Characterization of microbial community profiles associated with quality of Chinese strong-aromatic liquor through metagenomics.

AIMS: Microorganisms in fermentation pits (FPs) play key roles for Chinese-strong-aromatic-liquor (CSAL) production. However, the microbial community in the FPs is still poorly understood. Here, the aim of this study was to reveal the diversity and potential functions of microbiota in FPs. METHODS AND RESULTS: Sequencing-by-synthesis-based metagenomic sequencing and annotation results revealed that the microbiota of FPs was primarily composed of Firmicutes (54·6%), Euryarchaeota (15·3%), Bacteroidetes (10·1%), Gammaproteobacteria (5·8%), Opisthokonta (5·7%) and Unclassified_Bacteria (2·3%). And 133 genera were identified as the dominant genera of this fermentative food. Lactobacillus, Sedimentibacter, Syntrophomonas, Methanoculleus, Methanobacterium, Bacillus, Clostridium, Galactomyces, Candida, Pichia, Penicillium and Aspergillus were defined as active populations for biosynthesizing the characteristic volatile compounds of CSAL. The study also revealed that the microbial community structures changed significantly with different cellar ages and over different geographical regions. (i) The presence of Bacteroidetes was the most distinctive feature that characterized the different FPs ages. (ii) Distinct contents of Gammaproteobacteria and Euryarchaeota were observed at different positions in the FPs. (iii) Euryarchaeota markedly contributed to the generation of the character of the liquors with distinct geographical associations. CONCLUSIONS: This study demonstrated that the changes of microbial communities determined the different quality characteristics of CSAL. SIGNIFICANCE AND IMPACT OF THE STUDY: This research contributes to a deeper understanding of the FPs microbial composition and shows a new microbial resource for biotechnological applications.

The application of individual virtual nostalgic game design to the evaluation of cognitive function.

The aim of this study was to develop a task set based on personalized material for nostalgic experience, which could detect cognitive ability via a virtual experience system combined with Kinect somatosensory interactive operation applications without the user wearing any accessory input device. Fifty-nine subjects participated in the experiment. The receiver operating characteristic curve of the game system was statistically analyzed for determining the best cutoff-point in the cognitive function assessment. Correlation analysis and regression analysis were used to explore the correlations between the results and the clinical cognitive assessment scales. According to the MoCA scores, the results showed that the accuracy of the system was 86.4% in evaluating mild cognitive impairment. The system seems feasible and was strongly correlated with clinical cognitive assessment scales. We anticipate that daily use of our system could keep track of changes of cognitive function of the elderly in home life.

The proliferative and migratory effects of physical injury and stromal cell-derived factor-1α on rat cardiomyocytes and fibroblasts.

OBJECTIVE: This study aims to explore the effects of physical injury and stromal cell-derived factor-1α (SDF-1α) on the proliferation of cardiomyocytes and chemotactic effects of cardiomyocytes on the migration of cardiac fibroblasts. MATERIALS AND METHODS: Isolation and primary culture of rat cardiomyocytes and cardiac fibroblasts were performed; scratching was employed to induce physical injury on cells which were cultured with SDF-1α at different concentrations; proliferation ability of cardiomyocytes was checked with CCK-8 assay and migratory ability of cardiac fibroblasts under the chemotaxis of cardiomyocytes was detected with Transwell assay. RESULTS: SDF-1α enhanced the proliferation ability of cardiomyocytes with physical injury, especially at the concentration of 80 µg/L when the proliferation rate of cardiomyocytes increased most markedly. Moreover, physically injured cardiomyocyte that was cultured with SDF-1α significantly elevated migratory ability of cardiac fibroblasts, which tended to be more obvious along with the chemotactic culture time. CONCLUSIONS: SDF-1α enhanced the proliferation ability of cardiomyocytes with physical injury, and physically injured cardiomyocyte that was cultured with SDF-1α promoted the migration of cardiac fibroblasts.

A miniature lighted stylet for fast oral endotracheal intubation in rabbits.

Efficient oral endotracheal intubation of laboratory animals is a challenging technique in veterinary research. This study introduces a miniaturized lighted stylet for rabbit intubation. An experiment with repeated measures on two factors was used to assess the feasibility and efficacy of this method. The first factor compared stylet intubation vs. laryngoscopic intubation. The second compared three practitioners, one with prior experience and two without. Success rates on the initial attempt were not statistically different (χ(2)=2.46, P=0.12). The time difference between methods was significant (F=41.007, P<0.001), although the effect of practitioners was not (F=1.038, P=0.365). The mean±SD of the intubation time, combining results from the three practitioners, was 20.34±17.15s for the stylet method and 57.58±64.21s for the laryngoscopic method. The results of this study demonstrate that lighted stylet intubation is efficient, robust, and independent of practitioner experience.

Insulin promotes bone formation in augmented maxillary sinus in diabetic rabbits.

The role of insulin during the formation of bone in the augmented space of the maxillary sinus in patients with diabetes is unclear. The authors compared the differences in bone formation after maxillary sinus floor elevation in diabetic and healthy animals and evaluated the effects of insulin on osteogenesis and the differentiation and activities of the osteoblasts. 10 male Japanese white rabbits were divided into two groups after diabetic induction by a single injection of monohydrated alloxan and having maintained steady blood glucose levels. The groups included the diabetes mellitus group (DM; n=5) and the DM+insulin group (n=5); another five healthy rabbits comprised the control group. Maxillary sinus floor elevation was performed by grafting hydroxyapatite particles. Compared with the control group, the newly formed bone area, number of blood vessels and osteoblasts, collagen I content and serum osteocalcin levels were significantly decreased in DM rabbits (P<0.01). Insulin treatment reversed the decrease in bone formation, blood vessels, osteoblasts, collagen I and serum osteocalcin (P<0.01). Insulin treatment also promoted osteogenesis in the augmented space of the diabetic rabbits, which might have resulted from promotion of osteoblast differentiation and upregulation of neovascularization.

A novel four base-pair deletion within the Agamma-GLOBin gene promoter associated with slight increase of Agamma expression in adult.

We studied a Chinese family and revealed 5.4% and 3.2% fetal hemoglobin (HbF) with advantageously Agamma type in the mother and the daughter, respectively, using alkali denaturation assay and urea-Triton-acrylamide gel electrophoresis and high-performance liquid chromatography. The father's HbF was less than 0.5%. Large deletion was not observed within the beta-globin gene cluster by restriction endonuclease mapping. Characterization by the polymerase chain reaction (PCR) and DNA sequencing demonstrated the mother is a homozygote with a novel four base-pair "AAGC" (-226 to -223) deletion within the Agamma-globin gene promoter and the daughter is a heterozygote with this deletion. The deletion was not detected in the father. No any mutations were identified in the Ggamma promoter of all the subjects studied. We propose that the small deletion is associated with the slight increase of Agamma gene expression in adult.

Effects of adenosine A1-receptor activation on torsade de pointes in rabbits.

PURPOSE: We tested whether the adenosine A1 receptor agonist, R-PIA, suppressed torsade de pointes (TdP) induced by the delayed rectifier potassium channel blocker clofilium. Furthermore, we studied the underlying mechanism: beta-adrenergic antagonism or ATP-sensitive K+ channel (IK-ATP) opening. METHODS: In anesthetized rabbits, TdP was induced by simultaneous infusion of clofilium and the alpha1-adrenoceptor agonist methoxamine. Four groups were studied: (1) saline infusion after TdP induction; (2) R-PIA (1.3 mg/kg) infusion; (3) R-PIA infusion after propranolol (2 micromol/kg) pretreatment; (4) R-PIA infusion after glibenclamide (10 micromol/kg) pretreatment. RESULTS: TdP suppression rate was 0% in group 1, 78% in group 2 (p<0.01 vs. group 1), 67% in group 3 (p<0.05 vs. group 1, p = NS vs. group 2), 33% in group 4 (p = NS vs. group 1, p = 0.08 vs. group 2). TdP induction coincided with increased QT/QTc duration and QT dispersion. TdP suppression coincided with reduced QT dispersion, but further QT/QTc lengthening. CONCLUSIONS: R-PIA suppressed TdP, not by beta-adrenergic antagonism, but mostly by IK-ATP opening. QT dispersion correlated better with TdP induction/suppression than QT/QTc duration.

Bacillus popilliae endocarditis with prolonged complete heart block.

Bacillus popilliae, a fastidious, aerobic, gram-positive, spore-forming bacillus, has never been reported as a pathogen in human infectious diseases. We report the first case of a human infected by the pathogen B. popilliae, which presented as endocarditis involving the bicuspid aortic valve and complicated with prolonged (> 30 days; to our knowledge, the longest in the literature) complete heart block. Although surgery may be warranted by previous reports, the patient was successfully managed by medical treatment instead, because of the absence of evidence from various approaches that support the existence of perivalvular extension of infection.

Atrial flutter in the neonate and early infancy.

Atrial flutter is a rare arrhythmia in the neonate and early infancy. We retrospectively reviewed the clinical presentations, treatment and outcome of seven patients who presented clinically with atrial flutter. The age of onset ranged from 1 day to 3 months. Atrial flutter was diagnosed in the first 3 days of life in 4. Three cases presented as atrial flutter with 2:1 atrioventricular conduction and the remaining 4 with variable AV block. Heart failure was present in 3 patients and 6 patients showed normal intracardiac structure on echocardiography. Electrical cardioversion was attempted as the first treatment in 4 cases, followed by digoxin in three of the four. Digoxin was given as an initial therapy in 2 patients. One patient recovered spontaneously without treatment. In the 6 patients who received therapy, 5 converted to normal sinus rhythm within 2 days. The remaining patient had ventricular ectopic beats for about 4 months. Only 2 cases were maintained on oral digoxin for at least 4 months after discharge. No patient had a recurrence of atrial flutter during the follow-up period which ranged from 6 months to 7 years. We conclude that there is a good long-term prognosis for atrial flutter in the neonate. Digoxin and DC cardioversion may be effective as initial therapy. Long-term digoxin prophylaxis after conversion to sinus rhythm may be not necessary.

Late development of renal arteriovenous fistula following gunshot trauma--a case report.

A 43-year-old man presenting with symptoms of congestive heart failure, cardiomegaly, and impaired left ventricular (LV) function was diagnosed as having a huge left renal arteriovenous (AV) fistula. The AV fistula might be attributed to a gunshot wound suffered during his military service twenty years ago. Percutaneous transcatheter arterial embolization utilizing multiple spring coils in conjunction with cyanoacrylic glue successfully occluded the fistula, with subsequent improvement of LV function and reduction of LV size on his serial echocardiographic follow-up.

Electrophysiologic significance of discrete slow potentials in dual atrioventricular node physiology: implications for selective radiofrequency ablation of slow pathway conduction.

Atrioventricular (AV) node reentrant tachycardia is now routinely cured by selective radiofrequency ablation of slow AV node pathway conduction. However, debate remains concerning the optimum method for localizing the site at which radiofrequency energy should be delivered to eliminate slow-pathway conduction. Some investigators have proposed simple anatomy-guided ablations posteriorly near the ostium of the coronary sinus, whereas others suggest an electrophysiology-guided ablation using either recorded "slow potentials" or mapping of the retrograde atrial exit site of slow AV note pathway conduction when possible. To examine these issues, we systematically studied slow potentials recorded in the AV junction of patients undergoing radiofrequency catheter ablation for medically refractory AV node reentrant tachycardia. In 67 patients with the slow-fast form of AV note reentrant tachycardia, we performed detailed atrial mapping along the tricuspid annulus within the triangle of Koch. Two types of slow potentials were identified. Low-amplitude, low-frequency potentials, found in 48% of patients, were localized to the mid to posterior portions of the triangle of Koch, whereas high-amplitude, high-frequency potentials, observed in 22% of patients, were located only posteriorly near the ostium of the coronary sinus. In response to a bolus infusion of adenosine or incremental atrial pacing-induced AV node Wenckebach periodicity, the low-amplitude, low-frequency potentials showed an increased duration and further reduction in amplitude and frequency and often totally disappeared. In contrast, in spite of these maneuvers, the high-amplitude and high-frequency potentials remained unchanged. Of the 25 (37%) of 67 patients in whom the earliest retrograde atrial activation during ventriculoatrial slow AV nodal pathway conduction could be recorded, no patient exhibited low-amplitude, low-frequency potentials, and only 7 (28%) of 25 of these patients showed high-amplitude, high-frequency potentials. High-amplitude, high-frequency potentials persisted after successful radiofrequency ablation of slow pathway conduction. Fewer applications of radiofrequency energy were required for successful elimination of slow pathway conduction in patients in whom the retrograde atrial exit site of slow-pathway conduction could be localized, compared with those patients who only exhibited retrograde fast AV nodal pathway conduction. We conclude that high-amplitude, high-frequency potentials are part of atrial activity, whereas the origin of low-amplitude, low-frequency potentials is unclear and may represent either true intranodal biophysical electrical activity or merely artifact or far-field potentials. Regardless, the recording of high-amplitude or low-amplitude potentials is not required for successful ablation of slow-pathway conduction, although the ability to localize the retrograde atrial exit of slow-pathway conduction may assist in the ablation procedure.

Determination of ventricular vulnerable period and ventricular fibrillation threshold by use of T-wave shocks in patients undergoing implantation of cardioverter/defibrillators.

BACKGROUND: This study was designed to characterize the ventricular vulnerable period (VVP) and ventricular fibrillation (VF) threshold by use of T-wave shocks in patients undergoing implantation of cardioverter/defibrillators. A premature condensed shock applied during the VVP can induce VF. Most studies on the VVP and VF threshold have been conducted in animals rather than in humans. METHODS AND RESULTS: Twenty-one patients undergoing implantation of Medtronic PCD Jewel 7219D cardioverter/defibrillators because of ventricular tachycardia and/or VF were enrolled. All had structural heart disease. Their ages ranged from 42 to 85 years (mean, 69 +/- 11.3 years). Seventeen (80.9%) had atherosclerotic coronary artery disease. The right ventricle (RV) was driven at a cycle length (S1) of 400 ms, and monophasic shocks (S2) of 0.6 J were delivered through an RV apex lead (cathode) and a superior vena cava lead (anode) during the T wave of each cardiac cycle. The longest and shortest S1-S2 intervals that were capable of inducing sustained VF were defined as the outer and inner limits of the VVP at an energy level of 0.6 J, respectively. To determine the VF threshold, a shock of 0.2 J was applied at the midpoint of the VVP at 0.2-J increments until sustained VF was induced. The lowest energy setting capable of inducing sustained VF was defined as the VF threshold. Of the 21 patients, the VVP at an energy level of 0.6 J averaged 53.8 +/- 26.0 ms. Characteristically, the VVP started from the ascending limb of the T wave and ended at or slightly beyond the peak of the T wave, occupying 12.2 +/- 5.8% of the QT interval. The midpoint of the VVP used for determination of the VF threshold measured 0 to 90 ms (mean, 32.9 +/- 26.0 ms) before the peak of the T wave. Of the 21 patients, 16 (76.2%) had a VF threshold at < or = 0.2 J (estimated 57 V), 3 at 0.4 J (estimated 81 V), and 2 at 0.6 J (estimated 99 V). CONCLUSIONS: The VF threshold is low (< or = 0.2 J) in the majority of patients requiring implantation of cardioverter/defibrillators. Further studies are needed to define clinical usefulness of the study technique relative to its potential role for risk stratification and for assessing antifibrillatory properties of antiarrhythmic drugs in this subset group of patients.

Electrophysiologic mechanisms of the long QT interval syndromes and torsade de pointes.

PURPOSE: To review the current understanding of the mechanisms and treatment of the long QT interval syndromes and torsade de pointes. DATA SOURCES: Personal databases of the authors and a search of the MEDLINE database from 1966 to 1994. STUDY SELECTION: Experimental and clinical studies and topical reviews on the electrophysiologic mechanisms and treatment of torsade de pointes were analyzed. RESULTS: The long QT interval syndromes have been classified into acquired and hereditary forms, both of which are associated with a characteristic type of life-threatening polymorphic ventricular tachycardia called torsade de pointes. The acquired form is caused by various agents and conditions that reduce the magnitude of outward repolarizing K+ currents, enhance inward depolarizing Na+ or Ca2+ currents, or both, thereby triggering the development of early afterdepolarizations that initiate the tachyarrhythmia. The hereditary form appears to result from an abnormal response to adrenergic or sympathetic nervous system stimulation. At least some cases of the hereditary long QT interval syndromes may result from a single gene defect that alters the intracellular regulatory proteins responsible for the modulation of K+ channel function. Treatment of the acquired form is primarily directed at identifying and withdrawing the offending agent, although emergent therapy using maneuvers and agents that favorably modulate transmembrane ion currents can be lifesaving. In torsade de pointes associated with the hereditary long QT interval syndromes, early diagnosis leading to treatments designed to both shorten the QT interval and block the beta-adrenergic-induced instability of the QT interval is essential. CONCLUSIONS: The long QT interval syndromes and torsade de pointes are potentially life-threatening conditions caused by various agents, conditions, and genetic defects. The mechanisms responsible for these conditions and available treatment options for them are reviewed.