RNA-seq analysis of diet-driven obesity and anti-obesity effects of quercetin glucoside or epigallocatechin gallate in Drosophila adults.

OBJECTIVE: High-fat diet (HFD) feeding stimulates fat accumulation in mammals and Drosophila. In the present study, we examined whether simultaneous feeding of familiar anti-obesity drugs, quercetin glycosides (QG) and epigallocatechin gallate (EGCG), to Drosophila has the same suppressive effect on fat accumulation as previously reported in rats and mice. To understand the underlying molecular mechanisms of HFD diet-induced obesity and the suppression effect of the drugs, we performed transcriptome analyses. MATERIALS AND METHODS: We induced extra fat accumulation by feeding Drosophila fly food containing 20% coconut oil and quantified the triglyceride accumulated in flies. The effects of anti-obesity drugs were also evaluated. We isolated total RNA from each sample and performed RNA-seq analyses and quantitive Real Time-Polymerase Chain Reaction (qRT-PCR) to investigate altered gene expression. RESULTS: The mRNA levels of several genes involved in lipid metabolism, glycolysis/gluconeogenesis, and anti-oxidative stress changed in HFD-fed adults. Moreover, the levels altered in those fed an HFD with QG or EGCG. The qRT-PCR further confirmed the RNA-seq data, suggesting that the expression of five essential genes for lipid metabolism changed in HFD-fed flies and altered in the flies treated with anti-obesity drugs. The most remarkable alteration was observed in the dHSL gene encoding a lipase involved in lipid-storage after HFD feeding and HFD with QG or EGCG. These alterations are consistent with HFD-induced fat accumulation as well as the anti-obesity effects of the drugs in mammals, suggesting that the genes play an important role in anti-obesity effects. CONCLUSIONS: These are the first reports to date of entire profiles of altered gene expression under the conditions of diet-induced obesity and its suppression by anti-obesity drugs in Drosophila.

Evaluation of bedmaking-related airborne and surface methicillin-resistant Staphylococcus aureus contamination.

The number of airborne methicillin-resistant Staphylococcus aureus (MRSA) before, during and after bedmaking was investigated. Air was sampled with an Andersen air sampler in the rooms of 13 inpatients with MRSA infection or colonization. Sampling of surfaces, including floors and bedsheets, was performed by stamp methods. MRSA-containing particles were isolated on all the sampler stages-stage 1 (>7 microm diameter) to stage 6 (0.65-1.1 microm). The MRSA-containing particles were mostly 2-3 microm diameter before bedmaking and >5 microm during bedmaking. The number was significantly higher 15 min after bedmaking than during the resting period, but the differences in counts after 30 and 60 min were not significant. MRSA was detected on many surfaces. The results suggest that MRSA was recirculated in the air, especially after movement. To prevent airborne transmission, healthcare staff should exercise great care to disinfect inanimate environments. Further studies will be needed to confirm the level of MRSA contamination of air during bedmaking and establish measures for prevention of airborne transmission.

[Blockade of the obturator nerve in transurethral electroresection of urinary bladder tumors]. / Blockade des N. obturatorius bei transurethraler Elektroresektion von Harnblasentumoren.

Stimulation of obturator nerve during transurethral electroresection causes violent adductor muscle contraction, and is a major cause of inadvertent bladder perforation. General anesthesia with muscle relaxants is often required when the bladder tumor is in the area where the obturator nerve passes in close proximity to the inferolateral bladder wall. Recently obturator nerve block under spinal anesthesia during transurethral surgery have been reported in several papers, but the blockade is not completely reliable. Obturator nerve block using electrostimulator (neutracer) and insulated electroneedle (pole needle) was performed in 25 patients with bladder tumors during transurethral electroresection from October 1980 to December 1981. We herein describe the technique and results of local obturator nerve blockade. Use of neutracer and pole needle makes the obturator nerve block a completely reliable, safe and easy procedure.

[Effect on cerebral blood flow of midazolam during modified neurolept-anesthesia].

Midazolam (0.2 mg.kg-1) was administered to ten patients undergoing neurosurgical operation and its influence on CBF was studied under modified NLA. Simultaneously, the plasma concentration of midazolam was measured. Heart rate and mean arterial blood pressure showed no significant changes after injection in comparison with the control. Cerebral blood flow (CBF) decreased for about 15-20% after 5 minutes, 10 minutes and 15 minutes in comparison with the control. However, 30 minutes later, CBF showed a trend to return to the control. This change in CBF is related to the changes of cerebro-vascular resistance. We applied cerebral oxygen extraction fraction (OEF) to evaluate cerebral metabolism. OEF was constant, showing no significant changes. It is concluded that cerebral oxygen consumption (CMRO2) has decreased together with the decrease in CBF. The plasma concentration of midazolam was 250-300 ng.ml-1 or greater after 5 minutes, 10 minutes and 15 minutes. We think that the sedative dose of midazolam can also sufficiently reduce CBF and CMRO2. The results suggest that midazolam is a safe and effective agent to use for anesthesia and provides adequate sedation for patients with intracranial hypertension.

[Effects of controlled hypotension induced by prostaglandin E1 on the cerebral blood flow].

The effect of controlled hypotension induced by prostaglandin E1 (PGE1) on the cerebral blood flow (CBF) was studied in 14 patients undergoing neurosurgery. CBF was measured by thermal diffusion using a flow probe with a Peltier stack. PGE1 was injected i.v. continuously, at a dose of 0.05, 0.1 and 0.2 micrograms.kg-1.min-1. CBF tended to increase dose-dependently but not significantly by PGE1 administration. Cerebral vascular resistance was reduced significantly by every dose of PGE1 administered. Therefore, the results indicate that the cerebral vascular beds are dilated directly by PGE1. In conclusion, this study suggests that PGE1 can be used safely to control hypotension without reducing CBF during neurosurgery.

[General anesthesia with sevoflurane and vecuronium for patients with dystrophia myotonica and progressive muscular dystrophy].

A 9 year old male previously diagnosed as progressive muscular dystrophy whose serum CPK5430IU.l-1 was very high received general anesthesia. Before anesthesia, dantrolene sodium 2 mg.kg-1 was given. Anesthesia was induced with thiamylal 100 mg and vecuronium bromide 3 mg. Anesthesia was maintained with sevoflurane (0.5%) in nitrous oxide (66%) and oxygen (33%). The course of anesthesia was uneventful. The operative time was 80 minutes. At the end of the operation, the patient recovered smoothly from anesthesia. A 46 year old female with dystrophia myotonia also received general anesthesia. The patient was diagnosed as having this disease 26 years previously. Preoperatively, the patient was suspected to have cardiac damage. Anesthesia was induced with thiamylal 100 mg, fentanyl 100 micrograms, midazolam 5 mg and vecuronium bromide 4 mg, and maintained with sevoflurane (1.0%) in nitrous oxide (66%) and oxygen (33%). Anesthesia was uneventful, but at the end of the operation, the patient could not breath fully by herself. She was placed on a ventilator and observed carefully. The endotracheal tube was removed 150 minutes after the induction of anesthesia. In these two cases, sevoflurane and vecuronium bromide were used safely.

[A case of chronic masticator space abscess].

Different neoplasms and infections are known to involve the masticator space, but pathological diagnosis and treatment of these lesions are not always simple due to anatomical complexity. We treated a 66-year-old man with an abscess in the nasopharyngeal masticator space. Physical and CT findings resembled those of neoplastic lesion because the onset dated back 5 years and the patient was lacking in notable signs of infection. Surgery through the maxillary sinus to the lesion enabled us to confirm its pathology and drain pus, with subsequent cure. We noted periodontal infection of the mandibular molars accompanied with osteomyelitis as a cause of this abscess, so infected molars were extracted 13 days after surgery. The infection had spread upward along the mastication muscles, resulting in an abscess in both the upper masseter muscle and the lower temporalis muscle. Based on a review of the literature, most abscesses in the masticator space originate from the mandibular molar, while the most impressive physical finding varied between the submandibular region and temporal fossa, as did its acute or chronic clinical course. Such clinical manifestations appear to reflect the pattern of infection spread along the muscles of mastication and a pattern involving adjacent spaces. We emphasize diagnostic significance when assessing findings for each mastication muscle and mandibular bone depicted using computed tomography, magnetic resonance imaging, and bone-scan technetium.

Mitochondrial neurogastrointestinal encephalomyopathy associated with progressive hearing loss.

OBJECTIVE: We report a rare case of mitochondrial neurogastrointestinal encephalomyopathy with hearing loss. CASE REPORT: A 46-year-old woman presented with a three-year history of progressive, bilateral hearing loss and tinnitus. She had been suffering from unexplained abdominal pain and diarrhoea for 20 years. When first seen, her otoscopic findings were normal, and pure tone audiometry showed mild and moderate hearing loss in her right and left ears, respectively. She also had: bilateral ophthalmoparesis, neck and limb muscle weakness, and hypoactive deep tendon reflexes on neurological examination; diffuse leukoencephalopathy on magnetic resonance imaging of the brain; and markedly reduced leukocyte thymidine phosphorylase activity. On the basis of these findings, the patient was diagnosed with mitochondrial neurogastrointestinal encephalomyopathy. CONCLUSION: Mitochondrial neurogastrointestinal encephalomyopathy is an autosomal recessive disease caused by mutation of the thymidine phosphorylase gene, and is characterised by ophthalmoparesis, peripheral neuropathy, leukoencephalopathy, gastrointestinal symptoms and abnormal mitochondria in muscle cells. Current advances in genetic research may reveal a higher prevalence of mitochondrial disorders than had previously been thought. Otolaryngologists should be aware of mitochondrial neurogastrointestinal encephalomyopathy and other rare genetic disorders when managing patients with progressive hearing loss.