Four studies reported fair-to-moderate agreements between FRAIL-NH and FI, FP, and the Comprehensive Geriatric Assessment. Ten studies assessed the sensitivity and specificity of different FRAIL-NH cut-offs, with ≥8 having the highest sensitivity (94.1%) and specificity (82.8%) for classifying residents as frail based on FI, while two studies reported an optimal cut-off of ≥2 based on FI and FP, respectively. CONCLUSION: In seven years, the FRAIL-NH scale has been applied in 20 countries and adapted into three languages. Despite being applied with a range of cut-offs, FRAIL-NH was associated with higher care needs and demonstrated good agreement with other well-established but more complex scales. FRAIL-NH was predictive of adverse outcomes across different settings, highlighting its value in guiding care for frail residents in nursing homes.

Paracetamol treatment for patent ductus arteriosus: practice and attitudes in Australia and New Zealand.

Aim: To describe the current clinical practices and attitudes of neonatologists towards paracetamol treatment of PDA in Australia (AU) and New Zealand (NZ). Method: A web-based survey of all neonatologists registered under the 2017 Australia New Zealand Neonatal Network (ANZNN) was conducted. Results: The response rate for the survey was 67%, (141/210). Of those respondents, 37% stated their unit had a written policy outlining how to treat patent ductus arteriosus (PDA). Of the written policies, 53% mentioned paracetamol treatment. The majority of the respondents (70%) have prescribed paracetamol for PDA closure. When comparing between countries, 79% of AU respondents had compared with 44% of NZ respondents. Successful ductal closure in the infants who received paracetamol was anecdotally reported by 61% of respondents. The main reasons for clinicians not prescribing paracetamol were due to preferential NSAID use (61%) and lack of evidence to indicate efficacy (49%). Conclusion: Many neonatologists in AU and NZ have prescribed paracetamol for PDA closure. However, considerable practice variations exist. The results from this study suggest there may be a role for paracetamol in the treatment of PDA, however, further research is required to clarify the optimal use and provide evidence of efficacy.

The complete genome sequence and analysis of Corynebacterium diphtheriae NCTC13129.

Corynebacterium diphtheriae is a Gram-positive, non-spore forming, non-motile, pleomorphic rod belonging to the genus Corynebacterium and the actinomycete group of organisms. The organism produces a potent bacteriophage-encoded protein exotoxin, diphtheria toxin (DT), which causes the symptoms of diphtheria. This potentially fatal infectious disease is controlled in many developed countries by an effective immunisation programme. However, the disease has made a dramatic return in recent years, in particular within the Eastern European region. The largest, and still on-going, outbreak since the advent of mass immunisation started within Russia and the newly independent states of the former Soviet Union in the 1990s. We have sequenced the genome of a UK clinical isolate (biotype gravis strain NCTC13129), representative of the clone responsible for this outbreak. The genome consists of a single circular chromosome of 2 488 635 bp, with no plasmids. It provides evidence that recent acquisition of pathogenicity factors goes beyond the toxin itself, and includes iron-uptake systems, adhesins and fimbrial proteins. This is in contrast to Corynebacterium's nearest sequenced pathogenic relative, Mycobacterium tuberculosis, where there is little evidence of recent horizontal DNA acquisition. The genome itself shows an unusually extreme large-scale compositional bias, being noticeably higher in G+C near the origin than at the terminus.

Complete genome sequence of a multiple drug resistant Salmonella enterica serovar Typhi CT18.

Salmonella enterica serovar Typhi (S. typhi) is the aetiological agent of typhoid fever, a serious invasive bacterial disease of humans with an annual global burden of approximately 16 million cases, leading to 600,000 fatalities. Many S. enterica serovars actively invade the mucosal surface of the intestine but are normally contained in healthy individuals by the local immune defence mechanisms. However, S. typhi has evolved the ability to spread to the deeper tissues of humans, including liver, spleen and bone marrow. Here we have sequenced the 4,809,037-base pair (bp) genome of a S. typhi (CT18) that is resistant to multiple drugs, revealing the presence of hundreds of insertions and deletions compared with the Escherichia coli genome, ranging in size from single genes to large islands. Notably, the genome sequence identifies over two hundred pseudogenes, several corresponding to genes that are known to contribute to virulence in Salmonella typhimurium. This genetic degradation may contribute to the human-restricted host range for S. typhi. CT18 harbours a 218,150-bp multiple-drug-resistance incH1 plasmid (pHCM1), and a 106,516-bp cryptic plasmid (pHCM2), which shows recent common ancestry with a virulence plasmid of Yersinia pestis.

A comprehensive educational program improves clinical outcome measures in inner-city patients with asthma.

BACKGROUND: Despite improved understanding of the pathophysiology of asthma, morbidity and mortality continue to rise, with disproportionate increases occurring among urban, indigent minorities. New approaches in the management of asthma are therefore necessary to reverse these dramatic and costly trends. OBJECTIVE: To determine if patients who are admitted to the hospital with acute asthma and receive inpatient education will have improved outpatient follow-up and clinical outcome measures compared with those receiving conventional care. METHODS: Patients enrolled in the study had a primary admission diagnosis of asthma and were between ages 18 and 45 years. Exclusion criteria included comorbid disease, inability to speak English, absence of a telephone in the primary residence, or pregnancy. Seventy-seven patients admitted from the emergency department with asthma were randomized to either the inpatient educational program (IEP) or routine care (control group). Patients in the IEP received asthma education, bedside spirometry, a telephone call 24 hours after discharge, and scheduled follow-up in an outpatient asthma program within 1 week of discharge. Those individuals randomized to the routine management group received conventional inpatient asthma care and routine follow-up. RESULTS: The patients enrolled in the IEP had a markedly higher follow-up rate compared with outpatient appointments (60% vs. 27%; P = .01) and significantly fewer emergency department visits (P = .04) and hospitalizations (P = .04) for asthma in the 6 months following IEP intervention, as compared with control patients. This represented a substantial cost savings to the managed care organization. CONCLUSION: Our study suggests that an IEP in the treatment of indigent, inner-city patients hospitalized with asthma reduces the need for subsequent emergent care and improves outpatient follow-up in a cost-effective manner.

Rumors and gossip: a guide for the health care supervisor.

Rumor and gossip are long-standing means of communication among humans and are prevalent in health care settings in part due to the nature of the organization. Rumor and gossip may be negative or positive, and health care supervisors should monitor the grapevine and consider themselves personally responsible for transmitting accurate information whenever possible to ensure that rumor and gossip do not have a negative effect on the department or institution.

Rapid stimulation of EAAC1-mediated Na+-dependent L-glutamate transport activity in C6 glioma cells by phorbol ester.

C6 glioma cells were used as a model system to study the regulation of EAAC1-mediated Na(+)-dependent L-[3H]glutamate transport. Although a 30-min preincubation with forskolin had no effect on transport activity, preincubation with phorbol 12-myristate 13-acetate (PMA) increased transport activity two- to threefold. PMA caused a time-dependent and concentration-dependent increase in EAAC1-mediated L-[3H]glutamate transport activity. A 2-min preincubation with PMA was sufficient to cause more than a twofold increase in transport activity and the protein synthesis inhibitor cycloheximide had no effect on the increase. These data suggest that this increase is independent of protein synthesis. The EC50 value of PMA for stimulation of transport activity was 80 nM. Kinetic analyses demonstrated that the increase in transport activity was due to a 2.5-fold increase in Vmax with no change in Km. PMA also increased the transport of the nonmetabolizable analogue, D-[3H] aspartate to the same extent. In parallel assays, PMA did not, however, increase Na(+)-dependent glycine transport activity in C6 glioma. The inactive phorbol ester alpha-phorbol 12,13- didecanoate, did not stimulate L-[3H]glutamate transport activity, and the protein kinase C inhibitor chelerythrine blocked the stimulation caused by PMA. Okadaic acid and cyclosporin A, which are phosphatase inhibitors, had no effect on the stimulation of transport activity caused by PMA. The Ca2+ ionophore A23187 did not act synergistically to increase PMA stimulation. In previous studies, PMA caused a rapid increase in amiloride-sensitive Na(+)/H+ transport activity in C6 glioma. In the present study, pre- and coincubation with amiloride had no effect on the stimulation of transport activity caused by PMA. These studies suggest that activation of protein kinase C causes a rapid increase in EAAC1-mediated transport activity. This rapid increase in Na(+)-dependent L-[3H]-glutamate transport activity may provide a novel mechanism for protection against acute insults to the CNS.

Maintaining confidentiality: health care's ongoing dilemma.

Confidentiality of patient information is an ethical obligation of health care professionals. The exercise of confidentiality is not a simple process; it is dynamic rather than static and must be upgraded with changes in technology. This article discusses some of the common issues that arise in maintaining confidentiality in the health care environment, including spoken and written breaches of confidentiality, use of the computer, confidentiality as an ethical rather than legal obligation, and the use of programs in health care institutions to maintain confidentiality.

Comparison of Na+-dependent glutamate transport activity in synaptosomes, C6 glioma, and Xenopus oocytes expressing excitatory amino acid carrier 1 (EAAC1).

Several subtypes of sodium-dependent high affinity (SDHA) glutamate transporters have been pharmacologically differentiated in brain tissue. Recently, four distinct cDNAs (EAAC1, GLT1, GLAST, and EAAT4) encoding Na+-dependent glutamate transporters have been isolated, but the properties of some of these transporters do not fully match the properties of transport observed in brain tissue or astrocyte-enriched cultures. The purpose of the current investigation was to determine whether the pharmacological properties of EAAC1 parallel those observed in cortical or cerebellar synaptosomes, C6 glioma, or primary astrocyte-enriched cultures. EAAC1 cRNA was expressed in Xenopus oocytes, an expression system with no detectable endogenous Na+-dependent glutamate transport activity. EAAC1-mediated glutamate transport was >98% Na+ dependent, and the transport was saturable and consistent with a single site. Glutamate transport activates in EAAC1-injected oocytes and C6 glioma have similar Km values for glutamate (Km = 15-24 microM) and Na+ (apparent Km = 35-50mM), and these values markedly differ from those observed in rat synaptosomes (glutamate, Km = 1-5 microM; Na+, Km = 13-20 mM). Several excitatory amino acid analogues were tested as inhibitors of L-[3H] glutamate transport in oocytes expressing EAAC1 cRNA. The potencies of several compounds for inhibition of EAAC1-mediated transport differed from those previously observed in cerebellar synaptosomes and astrocyte-enriched cultures. Although EAAC1-mediated transport and cortical synaptosomal transport have similar pharmacological profiles, five excitatory amino acid analogues were > or= 3-fold more potent as inhibitors of transport into cortical synaptosomes than of transport into EAAC1-injected oocytes. For example, L-trans-pyrrolidine-2,4-dicarboxylate was approximately 5-fold more potent in cortical synaptosomes, and dihydrokainate was approximately 10-fold more potent in cortical synaptosomes than in EAAC1-injected oocytes. In contrast, all of the compounds examined inhibit transport observed in C6 glioma wtih potencies similar to that observed in oocytes injected with EAAC1 cRNA. Consistent with these data, C6 glioma expressed EAAC1- but not GLT1- and GLAST-like immunoreactivity. Although this immunoreactivity migrated as proteins of slightly different molecular masses in each system, treatment with N-glycosidase F shifted all proteins to a molecular mass consistent with that predicted from the cDNA sequence. In cortical synaptosomes, EAAC1-, GLT1-, and GLAST-like immunoreactives were apparent. These results indicate that (i) EAAC1 but not GLAST or GLT1 transporters are expressed in C6 glioma, (ii) synaptosomes contain a heterogeneous population of transporters, (iii) EAAC1 does not account for the pharmacology previously observed in cortical synaptosomes, and (iv) based on the pharmacology and tissue distribution of EAAC1, GLT1, GLAST, and EAAT4, it appears that there are additional glutamate transporter subtypes.

Tetanus: delay in diagnosis in England and Wales.

A 7 day delay occurred in the diagnosis of cephalic tetanus in a 69 year old woman who developed an ipsilateral facial palsy 5 days after a facial laceration. Cranial nerve palsies often precede trismus in this form of tetanus.

Subtypes of sodium-dependent high-affinity L-[3H]glutamate transport activity: pharmacologic specificity and regulation by sodium and potassium.

Some data suggest that the sodium-dependent, high-affinity L-glutamate (Glu) transport sites in forebrain are different from those in cerebellum. In the present study, sodium-dependent transport of L-[3H]Glu was characterized in cerebellum and cortex. In both cerebellar and cortical tissue, activity was enriched in synaptosomes. Approximately 100 excitatory amino acid analogues were tested as potential inhibitors of transport activity. Many of the compounds tested inhibited transport activity by < 65% at 1 mM and were not studied further. One group of compounds exhibited inhibition conforming to theoretical curves with Hill coefficients of 1 and were < 10-fold selective as inhibitors of transport activity. These included three of the putative endogenous substrates for transport: L-Glu, L-aspartate, and L-cysteate. Four of the compounds exhibited inhibition conforming to theoretical curves with Hill coefficients of 1 and were > 10-fold selective as inhibitors. These included beta-N-oxalyl-L-alpha,beta-diaminopropionate, alpha-methyl-DL-glutamate, (2S,1'S,2'S)-2-(carboxycyclopropyl)glycine, and (2S,1'S,2'S,3'S)-2-(2-carboxy-3-methoxymethylcyclopropyl)glycine. Data obtained with a few of the inhibitors were consistent with two sites in one or both of the brain regions. (2S,1'R,2'R)-2-(Carboxycyclopropyl)glycine (L-CCG-II) was identified as the most potent (IC50 = 5.5 microM) and selective (60-100-fold) inhibitor of transport activity in cerebellum. One of the potential endogenous substrates, L-homocysteate, was also a selective inhibitor of cerebellar transport activity. The data for inhibition of transport activity in cortex by both L-CCG-II and L-homocysteate were best fit to two sites. Kainate was equipotent as an inhibitor of transport activity, and in both brain regions the data for inhibition were best fit to two sites. The possibility that there are four subtypes of excitatory amino acid transport is discussed. Altering sodium and potassium levels affects cerebellar and cortical transport activity differently, suggesting that the differences extend to other recognition sites on these transporters.