Community Connectors (CCx): the strategies employed by peer to peer connectors to foster relationships with early years caregivers to improve universal early child health and development.

Blackpool is one of the most deprived Local Authority (LA) areas in England; in April 2015 the Blackpool Better Start (BBS) Partnership was allocated £45 million over 10 years from the Big Lottery Fund (BLF) as one of five 'A Better Start' initiative areas in England. The aim of the 'A Better Start' initiative is to improve outcomes for children from conception to 3 years of age. Co-designed by professionals and the community, the Community Connector (CCx) programme employs residents to directly engage caregivers of children, in seven of Blackpool's most socio-economically deprived wards. The CCx follow a socioecological framework which proposes that caregivers will be positively influenced to engage in early years activities because of connections to trained peers. Peer support models are commonly applied within targeted early years health settings (i.e., infant feeding support, literacy) yet their role to improve child outcomes at a universal level has received little attention. This paper focuses on caregiver-level evidence of the strategies employed by CCx - part of an early stage pilot study supported by Frontiers of Innovation, the Harvard Centre on the Developing Child's Research and Development platform.The study collated attendance data from Children's Centres, these are publically funded community centres providing information and activities for families with children 0-5 years of age. The study data included individual interactions between a CCx and caregiver over a 1 year period (1st April 2018 - 31st March 2019). A sampling frame was created from which a total of 22 interviews with caregivers were undertaken in early years community settings. The interview data was thematically analysed; the findings highlighted the mechanisms by which CCx served to mediate service and caregiver communication boundaries, negotiate access to spaces, and encouraged sustained engagement in longer term activities such as volunteering and training. Value was embedded by the CCx in their process of establishing and maintaining connections with caregivers through the 'everyday' conversations, their individualised approach and in demonstrating self-efficacy behaviours. Further research is required to review the impact of the CCx role in caregiver's recall of early years information, nevertheless the study provided important learning for establishing formalised CCx programmes elsewhere, and has implications for community health and early years policy and practice.

[The Médicins sans Frontières HIV/AIDS programme in Ukraine]. / Het hiv/aidsprogramma van Artsen zonder Grenzen in Oekraïne.

In 1999, Médicins sans Frontières started an HIV/AIDS programme in Ukraine, a country with an estimated 410,000 people with HIV (1.4% prevalence), including 53,000 in urgent need of antiretroviral therapy. Between 1999 and 2004, a comprehensive HIV/AIDS programme was implemented in close collaboration with the Ministry of Health in AIDS centres in Odessa, Mikolaev and Simferopol. Initial activities included prevention and treatment advocacy campaigns, which were later followed by prevention of mother-to-child transmission, treatment of opportunistic infections, antiretroviral therapy for infants and adults and palliative care. This programme has served as a model and has led to meaningful improvements in HIV/AIDS care in Ukraine. It demonstrates that adequate care for patients with HIV or AIDS is possible in countries like Ukraine.

An evaluation of germinating beans as a source of vitamin C in refugee foods.

OBJECTIVE: To assess whether germinating pulses and beans are a potential source of vitamin C in rations for refugee communities with poor vitamin C status. DESIGN: High pressure liquid chromatographic assessment of vitamin C content of a range of legumes following germination in light and dark and after cooking. RESULTS: Many species of pulses produced significant quantities of vitamin C up to five days following germination in both light and dark although cooking caused a marked loss of ascorbate. CONCLUSION: Germination of approximately half of the seeds of the pulse constituents of many basic rations would be likely to generate, within a 3-5 d germination period, sufficient ascorbate to provide the 10 mg needed to protect adults against the development of scurvy.

Micronutrient status of the besieged residents of Sarajevo: May 1993.

OBJECTIVE: To assess micronutrient status indices in blood and plasma of subjects subjected to siege conditions. DESIGN: Whole blood and serum samples were taken from subjects, sampled from 30 clusters in four Municipal Areas of Sarajevo. The blood samples were flown, under appropriate refrigeration, to the UK for analysis. SETTING: The study was conducted in besieged Sarajevo and laboratory analyses were carried out at Department of Clinical Chemistry, Aberdeen Royal Infirmary and at Rowett Research Institute, Aberdeen, Scotland. SUBJECTS: 202 subjects, aged from 1 to 82 years were included in the sample. INTERVENTIONS: Serum folate, ferritin, transferrin, retinol, retinol-binding protein, beta-carotene, alpha-tocopherol, 25-hydroxycholecalciferol, C-reactive protein, haemoglobin and mean corpuscular volume of blood were determined. Micronutrient status was assessed by comparison with a range of values derived from multinational data sets from both pathologically malnourished and normal subjects. RESULTS: Haemoglobin, ferritin, folate, retinol and 25-hydroxycholecalciferol levels were lower in the Sarajevan sample than in normal reference populations. Serum alpha-tocopherol was low in children and adolescents while a low beta-carotene level probably reflected the scarcity of green vegetables. No consistent evidence of protein/energy deficits were detected. CONCLUSIONS: Data for retinol binding protein and transferrin, when considered in association with BMI and Z-score data, provided no significant evidence of protein-energy undernutrition. However, the prevailing food aid rations failed to maintain adequate reserves of several micronutrients, particularly iron, folate and vitamin D. The significance of low values for serum retinol and beta-carotene and of low serum alpha-tocopherol in children must be investigated further.

Reduction of radiocaesium absorption by sheep consuming feed contaminated with fallout from Chernobyl.

Two compounds, a zeolite, clinoptilolite, and a ferrocyanide, potassium hexacyanocobalt (II) ferrate (II), were found to be the most effective adsorbers of caesium in vitro. When used in vivo they significantly reduced the absorption of caesium by sheep fed contaminated herbage. These compounds did not alter the rate of excretion of pre-absorbed caesium, which varied with the time from cessation of contamination.

Copper deficiency and tissue glutathione concentration in the rat.

Copper deficiency in rats increased renal vein and arterial (heart) plasma GSH concentration by approximately 50%. There was no change in plasma GSSG concentration. Renal vein plasma GSSG/GSH ratio was decreased in copper deficiency, which is consistent with previous reports showing a copper-dependent thiol oxidase activity in the renal basement membrane. No change occurred in arterial plasma GSSG/GSH ratio. Hepatic GSH concentrations were also elevated by 50% in copper deficiency, GSSG concentrations were unaffected, but GSSG/GSH ratio was depressed. Renal and cardiac tissue GSH and GSSG were unaffected by copper deficiency. The decreased SOD activity and GSH-Px activity observed in copper deficiency may contribute to increased hepatic and plasma GSH concentrations.

Biochemical and physiological indicators of mineral status in animals: copper, cobalt and zinc.

The value of estimates of trace element requirements or of data on tissue trace element content for identifying and controlling trace element-related disorders is often limited by inadequate data on the relationships of such criteria to physiological performance. Investigations of metabolic events initiating early pathological responses to deficiency are beginning to suggest more effective indicators of physiologically relevant abnormalities in trace element intake or status. Progress in studies of metabolic responses to deficiencies of copper, cobalt and zinc is reviewed.

Stimulation of peroxidation in rat liver microsomes by (copper, zinc)-metallothioneins.

The abilities of pig liver (copper, zinc) metallothionein I and rat liver zinc metallothionein II to modify lipid peroxidation in incubations of liver microsomes have been compared with the activities of reduced glutathione, mannitol, quinacrine, EDTA, dimethyl-pyrroline-N-oxide and phenyl-butyl-nitrone. Lipid peroxidation was determined by assay of thiobarbituric acid reactive substance formation in incubations of microsomes with iron/ADP or a mixture of xanthine and xanthine oxidase. Zinc metallothionein II had no effect on the extent of peroxidation in either system but (copper, zinc) metallothionein I caused a stimulation of peroxidation initiated by xanthine and xanthine oxidase, all other compounds tested were inhibitory. Gel exclusion chromatography of incubations of (copper, zinc) metallothionein I with xanthine and xanthine oxidase revealed aggregation of the metalloprotein. This may have exposed copper in a form capable of initiating peroxidation.

Tissue damage in vitamin E deficient rats is not detected by expired ethane and pentane.

Despite evidence for tissue damage in vitamin E deficient rats, no discernible difference in ethane and pentane production was apparent compared with controls. It is suggested that other sources of hydrocarbons may mask hydrocarbon production from peroxidation of polyunsaturated fatty acid components of cell membranes, or that tissue damage occurs before peroxidation of the polyunsaturated fatty acids.

Use of ammonium tetrathiomolybdate in the treatment of copper poisoning in sheep.

Intravenous administration of ammonium tetrathiomolybdate (three doses on alternate days) appeared to be an effective means of containing the acute phase of copper toxicity in sheep, whether this arose from continuous ingestion of high copper feeds or by injudicious use of copper preparations for the control of copper deficiency. No adverse effects were recorded on lamb numbers, birth weight or survival of lambs born to ewes of normal to low copper status when the treatment was applied at sensitive periods of the reproductive cycle. Decreases in 'available' plasma copper and in liver damage occurred rapidly in response to intravenous tetrathiomolybdate and it is suggested that all animals at risk be treated.

Effects of dietary copper, cadmium, iron, molybdenum and manganese on selenium utilization by the rat.

The possible antagonistic effects of different dietary concentrations of copper (1.3-200 mg/kg), cadmium (1-5 mg/kg), iron (20-500 mg/kg), molybdenum (0.3-50 mg/kg) and manganese (0.2-200 mg/kg) on selenium utilization by the rat were studied by the measurement of the absorption and organ distribution of dietary selenium as [75Se]selenite and by effects on organ glutathione peroxidase (GSH-Px: EC 1.11.1.9) activity. Although a high concentration of copper (200 mg/kg) in the diet did not alter the percentage absorption and total-body retention of doses of 75SeO3(2)- by rats, after such treatment tissue 75Se distribution was changed and was lower total selenium in some tissues. After copper treatment (200 mg/kg diet) GSH-Px activity of liver, testis, kidney and whole blood was also lower. Dietary cadmium, iron, molybdenum and manganese at the concentrations investigated had no significant effects on selenium metabolism. Thus it is unlikely that copper, cadmium, iron, molybdenum and manganese at normal dietary concentrations will have a major effect on selenium metabolism in the rat, especially if adequate amounts of selenium are being consumed.

Studies on the effects of copper deficiency on rat liver mitochondria. II. Effects on oxidative phosphorylation.

Effects of dietary copper deficiency in rats on respiratory enzymes of isolated rat liver mitochondria have been studied. After 2 weeks of Cu-depletion, cytochrome c oxidase (EC 1.9.3.1) activity had declined by 42% and between 4 and 8 weeks exhibited between 20 and 25% of the activity of control mitochondria. Activities of NADH cytochrome c reductase (EC 1.6.99.3) and succinate cytochrome c reductase (EC 1.3.99.1), were unaffected initially but declined by 32 and 46%, respectively, after 8 weeks of Cu-depletion. After 4 weeks there was a significant (34%) decline in succinate supported state 3 respiration with only a modest (18%) decline in state 4 respiration. The ADP:O ratio was unaffected by Cu-depletion after 6 and 8 weeks of dietary Cu-restriction. State 3 respiration was significantly reduced after 6 weeks when glutamate/malate or beta-hydroxybutyrate were used as substrates, whereas state 4 respiration and ADP:O ratios were unaffected. The fall in state 3 respiration was of sufficient magnitude at 8 weeks to cause a significant decline in the respiratory control ratio with all substrates. Comparisons between the relative activities of cytochrome c oxidase and reductase activities in Cu-deficient preparations, the relatively specific effect of the deficiency on state 3 respiration with all substrates tested and the ability to increase significantly oxygen consumption in excess of maximal state 3 respiration by the uncoupler 2,4-dinitrophenol suggest that the defect in Cu-deficient mitochondria cannot be attributed solely to the decreased activity of cytochrome c oxidase.

Studies on the effects of copper deficiency on rat liver mitochondria. I. Changes in mitochondrial composition.

As part of an investigation of the lesions of copper (Cu) deficiency a study was undertaken of the copper, iron, cytochrome and fatty acid composition of liver mitochondria from Cu deficient and Cu-adequate control rats. Cu concentrations were significantly decreased in whole liver, liver mitochondria and in blood plasma. Total iron was significantly increased in whole liver but remained at the normal level in mitochondria. Cytochrome c oxidase (EC 1.9.3.1) and its component cytochromes a and a3 were significantly reduced in liver mitochondria from Cu-deficient rats, whereas there was no effect on the concentration of cytochromes b, c1 and c. Evidence from comparisons between cytochrome c oxidase activity and the amount of enzyme present, as assessed from the mitochondrial cytochrome a and a3 content, suggests that in addition to an absolute loss of enzyme, Cu-deficiency adversely affects the efficiency of the residual enzyme. Severe Cu deficiency had no effect on 'ageing' or 'swelling' properties of liver mitochondria, indicating no marked effects on fatty acid composition. Fatty acid analyses demonstrated a slight but significant increase in docosapentenoic acid (22:5) of Cu-deficient mitochondria, but since this represents a minor component there was no change observed in the 'unsaturation index'. It was concluded that, in contrast to previous reports, Cu deficiency of the severity reported did not have a deleterious effect on the integrity and permeability of the inner mitochondrial membrane as exemplified by any qualitative modification of fatty acid constitution per se.

The effects of dietary sulfur on selenium utilization by the rat.

The antagonistic effects of S on Se utilization were studied by measurement of tissue Se concentrations and glutathione peroxidase (GSHpx, E.C.1.11.1.9) activities in rats offered Torula yeast-based diets supplemented with sodium sulfate to provide 1.5, 3, or 5 g S/kg diet. Increasing sulfur concentrations in the diet caused small but significant decreases in GSHpx activity of liver, spleen, heart, lung small intestine, and skeletal muscle. Also significantly decreased were Se concentrations in liver and hair. Dietary sulfur content had no significant effect on body weight gain of the rats. With an adequate supply of Se in the diet, there are probably no major deleterious effects of dietary S on Se metabolism in the rat.

Selenium utilization by sheep given diets differing in sulfur and molybdenum content.

The effects of differing dietary concentrations of sulfur (0.4, 1.8, and 3.9 g/kg diet) or Mo (0.3, 3, and 5 mg/kg diet) on Se utilization, were studied in Suffolk × Finn-Dorset ewes. Se concentrations and glutathione peroxidase (E.C.1.11.1.9) activity were measured in tissues of the ewes being repleted with Se or depleted of Se in the presence of the proposed antagonists. Evidence for an antagonism between dietary S and Se was found with an inverse relationship between dietary S concentrations and the Se concentrations of liver and wool, and glutathione peroxidase activity in the liver. Molybdenum (0.3, 3, or 5 mg) in diets of the sheep (0.01 or 0.03 mg Se/kg dry matter) had no significant effects on tissue Se concentrations or glutathione peroxidase activities. With an adequate supply of Se in the diet, there are probably no major effects of S on Se availability and metabolism in the sheep. Within dietary concentrations tested, dietary Mo does not influence utilization of Se by the sheep.

Zinc absorption in celiac disease and dermatitis herpetiformis: a test of small intestinal function.

The increments in plasma zinc concentrations after an oral dose of elemental zinc (50 mg) as the sulphate were used to assess the intestinal absorption of the metal in 11 patients with dermatitis herpetiformis (DH) before starting a gluten-free diet, 12 patients with newly diagnosed celiac disease (CD), 10 patients known to have CD, and 15 healthy volunteers. The areas under the plasma zinc increment curve plotted against time were determined for 3 (AUC3) and 6 (AUC6) h. The AUC3 in healthy volunteers was 401 +/- 48 mumol 1(-1) 3 h (mean +/- SD); it was reduced in newly diagnosed CD 187 +/- 76 mumol 1(-1) 3 h (p less than 0.001), and in dermatitis herpetiformis 206 +/- 87 mumol 1(-1) 3 h (p less than 0.01); but it was normal in the known CD 396 +/- 204 mumol 1(-1) 3 h, the wide variation reflecting the variable compliance with a previously instituted gluten-free diet. The AUC6 was similarly affected, healthy volunteers 700 +/- 111 mumol 1(-1) 6 h, new CD 380 +/- 169 mumol 1(-1) 6 h (p less than 0.01); dermatitis herpetiformis 471 +/- 107 mumol 1(-1) 6 h (p less than 0.01); known CD 725 +/- 380 mumol 1(-1) 6 h. The AUC3 was more consistently abnormal than conventional tests of small intestinal function. In a prospective study the AUC3 and AUC6 improved and reflected compliance with a gluten-free diet.

Thiomolybdates in rumen contents and rumen cultures.

Examination of direct and (Cu)-difference spectra of i) the aqueous supernatants of in vitro cultures of bovine rumen contents incubated with MoO42- and potential sources of S2- and ii) samples drawn directly from the rumen of animals receiving high Mo diets yielded evidence of the presence of thiomolybdates. Only MoS42- was detected in the soluble phase of in vitro cultures. Although intense and variable background absorbance precluded full characterization of thiomolybdate species in samples drawn directly from the rumen, both spectral data and the biochemical and clinical responses of animals given high Mo diets were consistent with the conclusion that MoS42- rather than MoOS32- was the predominant thiomolybdate species present in the aqueous phase. Addition of Ca2+ either to rumen cultures before incubation or as a supplement to diets high in MoO42- content inhibited the appearance of MoS42- in the aqueous phase. Evidence of the sequestration of MoS42- and MoOS32- by particulate or microbial fractions of rumen contents is considered in relation to the inhibitory action of Mo upon Cu absorption by ruminants.

Uteroplacental dysfunction and prostaglandin metabolism in zinc deficient pregnant rats.

Relationships between perinatal mortality, disrupted utero-placental function and prostaglandin metabolism have been studied in Zn-deficient rats. Uterine contractility in vitro, placental blood flow in vivo, and uterine and placental prostaglandin synthesis from [1-14C] arachidonic acid in vitro were investigated at day 22 of pregnancy. High amplitude uterine contractions were almost completely eliminated and utero-placental blood flow was decreased by 85% by Zn deficiency. Synthesis of [1-14C]-prostaglandin E2, F2 alpha and 6-keto-F1 alpha from [1-14C] arachidonic acid decreased significantly in uterine tissue but increased in placentae. These possibly inter-related effects may contribute to the high perinatal mortality observed in Zn deficiency.

Studies on the role of zinc in parturition in the rat.

1. Pregnant rats were fed either low (less than 1 p.p.m.) Zn or control (40 p.p.m. Zn) diets from day 10 of gestation. They were killed at intervals during the last 96 h preceding the normal time for onset of parturition, and differences in plasma progesterone, oestradiol-17 beta and ovarian 20 alpha-hydroxysteroid dehydrogenase were assessed. 2. Gestation was prolonged in Zn-deficient rats. 3. Although the preparturient decline in plasma progesterone began at the same time in all groups, at term, plasma progesterone concentration in Zn-deficient rats remained significantly higher than in normal females. 4. Induction of ovarian 20 alpha-hydroxysteroid dehydrogenase activity was delayed by about 8 h by Zn deficiency. This delay was not observed if prostaglandin F2 alpha was injected previously. 5. The results suggest a Zn-dependent step(s) in uterine synthesis and/or release of prostanoids.