Improving the nutritional intake of hospital patients: how far have we come? A re-audit.

BACKGROUND: Malnutrition affects up to 33.6% of hospitalised patients, with consequences that are detrimental for both patients and healthcare providers. In 2015, an audit demonstrated inadequate nutritional provision and consumption by hospitalised patients, comprising a major risk factor for malnutrition. This re-audit evaluates whether patients are meeting recommended energy and protein standards and estimated individual requirements, subsequent to food service improvements since 2015. METHODS: Patients (n = 111) were included from a South West hospital, and Malnutrition Universal Screening Tool scores (MUST) categorised patients as 'nutritionally well' (MUST 0) or 'nutritionally vulnerable' (MUST ≥ 1). Individual energy and protein requirements were estimated using weight-based equations. Nutritional intakes were assessed via 24-h dietary recall and compared against the British Dietetic Association's Nutrition and Hydration Digest standards, as well as estimated individual requirements. RESULTS: In total, the Digest standards for energy and protein were met by 35% and 63% of patients respectively, which is an increase of 19% and 36% since 2015. 'Nutritionally well' patients were more likely to meet nutrient standards for protein (62%) than estimated individual requirements (30%) (P ≤ 0.001). 'Nutritionally vulnerable' patients were more likely to meet estimated individual requirements for energy (60%) than the Digest standards (30%) (P = 0.047). CONCLUSIONS: The proportion of patients meeting the Digest standards has increased considerably following numerous food service changes. Nutritional training for housekeepers, energy/protein-dense snacks and drinks, and fortified dietary items may further increase nutritional intakes. Additionally, as a result of discrepancies between the Digest standards and individual estimated requirements, more research is required to identify the most appropriate auditing standards that reflect best practice.

Storage and retrieval of collective excitations on a long-lived spin transition in a rare-earth ion-doped crystal.

Robust, long-lived optical quantum memories are important components of many quantum information and communication protocols. We demonstrate coherent generation, storage, and retrieval of excitations on a long-lived spin transition via spontaneous Raman scattering in a rare-earth ion-doped crystal. We further study the time dynamics of the optical correlations in this system. This is the first demonstration of its kind in a solid and an enabling step toward realizing a solid-state quantum repeater.

Ethnic differences in osteocalcin gamma-carboxylation, plasma phylloquinone (vitamin K1) and apolipoprotein E genotype.

OBJECTIVE: To investigate plasma osteocalcin gamma-carboxylation and its relationship to plasma phylloquinone concentration and apolipoprotein E (apoE) genotype in women from three ethnic groups with differing osteoporotic fracture risk. DESIGN AND SUBJECTS: Fasted blood samples were collected from postmenopausal Gambian (n=50), British (n=31) and Chinese women (n=23), and 11 premenopausal women in each group from three cross-sectional studies. RESULTS: After adjustment for total osteocalcin, plasma undercarboxylated osteocalcin (adjusted ucOC) was lowest in Chinese and highest in British women postmenopause (British vs Chinese 103% higher, P<0.0001; Gambian vs Chinese 66% higher, P<0.01). No differences were observed premenopause. Within each ethnic group, adjusted ucOC was similar pre- and postmenopause. Postmenopause, plasma phylloquinone was higher in Chinese women (1.0 ng/ml) than in British (0.31 ng/ml) and Gambian women (0.36 ng/ml) (P<0.0001). Premenopause, plasma phylloquinone was higher in Gambian and Chinese women (0.6 ng/ml) than in British women (0.3 ng/ml; P=0.01). Plasma phylloquinone and adjusted ucOC were inversely related in postmenopausal British women (R2=32.4%; P=0.0008). ApoE4 frequency was Gambian 32.6%, British 13.8% and Chinese 6%. A lower adjusted ucOC was associated with apoE2 genotype in British and Chinese women. Ethnic differences in adjusted ucOC persisted after adjustment for phylloquinone and apoE genotype. CONCLUSION: These preliminary data indicate suboptimal vitamin K status in postmenopausal British compared to Chinese and Gambian women. Ethnic differences in apoE genotype may also influence osteocalcin gamma-carboxylation status. The study highlights the need for larger epidemiological investigations of ethnic differences in vitamin K status and the possible implications to bone health.

The effects of estrogen on osteoprotegerin, RANKL, and estrogen receptor expression in human osteoblasts.

Estrogen is essential for bone growth and development and for the maintenance of bone health in adulthood. The cellular responses of osteoblasts and osteoclasts to estrogen are initiated via two high-affinity receptors (ERs). Osteoblasts synthesize RANKL (receptor activator of NF-kappaB ligand), necessary for osteoclast formation and function, and osteoprotegerin (OPG), its decoy receptor. To investigate the effects of estrogen on the expression of OPG, RANKL, and ERs in human osteoblasts, cells were cultured with physiological (10(-10) M) and high-dose (10(-7) M) 17beta-estradiol for 24 and 48 h. Proteins and corresponding mRNA levels were quantitatively determined by immunocytochemistry and RT-PCR. OPG expression was significantly increased three- and sevenfold at 24 h with 10(-10) M (P < 0.05) and 10(-7) M (P < 0.01) estradiol, respectively, compared to untreated cells. Similar but smaller increases were seen at 48 h (P < 0.05). Osteoblasts treated with estradiol demonstrated increased RANKL protein expression at 24 h (P < 0.05), but this was not maintained at 48 h. ERalpha expression was significantly increased by high-dose estradiol (P < 0.01) at 24 h and dose-dependently increased at 48 h (P < 0.01), while ERbeta was only increased at 24 h (P < 0.01). The estrogen-induced protein expression of ER, OPG, and RANKL was abrogated when cells were cultured in the presence of the estrogen antagonist ICI 182780. mRNA levels at 24 h demonstrated a significant suppression of RANKL with the low-dose but not the high dose. ERalpha mRNA but not ERbeta expression was up-regulated by estrogen. Our results suggest that estrogen may exert its anti-resorptive effects on bone, at least in part, by stimulating ER and OPG expression in osteoblasts.

Mechanisms by which high-dose estrogen therapy produces anabolic skeletal effects in postmenopausal women: role of locally produced growth factors.

Conventional hormone replacement therapy acts primarily by preserving bone, but cannot restore lost bone in women with established osteoporosis. Studies in rodents have shown that high doses of estrogens have anabolic skeletal effects, and recent observations in a group of women treated long term with high doses of estrogen indicated that similar effects occur in humans. This study examines the hypothesis that locally produced growth factors, including transforming growth factor-beta (TGF-beta) and platelet-derived growth factors (PDGFs), are involved in mediating the anabolic effects of high-dose estrogen. Transiliac-crest bone biopsies were taken from ten women, aged 52-67 years (mean 58 years), who had been treated with high-dose estrogen for 15 years. Control samples were obtained from four age-matched postmenopausal women not receiving estrogen therapy. TGF-betas and PDGFs were analyzed for mRNA and protein expression by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry. Results showed both TGF-beta1 and -beta2 mRNA, expressed as a ratio to GAPDH, were increased in the estrogen-treated group with an eightfold increase for TGF-beta1 (0.258 +/- 0.246 [mean +/- SD] vs. 0.032 +/- 0.053 in the control group, p = 0.02) and a twofold increase for TGF-beta2 (p = n.s.). TGF-beta3 analysis showed only negligible amounts in both groups. Protein expression levels for TGF-beta1, -beta2, -betaRI and -RII were higher in the estrogen-treated group than in controls, the most marked effects being seen for TGF-beta1. PDGF-A protein expression was also significantly higher in osteoblasts and osteocytes in women treated with estrogen, whereas PDGF-B showed only modest differences. The percentage of bone surface occupied by osteoclasts, as determined by tartrate-resistant acid phosphatase (TRAP) staining, was significantly reduced in the estrogen-treated group (p = 0.001). These results demonstrate that high-dose estrogen therapy is associated with increased TGF-beta, TGF-betaR, and PDGF synthesis and decreased osteoclast activity, consistent with the hypothesis that these growth factors may mediate the actions of estrogen in bone.

Colocalization of glucocorticoid and mineralocorticoid receptors in human bone.

Osteoporosis is a poorly understood but common complication of glucocorticoid therapy. The actions of glucocorticoids are mediated via glucocorticoid receptors (GRs), but in vitro, glucocorticoids also can bind to mineralocorticoid receptors (MRs). It is not known if MR protein is present in human bone and little is known of GR isoform expression (GRalpha and GRbeta). GR and MR protein expression and possible sites of action were investigated in neonatal rib and adult iliac crest biopsy specimens using antibodies specific for MR, GRalpha, and GRalphabeta. Colocalization [MR GRalpha] [MR GRalphabeta] was performed using fluorescent-conjugated secondary antibodies. GRalpha, GRbeta, and MR show distinct but overlapping patterns of expression, suggesting important functions for each receptor type. Osteoclasts showed no staining for GRalpha but strong staining for GRalphabeta, indicating expression of GRbeta and a specific role in addition to antagonizing the transcriptional activity of GRalpha. MR also was observed in osteoclasts and colocalized with GRalphabeta. Coexpression of MR, GRalpha, and GRalphabeta was seen in osteoblasts. Reverse-transcription-polymerase chain reaction (RT-PCR) of cultured osteoblast RNA confirmed expression of both GRalpha and GRbeta. Osteocytes stained with MR, GRalpha, and GRalphabeta antibodies but to a lesser degree than osteoblasts. In the neonatal rib cartilage, staining for GRalpha, GRalphabeta, and MR was present in approximately one-half of the resting and hypertrophic chondrocytes and in most of proliferating chondrocytes and chondrocytes within the mineralizing matrix. Identification of MR raises the possibility that the physiological and pharmacologic effects of glucocorticoids on bone may be mediated via MR as well as GR and that GRalpha, GRbeta, and MR synergize to influence corticosteroid metabolism in human bone.

Estrogen receptors alpha and beta are differentially expressed in developing human bone.

Estrogen plays an essential role in the development and maintenance of the skeleton; its effects are mediated via interactions with two estrogen receptor (ER) subtypes, alpha and beta. The aim of this study was to establish the cellular distribution of ERalpha and ERbeta in neonatal human rib bone. ERalpha and ERbeta immunoreactivity was seen in proliferative and prehypertrophic chondrocytes in the growth plate, with lower levels of expression in the late hypertrophic zone. Different patterns of expression of the two ERs were seen in bone. In cortical bone, intense staining for ERalpha was observed in osteoblasts and osteocytes adjacent to the periosteal-forming surface and in osteoclasts on the opposing resorbing surface. In cancellous bone, ERbeta was strongly expressed in both osteoblasts and osteocytes, whereas only low expression of ERalpha was seen in these areas. Nuclear and cytoplasmic staining for ERbeta was apparent in osteoclasts. These observations demonstrate distinct patterns of expression for the two ER subtypes in developing human bone and indicate functions in both the growth plate and mineralized bone. In the latter, ERalpha is predominantly expressed in cortical bone, whereas ERbeta shows higher levels of expression in cancellous bone.

Megakaryocyte population in human bone marrow increases with estrogen treatment: a role in bone remodeling?

Skeletal effects of conventional hormone replacement therapy (HRT) are predominately antiresorptive, while high doses of estrogen have anabolic effects. The mechanisms mediating these effects are unclear but may involve cells in the bone marrow. We have investigated the in vivo effects of estrogen on the megakaryocyte (MK) population in bone marrow in 10 postmenopausal women before and after 2 years of conventional HRT, in 11 women after long-term, high-dose estradiol therapy, and in 2 premenopausal and 4 postmenopausal women who had received no previous estrogen treatment. Transiliac crest biopsies were halved and either decalcified and paraffin wax embedded for immunolocalization studies or dehydrated and embedded in LR White resin for histology. MKs were identified morphologically, and the bone marrow cell population and MK number quantified by cell counting in a defined area of view (1 mm(2)) from 5 randomly selected fields of bone marrow. Compared with pretreatment values, significantly higher MK numbers were found after conventional HRT treatment (before treatment, mean +/- SEM; 7.3 +/- 1.1 vs. after treatment, 18.0 +/- 1.6/5 mm(2); p < 0.0001), while the greatest MK number was associated with long-term, high-dose estradiol treatment (32.8 +/- 2.1/5 mm(2); p < 0.0001). Total bone marrow cell number did not differ significantly between groups. Immunolocalization studies revealed more intense estrogen receptor (ER)beta expression in MKs in the high-dose estradiol-treated group but similar levels of weak ERalpha staining in MKs in the control and high-dose estrogen-treated groups. Positive immunoreactivity for transforming growth factor (TGF)beta1, 2, and 3 and TGFbeta receptor I, II, and III was detected in MKs, with more intense staining being demonstrated in the high-dose estradiol-treated group, particularly for TGFbeta2 and TGFbetaRI and II. Our results demonstrate an increase in the MK population in bone marrow from women treated with estrogen. The ability of MKs to express ERs and synthesise TGFbeta, a potent mitogen in osteoblast differentiation, suggests that these cells may play a role in mediating estrogen-induced effects on bone.

Bone changes after 3 mo of lactation: influence of calcium intake, breast-milk output, and vitamin D-receptor genotype.

Factors influencing the change in bone mineral after 3 mo of lactation were investigated in 47 breast-feeding mothers, 11 formula-feeding mothers, and 22 nonpregnant, nonlactating control subjects. At 6-8 wk postpartum, the breast-feeding group had a mean (+/-SD) calcium intake of 34.8+/-13.2 mmol/d and breast-milk volume, calcium concentration, and calcium output of 0.865+/-0.230 L/d, 7.41+/-1.25 mmol/L, and 6.41+/-2.00 mmol/d, respectively. There was no relation between calcium intake and any breast-milk variable. Dual-energy X-ray absorptiometry of the whole body, spine, hip, and forearm was performed at 0.5 and 3 mo. There were significant decreases in bone mineral content at the spine (3.96%; 95% CI: 4.86%, 3.06%), femoral neck (2.39%; 95% CI: 3.61%, 1.17%), total hip (1.51%; 95% CI: 2.45%, 0.60%), and whole body (0.86%; 95% CI: 1.29%, 0.43%) in breast-feeding mothers but not in formula-feeding mothers or nonpregnant, nonlactating women. These changes were not related to calcium intake, breast-milk calcium concentration, vitamin D-receptor genotype, postpartum weight change, or use of the progesterone-only contraceptive pill. After adjustment for bone area, breast-milk volume and height were identified as significant predictors at the spine, such that greater decreases were associated with taller mothers (P = 0.007) and those with greater breast-milk volume (P = 0.001). This finding suggests that the marked bone mineral changes observed in breast-feeding mothers represented a physiologic response to lactation that was independent of dietary calcium supply.