Search

Participatory organizational interventions offer an effective way to promote occupational safety and health. Despite an increasing number of studies, a common definition of participatory organizational interventions has yet to be established. Therefore, we aimed to form a definition using the following process. First, we developed a tentative draft definition of organizational interventions and participatory elements, based on the relevant literature. The tentative definition was revised in several rounds of an extensive discussion by the authors. This resulted in the draft definition. We asked 15 selected international experts in occupational safety and health to review and comment on the draft definition. We carefully reviewed their comments, and formulated our final proposed definition. To summarize the key points of the final version of the definition, organizational interventions are planned actions that primarily directly target working conditions with the aim of promoting and maintaining of the highest degree of physical, mental, and social well-being of workers in all occupations. In addition, as participatory elements of organizational interventions in the final definition, ideally, all workers participate in every step of the intervention, while participating in part of the steps of the intervention in some cases. Furthermore, in principle, all workers participate in each step of intervention, while it is also acceptable that only elected representatives among workers participate in the intervention.

Participatory organizational interventions offer an effective way to promote occupational safety and health. Despite an increasing number of studies, a common definition of participatory organizational interventions has yet to be established. Therefore, we aimed to form a definition using the following process. First, we developed a tentative draft definition of organizational interventions and participatory elements, based on the relevant literature. The tentative definition was revised in several rounds of an extensive discussion by the authors. This resulted in the draft definition. We asked 15 selected international experts in occupational safety and health to review and comment on the draft definition. We carefully reviewed their comments, and formulated our final proposed definition. To summarize the key points of the final version of the definition, organizational interventions are planned actions that primarily directly target working conditions with the aim of promoting and maintaining of the highest degree of physical, mental, and social well‐being of workers in all occupations. In addition, as participatory elements of organizational interventions in the final definition, ideally, all workers participate in every step of the intervention, while participating in part of the steps of the intervention in some cases. Furthermore, in principle, all workers participate in each step of intervention, while it is also acceptable that only elected representatives among workers participate in the intervention.

Large placental chorioangioma is a rare but serious complication of pregnancy. To our knowledge, this case is the first reported diagnosis of consumption coagulopathy in a fetus using fetal blood sampling (FBS) during pregnancy complicated by placental chorioangioma. A 25-year-old woman, primigravida, was referred to our hospital at 29 weeks of gestation for placental chorioangioma. At 34+1 gestation, polyhydramnios and hyperdynamic circulation were observed in the fetus. FBS demonstrated microangiopathic hemolytic anemia and the presence of consumption coagulopathy. Cesarean section was performed at 34+4 gestation because fetal maturation was expected. A female infant weighing 2158 g was born, with Apgar scores of 6 and 8 at 1 and 5 min, respectively. Neonatal blood sampling results were similar to those of FBS. The infant was treated for hyperdynamic cardiac function, hemolytic anemia, and consumption coagulopathy on mechanical ventilation in the neonatal intensive care unit and recovered fully. When fetal anemia is suspected in a case of large placental chorioangioma, the possibility of developing consumption coagulopathy during the fetal period should be considered.

Cardiotrophin-1 (CT-1) is a potent cytokine that stimulates the assembly of sarcomeric units in series in cardiomyocytes through gp130 signaling, resulting in myocardial cell hypertrophy. To clarify the role of CT-1 and the gp130-signaling pathway during ventricular remodeling after myocardial infarction, we examined the expression of CT-1 and gp130 in a rat model of myocardial infarction. At 1, 3, 7, 14, 28 and 56 days (n=12 for each group) after ligation of a coronary artery, tissue samples were obtained from infarct tissue, the ventricular septum and the right ventricle. All animals developed large myocardial infarctions, with infarct sizes ranging from 39.8% to 50.3%. Progressive left ventricular dilatation and inadequate hypertrophy of the surviving myocardium were confirmed by echocardiography. CT-1 and gp130 mRNA levels were determined by semiquantitative reverse transcription-polymerase chain reaction using 1 or 5 μg of total RNA followed by Southern blotting. The densitometric analysis of the Southern blots revealed a significant increase in CT-1 and gp130 mRNA levels (P<0.01) compared with those of the sham-operated rats at 1, 3, 7, 14, 28 and 56 days post-infarct in the infarct area, the ventricular septum (non-infarcted area) and right ventricle. The protein levels of CT-1 and gp130, determined by Western blot analysis, were significantly increased (P<0.05) compared with those of sham-operated rats, peaked during the acute stage and declined thereafter in the three regions described above. Immunohistochemical staining showed that CT-1 and gp130-immunoreactivities were detected in cardiomyocytes and fibroblast-like cells and that the intensity of staining was increased at 7 days post-infarct compared with that in sham-operated rats. An augmented CT-1 and gp130 system thus appears to play an important role during ventricular remodeling after myocardial infarction.

We have cloned a cDNA encoding rat neutrophil inducible nitric oxide synthase (iNOS). The amino acid sequence of the iNOS in the rat neutrophils was 95% identical to that in the mouse macrophages, and the difference between the two sequences was most likely the result of species variability. Moreover, the iNOS in the rat neutrophils was 99% identical in amino acid sequence to that in the rat hepatocytes and vascular smooth muscle cells (VSMC). Northern blot analysis of total RNA from both rat macrophages and neutrophils showed a single band above 4 kilo-nucleotides. These findings suggest that iNOS in rat neutrophils, macrophages, hepatocytes, and VSMC are almost identical in the primary structure.

Acute kidney injury (AKI) is characterized by mitochondrial dysfunction and activation of the innate immune system. The cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) pathway detects cytosolic DNA and induces innate immunity. Here, we investigate the role of mitochondrial damage and subsequent activation of the cGAS-STING pathway using a genetically engineered animal model of cisplatin-induced AKI and cultured tubular cells. Cisplatin induced mtDNA leakage into the cytosol—probably through BCL-2-like protein 4 (BAX) pores in the mitochondrial outer membrane—in tubules, with subsequent activation of the cGAS-STING pathway, thereby triggering inflammation and AKI progression, which is improved in STING-deficient mice. STING knockdown in cultured tubular cells ameliorates inflammatory responses induced by cisplatin. mtDNA depletion and repletion studies support tubular inflammatory responses via the cGAS-STING signal activation by cytosolic mtDNA. Therefore, we conclude that mitochondrial dysfunction and subsequent activation of the mtDNA-cGAS-STING pathway is a critical regulator of kidney injury.