Deforestation reduces fruit and vegetable consumption in rural Tanzania

Strategies to improve food and nutrition security continue to promote increasing food via agricultural intensification. Little (if any) consideration is given to the role of natural landscapes such as forests in meeting nutrition goals, despite a growing body of literature that shows that having access to these landscapes can improve people’s diets, particularly in rural areas of low- and middle-income countries. In this study, we tested whether deforestation over a 5-y period (2008–2013) affected people’s dietary quality in rural Tanzania using a modeling approach that combined two-way fixed-effects regression analysis with covariate balancing generalized propensity score (CBGPS) weighting which allowed for causal inferences to be made. We found that, over the 5 y, deforestation caused a reduction in household fruit and vegetable consumption and thus vitamin A adequacy of diets. The average household member experienced a reduction in fruit and vegetable consumption of 14 g⋅d⁻¹, which represented a substantial proportion (11%) of average daily intake. Conversely, we found that forest fragmentation over the survey period led to an increase in consumption of these foods and dietary vitamin A adequacy. This study finds a causal link between deforestation and people’s dietary quality, and the results have important implications for policy makers given that forests are largely overlooked in strategies to improve nutrition, but offer potential “win–wins” in terms of meeting nutrition goals as well as conservation and environmental goals.

The challenge of achieving food and nutrition security for the worlds’ growing population while also minimizing and reversing damage to the natural environment is unprecedented. The dominant narrative on how to achieve food and nutrition security continues to be centered on intensifying agricultural production to produce more food (1–3). While agricultural intensification is undoubtedly a key reason we have kept pace with food demands and ended hunger for millions of people over the past decades, it has led to a preoccupation with dietary energy (calories), and thus the production of staple grains which provide the majority of calories globally (4, 5). The focus on staple foods has resulted in dietary quality and diversity being overlooked, despite the fact that far more people suffer from micronutrient deficiency than undernourishment (6–8). Likewise, agricultural intensification is a leading driver of environmental degradation (9–11). There has been much research in recent years examining the impact of different diets on land use (12–15), but less attention has been given to the reverse of this relationship: How do landscapes affect diets? A growing body of literature has examined this relationship with a focus on the linkages between forests and diets in low- and middle-income countries. This relatively new field of research has important implications for strategies to achieve food and nutrition security worldwide, particularly for rural areas in low- and middle-income countries where there are strong connections between livelihoods and landscapes, and undernourishment is most prevalent.Forests provide critical ecosystem services that benefit human populations in several ways, such as the provision of food and fiber, and climate and water regulation (16), with an estimated 1.5 billion forest-proximate people worldwide (i.e., living within 5 km of a forest) (17). Forests can improve people’s diets via four key pathways (18, 19). The most direct way is via the provision of wild forest foods, which most often include fruits, vegetables, mushrooms, and animal products (i.e., bushmeat and insects), all of which tend to be high in essential micronutrients (20–22). The second pathway is via income generation from the sale of forest foods and other nontimber forest products (NTFPs), which can improve livelihoods and facilitate the purchase of nutritious foods from markets (23, 24). The third pathway is via the flow of ecosystem services from forests into surrounding agricultural landscapes (e.g., forests can contribute to soil formation and nutrient cycling, and increase pollination) which can increase and/or diversify production (25). The final pathway is the provision of fuelwood for cooking, which is a key (but often overlooked) pathway that can improve nutrition by facilitating the preparation of a range of foods, particularly those with long cooking times (26, 27).The majority of studies have found a positive relationship between living near (having access to) forests and several measures of diet, nutrition, and food security outcomes. Most studies use metrics of diet quality such as dietary diversity scores or consumption of certain nutritious food groups. Very few studies have examined more detailed measures of dietary quality such as energy and nutrient intakes (28–30), and only one study has examined these in relation to forest cover using multivariate regression (31). Moreover, the majority of studies examine the relationship between forests and diet quality at a single point in time. Two studies have examined the relationship between diets and previous forest loss (32, 33), but no studies, to date, have used longitudinal data to understand concurrent changes in forests and diets over time. In this sense, most studies have only been able to identify associations between forests and diets as opposed to causal relationships. Furthermore, only one study, to date, has examined how the spatial arrangement of forests (as opposed to just forest amount) can affect people’s diets (34), finding that forest configuration may be as important as forest amount for dietary quality.This study aimed to advance the current knowledge on the forest–diet relationship in three main ways:

• 1)By using panel data and a rigorous estimation method which combines covariate balancing generalized propensity score (CBGPS) weighting with two-way fixed-effects regression, we were able to test the causal impact of forest changes on diets, which no studies, to our knowledge, have done. We were also able to explore the causal mechanisms by which forest cover change is hypothesized to affect people’s diets (the direct consumption pathway, the income pathway, and the ecosystem services pathway).
• 2)Most existing studies rely on measures such as dietary diversity scores and consumption of nutritious food groups as proxies for overall diet quality. In addition to these, we also quantified household energy and nutrient adequacy levels in order to gain a better understanding of how forests can affect people’s diets.
• 3)We considered not just forest amount but also the spatial arrangement of forests in relation to diet quality, which only one study has done, to date (34). Thus, this study aimed to extend this research to examine whether changes in forest configuration [in terms of fragmentation (35)] were related to people’s dietary quality.

     

Elliptical posts allow for detailed control of non-equibiaxial straining of cell cultures

BackgroundA modification of the Flexcell system that allows imposition of homogenous, controlled non-equibiaxial strains to cell cultures is developed and experimentally validated. The Flexcell system by default applies equibiaxial strain to cell cultures, meaning no shear strain, while soft tissue cells in vivo are subjected to a range of mechanical deformations including shear strain caused by activities of daily living. Shear strains are suspected to play an important role in tissue necrosis.MethodThe Flexcell system was redesigned using a finite element model in order to obtain large areas of the membrane in a controlled, uniform non-equibiaxial strain state.ResultsThe redesign was manufactured and the resulting strains were experimentally validated by means of image analysis methods. The results showed that the system could be used for experiments varying the shear strain.ConclusionThe result allows scientists and experimentalists to apply detailed control of the strain tensor applied to tissue samples in two dimensions.     

The Influence of Beta-Blocking Agents on Plasma Volume and Extracellular Volume in Ischaemic Heart Disease

Plasma volume and extracellular volume (sodium space) were found to be unchanged during treatment with propranolol (nine patients) and practolol (four patients) for well-compensated ischaemic heart disease. The volumes were determined before treatment and 2 days and 3 months after optimal dose for each patient was reached.     

The cholinomimetic agent carbachol induces headache in healthy subjects

The parasympathetic nervous system is likely to be involved in migraine pathogenesis. We hypothesized that the cholinomimetic agonist carbachol would induce headache and vasodilation of cephalic and radial arteries. Carbachol (3 µg/kg) or placebo was randomly infused into 12 healthy subjects in a double-blind crossover study. Headache was scored on a verbal rating scale from 0–10. Velocity in the middle cerebral artery (V_MCA) and diameter of the superficial temporal artery (STA) and radial artery (RA) were recorded. Nine participants developed headache after carbachol compared with three after placebo. The area under the curve for headache was increased after carbachol compared with placebo both during infusion (0–30 min) ( P  = 0.042) and in the postinfusion period (30–90 min) ( P  = 0.027). Carbachol infusion caused a drop in V_MCA ( P  = 0.003) and an increase in STA diameter ( P  = 0.006), but no increase in the RA diameter ( P  = 0.200). In conclusion, the study demonstrated that carbachol caused headache and dilation of cephalic arteries in healthy subjects.     

Randomised clinical trials in the Scandinavian Journal of Rheumatology

OBJECTIVE: To identify all reports of randomised clinical trials in the Journal and compare our findings with reports available in Medline. METHODS: We handsearched the Scandinavian Journal of Rheumatology with supplements for the years 1955-1997 to identify reports of randomised clinical trials and controlled clinical trials. RESULTS: We identified 445 trial reports. In Medline, 134 of these trials (30%) were indexed as randomised or controlled trials; an additional 50 trials (11%) were available in Medline but were indexed differently. Thus, 261 of the trials (59%) we identified were not indexed in Medline; most of these trials were published in supplements to the Journal. CONCLUSION: Handsearching of medical journals for randomised trials can be a worthwhile effort. Clinicians and patients will become better informed about the value of different treatment options and researchers will reduce their risk of performing trials that are unnecessary.     

Studies on singlet oxygen formation and UVA light-mediated photobleaching of the yellow chromophores in human lenses

The protein-bound chromophores, which increase with aging in the human lens, act as UVA sensitizers, producing almost exclusively singlet oxygen in vitro. Direct irradiation of whole, aged human lenses with high intensity UVA light (200 mW cm(-2) for 24 hr), however, failed to produce singlet oxygen damage, as evidenced by the lack of either His or Trp photodestruction. Total homogenates of human lenses prepared in a cuvette under air did show destruction of His and Trp residues by UVA light, but no destruction was seen when equivalent homogenates were prepared under argon. These data are consistent with the idea that the low oxygen levels in the lens prevent singlet oxygen damage in vivo.UVA irradiation of aged human lenses in culture caused an extensive photobleaching of the yellow chromophores. A time course indicated that the photobleaching increased with time, with significant color loss apparent after 6 hr. Homogenization of the irradiated and dark control lenses in 6 M guanidine-HCl, followed by determination of the difference spectrum, showed approximately 50% bleaching of compounds with a lambda(max) at 355 nm. Similarly, fluorophores with a lambda(max) for excitation of 355 nm and for emission of 420 nm were 50% destroyed by the UVA light. Similar results were obtained in vitro by the anaerobic irradiation of a sonication-solubilized WI fraction from type II brunescent cataracts and from aged human lenses. In this system, there was an initial bleaching of 15% after 30 min of irradiation, followed by a slow increase over the next 6 hr to a final bleaching of 30%. The addition of 1.0 m M ascorbic acid, but not 1.0 m M glutathione (GSH), increased the photobleaching to 60% under argon, and the loss of ascorbate could be detected under these anaerobic conditions. In the presence of air, UVA light produced no photobleaching, but rather caused a three-fold increase in absorbance at 345 nm, which was prevented by the inclusion of 1.0 m M ascorbic acid and almost 50% inhibited by 1.0 m M GSH.The data are consistent with the conversion of the triplet state of the sensitizers to anion and cation radicals in the absence of oxygen. Photobleaching may occur either by dismutation of the anion radical or by reduction of the anion radical by ascorbate via type I chemistry. UVA irradiation of an enriched fraction of sensitizers from a proteolytic digest from type II cataract lenses produced a 63% bleaching at 330 nm in the absence of oxygen, and the almost complete loss of the A(330) absorbing and 350/450 nm fluorescent peaks upon HPLC separation. This loss correlated with the loss of the ability of the irradiated fraction to produce singlet oxygen in vitro upon subsequent UVA irradiation.     

Free and glucuronidated olanzapine serum concentrations in psychiatric patients: influence of carbamazepine comedication

The influence of carbamazepine on the glucuronidation of the antipsychotic olanzapine was studied in a group of psychiatric patients. Steady-state serum concentrations of free and glucuronidated olanzapine were measured in 31 psychiatric patients in monotherapy (dose range, 2.5-30 mg/d; median, 15 mg/d) and in 16 patients being comedicated with carbamazepine (dose range, 5-50 mg/d; median, 20 mg/d). The concentrations were determined by HPLC with and without acid hydrolysis of glucuronidated olanzapine. For the monotherapy group, the concentrations of free and glucuronidated olanzapine ranged from 0 nmol/L to 292 nmol/L (median, 94 nmol/L) and from 0 nmol/L to 180 nmol/L (median, 27 nmol/L), respectively. The serum concentrations of the carbamazepine-treated group ranged from 21 nmol/L to 310 nmol/L (median, 81 nmol/L) and from 0 to 376 nmol/L (median, 57 nmol/L) for free and glucuronidated olanzapine, respectively. Two patients with outlying values were excluded from further analysis. The median concentration-to-daily dose ratios (C/D) of free and glucuronidated olanzapine in the monotherapy group were 5.8 nmol/L/mg and 2.2 nmol/L/mg, respectively (n =30). The corresponding values for the group comedicated with carbamazepine were 3.6 and 3.1 nmol/L/mg (n =15). Thus, the median C/D of free olanzapine in the carbamazepine group was 38% lower than that of the monotherapy group (P <0.01), confirming that carbamazepine accelerates the metabolism of olanzapine. Further, for the carbamazepine group the median glucuronidated olanzapine fraction constituted 79% of the free fraction compared with 43% for the monotherapy group (P <0.01), which suggests that an increased rate of olanzapine glucuronidation contributes to the increased rate of metabolism of olanzapine induced by carbamazepine.