Priming with atracurium efficiently suppresses etomidate-induced myoclonus

IntroductionEtomidate is a hypnotic drug widely used as an intravenous anesthetic induction agent. The incidence of etomidate-induced myoclonus has been reported as much as 50–80% after induction making it an undesirable drug for induction.ObjectiveOur aim is to use a priming dose of atracurium to suppress etomidate-induced myoclonus during induction of anesthesia.MethodsIn a double-blinded clinical trial 80 patients were randomly given either atracurium (20% of ED95 × kg) or saline as a priming agent. Then, induction of anesthesia was performed using 0.4 mg/kg etomidate. Age, weight, body mass index, bispectral index (BIS) monitor, and duration and grade of myoclonus were recorded.ResultsThe demographic characteristics, age, body mass index, BIS score, and weight were not significantly different between the atracurium (ATRA) priming group and control groups. The binomial regression model showed that BMI was an independent predictor variable for myoclonus (OR: 2.1, CI 95%: 1.7–7.5, p = 0.032). In this model, adjusted odds ratios (OR) of myoclonus (multivariate logistic regression analysis) in the control group was 6.6 (95% CI: 1.5–9.7, p = 0.013).ConclusionLow-dose atracurium priming could effectively suppress etomidate-induced myoclonus.     

Biased Homozygous Haplotypes Across the Human Caveolin 1 Upstream Purine Complex in Parkinson’s Disease

The alpha-synuclein–caveolin 1 axis is suggested to be of role in the pathogenesis of Parkinson’s disease in cell line models. The objective of this study was to analyze the homozygous haplotype compartment of the human caveolin 1 gene upstream purine complex in patients afflicted with Parkinson’s disease. This complex was screened in patients with Parkinson’s disease (n?=?141) and compared with a group of controls (n?=?760) using polymerase chain reaction and sequencing. The expression activity of the homozygous haplotypes was then examined using luciferase Dual-Glo system in human neuronal cell line, LAN-5. Six haplotypes were found to be homozygous in the patients, and not in the control pool (Fisher exact p?<?1?×?10^?6). Three of those haplotypes were specific to Parkinson’s disease (Fisher exact p?<?0.002), and the remaining three overlapped with homozygous haplotypes in Alzheimer’s disease and multiple sclerosis (Fisher exact p?<?0.002). The disease haplotypes contained motif lengths that were nonexistent in the control homozygous haplotype pool and significantly increased gene expression (p?<?9?×?10^—6). We conclude that skew in the caveolin 1 purine complex homozygous haplotype compartment and an additive effect of those haplotypes may be linked with Parkinson’s disease.     

Antilipolytic effects of 1,8‐naphthyridine derivatives β‐adrenoceptor antagonists in rat white adipocytes

The rat fat cell β‐adrenoceptors were investigated by studying the effects of new 1,8‐naphthyridine derivatives synthesized starting from 7‐amino‐2‐chloro‐3‐phenyl‐1,8‐naphthyridine on lipolysis induced by isoprenaline, and alprenolol. Lipolysis induced by isoprenaline agonist was competitively antagonized by the 1,8‐naphthyridine analogue with a 7‐hydroxy‐2‐(4′‐methoxybenzylamine)‐6‐nitro‐3‐phenyl substituent designated as 3 . In contrast, 10, 50, and 100 μm of 7‐methoxy and 7‐ethoxy derivatives did not modify the concentration–response curve of isoprenaline. A rightward shift of the curve was, however, observed with 50 μm of a 7‐methoxy‐2‐(4′‐methoxybenzylamine)‐6‐amino‐3‐phenyl substituent designated as 10 . The selective β₁‐AR antagonist, 7‐hydroxy‐4‐morpholinomethyl‐2‐piperazino‐1,8‐naphthyridine slightly reduced isoprenaline‐induced lipolysis only at high doses. Alprenolol‐mediated lipolytic effect was antagonized by derivative 3 , 10 and the selective β₃‐AR antagonist SR 59,230A, but resistant to the selective β₁‐AR antagonist 7‐hydroxy‐4‐morpholinomethyl‐2‐piperazino‐1,8‐naphthyridine. The results provide preliminary pharmacological evidence for the antilipolytic effect of the newly synthesized 1,8‐naphthyridine derivatives on rat fat cells. The analogues designated as 3 and 10 were the most potent antagonists of this series.     

Hospital-acquired infections in a tertiary hospital in Iran before and during the COVID-19 pandemic

Wiener Medizinische Wochenschrift - Infection prevention protocols are the accepted standard to control nosocomial infections. These protective measures intensified after the coronavirus 2019...     

Photobiomodulation therapy reduces apoptotic factors and increases glutathione levels in a neuropathic pain model

Neuropathic pain (NP) is caused by damage to the nervous system due to reactive oxygen spices (ROS) increase, antioxidants reduction, ATP production imbalance, and induction of apoptosis. In this investigation, we applied low-level laser 660 nm (photobiomodulation therapy) as a new strategy to modulate pain. In order to study the effects of photobiomodulation therapy (660 nm) on NP, chronic constriction injury (CCI) model was selected. Low-level laser of 660 nm was used for 2 weeks. Thermal and mechanical hyperalgesia were measured before and after surgery on days 7 and 14, respectively. Paw withdrawal thresholds were also evaluated. Expression of p2x3, Bax, and bcl2 protein was measured by western blotting. The amount of glutathione (GSH) was measured in the spinal cord by continuous spectrophotometric rate determination method. The results are presented as mean?±?SD. Statistical analysis of data was carried out using SPSS 21. CCI decreased the pain threshold, 2-week photobiomodulation therapy significantly increased mechanical and thermal threshold, decreased P2X3 expression (p?<?0.001), and increased bcl2 expression (p?<?0.01), but it was not effective on the Bax expression. We speculated that although photobiomodulation therapy increased ROS generation, it increased antioxidants such as GSH. Increase in bcl2 is another mitochondrial protection mechanism for cell survival and that pain relief and decrease in P2X3 expression confirm it.     

Systemic markers of microvascular disease and bone mineral density in older adults

Summary

Here we report that abnormal brain white matter and, to a lesser extent, albuminuria are associated with reduced bone mineral density in the hip, spine, and total body in men and women. These findings may explain the increased hip fracture risk reported in some studies in association with microvascular disorders.

Introduction

Markers of microvascular disease have been individually associated with increased risk of osteoporotic fractures in some studies. Here, we examine whether these markers are associated with reduced bone mineral density (BMD) individually and together.

Methods

BMD testing using dual x-ray absorptiometry of the hip, lumbar spine, and total body was performed in 1473 participants from the Cardiovascular Health Study (mean age ~ 78 years): 1215 were assessed for urinary albumin-creatinine ratio, 944 for abnormal white matter disease (AWMD) by brain MRI, and 541 for retinal vascular disease with fundus photographs. Linear regression models were used to evaluate the cross-sectional association of each marker with BMD accounting for potentially confounding factors.

Results

AWMD was associated with lower hip, spine, and total body BMD in women (β ?3.08 to ?4.53; p < 0.01 for all) and lower hip and total body BMD in men (β ?2.90 to ?4.24; p = 0.01–0.03). Albuminuria was associated with lower hip (β ?3.37; p = .05) and total body (β ?3.21; p = .02) BMD in men, but not in women. The associations of AWMD and albuminuria with BMD persisted with mutual adjustment and appeared to be additive to each other. Retinal vascular disease was not associated with BMD in men or women.

Conclusion

AWMD and, to a lesser extent, albuminuria were independently associated with lower BMD, suggesting that microvascular disease may play a role in the pathogenesis of reduced BMD. These findings need to be confirmed by longitudinal studies.

     

Assessing the Validity of Western Measurement of Online Risks to Children in an Asian Context

Before the advent of the Internet, television and film was the only audio-visual medium to which most children were exposed. The risks were primarily limited to children being exposed to sexual and violent materials, the nature of which were known and easy to control. Nowadays, children are surrounded by a variety of digital media and are exposed to different risks, many of which are still unknown. The Internet is fully integrated into children’s daily lives, along with the potential risks. The present study aimed to (i) describe the level of risks children are exposed to, and (ii) test the measurement validity of a total of 45 items assessing nine scales of online risk to children that were adapted from studies carried out in Europe and the United States. The study comprised 420 schoolchildren. The results showed that children were more exposed to ‘unwanted exposure to pornography’ and less to ‘conduct risk’ (e.g., accidental illegal downloading; creating profiles on inappropriate websites). Boys and older children were more exposed to the risks compared to girls and younger children. The study validated five dimensions (inappropriate materials, sexting, contact-related risks, risky online sexual behavior, and bullying/being bullied) assessing online risk to children by using exploratory and confirmatory factor analyses. The study found that scales developed in Europe and the United States are not wholly suitable to an Asian context and needed to be modified. Further investigation to classify online risks to children and offer a solutions to reducing the online risks.