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BackgroundYamakagashi venom is a prothrombin activator, leading to disseminated intravascular coagulation. We report a fatal case of severe coagulopathy from head trauma assumed to be caused by a yamakagashi bite.Case presentationAn 80-year-old man fell and developed systemic tonic–clonic convulsions. Head computed tomography revealed brain contusion and acute subdural hematoma. Physical examination revealed two bite marks with persistent bleeding on the right lower leg. The patient stated that he had been bitten by some creature 3 days prior, but the bite was left untreated. Laboratory tests showed fibrinogen levels below the detection limit. Although eighteen units of fresh frozen plasma were administered for coagulopathy, fibrinogen levels did not improve. He died about 18 h after a head injury.ConclusionIn this case of a yamakagashi bite with active bleeding due to trauma, early administration of yamakagashi antivenom should be considered to control coagulopathy.

We previously evaluated the antioxidative effects of astaxanthin intake in the aqueous humor by measuring reactive oxygen species-related parameters, including O(2)(•−) scavenging activity, H(2)O(2) level, and total hydroperoxides level. In this study, we analyzed the antioxidative effects of astaxanthin in relation to age in 16 males and 19 females (average age 71.3 and 70.6, respectively) who underwent bilateral cataract surgery on one side before and the other side after astaxanthin intake (6 mg/day for 2 weeks). None of the parameters correlated with age before astaxanthin intake, but only total hydroperoxides level was significantly correlated after the astaxanthin intake (r = 0.4, p

We explored the effect of astaxanthin on vascular endothelial growth factor in the aqueous humor, by measuring vascular endothelial growth factor levels and oxidation-related parameters, including O2 (•-) scavenging activity, H2O2 level, and total hydroperoxide level in the aqueous humor, obtained from 35 patients before and after astaxanthin administration. We evaluated the relationship between vascular endothelial growth factor and the oxidation-related parameters as well as the patient's diabetic status, age, and sex. Vascular endothelial growth factor levels did not change significantly but O2 (•-) scavenging activity and total hydroperoxide level significantly (p

Astaxanthin (ASTX) is a xanthophyll carotenoid produced by Haemococcus pluvialis, and is found in microalgae, plankton, krill and other seafood. ASTX has strong antioxidant activity, which is an attractive nutraceutical for further investigation in diabetes, lipid profile, and atherosclerotic cardiovascular disease where antioxidant cellular protection may be of clinical benefit. We already reported the effects of astaxanthin (randomized, double-blind, placebo-controlled study) on glucose metabolism and lipid profile in 44 healthy volunteers in the 10th Asia Pacific Conference on Clinical Nutrition 2017. Here we report the effects of ASTX on glucose metabolism in 29 subjects whose HbA1c was from 5.6 % to 6.4 % at baseline. Data of 75g OGTT and HbA1c in 29 subjects (16 in ASTX group and 13 in Placebo group) were analyzed. After ASTX (12mg/day) supplementation for 12 weeks, the glucose level at 30 min by 75g OGTT was significantly decreased compared to before. The level of HbA1c was also significantly decreased compared to before. Furthermore, we assessed indices of insulin resistance derived from OGTT. Both Matsuda index and hepatic insulin resistance were improved after ASTX (12mg/day) supplementation, although muscle insulin sensitivity index was unchanged. Our results suggest that ASTX might have beneficial effects on the prevention of diabetes in subjects whose HbA1c was from 5.6 % to 6.4 %, including subjects with prediabetes. Disclosure M. Urakaze: Research Support; Self; Fuji Chemical Industry Co., Ltd.. C. Kobashi: None. Y. Satou: None. M. Takagi: None. K. Shigeta: None. M. Toshima: Research Support; Self; Fuji Chemical Industry Co., Ltd. J. Takahashi: Employee; Self; Fuji Chemical Industry Co., Ltd. M. Nishida: Other Relationship; Self; Fuji Chemical Industry Co., Ltd..

Astaxanthin (ASX), an oxygenated carotenoid (xanthophyll), has previously been shown to exert ameliorative effects on obesity and insulin resistance, but the underlying mechanisms were not clearly elucidated. In the present study, we investigated whether ASX serves as a novel selective peroxisome proliferator-activated receptor (PPAR) γ modulator. Analyses of PPARγ binding by CoA-BAP assays revealed that ASX bound to PPARγ in a dose-dependent manner. However, ASX was unable to activate transcription in PPARγ reporter assays, although it antagonized transcriptional activation by the PPARγ agonist rosiglitazone (RGZ). When the molecular interactions between PPARγ and three coactivators were examined, ASX increased the interactions of PPARγ with transcriptional intermediary factor 2 (TIF2) and steroid receptor coactivator-1 (SRC-1), but not cAMP responsive element-binding protein (CREB)-binding protein (CBP). In addition, ASX effectively blocked the increase in CBP recruitment to PPARγ mediated by RGZ. ASX alone did not stimulate 3T3-L1 cell differentiation, although it antagonized 3T3-L1 cell differentiation and lipid accumulation induced by RGZ, similar to the PPARγ antagonist GW9662. When the effects of cotreatment of 3T3-L1 cells with ASX and RGZ were determined based on the mRNA levels of PPARγ target genes, ASX effectively reduced the mRNA levels of aP2 and lipoprotein lipase, but not CD36. Intriguingly, ASX was capable of inducing PPARγ target genes such as liver X receptor, CD36 and ABCA1 in thioglycollate-elicited peritoneal macrophages. Collectively, the present findings indicate that ASX is a novel selective PPARγ modulator that acts as an antagonist or agonist depending on the cell context.

In this study, the effect of dietary antioxidants, such as astaxanthin and Flavangenol®, and a combination of both, in counteracting oxidative stress in streptozotocin-induced diabetes was investigated. Streptozotocin-induced diabetic rats were divided into four groups: control, astaxanthin, Flavangenol, and combined astaxanthin and Flavangenol (mix group). Each group other than the control group was fed with an astaxanthin diet (0.1 g/kg), Flavangenol diet (2.0 g/kg), or an astaxanthin (0.1 g/kg)-Flavangenol (2.0 g/kg) mixture diet, respectively. After 12 weeks of feeding, the results showed that the lipid peroxide levels of plasma and lens and the plasma triglyceride (TG) level in the mix group were significantly decreased by 44%, 20%, and 20%, respectively, compared with the control group. In the mix group, lipid peroxidation was also significantly reduced by 70% in the liver and 20% in the kidney compared with the control group. Furthermore, the level of urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the mix group was significantly lower, 36%, than the control group. The α-tocopherol concentrations in the plasma, liver, and kidney in the astaxanthin and mix groups were significantly higher, 3-9 times, than in the control group. The degree of cataract formation in the Flavangenol and mix groups tended to be lower than the control group. These results indicate that the combination of astaxanthin with Flvangenol has an improved protective effect on oxidative stress associated with streptozotocin-induced diabetes than either agent used alone. Thus, this combination may be beneficial in preventing the progression of diabetic complications.

Effects of astaxanthin (AX) derived from H. pluvialis on human blood rheology were investigated in 20 adult men with a single-blind method. The experimental group was 57.5 +/- 9.8 years of age and the placebo group was 50.8 +/- 13.1 years of age. A blood rheology test that measures whole blood transit time was conducted using heparinized blood of the volunteers by a MC-FAN apparatus (microchannel array flow analyzer). After administration of AX 6 mg/day for 10 days, the values of the experimental group were decreased from 52.8 +/- 4.9 s to 47.6 +/- 4.2 s (p

The present study was performed to investigate the effect of astaxanthin in combination with other antioxidants against oxidative damage in streptozotocin (STZ)-induced diabetic Osteogenic Disorder Shionogi (ODS) rats. Diabetic-ODS rats were divided into five groups: control, astaxanthin, ascorbic acid, alpha-tocopherol, and tocotrienol. Each of the four experimental groups was administered a diet containing astaxanthin (0.1 g/kg), in combination with ascorbic acid (3.0 g/kg), alpha-tocopherol (0.1 g/kg), or tocotrienol (0.1 g/kg) for 20 wk. The effects of astaxanthin with other antioxidants on lipid peroxidation, urinary 8-hydroxy-2-deoxyguanosine (8-OHdG) excretion, serum creatinine (Cr) level, creatinine clearance (Ccr), and urinary protein content were assessed. The serum lipid peroxide levels and chemiluminescent (CL) intensity in the liver of the alpha-tocopherol and tocotrienol groups were significantly reduced in comparison to that of the control group. In the alpha-tocopherol group, urinary 8-OHdG excretion, serum Cr level, Ccr, urinary albumin excretion, and urinary protein concentration were significantly decreased as compared with those in the control group. Additionally, the CL intensity in the kidney of the alpha-tocopherol group was significantly lower, but that of the ascorbic acid group was significantly higher than that in the control group. These results indicate that dietary astaxanthin in combination with alpha-tocopherol has an inhibitory effect on oxidative stress. On the other hand, our study suggests that excessive ascorbic acid intake increases lipid peroxidation in diabetic rats.

The present study was designed to determine the effect of astaxanthin on endurance capacity in male mice aged 4 weeks. Mice were given orally either vehicle or astaxanthin (1.2, 6, or 30 mg/kg body weight) by stomach intubation for 5 weeks. The astaxanthin group showed a significant increase in swimming time to exhaustion as compared to the control group. Blood lactate concentration in the astaxanthin groups was significantly lower than in the control group. In the control group, plasma non-esterfied fatty acid (NEFA) and plasma glucose were decreased by swimming exercise, but in the astaxanthin group, NEFA and plasma glucose were significantly higher than in the control group. Astaxanthin treatment also significantly decreased fat accumulation. These results suggest that improvement in swimming endurance by the administration of astaxanthin is caused by an increase in utilization of fatty acids as an energy source.

Oxidative stress induced by hyperglycemia possibly causes the dysfunction of pancreatic beta-cells and various forms of tissue damage in patients with diabetes mellitus. Astaxanthin, a carotenoid of marine microalgae, is reported as a strong anti-oxidant inhibiting lipid peroxidation and scavenging reactive oxygen species. The aim of the present study was to examine whether astaxanthin can elicit beneficial effects on the progressive destruction of pancreatic beta-cells in db/db mice--a well-known obese model of type 2 diabetes. We used diabetic C57BL/KsJ-db/db mice and db/m for the control. Astaxanthin treatment was started at 6 weeks of age and its effects were evaluated at 10, 14, and 18 weeks of age by non-fasting blood glucose levels, intraperitoneal glucose tolerance test including insulin secretion, and beta-cell histology. The non-fasting blood glucose level in db/db mice was significantly higher than that of db/m mice, and the higher level of blood glucose in db/db mice was significantly decreased after treatment with astaxanthin. The ability of islet cells to secrete insulin, as determined by the intraperitoneal glucose tolerance test, was preserved in the astaxanthin-treated group. Histology of the pancreas revealed no significant differences in the beta-cell mass between astaxanthin-treated and -untreated db/db mice. In conclusion, these results indicate that astaxanthin can exert beneficial effects in diabetes, with preservation of beta-cell function. This finding suggests that anti-oxidants may be potentially useful for reducing glucose toxicity.

Oxidative stress is implicated as an important mechanism by which diabetes causes nephropathy. Astaxanthin, which is found as a common pigment in algae, fish, and birds, is a carotenoid with significant potential for antioxidative activity. In this study, we examined whether chronic administration of astaxanthin could prevent the progression of diabetic nephropathy induced by oxidative stress in mice. We used female db/db mice, a rodent model of type 2 diabetes, and their non-diabetic db/m littermates. The mice were divided into three groups as follows: non-diabetic db/m, diabetic db/db, and diabetic db/db treated with astaxanthin. Blood glucose level, body weight, urinary albumin, and urinary 8-hydroxydeoxyguanosine (8-OHdG) were measured during the experiments. Histological and 8-OHdG immunohistochemical studies were performed for 12 weeks from the beginning of treatment. After 12 weeks of treatment, the astaxanthin-treated group showed a lower level of blood glucose compared with the non-treated db/db group; however, both groups had a significantly high level compared with the db/m mice. The relative mesangial area calculated by the mesangial area/total glomerular area ratio was significantly ameliorated in the astaxanthin-treated group compared with the non-treated db/db group. The increases in urinary albumin and 8-OHdG at 12 weeks of treatment were significantly inhibited by chronic treatment with astaxanthin. The 8-OHdG immunoreactive cells in glomeruli of non-treated db/db mice were more numerous than in the astaxanthin-treated db/db mice. In this study, treatment with astaxanthin ameliorated the progression and acceleration of diabetic nephropathy in the rodent model of type 2 diabetes. The results suggested that the antioxidative activity of astaxanthin reduced the oxidative stress on the kidneys and prevented renal cell damage. In conclusion, administration of astaxanthin might be a novel approach for the prevention of diabetes nephropathy.

The healing of fracture has an important connection with the condition of lateral dislocation. On the other hand, it is inaccurate to guess only by looking at the X-ray films of the lateral dislocation of fracture of long bone with naked eyes.Authors designed a new mathematical measurement as follows:As shown in Fig. I, the distances between lateral faces (M & N) and the lengths of riding parts (X & Y) at both ends of the broken bone are determined at two X-ray films projected from such directions as to intersect at right angles.With the Ratios of these lengths to distances, (X/M, Y/N) ratio (d) of the sagittal length of the riding part to the diameter of the broken bone is obtained from the graphs in Fig. II drawn by previous calculation.Ratio (D) of area of the riding part to the cross-section of the broken bone is showed as a function of ratio (d) on the oblique line in Fig. II.

The present investigation was undertaken to examine the recovery of functions, spontaneous EEG activity and cerebral ATP content during blood recirculation following cerebral ischemia in rats. The ischemia was induced by bilateral carotid artery 30 min-occlusion 24 hr after the permanent electrocauterization of bilateral vertebral arteries. EEG spectral analysis was performed by the Berg transform. The recovery of EEG activity was assessed by the time elapsing from the onset of blood recirculation until the delta (0.5-4 Hz), theta (4-8 Hz), alpha (8-13 Hz) or beta (13-32 32 Hz) band reappeared and the relative proportion of the four bands at 45 and 60 min after recirculation. Following the 20 min recirculation, the brains were frozen in situ with liquid nitrogen and then stored at -80 degrees C for later extraction for analysis. Concentrations of ATP in the cerebral cortex were determined with enzymatic methods. In animals administered FO-1561 (10 approximately 100 mg/kg, i.v.) simultaneously with blood recirculation, the reduction of time elapsing until reappearance of the theta, alpha and beta bands, the decrease in proportion of the delta band and the increase in that of the theta, alpha and beta bands which indicated the facilitation of transition to the normal state were observed. In animals administered FO-1561 (100 mg/kg), the improvement of ATP content was detected. These results demonstrate that FO-1561 may have a beneficial effect on the recovery from dysfunctions due to cerebrovascular disorder.

Effects of S-adenosyl-L-methionine (SAMe) on deficits in a trained delayed response task or trained hand movement tasks after lesions in bilateral dorsolateral prefrontal cortices or the hand-arm area of the unilateral motor cortex in monkeys were studied. Lesions disturbed the delayed response task or hand movement tasks moderately or severely for 1 week to several months depending on the extent of the lesion and nature of the task. Although treatment with small doses of SAMe (10 mg/kg/day, i.m.) had no effect on these disturbances, treatment with moderate doses of SAMe (20 or 30 mg/kg/day, i.m.) reduced impairments and promoted recovery from both disturbances. Pretreatment with SAMe (30 mg/kg/day, i.m.) facilitated recovery from delayed response task deficits due to administration of reserpine (0.3 mg/kg, i.m.) in monkey with bilateral prefrontal cortical lesions, but not in intact monkey. The data suggest that SAMe improves recovery from behavioral disturbances due to brain damage, and this is partly due to increased monoamine turnover rate.