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Many breeding colonies of Procellariiformes have been threatened with extinction. Chick translocation has been shown to be an effective method for establishing new “safer” colonies of burrow-nesting species, but techniques for surface-nesting species have not been fully developed. The entire breeding population of the threatened Short-tailed Albatross Phoebastoria albatrus is restricted to two sites, Torishima Island and the Senkaku Islands, and neither site is secure due to volcanic activity or political instability. The Short-tailed Albatross Recovery Team has recommended facilitating the recovery of this species by establishing at least one additional colony through the translocation and hand-rearing of chicks at a safe historical breeding site. To evaluate the feasibility of this approach, we hand-reared 10 post-guard phase chicks of two related species in 2006–2007: Laysan Albatross P. immutabilis translocated from Midway Atoll to Kaua’i Island, Hawai’i and Black-footed Albatross P. nigripes translocated from a nearby islet in the Ogasawara (Bonin) Islands to Mukojima Island, Japan. In these pilot studies, 40% of Laysan Albatross chicks and 90% of Black-footed Albatross chicks fledged successfully. Following this groundwork, 40 post-guard phase Short-tailed Albatross chicks were translocated from Torishima Island to Mukojima Island in February 2008–2010 and hand-reared to fledging. Their fledging success has been 100% in all three years. Fledging body sizes were similar or greater in hand-reared chicks at the release site than parent-reared chicks on Torishima Island. There were significant differences in levels of some blood chemistry parameters between pre-fledging hand-reared and parent-reared chicks. The techniques developed in our studies have broad-reaching implications for the future conservation of threatened populations of other surface-nesting seabirds.
The aim of the present study was to examine the effects of cobalamin (Cbl) on the activity and expression of l-methylmalonyl-CoA mutase (MCM) in rat liver and cultured COS-7 cells. The MCM holoenzyme activity was less than 5 % of the total (holoenzyme+apoenzyme) activity in the liver although rats were fed a diet containing sufficient Cbl. When weanling rats were maintained on a Cbl-deficient diet, the holo-MCM activity became almost undetectable at the age of 10 weeks. In contrast, a marked increase in the total-MCM activity occurred under the Cbl-deficient conditions, and at the age of 20 weeks it was about 3-fold higher in the deficient rats than in the controls (108 (sd 14·5) v. 35 (sd 8·5) nmol/mg protein per min (n 5); P < 0·05). Western blot analysis confirmed that the MCM protein level increased significantly in the Cbl-deficient rats. However, the MCM mRNA level, determined by real-time PCR, was rather decreased. When COS-7 cells were cultured in a medium in which 10 % fetal bovine serum was the sole source of Cbl, holo-MCM activity was barely detected. The supplementation of Cbl resulted in a large increase in the holo-MCM activity in the cells, but the activity did not exceed 30 % of the total-MCM activity even in the presence of Cbl at 10 μmol/l. In contrast, the total-MCM activity was significantly decreased by the Cbl supplementation, indicating that Cbl deficiency results in an increase in the MCM protein level in COS-7 cells as well as in rat liver.
The aim of the present study was to elucidate the mechanism of the vitamin B12 deficiency-induced changes of the serine dehydratase (SDH) and tyrosine aminotransferase (TAT) activities in the rat liver. When rats were maintained on a vitamin B12-deficient diet, the activities of these two enzymes in the liver were significantly reduced compared with those in the B12-sufficient control rats (SDH 2·8 (sd 0·56) v. 17·5 (sd 6·22) nmol/mg protein per min (n 5); P < 0·05) (TAT 25·2 (sd 5·22) v. 41·3 (sd 8·11) nmol/mg protein per min (n 5); P < 0·05). In the B12-deficient rats, the level of SDH induction in response to the administration of glucagon and dexamethasone was significantly lower than in the B12-sufficient controls. Dexamethasone induced a significant increase in TAT activity in the primary culture of the hepatocytes prepared from the deficient rats, as well as in the cells from the control rats. However, a further increase in TAT activity was not observed in the hepatocytes from the deficient rats, in contrast to the cells from the controls, when glucagon was added simultaneously with dexamethasone. The glucagon-stimulated production of cAMP was significantly reduced in the hepatocytes from the deficient rats relative to the cells from the control rats. Furthermore, the glucagon-stimulated adenylyl cyclase activity in the liver was significantly lower in the deficient rats than in the controls. These results suggest that vitamin B12 deficiency results in decreases in SDH and TAT activities correlated with the impairment of the glucagon signal transduction through the activation of the adenylyl cyclase system in the liver.
In this paper, we demonstrate that high temperature and short time EBAS annealing is effective to obtain low sheet resistance without surface roughening in heavily Al-implanted 4H-SiC (0001) samples (Al concentration: 1.0 × 1021 /cm3, thickness: 0.3 microns, total dose: 2.6 × 1016 /cm2). The sheet resistance and rms surface roughness of the sample annealed at 1800 °C for 0.5 min is estimated to be 4.8k ohm/sq. and 0.82 nm, respectively. Also, we discuss the advantage of EBAS annealing for the suppression of surface roughening during annealing.
A large quantity of the jellyfish, Aurelia aurita, invade cooling water systems and cause serious problems at several electric power stations in Japan. In the present study, we examined intra—species genetic variation of A. aurita in Wakasa Bay, Japan in order to estimate the original polyp habitat of the adult medusae invading electric power stations. Total DNA was extracted from the adult medusae and the wild polyps, and polymerase chain reaction (PCR) was performed using the specific primers for amplification of nuclear internal transcribed spacer one (ITS-1) and mitochondrial cytochrome oxidase c subunit 1 (CO1). Then the DNA sequences of the PCR products were compared. The results showed genetic polymorphism of A. aurita in Wakasa Bay and locally specific frequency of each haplotype. The haplotype frequency, especially in CO1, of the adults collected at one of the power stations in Wakasa Bay was similar to that of the polyp colonies at harbours in the embayed area, not at another harbour in the western entrance of the bay. The polymorphic analysis is, therefore, thought to be useful for the determination of original polyp habitat as source of the adult medusae in relatively limited regions such as Wakasa Bay.
In rats, in contrast with human subjects who develop megaloblastic anaemia due to vitamin B12 deficiency, haematological abnormalities with anaemia were not observed under normoxic conditions even though plasma vitamin B12 concentration was reduced to <15 % of a normal concentration by depleting dietary vitamin B12. To elucidate whether erythropoiesis was affected by vitamin B12 deficiency in rats, these vitamin B12-deficient rats were exposed to hypoxia (10·5 % O2) to stimulate erythropoiesis. In the vitamin B12-sufficient control rats, erythrocyte count was significantly (P<0·05) increased 1 week after starting the hypoxic exposure. However, the hypoxia-induced erythropoiesis was affected by vitamin B12 deficiency, and no significant increase in the erythrocyte count was observed even after 6-week exposure to hypoxia in the vitamin B12-deficient rats. In the vitamin B12-deficient rats in hypoxia, erythrocytes became abnormally enlarged, and haemoglobin concentration in peripheral blood was increased in proportion to the increase of mean corpuscular volume. However, the level of the increase in the haemoglobin concentration was significantly (P<0·05) lower in the vitamin B12-deficient rats compared with that in the -sufficient controls. In addition, in the vitamin B12-deficient rats, in contrast to the -sufficient rats, serum erythropoietin concentration was not normalized even after 6-week exposure to hypoxia. These results indicate that a megaloblastic anaemia-like symptom is induced when the vitamin B12-deficient rats are exposed to hypoxia.
The aims of this study were to determine the types of chronic-stage EEG abnormalities that exist and to clarify their relation to neurodevelopmental outcome in preterm infants. We evaluated 183 preterm infants with gestational ages of less than 33 weeks (mean age 29.2 weeks) and weighing less than 2000g (mean weight 1275g). The first EEG was performed within 72 hours of life; thereafter, EEG was performed once every 1 to 4 weeks until the infant reached a post-conceptional age of 40 to 42 weeks. Two kinds of EEG abnormalities, acute- and chronic-stage abnormalities, were evaluated and we assessed mainly the latter. Chronic-stage EEG abnormalities were divided into two patterns: disorganized and dysmature. Periventricular leukomalacia (PVL) and intraventricular haemorrhage (IVH) were diagnosed on the basis of ultrasound findings. Psychomotor development was examined every 3 months after discharge until at least 18 months of the infants' corrected age. Disorganized and dysmature patterns were observed in 52 and 28 infants respectively. Among the 52 infants with disorganized patterns, PVL was observed in 31 and IVH in seven infants. Thirty-nine infants had cerebral palsy (CP). Twenty-six achieved normal cognitive development. Of the 28 infants with dysmature patterns, PVL was seen in one and IVH in 11 infants. CP was seen in five infants. Only eight infants achieved normal cognitive development. Gestational age and birthweight were significantly lower in infants with dysmature patterns than in those with disorganized ones. Results indicate that types of chronic-stage EEG abnormalities are related to types of neurological sequelae and are useful for assessing the mode of brain injury in preterm infants.
Quantitative analyses of cross-sectional areas of the thalami, caudate nuclei, and lentiform nuclei were performed in 29 preterm infants (16 males, 13 females; mean age 29.6 weeks, age range 27 to 24 weeks,) with periventricular leukomalacia (PVL). MRI was carried out in the infants between 9 and 18 months of corrected age and in 16 control infants. Bilateral thalami, caudate nuclei, lentiform nuclei, cerebral hemispheres, and cerebellum were measured by computer. Ratios of the areas of the thalami (Th), caudate nuclei (Ca), lentiform nuclei (Le), and cerebral hemispheres (CH) to that of the cerebellum (Ce) were calculated in each infant. The ratio of Th:Ce was significantly smaller in infants with moderate and severe PVL than in the control group bilaterally. Abnormal intensity areas were not observed in the thalami in any infants with PVL. CH:Ce was also smaller in infants with severe PVL than in the control group. No significant difference was observed between the groups in ratios Le:Ce or Ca:Ce. Results of our study suggest that the volume of the thalami is reduced and that thalamic involvement is present in infants with white matter lesions who have moderate to severe PVL.
To clarify the bioavailability of vitamin B12 in lyophylized purple laver (nori; Porphyra yezoensis), total vitamin B12 and vitamin B12 analogue contents in the laver were determined, and the effects of feeding the laver to vitamin B12-deficient rats were investigated. The amount of total vitamin B12 in the dried purple laver was estimated to be 54.5 and 58.6 (SE 5.3 and 7.5 respectively) ΜG/100 g dry weight by lactobacillus bioassay and chemiluminescent assay with hog intrinsic factor respectively. the purple laver contained five types of biologically active vitamin b12 compounds (cyano-, hydroxo-, sulfito-, adenosyl- and methylcobalamin), in which the vitamin b12 coezymes (adenosyl- and methylcobalamin) comprised about 60 % of the total vitamin b12. when 9-week-old vitamin b12-deficient rats, which excreted substantial amounts of methylmalonic acid (71.7(se 20.2) μmol/d) in urine, were fed the diet supplemented with dried purple laver (10 μg/kg diet) for 20 d, urinary methylmalonic acid excretion (as an index of vitamin B12 deficiency) became undetectable and hepatic vitamin B12 (especially adenosylcobalamin) levels were significantly increased. These results indicate that vitamin B12 in dried purple laver is bioavailable to rats.
Most neonatal seizures are occasional seizures and not true epilepsy. This study investigates seizure types of true neonatal epilepsies and their evolution with development. Seventy-five children with epilepsies of onset within 1 month of life, who were examined between 1970 and 1995, and whose seizure types could be confirmed with ictal EEG recordings, were studied. The patients were followed up for a minimum of 3 years and the evolution of epileptic syndromes was investigated. Sixty-three (84%) of 75 patients had partial seizures, while nine had generalized seizures, and only three had both generalized and partial seizures. Twenty-three of 24 neonates with benign familial or non-familial neonatal convulsions presented with partial seizures; these syndromes should not necessarily be categorized into generalized epilepsy as they are in the present International Classification. Age-dependent changes were a common feature of symptomatic neonatal epilepsies. Eighteen (41%) of 44 patients with symptomatic epilepsies of neonatal onset developed West syndrome in infancy. Fifteen (83%) of these 18 patients presented with symptomatic localization-related epilepsy in the neonatal period. In seven of these 15 patients, West syndrome was followed by localization-related epilepsy. Symptomatic localization-related epilepsy with transient West syndrome in infancy is another type of age-dependent epileptic syndrome.
To clarify the relationship between intracellular concentrations of methylmalonic acid and metabolic and growth inhibition in vitamin B12-deficient rats, hepatic methylmalonic acidlevels were assayed and inhibition of glucose and glutamic acid metabolism by methylmalonic acid was studied in isolated hepatocytes. Vitamin B12-deficient rats (14 weeks old) excreted more urinary methylmalonic acid and had lower body weights than the control rats. Hepatic methylmalonic acid levels (3·6 (SD 1·30)–5·3 (SD 0·51) µmol/g tissue; 7·9 (SD 2·90)–11·8 (SD 1·14) mM) were increased and correlated with the extent of the growth retardation during vitamin B12-deficiency. Isolated hepatocytes and mitochondria from normally fed rats were labelled with [14C(U)]glucose and [14C(U)]glutamic acid respectively, in the presence or absence of 5mM-methylmalonic acid. Although methylmalonic acid did not affect the incorporation of 14C into protein and organic acid fractions in the hepatocytes, it inhibited 14CO2 formation (an index of glucose oxidation by the Krebs cycle) by 25% and incorporation of 14C into the amino acid fractionby 30%. In the mitochondria, methylmalonic acid inhibited 14CO2, formation (indicating glutamic acid oxidation by the Krebs cycle) by 70%, but not the incorporation of 14C into the protein fraction. The incorporation of 14C into the organic acid fraction was significantly stimulated by the addition of methylmalonic acid. These results indicate that the unusual accumulation of methylmalonic acid caused by vitamin B12-deficiency disrupts normal glucose and glutamic acid metabolism in rat liver, probably by inhibiting the Krebs cycle.
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