Background
Malnutrition may worsen clinical outcomes in stroke patients. Few malnutrition screening tools have been validated in the rehabilitation setting. The present study aimed to assess the ...concurrent and predictive validity of two malnutrition screening tools.
Methods
We retrospectively collected scores for the Mini Nutritional Assessment Short‐Form (MNA‐SF) and the Geriatric Nutritional Risk Index (GNRI) in consecutive stroke patients aged ≥65 years in a rehabilitation hospital. Concurrent validity was confirmed against the European Society for Clinical Nutrition and Metabolism diagnostic criteria for malnutrition (ESPEN‐DCM). Malnutrition risk within the ESPEN‐DCM process was assessed using the Malnutrition Universal Screening Tool. Cut‐off values with maximum Youden index, and with sensitivity (Se) >90% and specificity (Sp) >50%, were defined as appropriate for identification and screening of malnutrition, respectively. The Functional Independence Measure and discharge destination were used to explore predictive validity.
Results
Overall, 420 patients were analysed. Of these, we included 125 patients in the malnutrition group and 295 in the non‐malnutrition group based on the ESPEN‐DCM. Cut‐off values for the identification and screening of malnutrition were 5 (Se: 0.78; Sp: 0.85) and 7 (Se: 0.96; Sp: 0.57) for the MNA‐SF; 92 (Se: 0.74; Sp: 0.84) and 98 (Se: 0.93; Sp: 0.50) for the GNRI, respectively. The GNRI predicted discharge to acute care hospital, whereas the MNA‐SF did not predict all outcome measures.
Conclusions
The MNA‐SF and the GNRI have a fair concurrent validity in stroke patients, although lower cut‐off values than currently used were required for the MNA‐SF. The GNRI exhibits good predictive validity for discharge destination.
We examined the effect of aspirin as a substitute for exercise in inducing urticaria/anaphylaxis in three patients with food‐dependent exercise‐induced anaphylaxis (FDEIA). Two of the patients had ...specific IgE antibodies to wheat and the other had antibodies to shrimp. Administration of aspirin before ingestion of food allergens induced urticaria in one patient and urticaria and hypotension in another, while aspirin alone or food alone elicited no response. The third patient developed urticaria only when he took all three items, i.e. aspirin, food and additional exercise, whereas provocation with any one or or two of these did not induce any symptoms. These findings suggest that aspirin upregulates type I allergic responses to food in patients with FDEIA, and further shows that aspirin synergizes with exercise to provoke symptoms of FDEIA. This is the first report of a synergistic effect of aspirin in inducing urticaria/anaphylaxis, which was confirmed using challenge tests in patients with FDEIA.
Summary
Recently, the axonal‐SMN (a‐SMN) protein, which is generated by the gene responsible for spinal muscular atrophy (SMA), SMN, has been reported. Surprisingly, the a‐SMN transcript includes the ...entire sequence of SMN intron 3. We had expected a high frequency of insertion/deletion mutations at a polyadenine tract in this intron, since simple repetitive sequence motifs are prone to mutations. Such mutations could change the C‐terminal structure of the a‐SMN protein. However, our study showed that almost all individuals, including healthy individuals, SMA patients and SMA‐like patients, carried only alleles with a normal polyadenine tract. Hypomutability of the polyadenine tract in SMN intron 3 suggests the existence of transcriptional mechanisms preventing alterations to the open reading frame of axonal SMN and not allowing variability in the protein structure of a‐SMN.
Tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) is an adapter protein that links signals from members of the TNFR superfamily and Toll/IL-1 receptor family to activation of ...transcription factors NFκB and AP-1. Analysis of TRAF6-deficient mice revealed that TRAF6 is essential for normal bone formation and establishment of immune and inflammatory systems. Here we report that TRAF6 deficiency results in defective development of epidermal appendixes, including guard hair follicles, sweat glands, sebaceous glands of back skin, and modified sebaceous glands such as meibomian glands, anal glands, and preputial glands. Except the sebaceous gland impairment, these abnormal phenotypes are identical to those observed in Tabby (Ta), downless (dl), and crinkled (cr) mice, which are models of hypohidrotic (anhidrotic) ectodermal dysplasia in human. β-catenin and mucosal addressin cell adhesion molecule-1, an early marker of developing guard-hair follicles is absent in the skin of TRAF6-deficient embryos. Thus, TRAF6 is essential for development of epidermal appendixes. TRAF6 does not associate with the cytoplasmic tail of the dl protein (DL)/ectodysplasin receptor (EDAR) receptor, which, when mutated, results in hypohidrotic (anhidrotic) ectodermal dysplasia. However, TRAF6 associates with X-linked ectodysplasin-A2 receptor (XEDAR) and TNFR super family expressed on the mouse embryo (TROY/toxicity and JNK inducer (TAJ), which are EDAR-related members of the TNFR superfamily that are expressed at high level in epidermal appendixes. Furthermore, TRAF6 is essential for the XEDAR-mediated NFκB activation. Our results suggest that TRAF6 may transduce signals emanating from XEDAR or TROY/TAJ that are associated with development of epidermal appendixes.
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