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米飯の原料となる精白米は，品種，産地，栽培方法，貯蔵環境等の様々な因子が品質に影響を与えている。本研究では，島根県産米の‘きぬむすめ’の米飯の保存条件の違いによる品質について比較検討を行った。‘きぬむすめ’の精白米を洗米後浸漬させた後，炊飯し保存条件を変えた米飯の物理特性，外観（形状），水分含量を測定した。その結果，保温8 時間後の米飯の物理特性は，炊飯直後の米飯と比較して有意に硬く，表面の付着性や，弾力性が強く，食味評価の指標とされるバランス値（粘り／硬さ）は低い値を示した。また，保温8 時間後の米飯の外観特性は，炊飯直後の米飯と比較して，有意に粒長や粒厚において低い値を示した。-30℃で冷凍保存1 週間後および冷凍保存1 か月後に再加熱した米飯の物理特性は，ともに炊飯直後の米飯と比較して有意に硬く，粘りやバランス値（粘り／硬さ）が低く，付着性や凝集性，弾力性は有意に高い値を示した。-30℃で冷凍保存1 週間後および冷凍保存1 か月後に再加熱した米飯の外観特性は，ともに炊飯直後の米飯と比較して，粒長，粒幅，粒厚，重さともに有意に低い値を示した。以上より，保存条件の違いが米飯の物理特性や外観特性に影響する可能性が示唆された。

島根県では，鹿や猪による農産物の被害が広範囲に及び，今後さらに拡大することが懸念されている。また，捕獲したジビエ（野生鳥獣の食肉）の活用は，農産物の被害を減らすだけでなく，ジビエのブランド化を通じて地域経済の活性化や新たな雇用創出につながる。本稿では，鹿や猪による被害や捕獲状況を把握するとともに，出雲北山地域において捕獲された鹿肉の解体および活用の現状調査および，産学官連携により島根県の食文化に関連した商品開発を行い，県内外への販路拡大を行った一連の地域貢献活動について報告する。

米飯の原料となる玄米もしくは精白米における品質には，品種，産地，栽培方法，貯蔵環境等の様々な影響因子が関わっている。本研究では，島根県産米の品種，栽培方法の違いにより物理特性および外観（形状）にどのような違いがあるのかについて比較検討を行った。島根県産 ‘コシヒカリ’，‘つや姫’，‘きぬむすめ’，‘イセヒカリ’ を使用し，精白米を洗米後1.5 時間浸漬させた後，炊飯した。物理特性は，圧縮試験機（タケトモ電機社製）を用いて，一粒を円柱形プランジャーで高圧縮試験を行い，硬さ・粘り・付着性・弾力性・凝集性を測定した。また，外観（形状）はノギスを用いて計測した。その結果，島根県産米の‘コシヒカリ’と比較して，‘つや姫’，‘きぬむすめ’は，食味評価の指標とされるバランス値（粘り/ 硬さ）が有意に高いことが認められた。また，形状においては‘コシヒカリ’と比較して，‘つや姫’，‘きぬむすめ’は粒が有意に長いことが認められた。‘コシヒカリ’‘つや姫’の有機栽培米は，慣行栽培米と比較して有意に柔らかいことが認められた。‘イセヒカリ’は，‘コシヒカリ’と比較して，すべての項目において差が認められなかった。以上より，品種や栽培方法の違いにおいて米飯の物理特性や形状が異なることが示唆された。

島根県の低出生体重児の出生割合は高いことが報告されており、児の将来において様々なリスクの可能性がある。 我々は、島根県内の妊婦に対して栄養摂取状況の調査を行い、低出生体重児との関連性について検討している。本研究では、妊娠初期における妊婦29 名に食物摂取頻度調査を行い、体格指数（Body Mass Index（BMI））の区分および妊娠後の欠食状況の違いによる栄養素摂取量および食品群別摂取量を算出し検討した。非妊娠時BMI が低い群は、エネルギー、炭水化物、ナトリウム、マンガン、鉄、食物繊維の摂取量が多いことが示唆された。また、妊娠初期の妊婦の44.8％が週一回以上の欠食をし、その結果、栄養素の多くが推奨量に満たないことが示唆された。

島根県における妊娠初期の妊婦の栄養摂取状況を明らかにすることを目的とし、分娩歴による違いがあるかに注目して研究を行った。妊娠10 週から12 週の妊婦29 名に食物摂取頻度調査を行い、初産婦（15名）、経産婦（14 名）の２群に分けて比較した。各種栄養素摂取量および食品群別栄養素摂取量については、２群間で有意な差はみられなかった。食品群別摂取量の「嗜好品飲料類」について、初産婦の摂取量が有意に多かった。栄養素摂取量の多くが２群とも平均必要量に満たないことが明らかになった。

過疎地でのイノシシやシカの増加による農作物への被害増加で、イノシシやシカ捕獲の必要性が叫ばれている。また、 最近イノシシやシカ肉を使った「ジビエ料理」がブームになっており、高蛋白低脂肪の肉として注目を浴びつつある。本稿では出雲北山山地のニホンジカについて、文献及び先進地視察でのインタビュー結果と最近加齢性筋肉減弱現象として注目をされているサルコペニア予防の食事としての可能性として考察する。

To reduce the risk of neural tube defects, studies have been conducted on female students of medical services, nutritional science, and nursery education that investigated the awareness of folic acid by using questionnaires. Many investigators have suggested the need to provide detailed information about the awareness of folic acid and knowledge about folic acid intake and neural tube defect risk reduction. The dietary habits of female students showed a positive correlation with their estimated folic acid intake, suggesting that improvements in dietary habits are associated with the consumption of folic acid. The importance of folic acid intake must be more aggressively promoted among female students. Thus, many learning opportunities should be provided for such students to help increase their folic acid intake.

Nutrition has been suggested as an important environmental factor other than viruses and chemicals in the pathogenesis of type 1 diabetes (T1D). Whereas various maternal dietary nutritional elements have been suggested and examined in T1D of both humans and experimental animals, the results largely remain controversial. In a series of studies using T1D model nonobese diabetic (NOD) mice, maternal dietary n-6/n-3 essential fatty acid ratio during pregnancy and lactation period, that is, early life stages of the offspring, has been shown to affect pathogenesis of insulitis and strongly prevent overt T1D of the offspring, which is consistent with its preventive effects on other allergic diseases.

To reduce the risk of neural tube defects, studies have been conducted on female students of medical services, nutritional science, and nursery education that investigated the awareness of folic acid by using questionnaires. Many investigators have suggested the need to provide detailed information about the awareness of folic acid and knowledge about folic acid intake and neural tube defect risk reduction. The dietary habits of female students showed a positive correlation with their estimated folic acid intake, suggesting that improvements in dietary habits are associated with the consumption of folic acid. The importance of folic acid intake must be more aggressively promoted among female students. Thus, many learning opportunities should be provided for such students to help increase their folic acid intake.

Neuropeptide Y (NPY) is expressed in the developing central nervous system, however, its role in the brain development remains unclear. In this study, C57/B6 mice were intraperitoneally administered 1 nmol/capita/day of NPY, 10 nmol/capita/day of an NPY-receptor 1-specific antagonist (Y1R-A), or NPY and Y1R-A simultaneously (NPY + Y1R-A) from postnatal day (P) 7 to P14. Recombinant NPY reached the P14 cerebrum in 1 hour. These treatments didn't significantly affect body weight gain or P14 brain weight. The ratio of myelinated axons to total axons in the parietal cerebrum was significantly higher in the NPY group than in the control group. The expression of myelin basic protein ( MBP )-mRNA in the cerebrum was significantly higher in the NPY group than in the control group and was significantly lower in the NPY + Y1R-A group than in the NPY group, while it was significantly higher in the NPY + Y1R-A group than in the control group. In cultured oligodendroglioma-derived B12 cells, NPY didn't influence the MBP -mRNA expression, while neurotrophin 3 (NT3) increased MBP mRNA via receptor-type tyrosine kinase type C (Trk C). NPY administration significantly increased NT3 -mRNA expression in the P14 cerebrum as deduced by quantitative real-time PCR. The change in phosphorylated Trk C (P-Trk C) was proportional to that of the NT3 -mRNA expression, and the proportion of P-Trk C was higher in the NPY group than in the control group. These results suggest that NPY, partially via Y1R, induces NT3 which, via Trk C phosphorylation, accelerates myelination by oligodendrocytes in the mouse brain during the neonatal period.

Morphological studies of congenital anomalies have mainly focused on abnormal shape (i.e. malformation) and thus on disturbed organogenesis. However, in regard to postnatal functions of organs that develop through branching mechanisms, organ size is another important morphological feature. These organs consist of a large number of structural and functional units, such as nephrons in the kidney, and the total number of these units, that is approximately proportional to the organ size, has been shown to vary widely among individuals. Organ-specific cells are differentiated and organized to form structural units and realize organ-specific functions during the histogenetic period (i.e. from mid-gestation to the early postnatal period). The total number of units is attained at the end of histogenesis and determines the total functional capacity, including the functional reserve of the organ, and thus may be related to predispositions to postnatal organ-based diseases, because the functional reserve decreases during the course of life and eventually become short of the minimum requirement of each organ. Therefore, it may be hypothesized that a smaller number of units of organs at the end of histogenesis is one of the predisposing factors for postnatal diseases (i.e. a form of unnoticed but late-manifested congenital anomalies), in this era of extended longevity. However, the mechanisms that control the total number of units in each organ during histogenesis and the possible relationship among the numbers of units in different organs remain unknown. Here, we review our trials based on the above hypothesis in order to (1) mathematically analyze the morphometric data of the different organs in fetuses to elucidate relationship among developing organs, (2) analyze the developing neuro-immuno-endocrine network as a series of mechanisms to systemically correlate the histogenesis of multiple organs, and (3) examine the maternal environment, including dietary fat, as a factor to influence histogenesis and thus the predisposition to type 1 diabetes.

To clarify the cytogenetic effects of glucose and ketone bodies on the pathogenesis of diabetes-associated congenital anomalies, we cultured cells from gestation-day-8 ICR mouse embryos under the diabetic condition. Cells were cultured in the medium with glucose (300 mg/dL) plus DL-2-hydroxybutyric acid (32 mM) (G + B group), glucose alone (G group), or neither of them (C group) for 5 days. At the end of the culture, cells were analyzed for the chromosomes. After 3-4 days culture, when the living cells grew into a mono-layered sheet, cells floating in the medium were observed and showed morphological features of apoptosis. Ratio of the floating cells was significantly higher in the G + B group than in the G or C group (P < 0.05), suggesting the deleterious effect of glucose and ketone body. Polyploidy was observed in the cultured cells more frequently in the G + B group (64.1%) than in the G group (49.0%), which was higher than the C group (20.5%) (G + B vs G: P < 0.05, G vs C: P < 0.001). The higher ratio of the polyploidy, but not of the aneuploidy, in the G + B and G groups suggested the specific effect of glucose and ketone body for inducing polyploidy. These results suggest that diabetic condition causes polyploidy in cultured embryonic cells.

Leptin is an obese gene product, and leptin-deficient ob/ob mice develop hyperphagia and reduced locomotor activity. Leptin is thought to be related to brain development, because leptin receptors are widely expressed in the brain, and because brain weight as well as brain protein and DNA contents were reduced in adult ob/ob mice. In this study, we investigated the effect of leptin on the fetal cingulate cortex, since the leptin receptor is expressed in the neurons of the cingulate cortex, which is involved in emotion as well as in sensory, motor, and cognitive processes. The ob/ob fetuses had more pycnotic cells than wild-type fetuses in the cingulate cortex at embryonic day (E) 18. Many pycnotic cells were observed in the intermediate zone of the cingulate cortex. Most cells observed in this area were neuronal lineage cells, while few undifferentiated cells and oligodendrocyte precursor cells were found. At E18 there was no significant difference in the rostrocaudal length of the corpus callosum, which contains the neuronal projection from the cingulate cortex, between ob/ob and wild-type fetuses. We also showed that the length of the cerebrum was greater and the width of the cerebrum and cerebellum were lesser in ob/ob fetuses than in wild-type at E16. These results suggest an increased cell death in neuronal lineage cells in the intermediate zone of the cingulate cortex in leptin-deficient ob/ob mice. Leptin deficiency may also alter the gross morphology of the brain in development, but not the formation of the corpus callosum.

Type 1 diabetes results from the destruction of pancreatic b-cells (insulitis). It is a multifactorial disease involving genetic and environmental factors, including the maternal environment. Viruses have also been implicated in the pathogenesis of human type 1 diabetes as well as in its model non-obese diabetic (NOD) mice during the perinatal period, as endogenous viruses and/or as infectious agents vertically transmitted from mothers. However, the role of virus as genetic or environmental factor and its interaction with other maternal factors remain unclear. In a series of experiments, we transplanted preimplantation-stage NOD embryos into the uterus of recipient Institute of Cancer Research (ICR) mice, which are without diabetic genetic predisposition, and NOD mice, which did not exhibit overt diabetes during the experiment, and designated offspring as NOD/ICR and NOD/NOD, respectively. We previously observed that NOD/ICR offspring developed insulitis significantly earlier than NOD/NOD offspring. To assess the role of viruses in the development of insulitis, we examined the appearance of viral particles and expression of retroviruses between NOD/ICR and NOD/NOD. NOD/ICR showed earlier expression of env region of the xenotropic type C retrovirus by polymerase chain reaction analysis than NOD/NOD, while the retrovirus-like particles were observed in the islet b-cells similarly in both groups by electron microscopy. Serum corticosterone level, which is suggested to enhance retroviral induction, was significantly higher in the ICR than in the NOD surrogate mothers. These findings suggest that the observed virus is endogenous and that maternal environmental factors, including hormone levels, affect the induction of endogenous viruses and cause the earlier onset of insulitis.

EXTL3 encodes alpha1,4-N-acetylglucosaminyltransferases I and II enzymes, which are involved in chain initiation and elongation of heparan sulfate (HS) biosynthesis. HS proteoglycans are critically involved in a variety of biological phenomena at various levels of complexity in adult and embryonic lives. Dedicated functions of HS proteoglycans are due to variable HS chains that interact with different cellular proteins, and can be regulated by their synthesizing enzymes. EXTL3 protein is also a putative receptor for Reg protein, a growth signal mediator for the beta-cells of the pancreas. The present Northern blot analysis revealed two EXTL3 transcripts (6.2 and 3.4 kb), which were differentially expressed in different mouse adult tissues. The strongest expression was in the adult brain and pancreas. In the adult pancreas, a comparable intensity of both signals was detected. In the embryonic pancreas, the longer transcript was predominant, and showed a biphasic expression pattern with a peak at E11.5, whereas the shorter one showed a steady level of expression throughout the whole period of pancreatic development. By in situ hybridization, the acini of adults and embryos were strong positive for EXTL3 mRNA. Mature islets of Langerhans gave a weak signal, whereas the developing islets showed moderately positive reaction albeit less intense than the acini. In situ hybridization revealed a wide and differential expression pattern of EXTL3 mRNA in embryonic tissues. At the early stages, intense reaction was found in the developing neurons of the brain and spinal cord and in the epithelia of the developing GIT, pancreas, liver and kidney of embryos. Our data suggested that EXTL3 expression is developmentally regulated, and may contribute to the regulated production of HS in different adult and embryonic tissues.

Although chromosomal segregation at meiosis I is the critical process for genetic reassortment and inheritance, little is known about molecules involved in this process in metazoa. Here we show by utilizing doublestranded RNA (dsRNA)-mediated genetic interference that novel protein kinases (Ce-CDS-1 and Ce-CDS-2) related to Cds1 (Chk2) play an essential role in meiotic recombination in Caenorhabditis elegans. Injection of dsRNA into adult animals resulted in the inhibition of meiotic crossing over and induced the loss of chiasmata at diakinesis in oocytes of F1 animals. However, electron microscopic analysis revealed that synaptonemal complex formation in pachytene nuclei of the same progeny of injected animals appeared to be normal. Thus, Ce-CDS-1 and Ce-CDS-2 are the first example of Cds1-related kinases that are required for meiotic recombination in multicellular organisms. Protein kinases play crucial roles in the regulation of a wide variety of cellular functions. A novel family of protein kinases, bearing a phosphospecific protein-protein interaction motif, the forkhead-associated (FHA) domain (11), has been identified and shown to be involved in checkpoint regulation and DNA repair induced by DNA damage (16). Protein kinases belonging to this family include Saccharomyces cerevisiae Rad53, Dun1, and Mek1p (MRE4), Schizosaccharomyces pombe Cds1

Environment factors, including maternal or infant dietary nutrition have been reported to have an influence on the pathogenesis of type 1 diabetes. In the present study, to investigate the effect of maternal or post-weaning offspring's nutrition, in particular the essential fatty acid ratio (n-6/n-3) on the development of type 1 diabetes, we prepared two kinds of chows with n-6/n-3 ratios of 3.0 (L) and 14.5 (H), and provided them to mothers of non-obese diabetic (NOD) mice during gestation and lactation and to the offspring after weaning. The n-6/n-3 ratios in breast milk and erythrocyte membrane of NOD offspring became nearly the same with that of the maternal diet at 2 weeks after birth. In the L chow-fed offspring from L chow-fed mother (LLL), levels of insulitis were higher than those in the H chow-fed offspring from H chow-fed mother (HHH) at 4 weeks of age, while the levels in the LLL offspring became lower than those in the HHH after 6 weeks. Early insulin autoantibody expressions were found from 2 to 6 weeks in the HHH offspring, but not in the LLL. The LLL offspring exhibited strong suppression of overt diabetes development in regard to the onset and accumulated incidence of diabetes compared to the HHH. The study with combined L and H chows during gestation, lactation in mother and in post-weaning offspring revealed that only the LLH chow significantly suppressed the development of diabetes with similar kinetics to LLL chow, although the other combinations may delay the onset of diabetes. The present findings suggest that n-6/n-3 ratio of the maternal diet during gestation and lactation rather than that of offspring after weaning strongly affects the development of overt diabetes in NOD mice.

Type 1 diabetes is a multifactorial disease involving genetic and environmental factors and results from the destruction of pancreatic islet β cells, virtually the only source of insulin. When the majority of β cells are lost, a 'honeymoon' period of variable length follows: namely, a fleeting phase of residual endogenous insulin production, during which glycemic control is achieved with modest or no doses of insulin. However, the remaining β cells are eventually lost, causing the individual to become insulin-dependent and to require long-term insulin therapy or islet transplantation. Here we show that NOD mice, a type 1 diabetes model, survived significantly longer when their diet was changed from one chow with a high essential fatty acid (EFA) ratio (n-6/n-3, 14.5) to another with a low n-6/n-3 ratio (3.0) within 6 days after the onset of overt diabetes (i.e. the 'honeymoon' period), than mice that were continuously fed with the chow with the high n-6/n-3 ratio. This effect was not observed when the chow was changed later than 9 days after the onset. Significantly larger number of islets remained with suggestive islet neogenesis from the pancreatic duct and pathological changes in renal glomeruli were significantly milder in NOD mice fed the chow with the low n-6/n-3 ratio within 6 days after the onset of overt diabetes than those continuously fed with the high-n-6/n-3-ratio chow. These findings indicate that a diet with a low n-6/n-3 ratio prolongs the 'honeymoon' period by retaining the β cell mass, suggesting its potential therapeutic merit.

Leptin is detected in the sera, and leptin receptors are expressed in the cerebrum of mouse embryos, suggesting that leptin plays a role in cerebral development. Compared with the wild type, leptin-deficient (ob/ob) mice had fewer cells at embryonic day (E) 16 and E18 and had fewer 5-bromo-2′-deoxyuridine+ cells at E14 and E16 in the neuroepithelium. Intracerebroventricular leptin injection in E14 ob/ob embryos increased the number of neuroepithelium cells at E16. In cultured neurosphere cells, leptin treatment increased Hes1 mRNA expression and maintained neural progenitors. Astrocyte differentiation was induced by low-dose (0.1 μg/ml) but not high-dose (1 μg/ml) leptin. High-dose leptin decreased Id mRNA and increased Ngn1 mRNA in neurosphere cells. The neuropeptide Y mRNA level in the cortical plate was lower in ob/ob than the wild type at E16 and E18. These results suggest that leptin maintains neural progenitors and is related to glial and neuronal development in embryos.

Type 1 diabetes, a multifactorial disease involving genetic and environmental factors, results from the destruction of pancreatic β-cells. The maternal environment has been suggested to be important in the development of diabetes. To assess the role of maternal factors in the development of insulitis and overt diabetes, we transplanted pre-implantation stage embryos of nonobese diabetic (NOD) mice, a model of type 1 diabetes, into the uterus of each recipient. Recipients were ICR and DBA/2J mice without diabetic genetic predisposition and NOD mice not exhibiting overt diabetes during the experiment; offspring were designated as NOD/ICR, NOD/DBA, and NOD/NOD, respectively; unmanipulated NOD offspring were also examined. NOD/ICR and NOD/DBA offspring developed insulitis significantly earlier than NOD/NOD offspring. However, overt diabetes was significantly suppressed in NOD/ICR and NOD/DBA offspring in comparison with NOD/NOD offspring. Insulin autoantibodies (IAAs) were undetectable in ICR and DBA/2J surrogate mothers and in NOD/ICR and NOD/DBA offspring at the onset of insulitis, suggesting that maternal factors other than transmitted IAAs induced the earlier onset. The present study indicates that altered maternal factors modify the immune response to islets, which in turn might affect the pathogenic course from insulitis to overt diabetes.

We previously showed that PSK, a biological response modifier, suppressed X-ray irradiation induced ocular anomalies in mouse embryos. In the present study, in mouse embryos irradiated at E7.5, PSK, when administered immediately after irradiation, suppressed mitosis and increased apoptosis as compared with embryos not treated with PSK at 12 hrs after irradiation. In the irradiated embryos, p53, which is normally expressed at a high level in early embryos, increased at 6 hrs and decreased at 12 hrs after irradiation. In the irradiated and PSK-treated embryos, the p53 level did not change at 6 hrs, increased at 12 hrs and decreased at 24 hrs after irradiation. This timing of PSK-induced delayed increase of p53 coincided with that of the PSK-induced decrease in mitosis and increase in apoptosis. These results suggested that PSK modified the p53 level and affected cell proliferation and apoptosis, which might contribute to the suppression of teratogenesis.

Chromosomes of Slc:ICR mouse blastocysts cultured under the diabetic condition were analyzed to clarify the effect of glucose and ketone body (DL-β-hydroxybutyric acid). In the group exposed to glucose plus ketone body or glucose alone, blastocysts showed higher incidences of chromosome abnormalities, especially numerical abnormalities such as aneuploidy and polyploidy, than in the control group (p < 0.01). The association of nucleolus organizing regions was increased in the blastocysts exposed to glucose plus ketone body, which seems to be related to the increase in numerical abnormalities. Structural abnormalities such as break and fragment were also observed, but there was no significant difference between the diabetic and nondiabetic conditions. These results from chromosome analysis of the cultured blastocysts suggest that the diabetic condition may directly cause chromosome abnormalities in early embryos, especially aneuploidies, and may thus induce duplications or deletions of genes. These chromosomal damages may disrupt the developmental programs for organogenesis and may be involved in diabetes-induced teratogenesis.