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We sequenced the complete mitochondrial genome of the fishfly species Acanthacorydalis fruhstorferi van der Weele (Megaloptera: Corydalidae). The genome, which was 15,286 bp in length, included a standard set of 13 protein-coding genes, 22 transfer RNA genes (tRNAs), two ribosomal RNA genes (rRNAs), and a putative A+T-rich region. The gene arrangement is identical to that of most common Megaloptera mitochondrial genomes. We analyzed the preferred codon usage of the protein-coding genes and predicted the secondary structures of all the RNA transcripts. In addition, a phylogenetic tree was constructed based on the sequences of the 13 protein-coding genes, and the results supported the current view of a close relationship between Megaloptera and Neuroptera. Our analyses suggest that complete mitochondrial genome sequences are a promising method to fully resolve the phylogenetic relationships within Megaloptera.

Obstructive Sleep Apnea and Obesity Hypoventilation Syndrome are two similar diseases. Obstructive Sleep Apnea has been receiving more and more attention while the diagnostic rate of Obesity Hypoventilation Syndrome is not high. Few studies directly evaluated the relationship between them. We systematically analyzed the relevance of the two diseases. MEDLINE®, EMBASE® and the Cochrane Library were carried out to find studies until May 2017. Pooled mean difference and 95% confidence interval were calculated to evaluate the value of clinical and physiologic variables in the prediction of Obesity Hypoventilation Syndrome. 9 Studies (n = 2085) fulfilled the predefined selection criteria. Totally 575 patients (28%) with Obesity Hypoventilation Syndrome were diagnosed from 2085 Obstructive Sleep Apnea patients. Among clearly diagnosed Obstructive Sleep Apnea patients, higher Body Mass Index levels(mean difference:4.72 kg/m2; 95% confidence interval: 4.26 to 5.17; p < 0.00001), higher Apnea-Hypopnea Index (mean difference: 8.36; 95% confidence interval: -3.88 to -2.84; p < 0.00001), greater neck circumference (mean difference:1.01; 95% confidence interval: 0.10 to 1.92; p = 0.03) and lower percent predicted FEV1 (mean difference:-10.28; 95% confidence interval:-11.33 to -9.22; p < 0.00001)were associated with the occurrence with obesity hypoventilation syndrome. We should be highly skeptical of obesity hypoventilation syndrome in Obstructive Sleep Apnea patients with these factors as early identification and appropriate treatment can improve prognosis.

Rational: Clinical and radiologic manifestations of pleural amyloidosis are non-specific. And it can easily be missed or misdiagnosed. Meanwhile, few studies document amyloidosis presenting with pulmonary infarcts at the same time. Hereby, we report a case of immunoglobulin light chain amyloidosis (AL) pleural amyloidosis with pulmonary embolism rarely reported. Patient concerns: A 66-year-old male patient who suffered recurrent pleural effusion for more than 6 months and coughed for 2 months was admitted to hospital for clear diagnosis and treatment. He was previously engaged in a job which exposed him to dust and talcum powder for a long time. He underwent right thoracentesis and anti-infective treatment before admission. The patient's cough and shortness of breath were slightly relieved. He still experienced pleural effusion and had symptoms of cough and shortness of breath. Diagnosis: Chest X-ray demonstrated bilateral pleural effusion. Chest computed tomography (CT) angiography demonstrated left lower pulmonary embolism. The thorascopy showed hyperaemia and black tissue of the parietal pleura, which were biopsied. The pathological diagnosis was amyloidosis. The final diagnosis of this patient was AL pleural amyloidosis and left lower pulmonary embolism. Intervention: During the hospitalization, the patient underwent thoracentesis several times without any conclusive diagnosis. After the diagnosis of pleural amyloidosis, the patient was repeatedly advised to undergo bone marrow biopsy and pleurodesis which the patient refused. For pulmonary embolism, Nadroparin calcium combined Warfarin were administered as anticoagulative therapy. Outcomes: The pulmonary embolism resolved 13 days after the anticoagulant therapy. The patient refused treatment for pleural effusion and requested for discharge. At the time of discharge, shortness of breath was relieved, and the pleural effusion had decreased. The patient was lost to follow-up. Lessons: Amyloidosis is a rare disease which can be ignored by many clinicians. It needs to be diagnosed promptly since the prognosis of amyloidosis is poor. Clinicians must improve relevant understandings of this kind of disease so as not to delay the diagnosis and treatment. We must be alert to the occurrence of embolic disease among amyloidosis patients. Last but not least, we should also think of the possibility of amyloidosis in patients with pulmonary embolism and recurrent pleural effusion.