Low expression of miR-409-3p is a prognostic marker for breast cancer.

OBJECTIVE: The present study aimed to clarify the expression pattern and prognostic role of miR-409-3p in breast cancer patients. MATERIALS AND METHODS: miR-409-3p levels in breast cancer tissues were tested by qRT-PCR. The chi-square test and Fishers exact tests were used to examine the associations between miR-409-3p expression and the clinicopathological characters. Overall survival (OS) was estimated using the Kaplan-Meier method. The univariable and the multivariable Cox regression analyses were used to evaluate independent prognostic factors. RESULTS: miR-409-3p expression in breast cancer specimens was observed to be decreased compared with matched normal breast tissues (p < 0.01). Additionally, low miR-409-3p expression in breast cancer tissues was significantly associated with the advanced TNM stage (p = 0.004), lymph node metastasis (p = 0.001), and poorer pathological differentiation (p = 0.026). The patients in the low miR-409-3p group had a shorter overall survival than those in the high miR-409-3p group (p < 0.001). Furthermore, the univariate and the multivariate analyses showed that miR-409-3p expression was an independent predictor of overall survival (p < 0.05). CONCLUSIONS: Our results revealed that miR-409-3p was related to the prognosis of patients with breast cancer and might be a promising predictor of miR-409-3p recurrence.

Comparison of two generalized transfer functions for measuring central systolic blood pressure by an oscillometric blood pressure monitor.

Central aortic systolic blood pressure (SBP-C) can be estimated from a cuff oscillometric waveform derived during the pulse volume plethysmography (PVP) by applying a device-specific aortic pressure-to-PVP waveform-generalized transfer function (A2P(GTF)). The present study compared the performance of an aortic-to-brachial pressure waveforms generalized transfer function (A2B(GTF)), which is independent of any PVP devices, with an A2P(GTF). Generalized transfer function of aortic-to-brachial (A2B(GTF)) and aortic-to-PVP (A2P(GTF)) were generated from the simultaneously obtained central aortic and brachial pressure waveforms recorded by a high-fidelity dual pressure sensor catheter, and the PVP waveform recorded by a customized noninvasive blood pressure monitor during cardiac catheterization in 40 patients, and were then applied in another 100 patients with simultaneously recorded invasive aortic pressure and noninvasively calibrated (using cuff SBP and diastolic blood pressures) PVP waveforms. The mean difference±s.d. between the noninvasively estimated and invasively recorded SBP-C was -2.1±7.7 mm Hg for A2B(GTF), which was not greater than that of -3.0±7.7 mm Hg for A2P(GTF) (P<0.01). In conclusion, SBP-C can be measured reliably using a noninvasive blood pressure monitor by applying either an A2P(GTF) or A2B(GTF) to a noninvasively calibrated PVP waveform. The performance of an A2B(GTF) is not inferior to that of an A2P(GTF).

Afferent nerve sensitivity is decreased by an iNOS-dependent mechanism during indomethacin-induced inflammation in the murine jejunum in vitro.

Evidence exists that visceral afferent sensitivity is subject to regulatory mechanisms. We hypothesized that afferent sensitivity is decreased in the small intestine during intestinal inflammation by an inducible nitric oxide synthase (iNOS)-dependent mechanism. C57BL/6 mice were injected twice with vehicle or 60 mg kg(-1) indomethacin subcutaneously to induce intestinal inflammation. Afferent sensitivity was recorded on day 3 from a 2-cm segment of jejunum in vitro by extracellular multi-unit afferent recordings from the mesenteric nerve bundle. In subgroups (n = 6), iNOS was inhibited selectively by L-N6-(1-iminoethyl)-lysine (L-NIL) given either chronically from day 1-3 (3 mg kg(-1) twice daily i.p.) or acutely into the organ bath (30 micromol L(-1)). The indomethacin-induced increase of macroscopic and microscopic scores of intestinal inflammation (both P < 0.05) were unchanged after pretreatment with L-NIL. Peak afferent firing following bradykinin (0.5 micromol L(-1)) was 55 +/- 8 impulse s(-1) during inflammation vs 97 +/- 7 impulse s(-1) in controls (P < 0.05). Normal firing rate was preserved following L-NIL pretreatment (112 +/- 16 impulse s(-1)) or acute administration of L-NIL (108 +/- 14 impulse s(-1)). A similar L-NIL dependent reduction was observed for 5-HT (250 micromol L(-1)) and mechanical ramp distension from 20 to 60 cmH(2)O (both P < 0.05). Intraluminal pressure peaks were decreased to 0.66 +/- 0.1 cmH(2)O during inflammation compared to 2.51 +/- 0.3 in controls (P < 0.01). Afferent sensitivity is decreased by an iNOS-dependent mechanism during intestinal inflammation which appears to be independent of the inflammatory response. This suggests that iNOS-dependent nitric oxide production alters afferent sensitivity during inflammation by interfering with signal transduction to afferent nerves rather than by attenuating intestinal inflammation.

The effect of data reduction by independent component analysis and principal component analysis in hand motion identification.

Both independent component analysis (ICA) and principal component analysis (PCA) were used in this study to evaluate their effects in data reduction in the hand motion identification using surface electromyogram (SEMG) and stationary wavelet transformation. The results indicate that both methods increase the number of training epochs of the artificial neural network. The unsupervised fast ICA reduces the number of SEMG channels from 7 to 4. However the hand motion identification rate using the reduced channels is significantly lower (p < 0.05). On the other hand, the PCA reduces the size of neural network by more than 70%. Moreover, the results of discrimination rate and neural network training epochs show no significant difference as compared to the results before PCA reduction. The result of this study demonstrates that using wavelet and PCA are effective pre-processing for surface EMG analysis. It can efficiently reduce the size of neural network and increase the discrimination rate for different hand motions.

Computer system for four-dimensional transesophageal echocardiographic image reconstruction.

This paper presents a system for reconstructing a four-dimensional (4D) heart-beating image from transesophageal echocardiographic (TEE) data acquired with a rotational approach. The system consists of the necessary processing modules for two-dimensional (2D) echocardiogram reformation and 3D/4D-image reconstruction. These include the modules of image decoding, image re-coordinating, and three-dimensional (3D) volume rendering. The system is implemented under PC platform with Windows 95 operating system (with Intel Pentium-166 CPU, 64 MB RAM on board, and 2.0 GB hard disk capacity). It takes 6 min to reconstruct a 4D echocardiographic data set. The resultant 2D/3D/4D echocardiographic image provide the tools for investigating the phenomenon of heart beating, exploring the heart structure, and reformatting the 2D echocardiograms in an arbitrary plane. The functions provided by the system can be applied for further studies, such as 3D cardiac shape analysis, cardiac function measurement, and so forth.

A graphic orientated data analysis system for hemodynamic research.

A software program to process and to extract physiological functional hemodynamics data has been developed and reported. The purpose of this software system is to process and capture cardiovascular hemodynamics and physiological functional data after data acquisition. The system utilized an interactive graphic display and script control to extract the data. With a minimum interface, it is capable of analyzing multiple channels of data and simultaneously obtaining the results. The extracted data includes global cardiovascular functional parameters and with script process the software will calculate stroke work from the pressure length relationship. The results are stored in files for further statistical analysis. The procedures are reliable and readily applicable to examine and analyze the acquired data with minimal observer bias.

A methodological improvement and system validation to obtain precise behavioral parameters for schedule-induced polydipsia.

A Schedule-Induced Polydipsia (SIP) animal behaviors monitor system was devised. The system included a software package to acquire data and to format the data storage of the animal behavior in the experiment was designed. Data analysis software will also extract the necessary information from recorded data. The SIP experimental apparatus consists of a number of subsystems. They are operant chambers, event counters, signal acquisition and storage system. The operant chamber is equipped with hopper, pellet and lick sensor and locomotion detector. The data acquisition and storage subsystem are custom designed that run on IBM-PC. The discrete time markers for pellet drop, bar pressing and licking water were recorded at 200 Hz. The image of rat locomotion was recorded at 10 Hz. A test of four different stages of animal to verify the accuracy of the system was reported in this article. The food-deprived rats that were exposed to the intermittent food schedule (1 per minute) exhibit an excess drinking behavior. The animal behaviors that were monitored during the scheduled events are adjunctive, facultative and terminal behavior. The volume of water intake was also recorded for reference. The real time data is stored chronologically into two types of data file. Therefore, a special data analysis procedure is designed to extract the results for off-line statistic analysis. The extracted parameters for animal behaviors analyzing including drinking efficiency, inter-lick intervals, number of drinking bursts, size of burst, temporal distribution of licking, temporal distribution of bar pressing and locomotion. The system can be employed in many different SIP studies such as investigating the effect of acute and chronic influence of amphetamine.

Pacing-induced left ventricular asynchronies in dogs with critical coronary stenosis: mechanisms and effect of anesthetics.

The mechanisms leading to left ventricular (LV) asynchronies are incompletely understood, and reports on the functional significance of asynchronies for the affected segments are conflicting. To characterize LV asynchronies, 16 anesthetized dogs with critical stenosis of the left anterior descending coronary artery (LAD) were instrumented to measure subendocardial contractile function (sonomicrometry) and the ECG in the LAD territory. The subendocardial ECG was also recorded from the anterior basal LV territory. Time of regional S wave arrival (TS) and time of onset of segment shortening were determined. The animals underwent atrial pacing with increasing frequencies until systolic LAD territory contractile dysfunction and eventual LV asynchronies were observed. Six animals without LAD stenosis served as controls to define the normal response (mean +/- 2.SD) to increasing pacing rates of systolic shortening and onset time of segment shortening (time difference between TS and onset of segment shortening). LAD contractile dysfunction was considered as a systolic shortening below the normal range, and LV asynchronies as an onset time of segment shortening above the normal range. When LV asynchronies occurred, onset time of segment shortening in the LAD territory was 80.1 +/- 4.9 ms versus 14.8 +/- 3.7 ms at control (P < 0.01); the time difference between S wave arrival in the LAD and circumflex territories, however, was unchanged. LV asynchronies were associated with marked LAD territory contractile dysfunction (systolic shortening of 9.6 +/- 0.8% v 21.0 +/- 1.9% at control, after systolic shortening of 31.3 +/- 3.8% v 9.0 +/- 2.6% at control; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute isovolemic hemodilution and blood transfusion. Effects on regional function and metabolism in myocardium with compromised coronary blood flow.

The use of isovolemic hemodilution to prevent adverse side effects of homologous blood transfusions has increased. The lowest level of hemoglobin that can be tolerated without regional myocardial dysfunction, however, had not been precisely defined for left ventricular myocardium with compromised coronary blood flow. This level was determined in our study in 19 dogs with critical stenosis of the left anterior descending coronary artery during graded isovolemic hemodilution. Regional function was assessed by sonomicrometry in the territory supplied by the left anterior descending coronary artery, as well as in two noncompromised left ventricular areas; oxygen extraction and consumption in the left anterior descending coronary artery region were assessed by analysis of anterior descending coronary venous oxygen saturation. The median lowest level of hemoglobin tolerated without contractile dysfunction of the territory supplied by the left anterior descending artery was 7.5 gm/dl, with lower and upper quartiles of 6 and 9 gm/dl. In addition to a marked increase in cardiac output and transstenotic left anterior descending flow, global cardiac and regional myocardial functions were unchanged at a hemoglobin level of 7.5 gm/dl, as compared with a control level of hemoglobin of 12.0 +/- 0.4 gm/dl. At a mean level of hemoglobin of 6.0 +/- 0.4 gm/dl, marked contractile dysfunction developed in the left anterior descending region: Systolic shortening decreased from 24.2% +/- 2.1% to 17.9% +/- 1.9% (p < 0.01); postsystolic shortening increased from 4.0% +/- 3.0% to 12.2% +/- 3.8% (p < 0.01); and in the left anterior descending region, oxygen consumption decreased. The increase of arterial level of hemoglobin by only 1.9 +/- 0.2 gm/dl restored contractile function in the left anterior descending region, regional oxygen consumption, and oxygen extraction across the left anterior descending region. Moderate isovolemic hemodilution is relatively well tolerated in left ventricular myocardium with compromised coronary blood flow, and hemodilution regional contractile dysfunction induced by hemodilution is reversible by minimal blood transfusion.

Validation of 133Xe clearance as a cerebral blood flow measurement technique during cardiopulmonary bypass.

133Xe clearance to measure cerebral blood flow (CBF) was examined in 10 dogs during cardiopulmonary bypass. As a reference method, a continuous Kety-Schmidt technique (CBFKS) with 133Xe as indicator was used. Extracranial tissue was removed to directly place the 133Xe detectors on the skull, and the head was covered with a 3 mm lead shield to minimize contamination of the 133Xe clearance curve with extracranial radiation. 133Xe detectors for the Kety-Schmidt technique were embedded in a shielded brass block to minimize interference with radiation from the animal's body. 133Xe clearance data were analyzed using stochastic (CBF10, CBF15, and CBFINF) and initial slope methods (CBFIS), and the results were compared with CBFKS using linear regression. CBF15 and CBFINF yielded similar CBF values as CBFKS (CBFKS = 0.97.CBF15-2.08, r = 0.92, p less than 0.01; CBFKS = 1.13.CBFINF-1.21, r = 0.92, p less than 0.01). CBF10 slightly overestimated CBFKS but still showed a close correlation to CBFKS (CBFKS = 0.89.CBF10-2.58, r = 0.92, p less than 0.01) and CBFIS considerably overestimated CBFKS (CBFKS = 0.60.CBFIS-1.27, r = 0.87, p less than 0.01). With extracranial contamination of the 133Xe clearance curve minimized, all 133Xe clearance techniques used to measure CBF were consistently related to CBFKS in a constant, significant manner. 133Xe clearance therefore is a valid method to assess CBF during cardiopulmonary bypass.

Influence of anesthesia on the threshold of pacing-induced ischemia.

Increased myocardial oxygen demand, induced by increased heart rate, may cause myocardial ischemia in the presence of significant coronary artery disease. Alterations in anesthetic depth or technique might put at risk or protect myocardium with compromised blood flow. In 20 dogs with critical left anterior descending coronary artery (LAD) stenosis, atrial pacing rates from 100 to 160 beats/min were achieved, with end-tidal halothane 0.7% (LowH) and 1.1% (HighH), end-tidal isoflurane 1.1% (LowI) and 1.5% (HighI), as well as with continuous fentanyl plus midazolam (FM) infusion anesthesia. Despite significantly different mean arterial and coronary perfusion pressures, rate-pressure product, and left ventricular dP/dtmax, the pacing rate at which systolic shortening decreased below the lower limit of the physiologic response, indicating regional dysfunction, was the same in all investigated anesthesia conditions (LowH: 127 +/- 4 beats/min; HighH: 128 +/- 5 beats/min; LowI: 125 +/- 4 beats/min; HighI: 122 +/- 5 beats/min; FM: 124 +/- 4 beats/min [mean +/- SEM], P greater than 0.05). None of the investigated anesthesia conditions either increased ischemia tolerance or showed a detrimental effect on myocardium with compromised coronary blood flow.

Effects of cardiopulmonary bypass and cardioplegia on regional and global cardiac actions of halothane in dogs.

Cardiopulmonary bypass (CPB) with aortic cross-clamping represents a controlled period of global cardiac ischemia. We hypothesized that CPB (asanguineous prime), with aortic cross-clamping and repeated cardioplegia, alters myocardial function, which would be manifested as an exaggerated myocardial depression caused by halothane after CPB. In nine dogs anesthetized with fentanyl and midazolam, halothane dose-response curves (0.0%-2.0%) were compared before and after CPB. A reduced mean arterial blood pressure (46.4 +/- 3.7 vs 85.8 +/- 5.9 mm Hg), associated with a marked hemodilution (hematocrit, 19% +/- 1% vs 41% +/- 2%), was observed after CPB. Cardiac output and systolic shortening were not significantly different after versus before CPB during fentanyl-midazolam anesthesia. Normalized to fentanyl-midazolam hemodynamics, halothane dose-response curves before and after CPB were identical for all variables except cardiac output, where halothane caused a slight but statistically significantly more pronounced decrease after CPB compared with before CPB. The effect of halothane on left ventricular function, therefore, is relatively unaffected by CPB with cardioplegia.