Acute respiratory distress after metofluthrin insecticide ingestion in a 19-month-old girl

Metofluthrin is a volatile pyrethroid insecticide. Despite being widely used as a safe household insecticide, it could cause severe systemic symptoms. A 19-month-old girl was taken to the emergency department after ingesting 1 mL of a mosquito repellent containing metofluthrin. After the arrival, the girl developed respiratory distress, which worsened progressively despite the administration of oxygen with nebulized salbutamol and budesonide. Additionally, she underwent application of high-flow nasal cannula, and administration of activated charcoal and systemic steroids. Her dyspnea gradually improved, and she was thus discharged on day 4 with oral prednisolone. All medications were discontinued 10 days after the discharge without any complication. Respiratory distress can develop after the ingestion of even a small amount of metofluthrin. Symptomatic and adjunctive steroid therapies can be effective therapeutic options

Grape seed proanthocyanidin extract inhibits glutamate-induced cell death through inhibition of calcium signals and nitric oxide formation in cultured rat hippocampal neurons

<p>Abstract</p> <p>Background</p> <p>Proanthocyanidin is a polyphenolic bioflavonoid with known antioxidant activity. Some flavonoids have a modulatory effect on [Ca²⁺]_i. Although proanthocyanidin extract from blueberries reportedly affects Ca²⁺buffering capacity, there are no reports on the effects of proanthocyanidin on glutamate-induced [Ca²⁺]_ior cell death. In the present study, the effects of grape seed proanthocyanidin extract (GSPE) on glutamate-induced excitotoxicity was investigated through calcium signals and nitric oxide (NO) in cultured rat hippocampal neurons.</p> <p>Results</p> <p>Pretreatment with GSPE (0.3-10 μg/ml) for 5 min inhibited the [Ca²⁺]_iincrease normally induced by treatment with glutamate (100 μM) for 1 min, in a concentration-dependent manner. Pretreatment with GSPE (6 μg/ml) for 5 min significantly decreased the [Ca²⁺]_iincrease normally induced by two ionotropic glutamate receptor agonists, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). GSPE further decreased AMPA-induced response in the presence of 1 μM nimodipine. However, GSPE did not affect the 50 mM K⁺-induced increase in [Ca²⁺]_i. GSPE significantly decreased the metabotropic glutamate receptor agonist (<it>RS</it>)-3,5-Dihydroxyphenylglycine-induced increase in [Ca²⁺]_i, but it did not affect caffeine-induced response. GSPE (0.3-6 μg/ml) significantly inhibited synaptically induced [Ca²⁺]_ispikes by 0.1 mM [Mg²⁺]_o. In addition, pretreatment with GSPE (6 μg/ml) for 5 min inhibited 0.1 mM [Mg²⁺]_o- and glutamate-induced formation of NO. Treatment with GSPE (6 μg/ml) significantly inhibited 0.1 mM [Mg²⁺]_o- and oxygen glucose deprivation-induced neuronal cell death.</p> <p>Conclusions</p> <p>All these data suggest that GSPE inhibits 0.1 mM [Mg²⁺]_o- and oxygen glucose deprivation-induced neurotoxicity through inhibition of calcium signals and NO formation in cultured rat hippocampal neurons.</p

Matrix Metalloproteinase-3 Causes Dopaminergic Neuronal Death through Nox1-Regenerated Oxidative Stress

In the present study we investigated the interplay between matrix metalloproteinase 3 (MMP3) and NADPH oxidase 1 (Nox1) in the process of dopamine (DA) neuronal death. We found that MMP3 activation causes the induction of Nox1 via mitochondrial reactive oxygen species (ROS) production and subsequently Rac1 activation, eventually leading to Nox1-derived superoxide generation in a rat DA neuronal N27 cells exposed to 6-OHDA. While a MMP3 inhibitor, NNGH, largely attenuated mitochondrial ROS and subsequent Nox1 induction, both apocynin, a putative Nox inhibitor and GKT137831, a Nox1 selective inhibitor failed to reduce 6-OHDA-induced mitochondrial ROS. However, both inhibitors for MMP3 and Nox1 similarly attenuated 6-OHDA-induced N27 cell death. RNAi-mediated selective inhibition of MMP3 or Nox1 showed that knockdown of either MMP3 or Nox1 significantly reduced 6-OHDA-induced ROS generation in N27 cells. While 6-OHDA-induced Nox1 was abolished by MMP3 knockdown, Nox1 knockdown did not alter MMP3 expression. Direct overexpression of autoactivated MMP3 (actMMP3) in N27 cells or in rat substantia nigra (SN) increased expression of Nox1. Selective knockdown of Nox1 in the SN achieved by adeno-associated virus-mediated overexpression of Nox1-specific shRNA largely attenuated the actMMP3-mediated dopaminergic neuronal loss. Furthermore, Nox1 expression was significantly attenuated in Mmp3 null mice treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Together we established novel molecular mechanisms underlying oxidative stress-mediated dopaminergic neuronal death in which MMP3 activation is a key upstream event that leads to mitochondrial ROS, Nox1 induction and eventual dopaminergic neuronal death. Our findings may lead to the development of novel therapeutic approach

Matrix Metalloproteinase-3 Causes Dopaminergic Neuronal Death through Nox1-Regenerated Oxidative Stress

In the present study we investigated the interplay between matrix metalloproteinase 3 (MMP3) and NADPH oxidase 1 (Nox1) in the process of dopamine (DA) neuronal death. We found that MMP3 activation causes the induction of Nox1 via mitochondrial reactive oxygen species (ROS) production and subsequently Rac1 activation, eventually leading to Nox1-derived superoxide generation in a rat DA neuronal N27 cells exposed to 6-OHDA. While a MMP3 inhibitor, NNGH, largely attenuated mitochondrial ROS and subsequent Nox1 induction, both apocynin, a putative Nox inhibitor and GKT137831, a Nox1 selective inhibitor failed to reduce 6-OHDA-induced mitochondrial ROS. However, both inhibitors for MMP3 and Nox1 similarly attenuated 6-OHDA-induced N27 cell death. RNAi-mediated selective inhibition of MMP3 or Nox1 showed that knockdown of either MMP3 or Nox1 significantly reduced 6-OHDA-induced ROS generation in N27 cells. While 6-OHDA-induced Nox1 was abolished by MMP3 knockdown, Nox1 knockdown did not alter MMP3 expression. Direct overexpression of autoactivated MMP3 (actMMP3) in N27 cells or in rat substantia nigra (SN) increased expression of Nox1. Selective knockdown of Nox1 in the SN achieved by adeno-associated virus-mediated overexpression of Nox1-specific shRNA largely attenuated the actMMP3-mediated dopaminergic neuronal loss. Furthermore, Nox1 expression was significantly attenuated in Mmp3 null mice treated with N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Together we established novel molecular mechanisms underlying oxidative stress-mediated dopaminergic neuronal death in which MMP3 activation is a key upstream event that leads to mitochondrial ROS, Nox1 induction and eventual dopaminergic neuronal death. Our findings may lead to the development of novel therapeutic approach

Phytohormone abscisic acid control RNA-dependent RNA polymerase 6 gene expression and post-transcriptional gene silencing in rice cells

RNA-dependent RNA polymerase 6 (RDR6) catalyses dsRNA synthesis for post-transcriptional gene silencing (PTGS)-associated amplification and the generation of endogeneous siRNAs involved in developmental determinations or stress responses. The functional importance of RDR6 in PTGS led us to examine its connection to the cellular regulatory network by analyzing the hormonal responses of RDR6 gene expression in a cultured cell system. Delivery of dsRNA, prepared in vitro, into cultured rice (Oryza sativa cv. Japonica Dongjin) cells successfully silenced the target isocitrate lyase (ICL) transcripts. Silencing was transient in the absence of abscisic acid (ABA), while it became persistent in the presence of ABA in growth medium. A transcription assay of the OsRDR6 promoter showed that it was positively regulated by ABA. OsRDR6-dependent siRNA(ICL) generation was also significantly up-regulated by ABA. The results showed that, among the five rice OsRDR isogenes, only OsRDR6 was responsible for the observed ABA-mediated amplification and silencing of ICL transcripts. We propose that ABA modulates PTGS through the transcriptional control of the OsRDR6 gene

Privacy Protection for Personal Health Device Communication and Healthcare Building Applications

This paper proposes a new method for protecting patient privacy when communicating with a gateway which collects bioinformation through using personal health devices, a type of biosensor for telemedicine, at home and in other buildings. As the suggested method is designed to conform with ISO/IEEE 11073-20601, which is the international standard, interoperability with various health devices was considered. We believe it will be a highly valuable resource for dealing with basic data because it suggests an additional standard for security with the Continua Health Alliance or related international groups in the future

A 4-year-old girl presenting with facial palsy, found to have increased delta neutrophil index, and diagnosed with acute myeloid leukemia with extramedullary infiltration

Although Bell’s palsy is the most common cause of facial palsy in children, some cases have potentially fatal causes. We report a rare case of isolated facial palsy in a 4-year-old girl whose diagnosis was acute myeloid leukemia with extramedullary infiltration. The findings of laboratory investigations were nonspecific at presentation except that the delta neutrophil index was 34.5% (reference range, 0%-5%). To avoid hasty diagnosis of Bell’s palsy in children with isolated facial palsy, vigilant differential diagnosis and workup are recommended

In-rich InGaN/GaN quantum wells grown by metal-organic chemical vapor deposition

Growth mechanism of In-rich InGaN/GaN quantum wells (QWs) was investigated. First, we examined the initial stage of InN growth on GaN template considering strain-relieving mechanisms such as defect generation, islanding, and alloy formation at 730 degrees C. It was found that, instead of formation of InN layer, defective In-rich InGaN layer with thickness fluctuations was formed to relieve large lattice mismatch over 10% between InN and GaN. By introducing growth interruption (GI) before GaN capping at the same temperature, however, atomically flat InGaN/GaN interfaces were observed, and the quality of In-rich InGaN layer was greatly improved. We found that decomposition and mass transport processes during GI in InGaN layer are responsible for this phenomenon. There exists severe decomposition in InGaN layer during GI, and a 1-nm-thick InGaN layer remained after GI due to stronger bond strength near the InGaN/GaN interface. It was observed that the mass transport processes actively occurred during GI in InGaN layer above 730 degrees C so that defect annihilation in InGaN layer was greatly enhanced. Finally, based on these experimental results, we propose the growth mechanism of In-rich InGaN/GaN QWs using GI.open9