Electron temperature and density probe for small aeronomy satellites.

A compact and low power consumption instrument for measuring the electron density and temperature in the ionosphere has been developed by modifying the previously developed Electron Temperature Probe (ETP). A circuit block which controls frequency of the sinusoidal signal is added to the ETP so that the instrument can measure both T(e) in low frequency mode and N(e) in high frequency mode from the floating potential shift of the electrode. The floating potential shift shows a minimum at the upper hybrid resonance frequency (f(UHR)). The instrument which is named "TeNeP" can be used for tiny satellites which do not have enough conductive surface area for conventional DC Langmuir probe measurements. The instrument also eliminates the serious problems associated with the contamination of satellite surface as well as the sensor electrode.

Leptin predicts a decline in moderate to vigorous physical activity in minority female children at risk for obesity.

UNLABELLED: What is already known about this subject Physical activity declines as children enter puberty. Leptin is cross-sectionally associated with physical activity, but there are conflicting findings on the magnitude and direction of this association. Leptin concentrations fluctuate during puberty, and may impact energy balance. What this study adds Leptin predicts the decline in physical activity during the start of puberty independent of central adiposity. Based on a median split of leptin, girls with low leptin levels have higher levels of physical activity than girls with high leptin levels at the start of puberty. Leptin levels at the start of puberty may provide a biological basis for the age-related physical activity decline in girls. BACKGROUND: Leptin may influence moderate to vigorous physical activity (MVPA) at the start of puberty. The direction and magnitude of this association are unclear. OBJECTIVES: To determine the effect of baseline leptin on MVPA over 1 year in minority girls at high risk for obesity. METHODS: Data came from TRANSITIONS, a longitudinal observational study on the age-related MVPA decline. Fifty peripubertal girls aged 8-11 years at baseline participated. Baseline leptin (ng mL(-1) ) was collected via a duplicated assay using a double antibody radio immune assay. MVPA (min d(-1) ) was measured using accelerometers for at least four 10-h days on a quarterly basis for up to 1 year. RESULTS: Continuous leptin was negatively related to MVPA (P = 0.001) independent of central adiposity at baseline and predicted the MVPA decline over 1 year (P = 0.002). For descriptive purposes, baseline leptin was dichotomized at the sample median into 'high leptin' and 'low leptin' categories to determine whether MVPA trajectories differed between these groups. Girls with 'low leptin' at baseline had significantly higher levels of MPVA at baseline, visit 1 and visit 2 compared to girls with 'high leptin'. CONCLUSIONS: High leptin levels predicted nearly a 12.6% decline in MVPA over 1 year. These findings provide support for the biological basis of declining MVPA as girls enter puberty.

Association between human opioid receptor genes polymorphisms and pressure pain sensitivity in females*.

This study examined the association between pressure pain sensitivity and various single nucleotide polymorphisms (SNPs) of human micro-, kappa-, and delta-opioid receptor (i.e. OPRM1, OPRK1, and OPRD1) genes in 72 healthy adult Taiwanese women of Han Chinese race. Pressure pain threshold and tolerance were measured by an algometer and polymorphisms of the opioid receptor genes determined from blood samples. Our data revealed that pressure pain threshold, but not tolerance, in subjects with the minor allele (termed 'GA') genotype of the IVS2+31G>A polymorphism of the OPRM1 gene was significantly higher than those with major allele (termed 'GG') genotype. Neither pressure pain threshold nor tolerance between major and minor alleles of other SNPs of the OPRM1, OPRK1, and OPRD1 genes were significantly different. These data suggest an association between the IVS2+31G>A SNP of the OPRM1 gene and pressure pain sensitivity in healthy adult females.

Synergic CSE1L/CAS, TNFR-1, and p53 apoptotic pathways in combined interferon-gamma/adriamycin-induced apoptosis of Hep G2 hepatoma cells.

Many cancers are chemotherapy-resistant. Chemotherapy combined with immunotherapy offers a potential avenue for the treatment of chemotherapy-resistant cancers. In this study, we investigated the apoptotic pathways induced by combined interferon-gamma/adriamycin treatment in Hep G2 cells. Our data showed that Hep G2 cells treated with combined interferon-gamma/adriamycin enhanced cell apoptosis in comparison with that of cells treated with adriamycin. Interferon-y increased TNFR-1, CSE1L/CAS (cellular apoptosis susceptibility protein), Bax, and Bad levels. Adriamycin increased p53 and Bax, but not TNFR- 1 and CAS levels. Interferon-y did not increase p53 accumulation; nevertheless it enhanced adriamycin-induced p53 accumulation. Overexpression of IRF-1 augmented the combined interferon-gamma/adriamycin-induced p53 accumulation. Interferon-gamma co-treatment increased the stability of p53 protein induced by adriamycin. Our data suggest that TNF-gamma may greatly enhance the combined interferon-gamma/chemotherapeutic drug-induced apoptosis of cancers. Our findings also indicate that CAS, TN-FR-1, p53, Bax, and Bad may be the targets for the interferon-y-based chemo-immunotherapy of the chemotherapy-resistant cancers.

Pre-operative measurement of heart rate variability predicts hypotension during general anesthesia.

BACKGROUND: Peri-operative hymodynamic instability is one of the major concerns for anesthesiologists when performing general anesthesia for individuals with autonomic dysfunction. The purpose of this study was to examine the potential usage of pre-operative measurement of heart rate variability (HRV) in identifying which individuals, with or without diabetes, may be at risk of blood pressure (BP) instability during general anesthesia. METHODS: We studied 46 patients with diabetes and 87 patients without diabetes ASA class II or III undergoing elective surgery. Participants' cardiovascular autonomic function and HRV were assessed pre-operatively, and hymodynamic parameters were monitored continuously intra-operatively by an independent observer. RESULTS: Only 6% of the participants were classified as having cardiovascular autonomic neuropathy (CAN) based on traditional autonomic function tests whereas 15% experienced hypotension. Total power (TP, P = 0.006), low frequency (LF, P = 0.012) and high frequency (HF, P = 0.028) were significantly lower in individuals who experienced hypotension compared with those who did not. Multivariate logistic regression analysis revealed that TP [odds ratio (OR) = 0.15, 95% confidence interval (CI) = 0.05-0.47, P = 0.001] independently predicted the incidence of hypotension, indicating that each log ms2 increase in total HRV lowers the incidence of hypotension during general anesthesia by 0.15 times. After stepwise multiple linear regression analysis (R2= 11.5%), HF (beta = -11.1, SE = 2.79, P < 0.001) was the only independent determinant of the magnitude of systolic blood pressure (SBP) reduction at the 15th min after tracheal intubation. CONCLUSIONS: Spectral analysis of HRV is a sensitive method for detecting individuals who may be at risk of BP instability during general anesthesia but may not have apparent CAN according to traditional tests of autonomic function.

Study of human exposure to particulate PAHs using personal air samplers.

Three common sources of environmental exposure to particulate polycyclic aromatic hydrocarbons (PAHs) in Taiwan were chosen for this study. They are smoke of incense burning, exhausts of motor vehicles, and fumes of charcoal burning. The campus environment without any specific PAH sources (nonpoint sources) was chosen as the control. The particulate PAH concentrations in the air samples containing smoke of incense burning were only slightly higher than those in the control. However, the total concentration of particulate PAHs in the air samples with exhausts of motor vehicles and fumes of charcoal burning was about 7.5 times and 22 times higher than those observed in the control, respectively. The mean inhalation amounts of particulate PAHs per unit time are very high both in samples with exhausts of motor vehicles (13.9 ng/min) and fumes of charcoal burning (38.1 ng/min). The exposure dose of 22 PAHs per day ranged from 3.18 to 18.0 microg/day under four exposure conditions. Moreover, the personal inhalation BaP(eq) levels are in the range of 0.4 to 1.55 microg/day.

Ceramide inhibits lipopolysaccharide-mediated nitric oxide synthase and cyclooxygenase-2 induction in macrophages: effects on protein kinases and transcription factors.

The goal of this study was to elucidate whether triggering the sphingomyelin pathway modulates LPS-initiated responses. For this purpose we investigated the effects of N-acetylsphingosine (C(2)-ceramide) on LPS-induced production of NO and PGE(2) in murine RAW 264.7 macrophages and explored the signaling pathways involved. We found that within a range of 10-50 microM, C(2)-ceramide inhibited LPS-elicited NO synthase and cyclooxygenase-2 induction accompanied by a reduction in NO and PGE(2) formation. By contrast, a structural analog of C(2)-ceramide that does not elicit functional activity, C(2)-dihydroceramide, did not affect the LPS response. The nuclear translocation and DNA binding study revealed that ceramide can inhibit LPS-induced NF-kappaB and AP-1 activation. The immunocomplex kinase assay indicated that IkappaB kinase activity stimulated by LPS was inhibited by ceramide, which concomitantly reduced the IkappaBalpha degradation caused by LPS within 1-6 h. In concert with the decreased cytosolic p65 protein level, LPS treatment resulted in rapid nuclear accumulation of NF-kappaB subunit p65 and its association with the cAMP-responsive element binding protein. Ceramide coaddition inhibited all the LPS responses. In addition, LPS-induced PKC and p38 mitogen-activated protein kinase activation were overcome by ceramide. In conclusion, we suggest that ceramide inhibition of LPS-mediated induction of inducible NO synthase and cyclooxygenase-2 is due to reduction of the activation of NF-kappaB and AP-1, which might result from ceramide's inhibition of LPS-stimulated IkappaB kinase, p38 mitogen-activated protein kinase, and protein kinase C.

Comparison of inhalation induction with 2%, 4%, 6%, and 8% sevoflurane in nitrous oxide for pediatric patients.

BACKGROUND: Sevoflurane is almost the idealest volatile anesthetic agent regarding inhalation induction of general anesthesia. Previous studies have established a role of sevoflurane in high concentration primed in the circuit for inhalation induction in pediatric patients. However, which concentration of sevoflurane is suitable has not yet been reported. This study was designed to compare the efficiency of different concentration of sevoflurane i.e. 2%, 4%, 6%, and 8% and with N2O in 50% oxygen for induction of anesthesia in pediatric patients and at the same time to evaluate the tolerance of patients. METHODS: One hundred and twenty children who were 3 to 10 years old, of ASA class I, were randomly assigned to receive either 2%, 4%, 6%, and 8% sevoflurane and N2O in 50% O2 for induction of anesthesia. The time to loss of eyelash reflex, responses of airway reflex, involuntary movement, and hemodynamic responses were recorded. RESULTS: Ninety-nine children completed the study. The times to loss of eyelash reflex with 2% in sequence to 8% sevoflurane were 114 +/- 21 s, 87 +/- 11 s, 75 +/- 6 s, and 48 +/- 8 s respectively. Incidence of airway reflex response including coughing, laryngospasm, and breath holding was the highest in the 8% group (P < 0.05). Inhalation induction with sevoflurane significantly decreased systolic as well as diastolic blood pressure compared with baseline blood pressure in all the four groups. The extent of decrease of blood pressure was within 20% range of baseline blood pressure in all groups. Significant increase of heart rate was only observed in the 4% and 6% groups. CONCLUSIONS: Sevoflurane 6% for inhalation induction apparently caused low incidence of adverse effects and hastened induction. We suggest that 6% sevoflurene is a concentration more practical for inhalation induction in pediatric patients.

Cycloheximide-induced cPLA(2) activation is via the MKP-1 down-regulation and ERK activation.

Extracellular signal-regulated kinase (ERK)-dependent phosphorylation is an important regulator for cytosolic phospholipase A(2) (cPLA(2)). In this study, we found that the protein synthesis inhibitor cycloheximide can potentiate thapsigargin-induced arachidonic acid (AA) release concomitant with ERK phosphorylation from murine RAW 264.7 macrophages. The cycloheximide effect is not due to the activation of p38 mitogen-activated protein kinase (MAPK) nor c-Jun NH(2)-terminal kinase (JNK), because the activator of both MAPKs anisomycin does not elicit AA release. Cycloheximide effect is additive to the tyrosine phosphatase inhibitor orthovanadate since these two stimuli induced sustained ERK activation respectively through inhibition of the translation and activity of MAPK phosphatase-1 (MKP-1).

Modulation of inducible nitric oxide synthase induction by prostaglandin E2 in macrophages: distinct susceptibility in murine J774 and RAW 264.7 macrophages.

Prostaglandin E2 (PGE2) is the major cyclooxygenase metabolite in macrophages with complex proinflammatory and immunoregulatory properties. In the present study, we have compared the modulatory role of PGE2/cAMP-dependent signaling on induced nitric oxide (NO) production in two murine macrophages, J774 and RAW 264.7. With no effect on NO release by itself, PGE2 co-addition with lipopolysaccharide (LPS) resulted in a concentration-dependent enhancement in NO release and inducible NO synthase induction in J774, but not in RAW 264.7, macrophages. The potentiation effect of PGE2 in J774 cells was still seen when applied within 9 h after LPS treatment. Whereas RAW 264.7 macrophages release PGE2 with greater extent than J774 macrophages in response to LPS, indomethacin and NS-398, upon abolishing LPS-induced PGE2 release, caused a more obvious inhibition of NO release from J774 than RAW 264.7 cells. Thus, we suggest a higher positive modulatory role of PGE2--either endogenous or exogenous--on NO formation in J774 cells. Supporting these findings, exogenous PGE2 triggers cAMP formation in J774 cells with higher potency and efficacy. Of interest, dBcAMP also elicits higher sensitivity in potentiating NO release in J774 cells. We conclude that the opposite effect of PGE2/cAMP signaling on macrophage NO induction depends on its signaling efficacy and might be associated with the difference in endogenous PGE2 levels.

Prevention of coughing induced by endotracheal tube during emergence from general anesthesia--a comparison between three different regimens of lidocaine filled in the endotracheal tube cuff.

BACKGROUND: "Deep" extubation, administration of intravenous (i.v.) narcotics, i.v. lidocaine and forestalling local spray of lidocaine have been used to help diminish coughing during emergence. However, the respective efficacy of these techniques has not been concluded. Sconzo et al. indicated that endotracheal tube (ETT) cuff might serve as a reservoir for local anesthetic. Alkalizing and warming are two techniques frequently used to increase in the proportion of uncharged drugs available. Matias indicated that alkalization could prompt a 63-fold increase of the rate of diffusion of lidocaine across the ETT cuff. Huang et al. also observed that alkalization together with warming could achieve a 118-fold increase further. However, the in vivo effects of ETT-cuff lidocaine have not been studied. METHODS: Eighty patients of ASA Class I-II undergoing elective surgeries were included. They were randomly assigned into four groups. After tracheal intubation, the ETT cuff was filled with one of the following solutions: normal saline 6 ml (Group A), 4% lidocaine 6 ml at room temperature (Group B), 4% lidocaine 5 ml + 7% sodium bicarbonate 1 ml at room temperature (Group C), and 4% lidocaine 5 ml + 7% sodium bicarbonate 1 ml warmed to 38 degrees C (Group D). Changes of vital signs as well as the times of coughing in the course of extubation and post-extubation complications were recorded. One way ANOVA (SPSS for windows) was used for data analysis. RESULTS: The respective number of coughing per patient in the experimental groups (Group B, C and D) was significantly less than the saline or control group (mean = 9.70, 9.15 and 3.95, respectively, p < 0.05). The incidence of sore throat in Group C and Group D was significantly less than the control group (35% and 25%, respectively, p < 0.05). Regarding the hemodynamic changes, systolic arterial pressure (SAP) and mean arterial pressure (MAP) were higher in Group B and C (p < 0.05) before extubation. CONCLUSIONS: Alkalized and warmed lidocaine prestored in the endotracheal tube (ETT) cuff can greatly reduce ETT-induced coughing and thus promote a smoother emergence from general anesthesia with endotracheal intubation.

Comparison of the cuffed oropharyngeal airway and laryngeal mask airway in spontaneous breathing anesthesia.

BACKGROUND: The cuffed oropharyngeal airway (COPA) is a modified Guedel airway with a cuff at its distal end and a standard 15 mm connector at its proximal end. This study was performed to determine if the COPA would offer any advantage over the laryngeal mask airway (LMA). METHODS: Eighty ASA class I to II adult patients scheduled for short elective procedures (less than 1 h) were randomly allocated into two groups. All patients were given atropine 0.01 mg/kg, fentanyl 2 micrograms/kg and propofol 2 mg/kg intravenously for induction of anesthesia. The COPA or LMA was inserted following the loss of eyelash reflex. If the jaw was not relaxed enough for insertion of a COPA or LMA, succinylcholine 1 mg/kg was given to facilitate the insertion. When correctly positioned, the cuff was immediately inflated with an appropriate volume. Gentle positive pressure ventilation was applied before spontaneous breathing resumed. Capnography was used to assess the patency of the airway. Anesthesia was maintained with isoflurane-N2O-O2 until the end of surgery. The success rate, vital signs, and adverse events were evaluated and compared. RESULTS: The success rate in the LMA group (95%) was higher than the COPA group (85%). The increase in circulatory response after the LMA insertion was greater than that after the COPA insertion (P < 0.05). Nine patients (22.5%) in the LMA group needed succinylcholine to facilitate insertion compared with only two patients (5%) in the COPA group. Additional manipulation was frequently (57.5%) needed after inserting the COPA to maintain the patency of the airways, but none needed so in the LMA group. Two patients had laryngospasms upon removal of the LMA, but none had laryngospasm in the COPA group. The incidence of sore throat in the LMA group was higher than in the COPA group (18% vs. 10%). CONCLUSIONS: We demonstrated that the COPA could be easily inserted without the need of muscle relaxants in most patients. But the COPA needed airway intervention to provide an effective airway in most patients. Compared with the LMA, the COPA caused less stimulation than the LMA.

The use of intranasal nitroglycerin to prevent pressor responses during intubation in general anesthesia--a comparison of various doses.

BACKGROUND: Intranasal nitroglycerin (NTG) was first reported to successfully prevent an increase in arterial blood pressure following laryngoscopy and tracheal intubation by Hill et al. Various different effective dosages of NTG have been reported. Grover et al. indicated 0.75 mg of intranasal NTG to be the most suitable dose. However, no definite conclusion has yet been made. This study was designed to compare the efficacy of four different dosages of intranasal NTG (0.3, 0.5, 0.75, and 1.0 mg) in preventing pressor responses to laryngoscopy and tracheal intubation during the induction of general anesthesia. METHODS: One hundred patients (ASA I or II) scheduled for elective surgery were included. These study subjects were divided into five groups and randomly assigned to four different dosages of intranasal NTG and a placebo. Each group consisted of 20 patients. The NTG solution was administered 1 min before the injection of thiopental. Systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP) and heart rate (HR) were recorded before the induction of anesthesia (T1), before laryngoscopy (T2), and at 0, 3, and 5 min after tracheal intubation (T3, T4, and T5 respectively). RESULTS: In patients who received a placebo (control group), there were significant increases in SAP, MAP, HR and rate-pressure-product (RPP) associated with tracheal intubation. Tachycardia was noted in all experimental groups. The increases in MAP associated with tracheal intubation were significantly less in patients who received NTG of 0.5 mg or more but not 0.3 mg. Although 0.5 mg of NTG did attenuate the increases in SAP after tracheal intubation, the increases in SAP of the other three experimental groups were no less than that of the control group. Rate-pressure-product (RPP) values of the experimental groups were noted to be equal to or higher than those of the control group during the period of study. Contrary to the results of the study conducted by Grover et al., 0.75 mg of NTG did not attenuate the pressor responses. CONCLUSIONS: Intranasal NTG does not attenuate the pressor responses to laryngoscopy and tracheal intubation.

[A proper size of endotracheal tube for infant and young child--a retrospective study in Mackay Memorial Hospital].

BACKGROUND: There are more than 2000 pediatric patients receiving surgery in Mackay Memorial Hospital each year. Most of these surgery were performed under general anesthesia with endotracheal tube; therefore choosing an appropriate size of endotracheal tube becomes an important issue in our daily practice. METHODS: Our principle is to choose an uncuffed Mallinckrodt endotracheal tube with a proper internal diameter (ID), ranging from 2.5 mm to 6.5 mm, which could be suitably and gently inserted into the trachea under full muscle relaxation. The tube would then be immediately removed and replaced with a smaller one if facing obvious resistance during intubation. After intubation, a leak test was applied to ascertain that there was no excessive gas leakage. We reviewed all anesthetic records of elective pediatric surgery in the recent 6 years, and the patients whose age above 8.5 years old and body weight (Wt) above 30 kg were excluded from this study. Using age (6476 cases) and Wt (6406 cases) as our parameters, we analyzed these data according to the distribution of each size of uncuffed endotracheal tube (UCETT) in different age and Wt intervals and compared them with the recommended Western reports. RESULTS: Our results revealed that (1) the UCETT size increases as age or Wt increases; (2) considerable spread of UCETT sizes for different age and Wt intervals and basically represent as normal distribution; (3) for the case of even age equal or above 2 years old (up to 8 years old), the ID of the most frequently used UCETT can be memorized as (18 + age in years) divided by 4 or the outer circumference (OC) of the Mallinckrodt UCETT (in French unit, Fr) = 19 + age in years; and (4) Wt as a parameter for tube size selection was as powerful as age (94.76% vs. 94.65%). CONCLUSIONS: From our results, we concluded that "whatever method of predicting tube size is used, tracheal tubes 0.5 mm larger and smaller should be available at the time of intubation so that the proper size can be chosen when the glottis is visualized."

Pulmonary edema induced by upper airway obstruction--report of 3 cases.

Pulmonary edema is a well-recognized complication of upper airway obstruction, and has been reported sporadically both in children and adults since 1977. Although the pathogenesis of pulmonary edema associated with upper airway obstruction is multifactorial, attention is primarily focused on excessive negative intrapleural and transpulmonary pressure produced by forceful inspiration against a closed glottis that results in transudation of fluid from the pulmonary capillary into the interstitial and alveolar spaces. We report 3 cases of pulmonary edema induced by upper airway obstruction after extubation following general anesthesia.

[4P- syndrome (Wolf-Hirschhorn syndrome) complicated with delay onset of malignant hyperthermia: a case report].

One 8-month-old female patient, weighted 5 kg, with congenital abnormality (4P- syndrome) underwent elective cheiloplasty for cleft lip and palate. Two hours later, with smooth anesthesia and operation, a life-threatening anesthetic complication of malignant hyperthermia occurred at pediatric intensive care unit. The immediate treatments were initially hyperventilating the patient with 100% O2 and cooling the patient with ice bags. Subsequently, intravenous dantrolene 2.5 mg/kg and symptomatic supportive care were administered successfully to treat the event. Upon reviewing the articles, we found that a congenital chromosome 4P deletion abnormality complicated with a delay onset of malignant hyperthermia has not been described previously.