Identification of non-coding RNA regulatory networks in pediatric acute myeloid leukemia reveals circ-0004136 could promote cell proliferation by sponging miR-142.

OBJECTIVE: Abnormal expression of circular RNAs (circRNAs) has been observed in various biological processes and cancer pathogenesis. However, the expression of circRNAs in pediatric acute myeloid leukemia (AML) remains largely unknown so far. PATIENTS AND METHODS: Twelve bone marrow samples from pediatric AML patients and healthy controls were analyzed using Agilent circRNA microarray (n = 6, respectively). The circRNAs profiles and regulatory networks were analyzed by integrated bioinformatics methods. Functional analysis (Gene Ontology and KEGG) was performed by KOBAS. The expression of circRNA in patient samples was validated via qRT-PCR assay (n > 30). Luciferase reporter assay was performed to validate the binding of miRNAs. CCK8 and colony formation assay were conducted to measure cell proliferation. RESULTS: A total of 273 circRNAs were upregulated in AML and 296 were downregulated (Fold change > 2, p-value < 0.05), the majority of these circRNAs were distributed among chr1, chr6, and chr16, while few in chr13 and chr21. Top 20 differentially expressed circRNAs were chosen to build circRNAs-miRNAs regulatory relationships. Bioinformatics algorithms indicated that circ-0004136 acts as a sponge for several pediatric AML-related miRNAs. Target genes involved in the circ0004136-miRNA-mRNA network were enriched in leukemia-related functions and signaling pathways. Circ-0004136 was found to be significantly upregulated in pediatric AML and could sponge AML-related miRNAs, including miR-29a and miR-142. Furthermore, circ-0004136 was demonstrated to promote the proliferation of AML by sponging miR-142. CONCLUSIONS: Taken together, this study revealed the circRNAs expression profile and regulatory networks of circRNAs-miRNAs-mRNAs in pediatric AML for the first time. Circ-0004136 was significantly upregulated in pediatric AML and could promote cell proliferation by sponging miR-142.

Relating surface roughness and magnetic domain structure to giant magneto-impedance of Co-rich melt-extracted microwires.

Understanding the relationship between the surface conditions and giant magneto-impedance (GMI) in Co-rich melt-extracted microwires is key to optimizing their magnetic responses for magnetic sensor applications. The surface magnetic domain structure (SMDS) parameters of ~45 µm diameter Co69.25Fe4.25Si13B13.5-xZrx (x = 0, 1, 2, 3) microwires, including the magnetic domain period (d) and surface roughness (Rq) as extracted from the magnetic force microscopy (MFM) images, have been correlated with GMI in the range 1-1000 MHz. It was found that substitution of B with 1 at. % Zr increased d of the base alloy from 729 to 740 nm while retaining Rq from ~1 nm to ~3 nm. A tremendous impact on the GMI ratio was found, increasing the ratio from ~360% to ~490% at an operating frequency of 40 MHz. Further substitution with Zr decreased the high frequency GMI ratio, which can be understood by the significant increase in surface roughness evident by force microscopy. This study demonstrates the application of the domain period and surface roughness found by force microscopy to the interpretation of the GMI in Co-rich microwires.

Carcase composition of Taiwan simulated native chickens.

This study investigated the carcase composition of Taiwan simulated native chickens at different stages of growth. The results indicated that the carcases of male chickens exhibited significantly larger protein mass and water mass than those of females during weeks 7 to 20; as was the ash mass during weeks 8 to 20. However, the fat mass of the carcases of female chickens was larger than that of males during weeks 14 to 20. Separate regression equations were derived for the relationship between protein mass, fat mass, ash mass and water mass and both carcase weight and age of both male and female chickens.

Changes in resistance to mouth opening induced by depolarizing and non-depolarizing neuromuscular relaxants.

Mouth opening was measured in 43 children anaesthetized with isoflurane and paralysed with vecuronium or suxamethonium. Measurements of mouth opening were made for up to 10 min after loss of the adductor pollicis twitch and cessation of muscle fasciculations. In 22 patients receiving suxamethonium, a significant (P less than 0.001) reduction in mean mouth opening occurred in the 60 s after loss of twitch and cessation of fasciculations. Mouth opening reductions could last for up to 10 min after the loss of twitch, beyond the return of the twitch. One patient experienced "masseter spasm"; he did not develop malignant hyperpyrexia during 2.5 h of isoflurane anaesthesia. Patients receiving vecuronium showed a significant (P less than 0.0006) increase in mouth opening. In 20 subjects, mouth opening was generated with a small (1.67 N) and a larger (4.32 N) force. Proportionally equal reductions in mouth opening were obtained with either force after suxamethonium administration. Relatively equal increases with either force followed vecuronium administration. Isolated masseter spasm is not pathognomonic for malignant hyperpyrexia. If the diagnosis of malignant hyperpyrexia is contemplated, signs of hypermetabolism, such as increases in end-tidal carbon dioxide concentration during constant minute ventilation, should be sought.

The onset of ablation of the evoked adductor pollicis muscle twitch in children: a clinical perspective.

The time to loss of the adductor pollicis muscle response to ulnar nerve stimulation at 1 Hz (twitch) after succinylcholine, 1.5 mg.kg-1 intravenously (IV), or vecuronium, 0.1 mg.kg-1 (IV), administration was assessed visually in 134 children, age 2-13 yr, during clinically determined, deep halothane, enflurane and isoflurane anaesthesia. The overall time to twitch ablation and duration of succinylcholine's action is in agreement with published times obtained under controlled experimental conditions; the onset time following vecuronium is comparable to those observed during a similar anaesthetic background measured under controlled experimental conditions. Twitch ablation after succinylcholine was achieved in half the time needed following vecuronium regardless of anaesthetic agent. Succinylcholine's and vecuronium's onset time as well as succinylcholine's duration is adequately assessed by the outlined, simple clinical means. The choice of inhalation agent does not affect the time to visible twitch ablation in a clinically relevant manner; nor does it make an appreciable difference, in clinical terms, in succinylcholine's duration of action.

Increased masticatory muscle stiffness during limb muscle flaccidity associated with succinylcholine administration.

The resistance of mouth opening to a constant force of 1.7 N was measured in 44 pediatric subjects anesthetized with enflurane and paralyzed with succinylcholine or vecuronium. Measurements were made during a deep level of anesthesia before relaxant administration, immediately after the loss of the adductor pollicis muscle twitch and 45 s later. In 22 patients receiving succinylcholine, there was a significant reduction in mean mouth opening (from 16.9 +/- 2.8 to 12.6 +/- 4.3 to 13.0 +/- 4.3 mm; P less than 0.0005) and an increase in jaw stiffness (from 102.3 +/- 21.9 to 154.5 +/- 77.4 to 150.5 +/- 77.0 Nm/degree; P less than 0.02) immediately after disappearance of the evoked thenar muscle twitch, as well as 45 s later. In six patients receiving succinylcholine, measurements were continued at 1 min intervals; mouth opening reduction and jaw stiffness increase lasted up to 10 min and extended beyond the return of visible twitch. One patient had a reduction of mouth opening from 20 to less than 1 mm; his corresponding jaw stiffness changed from 83.4 to 3335.4 Nm/degree. This patient, considered by us to have masseter spasm, required several attempts at tracheal intubation due to an increased resistance to mouth opening, as did one other patient. Patients receiving vecuronium showed a significant (P less than 0.02) increase of mouth opening 45 s following loss of twitch (from 19.8 +/- 3.6 to 20.9 +/- 4.1 mm; jaw stiffness changed from 87.0 +/- 15.3 to 83.0 +/- 17.2 Nm/degree). Anesthesia and surgery proceeded normally; in most patients, in excess of 1 h.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of succinylcholine on mouth opening.

Mouth opening and the resistance to opening developed by the muscles of mastication were measured in 63 children anesthetized with halothane and relaxed with succinylcholine, pancuronium, or vecuronium. Measurement of mouth opening, induced by a constant test force, was made when each patient was deeply anesthetized, as judged by clinical parameters. Succinylcholine, vecuronium, or pancuronium was then administered. The mouth opening measurement was repeated immediately after the loss of limb muscle twitch response and 45 s following the loss of twitch response. For the 24 patients receiving succinylcholine, there was a significant reduction in mean mouth opening (P less than 0.0001) and a significant increase in jaw stiffness (P less than 0.0001) immediately after limb relaxation. Forty-five seconds after full limb relaxation was attained, the mean mouth opening was still reduced (P less than 0.0001) and the mean jaw stiffness was still increased (P less than 0.0003) in the succinylcholine group. Patients receiving either vecuronium or pancuronium did not show a significant change of mouth opening or jaw stiffness following limb relaxation. Three patients, who received succinylcholine, required several attempts at tracheal intubation due to increased resistance to mouth opening. Anesthesia and surgery proceeded in all patients. None of the patients developed malignant hyperthermia. In view of the fact that a reduction in mouth opening was a constant finding when succinylcholine was administered during halothane anesthesia, the assumption that isolated "masseter spasm" or jaw stiffness heralds malignant hyperthermia should be reconsidered.