When Japanese law goes pop

This article explores the extent to which the growth in law-themed popular culture since the turn of the century, especially television shows, signals a shift in popular attitudes towards law. Four decades of research into Japanese legal consciousness has called into question the extent to which there is a Japanese cultural aversion to Jaw, with most scholars expressing doubt over whether culture properly explains the comparatively low litigation rates in Japan compared to other industrialised nations. This article argues that popular culture, although not without its limitations, offers new clues into how legal consciousness is developing and changing in 21st Century Japan. The article concludes that popular culture paints a picture of a greater readiness by Japanese people to engage with Jaw, although scepticism remains about the law's promise to achieve justice and social solidarity.

Introduction: Mapping the Contours of East Asian Commercial Law for the Asian Century

The centre of economic gravity in the new century is shifting to the East. Since 200 1, according to the International Monetary Fund (IMF), Asia's contribution to world economic growth has matched that of the United States and Europe combined, and, since 2006, has even exceeded it (IMF, 20 I I; Neumann and Arora, 20 II ). This surge is easy to explain: China has emerged as a global super-power; Japan remains the third-largest world economy, despite only recently emerging from over twenty years of economic stagnation (The Age, 2013); South Korea and the ' tiger ' economies of Taiwan, Hong Kong and Singapore have achieved high-level economic development through capital investment and technological innovation; and Indonesia, Thailand, the Philippines and Malaysia have supplied riches in labour and resources to the regional economy (Macintyre and Naughton, 2005, p. 78). A growing middle class is lifting consumption. ‘Billions of Asians,' writes Mahbubani (2008, p. 3), 'are marching to modernity.’ This book examines scholarly interpretations for the role commercial law has played in East Asia's economic rise. At first blush, this might seem a daunting task. After all, as some theorists have argued, the East Asian experience is largely neglected in writings on Jaw generally and commercial law more broadly (Wolff, 20 12). This is because law, as a discipline, was largely forged in the prior European and American centuries; these 'Anglo-American moorings' ill-serve legal analysis in the new Asian Century (Cossman, 1997, p. 539).

Mutations in the gene encoding IFT dynein complex component WDR34 cause jeune asphyxiating thoracic dystrophy

Bidirectional (anterograde and retrograde) motor-based intraflagellar transport (IFT) governs cargo transport and delivery processes that are essential for primary cilia growth and maintenance and for hedgehog signaling functions. The IFT dynein-2 motor complex that regulates ciliary retrograde protein transport contains a heavy chain dynein ATPase/motor subunit, DYNC2H1, along with other less well functionally defined subunits. Deficiency of IFT proteins, including DYNC2H1, underlies a spectrum of skeletal ciliopathies. Here, by using exome sequencing and a targeted next-generation sequencing panel, we identified a total of 11 mutations in WDR34 in 9 families with the clinical diagnosis of Jeune syndrome (asphyxiating thoracic dystrophy). WDR34 encodes a WD40 repeat-containing protein orthologous to Chlamydomonas FAP133, a dynein intermediate chain associated with the retrograde intraflagellar transport motor. Three-dimensional protein modeling suggests that the identified mutations all affect residues critical for WDR34 protein-protein interactions. We find that WDR34 concentrates around the centrioles and basal bodies in mammalian cells, also showing axonemal staining. WDR34 coimmunoprecipitates with the dynein-1 light chain DYNLL1 in vitro, and mining of proteomics data suggests that WDR34 could represent a previously unrecognized link between the cytoplasmic dynein-1 and IFT dynein-2 motors. Together, these data show that WDR34 is critical for ciliary functions essential to normal development and survival, most probably as a previously unrecognized component of the mammalian dynein-IFT machinery.

Analytical study of osteoporosis of maxilla in ovariectomized rats

The project applied analytical facilities to characterize the composition and mechanical properties of osteoporosis in maxillary bone using an ovariectomized rat model. It was found that osteoporotic jaw bone contained different amount of trace elements in comparison with the normal bone, which plays a significant role in bone quality. The knowledge generated from the study will assist the treatment of jaw bone fracture and dental implant placement.

A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva

Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal dominant disorder of skeletal malformations and progressive extraskeletal ossification. We mapped FOP to chromosome 2q23-24 by linkage analysis and identified an identical heterozygous mutation (617G→A; R206H) in the glycine-serine (GS) activation domain of ACVR1, a BMP type I receptor, in all affected individuals examined. Protein modeling predicts destabilization of the GS domain, consistent with constitutive activation of ACVR1 as the underlying cause of the ectopic chondrogenesis, osteogenesis and joint fusions seen in FOP.

Mutation of perinatal myosin heavy chain

Veugelers et al. (July 29 issue)1 report on patients with the trismus–pseudocamptodactyly syndrome as having a “Carney complex variant.” Among more than 500 patients with the Carney complex in our database, there are none with the trismus–pseudocamptodactyly syndrome.2,3...

Treatment failure in celiac disease due to coexistent exocrine pancreatic insufficiency

A 17-year-old white adolescent had a history of chronic diarrhea, delayed puberty, and growth failure. Investigations excluded cystic fibrosis, Shwachman syndrome, and endocrine causes of growth failure. Severe steatorrhea was diagnosed from fecal fat studies, and a jejunal suction biopsy showed total villus atrophy, consistent with a diagnosis of celiac diseases. Following introduction of a gluten-free diet, his appetite and growth improved, but he continued to have abdominal discomfort and loose offensive bowel motions. One year later, severe steatorrhea was present. A repeat jejunal biopsy showed partial recovery of villus architecture. Serum immunoreactive trypsinogen level was low, which was highly suggestive of exocrine pancreatic failure. Results of quantitative pancreatic stimulation test confirmed the presence of primary pancreatic insufficiency. After introduction of oral pancreatic enzyme supplements with meals, his gastrointestinal symptoms resolved and growth velocity accelerated. Previously, primary pancreatic insufficiency has only been described in elderly patients with long-standing untreated celiac disease. This case, however, emphasizes that pancreatic failure can occur with celiac disease at any age. Determination of a serum immunoreactive trypsinogen level should be considered a useful screening tool for pancreatic insufficiency in patients with celiac disease who have not responded to a gluten-free diet.

Serum immunoreactive pancreatic lipase and cationic trypsinogen for the assessment of exocrine pancreatic function in older patients with cystic fibrosis

Indirect and qualitative tests of pancreatic function are commonly used to screen patients with cystic fibrosis for pancreatic insufficiency. In an attempt to develop a more quantitative assessment, we compared the usefulness of measuring serum pancreatic lipase using a newly developed enzyme-linked immunosorbent immunoassay with that of cationic trypsinogen using a radioimmunoassay in the assessment of exocrine pancreatic function in patients with cystic fibrosis. Previously, we have shown neither lipase nor trypsinogen to be of use in assessing pancreatic function prior to 5 years of age because the majority of patients with cystic fibrosis in early infancy have elevated serum levels regardless of pancreatic function. Therefore, we studied 77 patients with cystic fibrosis older than 5 years of age, 41 with steatorrhea and 36 without steatorrhea. In addition, 28 of 77 patients consented to undergo a quantitative pancreatic stimulation test. There was a significant difference between the steatorrheic and nonsteatorrheic patients with the steatorrheic group having lower lipase and trypsinogen values than the nonsteatorrheic group (P < .001). Sensitivities and specificities in detecting steatorrhea were 95% and 86%, respectively, for lipase and 93% and 92%, respectively, for trypsinogen. No correlations were found between the serum levels of lipase and trypsinogen and their respective duodenal concentrations because of abnormally high serum levels of both enzymes found in some nonsteatorrheic patients. We conclude from this study that both serum lipase and trypsinogen levels accurately detect steatorrhea in patients with cystic fibrosis who are older than 5 years but are imprecise indicators of specific pancreatic exocrine function above the level needed for normal fat absorption.

New records of the River Shark Glyphis (Carcharhinidae) reported from Cape York Peninsula, northern Australia

The distribution of the river shark Glyphis in northern Australia is extended with new records of occurrence in the Gulf of Carpentaria and a reassessment of historical survey data from Cape York Peninsula. Nine new specimens of Glyphis sp. A were collected in 2005 from the Weipa region on the Queensland coast of the Gulf of Carpentaria. A re-examination of archival records from 1978-86 marine and estuarine fish surveys in the Gulf of Carpentaria and along the northern Queensland East Coast allowed a further nineteen Glyphis specimens to be identified. Combined this gives twenty-eight new records of Glyphis specimens from the coasts of Cape York Peninsula, Queensland. Common habitat characteristics for all captures were turbid, shallow, fast running tidal water in the upper reaches of coastal rivers. The substrate was generally muddy and the rivers lined with mangrove. In all surveys the representation of Glyphis was low, being less than 1% of the total shark captures historically and 0.002 sharks 50 m net hour-1 in Weipa 2005. The size range captured was 1000-1800 mm total length historically and 705-1200 mm total length from Weipa 2005, with none recorded as sexually mature. Diagnostic characteristics of the Weipa specimens, identified as Glyphis sp. A, were: lower jaw teeth protruding and "spear-like"; second dorsal fin greater than half the height of the first dorsal fin; the snout relatively short and fleshy in the lateral view; pectoral fin ventral surface black in colouration; the precaudal vertebral count between 118 and 123; and the total vertebral count between 204 and 209.

Roy Kenzie Kiyooka

Roy Kenzie Kiyooka Canadian, born 1926 Roy Kiyooka was born in Moose Jaw, Saskatchewan in 1926. Throughout his career, he was known as a painter, photographer, sculptor, poet, musician, filmmaker and teacher. He studied at the Provincial Institute of Technology and Art in Calgary from 1946-49, and then at the Instituto Allende in Mexico in 1955. During the summers of 1958 - 1960 he attended the Emma Lake Workshops in Saskatchewan, where he worked closely with Barnett Newman and Clement Greenberg. In 1959 he executed his first series of abstract paintings, The Hoarfrost Series, which assume a disciplined minimal quality. In the late 1960's Kiyooka began to push beyond painting and created mixed media works, including collage, photography, film and poetry. Kiyooka’s art is born out of personal experience and through it he records his relationship to the surrounding landscape; a night in a motel, a trip to the coast, or hoarfrost on the trees. Through the unfolding of Kiyooka’s interior/exterior landscapes he shares his personal journeys with us all. The Art Gallery of Ontario's collection of Roy Kiyooka's work began with the purchase of two paintings; Barometer No. 2, in 1964 and Surya, in 1987.

Post capture necrosis of the feet caused by soft-catch traps – incidents, cause and prevention.

When recapturing satellite collared wild dogs that had been trapped one month previous in padded foothold traps, we noticed varying degrees of pitting on the pads of their trapped paw. Veterinary advice, based on images taken of the injuries, suggests that the necrosis was caused by vascular compromise. Five of six dingoes we recaptured had varying degrees of necrosis restricted only to the trapped foot and ranging from single 5 mm holes to 25% sections of the toe pads missing or deformed, including loss of nails. The traps used were rubber-padded, two–coiled, Victor Soft Catch #3 traps. The springs are not standard Victor springs but were Beefer springs; these modifications slightly increase trap speed and the jaw pressure on the trapped foot. Despite this modification the spring pressure is still relatively mild in comparison to conventional long spring or four-coiled wild dog traps. The five wild dogs developing necrosis were trapped in November 2006 at 5-6 months of age. Traps were checked each morning so the dogs were unlikely to have been restrained in the trap for more than 12 hours. All dogs exhibited a small degree of paw damage at capture which presented itself as a swollen paw and compression at the capture point. In contrast, eight wild dogs, 7-8 month-old, were captured two months later in February. Upon their release, on advice from a veterinarian, we massaged the trapped foot to get blood flow back in to the foot and applied a bruise treatment (Heparinoid 8.33 mg/ml) to assist restoring blood flow. These animals were subsequently recaptured several months later and showed no signs of necrosis. While post-capture foot injuries are unlikely to be an issue in conventional control programs where the animal is immediately destroyed, caution needs to be used when releasing accidentally captured domestic dogs or research animals captured in rubber-padded traps. We have demonstrated that 7-8 month old dogs can be trapped and released without any evidence of subsequent necrosis following minimal veterinary treatment. We suspect that the rubber padding on traps may increase the tourniquet effect by wrapping around the paw and recommend the evaluation of offset laminated steel jaw traps as an alternative. Offset laminated steel jaw traps have been shown to be relatively humane producing as few foot injuries as rubber-jawed traps.

Tadpole mouthpart depigmentation as an accurate indicator of chytridiomycosis, an emerging disease of amphibians

Chytridiomycosis is an emerging infectious disease of amphibians caused by the fungal pathogen Batrachochytrium dendrobatidis, and its role in causing population declines and species extinctions worldwide has created an urgent need for methods to detect it. Several reports indicate that in anurans chytridiomycosis can cause the depigmentation of tadpole tnouthparts, but the accuracy of using depigmentation to determine disease status remains uncertain. Our objective was to determine for the Mountain Yellow-legged Frog (Rana muscosa) whether visual inspections of the extent of tadpole mouthpart depigmentation could be used to accurately categorize individual tadpoles or R. muscosa populations as B. dendrobatidis-positive or negative. This was accomplished by assessing the degree of mouthpart depigmentation in tadpoles of known disease status (based on PCR assays). The depigmentation of R. muscosa tadpole mouthparts was associated with the presence of B. dendrobatidis, and this association was particularly strong for upper jaw sheaths. Using a rule that classifies tadpoles with upper jaw sheaths that are 100% pigmented as uninfected and those with jaw sheaths that are <100% pigmented as infected resulted in the infection status of 86% of the tadpoles being correctly classified. By applying this rule to jaw sheath pigmentation scores averaged across all tadpoles inspected per site, we were able to correctly categorize the infection status of 92% of the study populations. Similar research on additional anurans is critically needed to determine how broadly applicable our results for R. muscosa are to other species.

Molecular genetics of tooth agenesis

Congenital missing of teeth, tooth agenesis or hypodontia, is one of the most common developmental anomalies in man. The common forms in which one or a few teeth are absent, may cause occlusal or cosmetic harm, while severe forms which are relatively rare always require clinical attention to support and maintain the dental function. Observation of tooth agenesis is also important for diagnosis of malformation syndromes. Some external factors may cause developmental defects and agenesis in dentition. However, the role of inheritance in the etiology of tooth agenesis is well established by twin and family studies. Studies on familial tooth agenesis as well as mouse null mutants have also identified several genetic factors. However, these explain syndromic or rare dominant forms of tooth agenesis, whereas the genes and defects responsible for the majority of cases of tooth agenesis, especially the common and less severe forms, are largely unknown. In this study it was shown, that a dominant nonsense mutation in PAX9 was responsible for severe tooth agenesis (oligodontia) in a Finnish family. In a study of tooth agenesis associated with Wolf-Hirschhorn syndrome, it was shown that severe tooth agenesis was present if the causative deletion in 4p spanned the MSX1 locus. It was concluded that severe tooth agenesis was caused by haploinsufficiency of these transcription factors. A summary of the phenotypes associated with known defects in MSX1 and PAX9 showed that, despite similarities, they were significantly different, suggesting that the genes, in addition to known interactions, also have independent roles during the development of human dentition. The original aim of this work was to identify gene defects that underlie the common incisor and premolar hypodontia. After excluding several candidate genes, a genome-wide search was conducted in seven Finnish families in which this phenotype was inherited in an autosomal dominant manner. A promising locus for second premolar agenesis was identified in chromosome 18 in one family and this finding was supported by results from other families. The results also implied the existence of other loci both for second premolar agenesis and for incisor agenesis. On the other hand the results did not lend support for comprehensive involvement of the most obvious candidate genes in the etiology of incisor and premolar hypodontia. Rather, they suggest remarkable genetic heterogeneity of tooth agenesis. The available evidence suggests that quantitative defects during tooth development predispose to a failure to overcome a developmental threshold and to agenesis. The results of the study increase the understanding of the etiology and heredity of tooth agenesis. Further studies may lead to identification of novel genes that affect the development of teeth.

The Molecular Basis of Hydrolethalus Syndrome

Hydrolethalus syndrome (HLS) is a severe fetal malformation syndrome that is inherited by an autosomal recessive manner. HLS belongs to the Finnish disease heritage, an entity of rare diseases that are more prevalent in Finland than in other parts of the world. The phenotypic spectrum of the syndrome is wide and it is characterized by several developmental abnormalities, including hydrocephalus and absent midline structures in the brain, abnormal lobation of the lungs, polydactyly as well as micrognathia and other craniofacial anomalies. Polyhydramnios are relatively frequent during pregnancy. HLS can nowadays be effectively identified by ultrasound scan already at the end of the first trimester of pregnancy. One of the main goals in this study was to identify and characterize the gene defect underlying HLS. The defect was found from a previously unknown gene that was named HYLS1. Identification of the gene defect made it possible to confirm the HLS diagnosis genetically, an aspect that provides valuable information for the families in which a fetus is suspected to have HLS. Neuropathological findings of mutation confirmed HLS cases were described for the first time in detail in this study. Also, detailed general pathological findings were described. Since HYLS1 was an unknown gene with no relatives in the known gene families, many functional studies were performed in order to unravel the function of the gene and of the protein it codes for. Studies showed, for example, that the subcellular localization of the HYLS1 protein was different when the normal and the defective forms were compared. In addition, HYLS1 was shown to possess transactivation potential which was significantly diminished in the defective form. According to the results of this study it can be stated that HYLS1 most likely participates in transcriptional regulation and also in the regulation of cholesterol metabolism and that the function of HYLS1 is critical for normal fetal development.

Placental abruption : Studies on incidence, risk factors and potential predictive biomarkers

Placental abruption, one of the most significant causes of perinatal mortality and maternal morbidity, occurs in 0.5-1% of pregnancies. Its etiology is unknown, but defective trophoblastic invasion of the spiral arteries and consequent poor vascularization may play a role. The aim of this study was to define the prepregnancy risk factors of placental abruption, to define the risk factors during the index pregnancy, and to describe the clinical presentation of placental abruption. We also wanted to find a biochemical marker for predicting placental abruption early in pregnancy. Among women delivering at the University Hospital of Helsinki in 1997-2001 (n=46,742), 198 women with placental abruption and 396 control women were identified. The overall incidence of placental abruption was 0.42%. The prepregnancy risk factors were smoking (OR 1.7; 95% CI 1.1, 2.7), uterine malformation (OR 8.1; 1.7, 40), previous cesarean section (OR 1.7; 1.1, 2.8), and history of placental abruption (OR 4.5; 1.1, 18). The risk factors during the index pregnancy were maternal (adjusted OR 1.8; 95% CI 1.1, 2.9) and paternal smoking (2.2; 1.3, 3.6), use of alcohol (2.2; 1.1, 4.4), placenta previa (5.7; 1.4, 23.1), preeclampsia (2.7; 1.3, 5.6) and chorioamnionitis (3.3; 1.0, 10.0). Vaginal bleeding (70%), abdominal pain (51%), bloody amniotic fluid (50%) and fetal heart rate abnormalities (69%) were the most common clinical manifestations of placental abruption. Retroplacental blood clot was seen by ultrasound in 15% of the cases. Neither bleeding nor pain was present in 19% of the cases. Overall, 59% went into preterm labor (OR 12.9; 95% CI 8.3, 19.8), and 91% were delivered by cesarean section (34.7; 20.0, 60.1). Of the newborns, 25% were growth restricted. The perinatal mortality rate was 9.2% (OR 10.1; 95% CI 3.4, 30.1). We then tested selected biochemical markers for prediction of placental abruption. The median of the maternal serum alpha-fetoprotein (MSAFP) multiples of median (MoM) (1.21) was significantly higher in the abruption group (n=57) than in the control group (n=108) (1.07) (p=0.004) at 15-16 gestational weeks. In multivariate analysis, elevated MSAFP remained as an independent risk factor for placental abruption, adjusting for parity ≥ 3, smoking, previous placental abruption, preeclampsia, bleeding in II or III trimester, and placenta previa. MSAFP ≥ 1.5 MoM had a sensitivity of 29% and a false positive rate of 10%. The levels of the maternal serum free beta human chorionic gonadotrophin MoM did not differ between the cases and the controls. None of the angiogenic factors (soluble endoglin, soluble fms-like tyrosine kinase 1, or placental growth factor) showed any difference between the cases (n=42) and the controls (n=50) in the second trimester. The levels of C-reactive protein (CRP) showed no difference between the cases (n=181) and the controls (n=261) (median 2.35 mg/l [interquartile range {IQR} 1.09-5.93] versus 2.28 mg/l [IQR 0.92-5.01], not significant) when tested in the first trimester (mean 10.4 gestational weeks). Chlamydia pneumoniae specific immunoglobulin G (IgG) and immunoglobulin A (IgA) as well as C. trachomatis specific IgG, IgA and chlamydial heat-shock protein 60 antibody rates were similar between the groups. In conclusion, although univariate analysis identified many prepregnancy risk factors for placental abruption, only smoking, uterine malformation, previous cesarean section and history of placental abruption remained significant by multivariate analysis. During the index pregnancy maternal alcohol consumption and smoking and smoking by the partner turned out to be the major independent risk factors for placental abruption. Smoking by both partners multiplied the risk. The liberal use of ultrasound examination contributed little to the management of women with placental abruption. Although second-trimester MSAFP levels were higher in women with subsequent placental abruption, clinical usefulness of this test is limited due to low sensitivity and high false positive rate. Similarly, angiogenic factors in early second trimester, or CRP levels, or chlamydial antibodies in the first trimester failed to predict placental abruption.