[Analysis of risk factors and consequences for concurrent obstructive sleep apnea in chronic obstructive pulmonary disease patients].

Objective: To compare clinical characteristics between patients with chronic obstructive pulmonary disease (COPD) and COPD -OSA overlap, and to analyze the risk factors for OSA in patients with COPD. Methods: A total of 431 patients with COPD were divided into a COPD-OSA group with AHI>15 events/h or a COPD group with AHI ≤ 15 events/h according to the results of polysomnography, and their clinical characteristics were summarized. Risk factors for OSA overlap in COPD patients were identified by univariate and multivariate logistic regression analyses. Results: There were no significant differences in gender composition, dyspnea scale (mMRC) score, the numbers of acute exacerbations and hospitalizations in the last year, prevalence of coronary heart disease, or cor pulmonale or diabetes mellitus in the two groups (all P>0.05). Age, BMI, neck circumference, smoking index, COPD assessment test (CAT) score, the values of FEV(1) or FEV(1)%, FEV(1)/FVC ratios, and the prevalence of hypertension in the COPD-OSA group with AHI>15 events/h were significantly higher than in the COPD group with AHI ≤15 events/h, while the duration of COPD and the proportion of severe COPD were lower than the COPD group with AHI≤ 15 (P<0.05). The scores of Charlson Comorbidity Index, Epworth Sleepiness Scale (ESS) and Sleep Apnea Clinical Score (SACS) in the COPD-OSA group were significantly higher than in the COPD group with AHI≤ 15, with all P values<0.05. Risk factors for AHI>15 OSA coinciding in patients with COPD included BMI, neck circumference, ESS, SACS and CAT (P<0.05). Furthermore, BMI, ESS and CAT were independent risk factors for OSA in COPD patients (P<0.05). Compared with mild or moderate COPD cases, patients with severe COPD (FEV(1)%<50%) had a lower risk of having OSA (ß=-0.459, OR=0.632, 95% CI 0.401-0.997, P=0.048). Conclusions: Compared to COPD patients with AHI ≤ 15 events/h, OSA-COPD overlap patients (AHI>15 events/h) had a worse quality of life, more daytime sleepiness and higher prevalence of hypertension. BMI, ESS and CAT were independent risk factors for AHI>15 OSA in patients with COPD. The risk of having OSA in severe COPD patients was lower than cases with mild or moderate COPD.

[Application of three questionnaires in screening obstructive sleep apnea in patients with chronic obstructive pulmonary disease].

Objective: To evaluate the clinical value of three questionnaires [Sleep Apnea Clinical Score (SACS), Berlin Questionnaire (BQ), and Epworth Sleepiness Scale (ESS)] in screening obstructive sleep apnea (OSA) in patients with chronic obstructive pulmonary disease (COPD). Methods: A total of 198 patients with COPD were assessed the likelihood of OSA by using the SACS, BQ, ESS, which was confirmed by the overnight polysomnography (PSG). The receiver operating characteristic curve (ROC) and the calculated likelihood ratios were used to compare the values of three scoring systems in predicting OSA in COPD patients. Results: The patients had an average age of (65.5±9.3) years and 92.9% (184 cases) of which were male, 14 cases (7.1%) were female; 27 cases (13.6%) had a high probability of OSA by SACS assessment, 61 cases (30.8%) had a high probability screened by BQ, and 72 (36.4%) had OSA high probability by ESS. The diagnosis of OSA in 75 patients (37.9%) were confirmed by PSG. OSA did not be accurately predicted by ESS screening in patients with COPD, with a ROC curve area under the curve of 0.592 (95% CI: 0.509-0.674, P=0.053). BQ had an area under the ROC curve of 0.706 (95% CI: 0.626-0.779, P<0.001). However, the prediction of SACS was much better, with an area under the ROC curve of 0.810 (95% CI: 0.737-0.871, P<0.001). Conclusion: SACS is superior to BQ and ESS in predicting OSA in this group of patients with COPD.

[5-HT(2A) receptor/protein kinase C pathway in mediating long-term facilitation of carotid sinus nerve discharge in chronic intermittent hypoxia rats].

Objective: To explore the role of 5-HT(2A)R/PKC pathway in mediating long-term facilitation (LTF) of carotid sinus nerve (CSN) discharge in chronic intermittent hypoxia (CIH) rats. Methods: With number table, 24 adult SD rats were randomly divided into saline control group (group A, n=6), 5-HT(2A)R antagonist (ketanserin) group (group B, n=6), PKC inhibitor (PKC θ-pseudosubstrate) group (group C, n=6) and combined ketanserin with PKC θ-pseudosubstrate group (group D, n=6). All rats were placed into the animal chambers for CIH treatment, 8 h per day (from 9: 00 to 17: 00) for 4 consecutive weeks. 28 days later, 5 min × 3 times of stimulation with acute intermittent hypoxia (AIH) were given, after that, stable CSN discharge activities were recorded and compared before and after intravenous injection of saline (group A), ketanserin (group B), PKC θ-pseudosubstrate (group C) or ketanserin + PKC θ-pseudosubstrate (group D), respectively. Results: There were no significant difference in the baseline (before AIH stimulation) average peak amplitude of CSN discharge among the four groups (P>0.05). In group A, the amplitude of CSN discharge at 30 min and 60 min after AIH were (5.01 ± 0.53) µV and (4.95 ± 0.34) µV respectively, which were significantly higher than that before AIH (P<0.01). The results implied that the CSN LTF could be induced by AIH in CIH pre-treatment rats. In group B, the amplitude of CSN discharge at 30 min and 60 min after AIH were (3.79 ± 0.42) µV and (3.73 ± 0.46) µV, respectively, which were still significantly higher than that before AIH (P<0.01), showing that carotid sinus nerve LTF couldn't be completely blocked by 5-HT(2A)R antagonist in rats. After injection of PKC θ-pseudosubstrate or ketanserin + PKC θ-pseudosubstrate in group C or D, there were no significant differences in CSN discharge amplitude before and after AIH (P>0.01), suggesting that inhibition of PKC alone or 5-HT(2A)R/PKC pathway could completely block the LTF of CSN. Conclusion: 5-HT(2A)R/PKC pathway was involved in mediating long-term facilitation of carotid sinus nerve discharge in CIH rats.

Empirical model of total internal reflection from highly turbid media.

We demonstrate, to the best of our knowledge, a first accurate empirical model for reflectance measurements from highly turbid media over the full range of incident angles, i.e., for reflectivity values going from unity in the total internal reflection regime to nearly zero when almost all the light is transmitted. Evidence that our model is accurate is provided by extraction of the particle size, followed by independent verification with dynamic light scattering. Our methodology is in direct contrast with the prevalent approach in turbid media of focusing on only the critical angle region, which is just a small subset of the entire reflectance data.

Long noncoding LUCAT1 promotes cisplatin resistance of non-small cell lung cancer by promoting IGF-2.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding LUCAT1 promotes cisplatin resistance of non-small cell lung cancer by promoting IGF-2, by W. Wang, M.-L. Dong, W. Zhang, T. Liu, published in Eur Rev Med Pharmacol Sci 2019; 23 (12): 5229-5234-DOI: 10.26355/eurrev_201906_18188-PMID: 31298373" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18188.

Long noncoding LUCAT1 promotes cisplatin resistance of non-small cell lung cancer by promoting IGF-2.

OBJECTIVE: Drug-resistance remains a huge problem in the therapy of malignant tumors including non-small cell lung cancer (NSCLC). Several researches have proved that long noncoding RNAs (lncRNAs) contributes to drug-resistance in NSCLC. LncRNA LUCAT1 was explored to identify how it functions in the cisplatin-resistance of NSCLC patients. MATERIALS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect LUCAT1 expression in A549/DDP cells and A549 cells. Then, we conducted cell counting kit-8 (CCK-8) assay and flow cytometric analysis to detect the function of LUCAT1 on the resistance of NSCLC cells to cisplatin. Furthermore, the potential mechanism was explored by mechanism assays. RESULTS: LUCAT1 expression of A549/DDP cells was higher than paired A549 cells. Besides, cell apoptosis was inhibited, cell cycle distribution was changed, and resistance to cisplatin was promoted after LUCAT1 was overexpressed in A549 cells. Furthermore, the overexpression of LUCAT1 could upregulate the IGF-2 expression in A549/DDP cells. CONCLUSIONS: We suggest that LUCAT1 regulates cell cycle, cell apoptosis of NSCLC cells and the resistance to cisplatin through targeting IGF-2 and could be a possible target for NSCLC treatment.

Composition, physiochemical properties, nitrogen fraction distribution, and amino acid profile of donkey milk.

This study investigated the changes in chemical composition, nitrogen fraction distribution, and AA profile of milk samples obtained during lactation from the Jiangyue breed of donkey in Northwest China. Results showed that donkey milk contained 9.53% total solids, 1.57% protein, 1.16% fat, 6.33% lactose, and 0.4% ash on average, which is more similar to mare and human milk than to the milk of other mammals. Throughout the lactation investigated, pH and density were constant, protein and ash content showed an apparent negative trend (an increase in lactose content during 120 d postpartum, followed by a decrease), fat content exhibited wide variability, and variations in the content and percentage of whey protein, casein, and AA were small. The casein to whey protein ratio of 52:37 was between the lower value of human milk and the higher value of cow milk. Sodium dodecyl sulfate-PAGE results demonstrated that donkey milk is rich in beta-lactoglobulin and lysozyme. The percentages of 8 essential AA in protein of donkey milk were 38.2%, higher than those of mare and cow milk; donkey milk also had higher levels of serine (6.2%), glutamic acid (22.8%), arginine (4.6%), and valine (6.5%) and a lower level of cystine (0.4%).

Transcranial Doppler ultrasonography in neurosurgery: effects of intracranial tumour on right middle cerebral artery flow velocity during induction of anaesthesia.

The right middle cerebral artery flow velocity (MCAFV) was measured by transcranial Doppler ultrasonography in neurosurgical patients with and without intracranial tumours during anaesthetic induction and endotracheal intubation. With institutional and patient consent, 20 non-tumour and 85 tumour-bearing neurosurgical patients were enlisted. The right middle cerebral artery was insonated with a pulsed-wave range-gated transcranial Doppler at 2 MHz, and MCAFV was recorded via a video graphics printer. The mean MCAFV, pulsatility index, use of anaesthetic drugs, heart rate, mean arterial pressure, and endtidal CO2 were recorded on preinduction, postinduction, intubation, and 90 to 180 s postintubation. There was no demographic, systemic haemodynamic, or anaesthetic difference between groups except for a predominance of women in the tumour group. In all patients, mean arterial pressure and MCAFV demonstrated with time a significant decrease with anaesthetic induction, increase with endotracheal intubation, and decrease post intubation. The right MCAFV was significantly higher in both tumour and right-sided tumour patients compared to non-tumour patients. There was no difference in left-sided tumour patients compared to non-tumour patients. These data indicate that intracranial tumours have cerebrovascular effects, causing either hyperaemia or vasoconstriction, and that the effects of anaesthetic induction and intubation agree with previously reported effects on cerebral blood flow and intracranial pressure.

Anesthetic care during thiopental tests to evaluate epileptic patients for surgical therapy.

A thiopental test 2 weeks after insertion of intracranial electrodes may be used to evaluate patients with refractory epilepsy for surgical therapy. Barbiturates normally produce beta activity on the electroencephalogram. The absence of this response in a monitored brain region implies focal cerebral dysfunction. We describe a technique used to perform this test and the resultant morbidity. The thiopental test consists of intravenous injection of thiopental, 25 mg, every 30 s until either corneal reflexes are abolished, 1,000 mg of thiopental has been administered, or adverse events occur. In children, the dose is adjusted to approximately 0.3 mg/kg of thiopental every 20 s. A retrospective chart review was performed on 104 patients who underwent thiopental tests at the University of Pittsburgh Epilepsy Center. Records were systematically reviewed for thiopental dose, mean arterial blood pressure, heart rate, oxygen saturation in arterial blood, time to responsivity, need for airway intervention, and occurrence of nausea or vomiting. Thirty-six patients developed upper airway obstruction which required jaw lift maneuver, six patients were given 1,000 mg of thiopental without loss of corneal reflexes, and one patient briefly sustained an arterial saturation of 67%. Five patients exhibited electrographic seizures with clinical seizures evident in two patients. No permanent effects were evident in any patient as a consequence of the test. We conclude, with appropriate monitoring and personnel, that the thiopental test, as described, can be performed safely with acceptable morbidity.

Transcranial Doppler ultrasonography with induction of anesthesia for neurosurgery.

Intracranial hypertension can occur with induction of anesthesia; however, the clinical significance of this is unclear. We used transcranial Doppler (TCD) ultrasonography in neurosurgical patients during induction of anesthesia and endotracheal intubation to assess the incidence of high intracranial pressure (ICP) waveforms and to correlate TCD observations with specific anesthetics and anesthetic regimens. The middle cerebral artery was monitored by TCD during induction of anesthesia and endotracheal intubation in 196 patients undergoing elective neurosurgery. Middle cerebral artery blood flow velocity (MCABFV) and physiologic data were observed continuously and recorded at the following times: preinduction, induction, intubation, and postintubation. Induction with thiopental or etomidate decreased MCABFV, intubation increased MCABFV, and postintubation ventilation decreased MCABFV. MCABFV was higher throughout the induction sequence in the 92 patients with tumors. Although there were numerous individual exceptions, changes in mean arterial pressure correlated statistically with changes in MCABFV. No patient had an end-diastolic flow velocity of 0. We reached the following conclusions: (a) TCD is a straightforward modality that can be used to monitor dynamic cerebrovascular events during induction of anesthesia; (b) MCABFV is increased with brain tumors; (c) thiopental and etomidate rapidly decrease and intubation rapidly increases MCABFV; and (d) routine TCD monitoring for high ICP waveforms during anesthetic induction for routine elective neurosurgery appears to be unwarranted.

Note: refractive index sensing of turbid media by differentiation of the reflectance profile: does error-correction work?

A widely used method for determining refractive index postulates that the derivative of the angular profile for light reflected from the sample is maximum at the critical angle for total internal reflection (TIR). It is well-known that in turbid media this "differentiation method" yields errors in refractive index. Unexplained anomalies in previous error-calculations are eliminated if one uses a recent model of TIR which departs from traditional Fresnel theory. However we find that, in practical situations, the refractive index obtained by differentiation even after error-correction is significantly different from the best estimate for the refractive index obtained by curve-fitting the reflectance data. Thus the differentiation method lacks scientific validity in turbid media.

Vecuronium infusion requirements in children during halothane-narcotic-nitrous oxide, isoflurane-narcotic-nitrous oxide, and narcotic-nitrous oxide anesthesia.

We were interested in determining the infusion rate of vecuronium required to maintain approximately 95% neuromuscular blockade in children during halothane-narcotic-nitrous oxide (0.8% end-tidal concentration), isoflurane-narcotic-nitrous oxide (1.0% end-tidal concentration), or narcotic-nitrous oxide anesthesia. Neuromuscular blockade was monitored by recording the electromyographic activity (Datex NMT) of the adductor pollicis muscle resulting from supramaximal stimulation of the ulnar nerve at 2 Hz for 2 s at 10-s intervals. Effective vecuronium infusion requirements averaged 1.5 +/- 0.1 micrograms.kg-1.min-1 (mean +/- SEM) during isoflurane-narcotic-nitrous oxide anesthesia, 1.9 +/- 0.1 micrograms.kg-1.min-1 during halothane-narcotic-nitrous oxide anesthesia, and 2.4 +/- 0.3 micrograms.kg-1.min-1 during narcotic-nitrous oxide anesthesia. Infusion requirements significantly decreased after the first 30 min of infusion in the presence of both potent inhalation anesthetics, but did not change with time during narcotic-nitrous oxide anesthesia. There was no evidence of decreasing infusion requirements during prolonged vecuronium infusion (2.5 h). There was no difference in the rate of spontaneous or pharmacologically induced recovery between anesthetic groups. The mean recovery index (T25-75) after termination of the infusion was 13.7 min.

Clinical pharmacology of pipecuronium in infants and children during halothane anesthesia.

We determined the cumulative dose-response relations of pipecuronium in infants and children during nitrous oxidehalothane anesthesia. Neuromuscular blockade was monitored by recording the electromyographic activity of the adductor pollicis muscle resulting from supramaximal stimulation of the ulnar nerve at 2 Hz for 2 s at 10-s intervals. Patients were stratified into four groups according to age: 3 mo or older but not yet 6 mo (n = 10), 6 mo or older but not yet 12 mo (n = 10), 1 yr or older but not yet 3 yr (n = 10), and 3 yr or older but not yet 6 yr (n = 9). The mean ED50 of pipecuronium in these age groups was 18, 20, 21, and 24 micrograms/kg, respectively; the mean ED95 was 33, 38, 47, and 49 micrograms/kg, respectively. The ED95 of pipecuronium was statistically significantly less for the 3-6-mo-old patients than for children between 1 and 6 yr of age. Similarly, pipecuronium dosage requirements calculated on the basis of body surface area were significantly less in infants 3-12 mo of age than in children 1-6 yr of age. Thus, compared with children, infants appear to be more sensitive to the neuromuscular blocking effects of pipecuronium. Duration (T25) of action after cumulative dosing with pipecuronium was approximately 20 min in infants and 30 min in children. Spontaneous recovery indices were not prolonged in the younger patients. The average T25-75 recovery index was 27.1 +/- 9.6 min. There were no changes in cardiac rhythm, heart rate, or blood pressure attributable to pipecuronium during this study.

Clinical pharmacology of mivacurium chloride (BW B1090U) in children during nitrous oxide-halothane and nitrous oxide-narcotic anesthesia.

We determined the dose-response relationships of mivacurium (BW B1090U) in children (2-10 years) during nitrous oxide-halothane anesthesia (0.8% end-tidal) and during nitrous oxide-narcotic anesthesia. Neuromuscular blockade was monitored by recording the electromyographic activity of the adductor pollicis muscle resulting from supramaximal stimulation at the ulnar nerve at 2 Hz for 2 seconds at 10-second intervals. To estimate dose-response relationships, for each anesthetic background four subgroups of nine patients received single bolus doses of 20-120 micrograms/kg mivacurium. The ED50 and ED95 (estimated from linear regression plots of log-dose vs. probit of effect) were 52 micrograms/kg and 89 micrograms/kg during halothane anesthesia and 62 micrograms/kg and 103 micrograms/kg during narcotic anesthesia. Nine additional patients in each anesthetic group received 250 micrograms/kg mivacurium. Three of the 18 patients given 250 micrograms/kg mivacurium developed cutaneous flushing; in one of these mean arterial pressure decreased 32% for less than 1 minute; no significant changes in heart rate occurred. With the increase in mivacurium dose from 120 micrograms/kg to 250 micrograms/kg the times to onset of 90% and maximum neuromuscular block decreased by 0.5 to 1 minute, and the times to recovery of neuromuscular transmission to 5% (T5) or 25% (T25) increased by 2-4 minutes. The recovery index (T25-75) in patients anesthetized with halothane was 4.3 +/- 1.5 minute (mean +/- SD); the time to complete recovery (T4:1 greater than or equal to 0.75) was 19.8 +/- 7.4 minutes.

Clinical pharmacology of doxacurium chloride (BW A938U) in children.

The neuromuscular effects of doxacurium were studied in 26 children during halothane-nitrous oxide-oxygen anesthesia. Neuromuscular blockade was measured using electromyographic activity of the adductor pollicis muscle after supramaximal stimulation of the ulnar nerve at 2 Hz for 2 seconds at 10-second intervals. To estimate the cumulative dose-response relation, nine patients received incremental doses of doxacurium (2.5-10 micrograms/kg); nine patients received 27.5 micrograms/kg (the estimated ED95); eight patients received 50 micrograms/kg (1.8 X ED95). The ED25, ED50, ED75, and ED95 (estimated from linear regression plots of log dose vs probit of effect) were 11.5, 14.8, 19.0, and 27.3 micrograms/kg, respectively. Clinical duration (T25) was 27.8 +/- 10.3 (mean +/- SD) minutes at 1 X ED95 and 50.6 +/- 15.6 minutes at 1.8 X ED95. Time to recovery of the train-of-four ratio to 0.75 was 63.1 +/- 32.9 minutes at 1 X ED95 and 108.5 +/- 25.7 minutes at 1.8 X ED95. There were no significant changes in heart rate or mean arterial pressure after bolus administration of any dose of doxacurium.

Mivacurium infusion requirements in pediatric surgical patients during nitrous oxide-halothane and during nitrous oxide-narcotic anesthesia.

We were interested in determining the infusion rate of mivacurium required to maintain approximately 95% neuromuscular blockade during nitrous oxide-halothane (0.8% end-tidal) or nitrous oxide-narcotic anesthesia. Neuromuscular blockade was monitored by recording the electromyographic activity (Datex NMT) of the adductor pollicis muscle resulting from supramaximal stimulation of the ulnar nerve at 2 Hz for 2 s at 10-s intervals. Mivacurium steady-state infusion requirements averaged 315 +/- 26 micrograms.m-2.min-1 during nitrous oxide-halothane anesthesia and 375 +/- 19 micrograms.m-2.min-1 (mean +/- SEM) during nitrous oxide-narcotic anesthesia. Higher levels of pseudocholinesterase activity were generally associated with a higher mivacurium infusion requirement. During both anesthetics, younger age was associated with a higher infusion requirement when the infusion requirement was calculated in terms of micrograms.kg-1.min-1. This difference was not present when the infusion rate was calculated in terms of micrograms.m-2.m-1. There was no evidence of cumulation during prolonged mivacurium infusion. There was no difference in the rates of spontaneous or reversal-mediated recovery between anesthetic groups. After the termination of the infusion, spontaneous recovery to T4/T1 greater than or equal to 0.75 occurred in 9.8 +/- 0.4 min, with a recovery index, T25-75, of 4.0 +/- 0.2 min (mean +/- SEM). In summary, pseudocholinesterase activity is the major factor influencing mivacurium infusion rate in children during nitrous oxide-narcotic or nitrous oxide-halothane (0.8% end-tidal) anesthesia.