Medical benefits for workmen under social insurance in Japan

Japan was the first Asian country to introduce social insurance measures and she has expanded them during the last few decades. The first social insurance law was passed in 1922 dealing with worker's health insurance in general. It was followed by many schemes of social insurance. National Health Insurance in 1938, Seamen's Insurance in 1939, Employees' Pension Insurance in 1941 and so forth. After World War II the new Constitution was enacted by which the Japanese Government was made responsible for the provision of medical care services for the whole nation. At present approximately the whole population is covered by either one or more of the various social insurance schemes. The main social insurance programs are shown in Figure 1 and Table 1. Most of these insurance schemes are compulsory under Japanese law. Since it would be too difficult and complicated to explain all of these forms of social insurance in detail, we will discuss only about two schemes directly related to medical care services for the workers; namely, the Health Insurance Scheme for non. occupational diseases and disorders (sickness or injury off the job) and Workmen's Compensation Insurance for occupational diseases and disorders (sickness or injury on the job).</p

Bioinformatics Analyses Determined the Distinct CNS and Peripheral Surrogate Biomarker Candidates Between Two Mouse Models for Progressive Multiple Sclerosis

Previously, we have established two distinct progressive multiple sclerosis (MS) models by induction of experimental autoimmune encephalomyelitis (EAE) with myelin oligodendrocyte glycoprotein (MOG) in two mouse strains. A.SW mice develop ataxia with antibody deposition, but no T cell infiltration, in the central nervous system (CNS), while SJL/J mice develop paralysis with CNS T cell infiltration. In this study, we determined biomarkers contributing to the homogeneity and heterogeneity of two models. Using the CNS and spleen microarray transcriptome and cytokine data, we conducted computational analyses. We identified up-regulation of immune-related genes, including immunoglobulins, in the CNS of both models. Pro-inflammatory cytokines, interferon (IFN)-γ and interleukin (IL)-17, were associated with the disease progression in SJL/J mice, while the expression of both cytokines was detected only at the EAE onset in A.SW mice. Principal component analysis (PCA) of CNS transcriptome data demonstrated that down-regulation of prolactin may reflect disease progression. Pattern matching analysis of spleen transcriptome with CNS PCA identified 333 splenic surrogate markers, including Stfa2l1, which reflected the changes in the CNS. Among them, we found that two genes (PER1/MIR6883 and FKBP5) and one gene (SLC16A1/MCT1) were also significantly up-regulated and down-regulated, respectively, in human MS peripheral blood, using data mining

Expectant management of a herniated amniotic sac presenting as silent uterine rupture: a case report and literature review.

Foetal membranes bulging into the abdominal cavity is a unique initial manifestation of silent or complete uterine rupture during pregnancy. Since silent uterine rupture has potential risk for complete uterine rupture, which leads to acute life-threatening complications for both the mother and baby, it is difficult to determine whether to manage expectantly or surgically, including repair of the uterine wall or termination of the pregnancy, especially in the early second trimester. We present here a case of a herniated amniotic sac with overstretched uterine wall of the fundus presenting as silent uterine rupture, which was incidentally detected on routine ultrasonography at 18 weeks' gestation in a 38-year-old primigravida with a history of myomectomy for diffuse uterine leiomyomatosis. Magnetic resonance imaging examination revealed that the myometrium thickness was fully maintained at the site of the foetal membranes ballooning. The pregnancy was therefore managed expectantly and continued to successful delivery at 30 weeks' gestation. The precise assessment of the uterine wall may be essential to manage a herniated amniotic sac presenting as silent uterine rupture and to optimise the outcome of the pregnancy. We review all cases of a herniated amniotic sac out of focally overstretched uterine wall before 34 weeks' gestation

Transgenic Monkey Model of the Polyglutamine Diseases Recapitulating Progressive Neurological Symptoms

Age-associated neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and the polyglutamine (polyQ) diseases, are becoming prevalent as a consequence of elongation of the human lifespan. Although various rodent models have been developed to study and overcome these diseases, they have limitations in their translational research utility owing to differences from humans in brain structure and function and in drug metabolism. Here, we generated a transgenic marmoset model of the polyQ diseases, showing progressive neurological symptoms including motor impairment. Seven transgenic marmosets were produced by lentiviral introduction of the human ataxin 3 gene with 120 CAG repeats encoding an expanded polyQ stretch. Although all offspring showed no neurological symptoms at birth, three marmosets with higher transgene expression developed neurological symptoms of varying degrees at 3–4 months after birth, followed by gradual decreases in body weight gain, spontaneous activity, and grip strength, indicating time-dependent disease progression. Pathological examinations revealed neurodegeneration and intranuclear polyQ protein inclusions accompanied by gliosis, which recapitulate the neuropathological features of polyQ disease patients. Consistent with neuronal loss in the cerebellum, brain MRI analyses in one living symptomatic marmoset detected enlargement of the fourth ventricle, which suggests cerebellar atrophy. Notably, successful germline transgene transmission was confirmed in the second-generation offspring derived from the symptomatic transgenic marmoset gamete. Because the accumulation of abnormal proteins is a shared pathomechanism among various neurodegenerative diseases, we suggest that this new marmoset model will contribute toward elucidating the pathomechanisms of and developing clinically applicable therapies for neurodegenerative diseases.ArticleeNeuro.4(2):e0250(2017)journal articl