Cooperation between Japanese and Cambodian Dietitians in Setting up a Hospital Diet Management System.

Cambodia faces a considerably high percentage of the stunted under 5 (Unicef, 2014). Despite the National Nutrition Strategy Launched by the Ministry of Health in cooperation with development partners, nutrition improvement projects have not always been effective. It is generally said these issues are addressed in many other developing nations, and the literature largely documented that successful nutrition programmes are community-based programmes because of their sustainability and the intensive communications between health workers and beneficiaries. Learning from the past experiences, the Foundation for International Development/Relief organized a project team with a Cambodian dietitian and an experienced Japanese dietitian to implement a hospital diet programme for children from April 2006 to March 2014 in the National Pediatric Hospital (NPH) in Cambodia. The project has two objectives: establishing a hospital diet management system, and developing the capacity of NPH staff. Hospital food menus were created paying particular attention to Cambodian culture, eating habits and accessibility to the ingredients for the purpose of continuous supply. We have also put emphasis on the communication between dietitians and family members of the children to let them understand the importance of a nutritious diet. After 8 y of project implementation, the hospital diet management system was established providing 7 types of menu with nutritious diets. The final evaluation of the project showed that NPH staff have the intention to continue hospital food supply with their acquired knowledge and capacity. In practice, a Cambodian dietitian currently takes the initiative for a continuous nutritional diet in NPH. The key to this success is the collaboration between Japanese dietitians with experience and Cambodian dietitians with knowledge of Cambodian eating habits. Taking our experience into account, it is highly recommended to educate Cambodian dietitians, as they are extremely scarce, and to increase the awareness of health care staff towards the importance of nutrition management.

Neuroprotection following mild hypothermia after spinal cord ischemia in rats.

OBJECTIVE: We examined the hypothesis that a 1°C reduction in body temperature would reduce gray and white matter injury induced by spinal cord ischemia in rats. In addition, we evaluated the relationship between reactive astrogliosis and gray or white matter injury after spinal cord ischemia with a 1°C reduction in body temperature or normothermia. METHODS: Rats were randomly divided into hypothermia (1°C decrease in body temperature to 36.3°C), normothermia (37.3°C), and sham surgery groups (n=6/group). Hypothermia was induced 15 minutes before ischemia and maintained during ischemia. Animals were then rewarmed to normothermia. Spinal cord ischemia was induced by a balloon catheter in the thoracic aorta, and the proximal mean arterial blood pressure was maintained at 40 mm Hg for 14 minutes. Hind limb motor function was assessed at 2, 7, 14, 21, and 28 days after reperfusion. At 28 days after reperfusion, gray matter damage was assessed by counting the number of normal motor neurons and white matter damage by the extent of vacuolation. The glial fibrillary acidic protein (GFAP)-positive area fraction (GFAP%) was determined in white and gray matter structures to measure reactive astrogliosis. RESULTS: Compared with normothermia, hypothermia significantly improved hind limb function at all assessments (P<.01) and increased numbers of normal gray matter motor neurons (39±20 vs 99±13, respectively; P<.001), decreased the percentage area of white matter vacuolation (9.0%±2.7% vs 1.6%±1.3%, respectively; P=.001), and decreased the GFAP% in gray (P=.003) and white matter (P=.009). CONCLUSIONS: Prophylactic mild hypothermia (1°C reduction in body temperature) preserved hind limb motor function and reduced neuronal death, white matter vacuolation, and astrogliosis in gray and white matter induced by spinal cord ischemia in rats. Thus, mild hypothermia may be useful for perioperative management of thoracoabdominal aortic surgery.

Mechanisms for prostaglandin E2 formation caused by proteinase-activated receptor-1 activation in rat gastric mucosal epithelial cells.

Proteinase-activated receptor-1 (PAR1), a thrombin receptor, plays a protective role in gastric mucosa via prostanoid formation. Thus, we studied effects of PAR1 stimulation on prostaglandin E(2) (PGE(2)) formation in rat normal gastric mucosal epithelial RGM1 cells and analyzed the underlying signal transduction mechanisms. The PAR1-activating peptide (PAR1-AP) and thrombin increased PGE(2) release from RGM1 cells for 18h, an effect being suppressed by inhibitors of COX-1, COX-2, MEK, p38 MAP kinase (p38 MAPK), protein kinase C (PKC), Src and EGF receptor-tyrosine kinase (EGFR-TK), but not JNK and matrix metalloproteinase (MMP)/a disintegrin and metalloproteinases (ADAMs). PAR1-AP caused persistent (6h or more) and transient (5min) phosphorylation of ERK and p38 MAPK, respectively, followed by delayed reinforcement at 18h. PAR1-AP up-regulated COX-2 in a manner dependent on MEK and EGFR-TK, but not p38 MAPK. The PAR1-mediated persistent ERK phosphorylation was reduced by inhibitors of Src and EGFR-TK. PAR1-AP actually phosphorylated EGF receptors and up-regulated mRNA for heparin-binding-EGF (HB-EGF), the latter effect being blocked by inhibitors of Src, EGFR-TK and MEK. Heparin, an inhibitor for HB-EGF, suppressed PAR1-mediated PGE(2) formation and persistent ERK phosphorylation. These results suggest that PAR1 up-regulates COX-2 via persistent activation of MEK/ERK that is dependent on EGFR-TK activation following induction of HB-EGF, leading to PGE(2) formation. In addition, our data also indicate involvement of COX-1, PKC and p38 MAPK in PAR1-triggered PGE(2) formation. PAR1, thus stimulates complex multiple signaling pathways responsible for PGE(2) formation in RGM1 cells.

Accurate evaluation of the absorption maxima of retinal proteins based on a hybrid QM/MM method.

Here we improved our hybrid QM/MM methodology (Houjou et al. J Phys Chem B 2001, 105, 867) for evaluating the absorption maxima of photoreceptor proteins. The renewed method was applied to evaluation of the absorption maxima of several retinal proteins and photoactive yellow protein. The calculated absorption maxima were in good agreement with the corresponding experimental data with a computational error of <10 nm. In addition, our calculations reproduced the experimental gas-phase absorption maxima of model chromophores (protonated all-trans retinal Schiff base and deprotonated thiophenyl-p-coumarate) with the same accuracy. It is expected that our methodology allows for definitive interpretation of the spectral tuning mechanism of retinal proteins.

Decisive role of electronic polarization of the protein environment in determining the absorption maximum of halorhodopsin.

It is known that the absorption maximum of halorhodopsin is red shifted by 10 nm with the uptake of a chloride ion Cl(-). According to the X-ray structure, the ion is located at the position of the counterion of the chromophore, protonated retinal Schiff base. Thus, the direction of the observed spectral change is opposite to that expected from the pi-electron redistribution (an increase in the bond alternation) induced by the counterion. The physical origin of this abnormal shift is never explained in terms of any simple chemical analogues. We successfully explain this phenomenon by a QM/MM type of excitation energy calculation. The three-dimensional structure of the protein is explicitly taken into account using the X-ray structure. We reveal that the electronic polarization of the protein environment plays an essential role in tuning the absorption maximum of halorhodopsin.