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.

     

Complex tibial fractures are associated with lower social classes and predict early exit from employment and worse patient-reported QOL: a prospective observational study of 46 complex tibial fractures treated with a ring fixator

The long-term outcomes following complex fractures of the tibia are reported to carry a risk of knee pain, malalignment, articular injury and post-traumatic osteoarthritis. The main objective of this study was to account for the patient-reported quality of life (QOL) 12 months after ring fixator removal in patients with a complex tibial fracture. Secondary objectives included a review of the socio-economic characteristics of the patient group and the rate of return to work in the study period. A prospective follow-up study was conducted of 60 patients with complex fractures of the tibia treated with ring external fixation. Patient-reported outcomes, radiological outcomes and socio-economic status including employment status of the patients were obtained 12 months after frame removal. Forty-six patients completed the assessment 12 months after frame removal (77%). The mean age of the patient at the time of fracture was 54.6 years (range 31–86). There were 19 males and 27 females. At 12 months after frame removal, the mean EQ5D-5L index was 0.66 (CI 0.60–0.72). The mean EQ5D-5L VAS was 69 (CI 61–76). When this was compared to the established reference population from Denmark, the study population showed a significantly worse EQ5D-5L index. The majority of patients (87%) were in the lower social classes suggesting a higher degree of social deprivation in the study population. Twenty-seven per cent of patients who were employed prior to injury had returned to employment at approximately 19 months following fracture. The onset of post-traumatic osteoarthritis was present in the knee joint in 29% of patients following a proximal intra-articular fracture, whereas osteoarthritis was present at the ankle joint in 35% of patients following a distal intra-articular fracture 12 months after frame removal. This study indicates that at 12 months after frame removal there are poorer patient-reported QOL as when compared to reference populations. Furthermore, this study suggests that complex tibial fractures are associated with lower social classes and that only 27% of patients in this sample, who prior to injury were employed, had returned to employment at approximately 19 months after the injury.     

Is the risk of bipolar disorder in twins equal to the risk in singletons? A nationwide register-based study

BACKGROUND: A previous study demonstrated a higher rate of schizophrenia in dizygotic twins than in the general population, and a higher rate of schizophrenia in siblings of dizygotic twins than in siblings of monozygotic twins and singletons, pointing to a common genetic predisposition for dizygotic twinning and schizophrenia. The aim of the present study was to investigate whether these findings also apply to bipolar disorder. METHODS: Through record linkage between The Danish Twin Register, The Danish Psychiatric Central Register and The Danish Civil Registration System, the rate of bipolar disorder (diagnosed for the first time during admission to hospital) in dizygotic and monozygotic twins was compared with the rate in singletons, and the rate in siblings and parents of twins was compared with the rate in siblings and parents of singletons. RESULTS: The rate of bipolar disorder was the same in dizygotic twins, monozygotic twins and singletons as well as for parents and siblings of dizygotic twins, monozygotic twins and singletons. LIMITATIONS: The study is a register-based study, only including hospitalized patients. CONCLUSION: This study shows that there is an equal rate of bipolar disorder in twins and in singletons. Assuming that DZ twinning is under some genetic influence, a differential relationship between schizophrenia and DZ twinning on one hand and bipolar disorder and DZ twinning on the other hand may suggest differences in the genetic basis of the two diseases. The finding that the rate of bipolar disorder in monozygotic twins is the same as the rate of bipolar disorder in singletons supports studies finding no association between bipolar disorder and obstetric complications.     

Campylobacter coli isolates derived from chickens in Senegal: Diversity, genetic exchange with Campylobacter jejuni and quinolone resistance

We used the multilocus sequence typing (MLST) method to study the genetic diversity of Campylobacter coli isolated from chickens in Senegal, and to check the presence of genetic exchange with Campylobacter jejuni. In addition, we assessed the resistance of the isolates to ciprofloxacin and nalidixic acid, and their gyrA sequences. MLST revealed a low level of diversity and the absence of lineages among C. coli isolates. In addition, an exchange of alleles with C. jejuni was found. Twenty percent of the ciprofloxacin-resistant isolates lacked mutations within the quinolone resistance-determining region (QRDR) of GyrA. There was no link between quinolone resistance and sequence type (ST).     

A new multiplex PCR for easy screening of methicillin-resistant Staphylococcus aureus SCCmec types I–V

A multiplex PCR with four primer-pairs was designed to identify the five main known SCCmec types. A clear and easily discriminated band pattern was obtained for all five types. The SCCmec type was identified for 98% of 312 clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA). SCCmec type IV was by far the most common SCCmec type among both hospital- and community-acquired MRSA isolates in Denmark.     

Renin secretion from permeabilized juxtaglomerular cells requires a permeant cation

 The cytosolic concentration of chloride correlates directly with renin secretion from renal juxtaglomerular granular (JG) cells. In the present study, the mechanism by which chloride stimulates renin release was investigated in a preparation of permeabilized rat glomeruli with attached JG cells. An isosmotic increase in the concentration of chloride by 129 mM stimulated renin release 16- to 20-fold. Substitution of K⁺ by the impermeant cation N-methyl-d-glucamine (NMDG) abolished this response, while substitution with Na⁺ caused marginal inhibition. Substitution with Cs⁺ had no effect. Addition of sucrose, which permeates the secretory granules poorly, also abolished the stimulation of renin secretion by KCl. The response to KCl was not affected by K⁺-channel antagonists or by agonists of K⁺ channels. Chloride channel blockers were also without effect on the secretory response to KCl. When the ATP concentration was lowered from 1 to 0.1 mM renin release was stimulated, while an increase in the ATP concentration from 1 to 5 mM had no effect. Blockers of ATP-sensitive (K_ATP) channels did not modify the response to chloride. The present data suggest that chloride stimulates renin release after entry of KCl into the renin secretory granules which results in swelling and release of renin. Received: 3 July 1998 / Received after revision: 9 September 1998 / Accepted: 8 October 1998     

Characterization of a culturable "Gastrospirillum hominis" (Helicobacter heilmannii) strain isolated from human gastric mucosa

Spiral organisms were isolated from an antral gastric mucosal biopsy specimen from a dyspeptic patient with gastritis. Only corkscrew-shaped organisms resembling "Gastrospirillum hominis" ("Helicobacter heilmannii") but no Helicobacter pylori-like organisms were seen in histological sections. H. pylori was not cultured from specimens from this patient. On the basis of biochemical reactions, morphology, ultrastructure, and 16S DNA sequencing, the isolated "G. hominis" was shown to be a true Helicobacter sp. very similar to Helicobacter felis and the "Gastrospirillum" but was separate from H. pylori. "G. hominis" is a pleomorphic gram-negative cork-screw-shaped, motile rod with 3 to 8 coils and a wavelength of about 1 micrometer. In contrast to H. pylori, it has up to 14 sheathed flagellar uni- or bipolar fibrils but no periplasmic fibrils. "G. hominis" grows under microaerobic conditions at 36 and 41 degrees C on 7% lysed, defibrinated horse blood agar plates within 3 to 7 days and can be subcultured under microaerobic but not under anaerobic conditions on media similar to those used for H. pylori and H. felis. The small translucent colonies were, in contrast to those of H. felis, indistinguishable from those of H. pylori. "G. hominis" is, like H. pylori and H. felis, motile, is oxidase, catalase, nitrite, nitrate, and urease positive, and produces alkaline phosphatase and arginine arylamidase. Like H. pylori and H. felis, it is sensitive to cephalothin (30-microgram disc), resistant to nalidixic acid (30-microgram disc), and sensitive to most other antibiotics. The 16S DNA sequence clusters "G. hominis" together with "Gastrospirillum," H. felis, Helicobacter bizzozeronii, Helicobacter salmonii, Helicobacter nemestrinae, Helicobacter acinonychis, and H. pylori.     

Selective immunolesion of cholinergic neurons leads to long-term changes in 5-HT2A receptor levels in hippocampus and frontal cortex

Although loss of cholinergic neurons in the basal forebrain is considered a key initial feature in Alzheimer's disease (AD), changes in other transmitter systems, including serotonin and 5-HT_2A receptors, are also associated with early AD. The aim of this study was to investigate whether elimination of the cholinergic neurons in the basal forebrain directly affects 5-HT_2A receptor levels. For this purpose intraventricular injection of the selective immunotoxin 192 IgG-Saporin was given to rats in doses of either 2.5 or 5 μg. The rats were sacrificed after 1, 2, 4 and 20 weeks. 5-HT_2A protein levels were determined by western techniques in frontal cortex and hippocampus. A significant 70% downregulation in frontal cortex and a 100% upregulation in hippocampus of 5-HT_2A receptor levels were observed 20 weeks after the cholinergic lesion when using the highest dose of 192 IgG-Saporin. Our results show that cholinergic deafferentation leads to decreased frontal cortex and increased hippocampal 5-HT_2A receptor levels. This is probably a consequence of the interaction between the serotonergic and the cholinergic system that may vary depending on the brain region.     

CLEC-2 signaling via Syk in myeloid cells can regulate inflammatory responses

Myeloid cells express a plethora of C-type lectin receptors (CLRs) that can regulate immune responses. CLEC-2 belongs to the Dectin-1 sub-family of CLRs that possess an extracellular C-type lectin-like domain and a single intracellular hemITAM motif. CLEC-2 is highly expressed on mouse and human platelets where it signals via Syk to promote aggregation. We generated a monoclonal antibody (mAb) against mouse CLEC-2 and found that CLEC-2 is additionally widely expressed on leukocytes and that its expression is upregulated during inflammation. MAb-mediated crosslinking of CLEC-2 leads to hemITAM-dependent signaling via Syk, Ca(2+) and NFAT and, in myeloid cells, modulates the effect of toll-like receptor (TLR) agonists to selectively potentiate production of IL-10. A macrophage/dendritic cell-dependent increase in IL-10 is also observed in mice given anti-CLEC-2 mAb together with LPS. Collectively, these data indicate that CLEC-2 is expressed in myeloid cells and acts as a Syk-coupled CLR able to modulate TLR signaling and inflammatory responses.