Effects of a comprehensive nutrition education programme to change grade 4 primary-school students’ eating behaviours in China

Objective: As part of a national initiative to reduce child obesity, a comprehensive school-based nutrition education intervention to change eating behaviours among grade 4 primary-school students was developed, implemented and evaluated. Design: The intervention was developed by school staff, with technical assistance from outside health education specialists. The programme included school facility upgrades, school teacher/staff training, curriculum changes and activities for parents. Student scores on nine key eating behaviours were assessed prior to and after the programme. The quality of programme implementation in the schools was monitored by technical assistance teams. Setting: Shandong Province (high household income) and Qinghai Province (low household income), China. Three programme schools and three control schools in each province. Participants: Students in grade 4 (age 8–9 years). Results: There were significant positive changes in self-reported eating behaviour scores from pre- to post-assessment in programme schools. At post-test students in programme schools had significantly higher scores than students in control schools after controlling for other variables. The programme was more effective in the highincome province. Observations by the technical assistance teams suggested the programme was implemented more completely in Shandong. The teams noted the challenges for implementing and evaluating programmes like these. Conclusions: This intervention increased healthy eating behaviours among 4th graders in both provinces and had more effect in the more affluent province. Results suggest that a scaled-up initiative using existing school and public health resources could change eating practices in a large population over time. The intervention also provided lessons for implementing and evaluating similar nutrition programmes

A multicentre trial of voltaren in the treatment of rheumatoid arthritis

Voltaren, a compound with analgesic, anti-inflammatory and antipyretic properties, has been compared at two dose levels-25 mg t.d.s. and 50 mg t.d.s. with indomethacin 25 mg t.d.s. and acetylsalicylic acid 1 500 mg t.d.s. Ninety-one patients with definite or classical rheumatoid arthritis took part in this study. The trial was a doubleblind cross-over study, with each  medication being given for one week. Patients were washed out for one week prior to the first active treatment. Each patient received only two of the four possible treatments. Voltaren in a dose of 25 mg t.d.s. was found to improve the symptoms of rheumatoid arthritis to a greater degree than indomethacin or acetylsalicylic acid. Voltaren 50 mg t.d.s. evoked a greater response than acetylsalicylic acid and was at least as efficacious as indomethacin. Voltaren was better tolerated than either indomethacin or acetylsalicylic acid. The incidence of gastro-intestinal side-effects was similar with Voltaren and indomethacin, and half that produced by acetylsalicylic acid. Some evidence of possible drug interaction was found.S. Afr. Med. J., 48, 2013 (1974)

The effects of electrical hippocampal kindling of seizures on amino acids and kynurenic acid concentrations in brain structures

Our study demonstrated that the development of seizures during the electrically induced kindling of seizures is associated with significant changes in the concentration of kynurenic acid (KYNA) and its precursor, tryptophan (TRP). The primary finding of our study was an increase in KYNA levels and the KYNA/TRP ratio (a theoretical index of activity of the kynurenine pathway) in the amygdala and hippocampus of kindled animals. We also found decreases in the concentration of tryptophan in the hippocampus and prefrontal cortex. Changes in the concentration of KYNA and TRP in the amygdala were accompanied by a significant decrease in γ-Aminobutryic Acid (GABA) levels and an increase in the glutamate/GABA ratio. Moreover, we found a significant negative correlation between the local concentrations of KYNA and glutamate in the amygdala of kindled rats. However, there were no changes in the local concentrations of the following amino acids: glutamate, aspartate, glutamine, glycine, taurine and alanine. In conclusion, these new results suggest a modulatory influence of KYNA on the process of epileptogenesis, characterized by a negative relationship between the KYNA and glutamate systems in the amygdala

Coronavirus (COVID-19) infection in children at a specialist centre: outcome and implications of underlying ‘high-risk’ comorbidities in a paediatric population

Background: There is evolving evidence of significant differences in severity and outcomes of coronavirus disease 2019 (COVID-19) in children compared to adults. Underlying medical conditions associated with increased risk of severe disease are based on adult data, but have been applied across all ages resulting in large numbers of families undertaking social ‘shielding’ (vulnerable group). We conducted a retrospective analysis of children with suspected COVID-19 at a Specialist Children’s Hospital to determine outcomes based on COVID-19 testing status and underlying health vulnerabilities. Methods: Routine clinical data were extracted retrospectively from the Institution’s Electronic Health Record system and Digital Research Environment for patients with suspected and confirmed COVID-19 diagnoses. Data were compared between Sars-CoV-2 positive and negative patients (CoVPos / CoVNeg respectively), and in relation to presence of underlying health vulnerabilities based on Public Health England guidance. Findings Between 1st March and 15th May 2020, 166 children (<18 years of age) presented to a specialist children’s hospital with clinical features of possible COVID-19 infection. 65 patients (39.2%) tested positive for SARS-CoV-2 virus. CoVPos patients were older (median 9 [0.9 - 14] years vs median 1 [0.1 - 5.7.5] years respectively, p<0.001). There was a significantly reduced proportion of vulnerable cases (47.7% vs 72.3%, p=0.002), but no difference in proportion of vulnerable patients requiring ventilation (61% vs 64.3%, p = 0.84) between CoVPos and CoVNeg groups. However, a significantly lower proportion of CoVPos patients required mechanical ventilation support compared to CoVNeg patients (27.7 vs 57.4%, p<0.001). Mortality was not significantly different between CoVPos and CoVNeg groups (1.5 vs 4% respectively, p=0.67) although there were no direct COVID-19 related deaths in this highly preselected paediatric population. Interpretation COVID-19 infection may be associated with severe disease in childhood presenting to a specialist hospital, but does not appear significantly different in severity to other causes of similar clinical presentations. In children presenting with pre-existing ‘COVID-19 vulnerable’ medical conditions at a specialist centre, there does not appear to be significantly increased risk of either contracting COVID-19 or severe complications, apart from those undergoing chemotherapy, who are over-represented. Competing Interest Statement The authors have declared no competing interest. Funding Statement: Funding RI is funded by a British Heart Foundation Research Fellowship Grant. HH is funded by NIHR UCLH BRC and HDRUK, NJS is funded by GOSHCC and HDRUK. Role of the funding source The study sponsor / funders had no role or influence in study design, in the collection, analysis, and interpretation of data, in the writing of the report or in the decision to submit the paper for publicatio

TRIM37 interacts with PTEN to promote the growth of human T-cell acute lymphocytic leukemia cells through regulating PI3K/AKT pathway

BackgroundTRIM37 has been reported to be associated with the tumorigenesis of cancers. However, the role of TRIM37 in T-cell acute lymphoblastic leukemia (T-ALL) remains unclear. This study aimed to characterize the effect of TRIM37 on T-ALL.MethodsTRIM37 expression in T-ALL patients and T-ALL cell lines was determined by qRT-PCR and Western blot. Knockdown or overexpression of TRIM37 was conducted by transferring small-interfering TRIM37 or lentivirus-mediated transducing into T-ALL cells. CCK-8 assay and flow cytometry assay were conducted to analyze the proliferation and apoptosis of T-ALL cells. Co-immunoprecipitation experiments were conducted to investigate the relationship between TRIM37 and PTEN and the ubiquitination of PTEN.ResultsOur results suggested that TRIM37 expression was upregulated in the blood of T-ALL patients and T-ALL cell lines. Knockdown of TRIM37 noticeably inhibited the proliferation and promoted apoptosis of T-ALL cells. Ectopic expression of TRIM37 promoted the proliferation and suppressed the apoptosis rate of MOLT-4 cells and enhanced the phosphorylation of AKT. Moreover, TRIM37 interacted with PTEN and accelerated the degradation of PTEN via TRIM37-mediated ubiquitination in T-ALL cells. Moreover, TRIM37 reduced the sensitivity of T-ALL cells to bortezomib treatment. Additionally, PI3K/AKT signaling pathway was involved in the function of TRIM37 in T-ALL. TRIM37 contributed to the proliferation of T-ALL cells and reduced the susceptibility of T-ALL cells to bortezomib treatment through ubiquitination of PTEN and activating PI3K/AKT signaling pathway.ConclusionsOur study suggested that TRIM37 could be considered as a therapeutic target for T-ALL

Observation of anomalous decoherence effect in a quantum bath at room temperature

Decoherence of quantum objects is critical to modern quantum sciences and technologies. It is generally believed that stronger noises cause faster decoherence. Strikingly, recent theoretical research discovers the opposite case for spins in quantum baths. Here we report experimental observation of the anomalous decoherence effect for the electron spin-1 of a nitrogen-vacancy centre in high-purity diamond at room temperature. We demonstrate that under dynamical decoupling, the double-transition can have longer coherence time than the single-transition, even though the former couples to the nuclear spin bath as twice strongly as the latter does. The excellent agreement between the experimental and the theoretical results confirms the controllability of the weakly coupled nuclear spins in the bath, which is useful in quantum information processing and quantum metrology.Comment: 22 pages, related paper at http://arxiv.org/abs/1102.557

Quark masses and mixings in the RS1 model with a condensing 4th generation

We study the hierarchy of quark masses and mixings in a model based on a 5-dimensional spacetime with constant curvature of Randall-Sundrum type with two branes, where the Electroweak Symmetry Breaking is caused dynamically by the condensation of a 4th generation of quarks, due to underlying physics from the 5D bulk and the first KK gluons. We first study the hierarchy of quark masses and mixings that can be obtained from purely adjusting the profile localizations, finding that realistic masses are not reproduced unless non trivial hierarchies of underlying 4-fermion interactions from the bulk are included. Then we study global U(1) symmetries that can be imposed in order to obtain non-symmetric modified Fritzsch-like textures in the mass matrices that reproduce reasonably well quark masses and CKM mixings.Comment: Minor changes. Version accepted for publication in JHE

Interplay between pleiotropy and secondary selection determines rise and fall of mutators in stress response

Dramatic rise of mutators has been found to accompany adaptation of bacteria in response to many kinds of stress. Two views on the evolutionary origin of this phenomenon emerged: the pleiotropic hypothesis positing that it is a byproduct of environmental stress or other specific stress response mechanisms and the second order selection which states that mutators hitchhike to fixation with unrelated beneficial alleles. Conventional population genetics models could not fully resolve this controversy because they are based on certain assumptions about fitness landscape. Here we address this problem using a microscopic multiscale model, which couples physically realistic molecular descriptions of proteins and their interactions with population genetics of carrier organisms without assuming any a priori fitness landscape. We found that both pleiotropy and second order selection play a crucial role at different stages of adaptation: the supply of mutators is provided through destabilization of error correction complexes or fluctuations of production levels of prototypic mismatch repair proteins (pleiotropic effects), while rise and fixation of mutators occur when there is a sufficient supply of beneficial mutations in replication-controlling genes. This general mechanism assures a robust and reliable adaptation of organisms to unforeseen challenges. This study highlights physical principles underlying physical biological mechanisms of stress response and adaptation

Sphingosine-1-phosphate receptor 2 protects against anaphylactic shock through suppression of endothelial nitric oxide synthase in mice

Background: Sphingosine-1-phosphate receptor 2 (S1P2) is expressed in vascular endothelial cells (ECs). However, the role of S1P2 in vascular barrier integrity and anaphylaxis is not well understood. Endothelial nitric oxide synthase (eNOS) generates nitric oxide to mediate vascular leakage, compromising survival in patients with anaphylaxis. We recently observed that endothelial S1P2 inhibits Akt, an activating kinase of eNOS. Objective: We tested the hypothesis that endothelial S1P2 might suppress eNOS, exerting a protective effect against endothelial barrier disruption and anaphylaxis. Methods: Mice deficient in S1P2 and eNOS underwent antigen challenge or platelet-activating factor (PAF) injection. Analyses were performed to examine vascular permeability and the underlying mechanisms. Results: S1pr2 deletion augmented vascular leakage and lethality after either antigen challenge or PAF injection. PAF injection induced activation of Akt and eNOS in the aortas and lungs of S1pr2-null mice, which were augmented compared with values seen in wild-type mice. Consistently, PAF-induced increase in cyclic guanosine monophosphate levels in the aorta was enhanced in S1pr-null mice. Genetic Nos3 deletion or pharmacologic eNOS blockade protected S1pr2-null mice from aggravation of barrier disruption after antigen challenge and PAF injection. ECs isolated from S1pr2-null mice exhibited greater stimulation of Akt and eNOS, with enhanced nitric oxide production in response to sphingosine-1-phosphate or PAF, compared with that seen in wild-type ECs. Moreover, S1pr2-deficient ECs showed more severe disassembly of adherens junctions with augmented S-nitrosylation of β-catenin in response to PAF, which was restored by pharmacologic eNOS blockade. Conclusion: S1P2 diminishes harmful robust eNOS stimulation and thereby attenuates vascular barrier disruption, suggesting potential usefulness of S1P2 agonists as novel therapeutic agents for anaphylaxis. © 2013 American Academy of Allergy, Asthma & Immunology

S1P2, the G protein-coupled receptor for sphingosine-1- phosphate, negatively regulates tumor angiogenesis and tumor growth in vivo in mice

金沢大学医薬保健研究域医学系Sphingosine-1-phosphate (S1P) has been implicated in tumor angiogenesis by acting through the Gi-coupled chemotactic receptor S1P1. Here, we report that the distinct receptor S1P2 is responsible for mediating the G12/13/Rho-dependent inhibitory effects of S1P on Akt, Rac, and cell migration, thereby negatively regulating tumor angiogenesis and tumor growth. By using S1P2LacZ/+ mice, we found that S1P2 was expressed in both tumor and normal blood vessels in many organs, in both endothelial cells (EC) and vascular smooth muscle cells, as well as in tumor-associated, CD11b-positive bone marrow-derived cells (BMDC). Lewis lung carcinoma or B16 melanoma cells implanted in S1P2-deficient (S1P2-/-) mice displayed accelerated tumor growth and angiogenesis with enhanced association of vascular smooth muscle cells and pericytes. S1P2-/- ECs exhibited enhanced Rac activity, Akt phosphorylation, cell migration, proliferation, and tube formation in vitro. Coinjection of S1P2-/- ECs and tumor cells into wild-type mice also produced a relative enhancement of tumor growth and angiogenesis in vivo. S1P2-/- mice were also more efficient at recruiting CD11b-positive BMDCs into tumors compared with wild-type siblings. Bone marrow chimera experiments revealed that S1P2 acted in BMDCs to promote tumor growth and angiogenesis. Our results indicate that, in contrast to endothelial S1P1, which stimulates tumor angiogenesis, S1P 2 on ECs and BMDCs mediates a potent inhibition of tumor angiogenesis, suggesting a novel therapeutic tactic for anticancer treatment. ©2010 AACR