Inability to capture with increasing current strength: Is this near-field or far-field?

We present a case of wide-complex tachycardia in which the clinical electrophysiological diagnosis was considered to be bundle branch re-entry ventricular tachycardia. A series of ventricular entrainment attempts were performed from the left and right ventricular septum to confirm the diagnosis. Entrainment pacing with a general current output (10 mA) was performed from the right ventricular septum with manifest fusion and a post-pacing interval similar to tachycardia cycle length. Thereafter, another entrainment attempt with a greater current output (20 mA) was performed from the same site. Paradoxically, concealed fusion was demonstrated by selective RB capture only, though there was no clear "RB" potential seen. In this case, we attempt to explain and illustrate the mechanism of paradoxical near-field inability to capture with increasing current strength.

Supraventricular tachycardia with atrial activation earliest at the His bundle region-What is the mechanism?

A 70-year-old man with recurrent symptomatic supraventricular tachycardia was referred for catheter ablation. Atrial activation was earliest at the His bundle region with HA longer than AH.

A translational mouse model for investigation of the mechanism of preterm diffuse white matter injury.

Background: The increasing incidence of preterm birth has led to a global problem of adverse neurodevelopmental outcomes in preterm neonates as a result of brain injury. There is still a lack of models mimicking diffuse white matter injury (WMI) in preterm neonates that can be applied to transgenic mice. Methods: The right common carotid artery of the neonatal mouse was ligated on postnatal day 3 (P3) C57BL/6 mice and followed by 80, 90, or 100 min of hypoxia using a mixture of 10%±0.2% oxygen-nitrogen. The most suitable model was chosen by characterizing the effects of this hypoxic-ischemic insult on development of myelin, glial cell conditions, and neurological outcomes by hematoxylin-eosin (HE) staining performed at postnatal day 17 (P17), western blot measuring myelin basic protein (MBP) at postnatal day 10 (P10) and P17, immunofluorescence staining of MBP-neurofilament protein heavy chain (NFH), oligodendrocyte transcription factor-2 (Olig2)-adenomatous polyposis coli clone (CC1), glial fibrillary acidic protein (GFAP) and ionic calcium linker protein (Iba-1) at P17, electron microscopy observing myelin microstructure at postnatal day 52 (P52) and behavioral testing at postnatal day 45-50 (P45-P50). Results: The 90-min group showed neuroanatomical changes in the ipsilateral side of the brain, the 80-min group showed minor changes, and the 100-min group showed severe injury. Mice in the 90-min group subsequently showed marked activation of astrocytes, augmentation of microglia, a notable decrease in expression of MBP with a normal level of NFH, long-term cognitive dysfunction, and impairment of the myelin ultrastructure in adulthood. Conclusions: In conclusion, a mouse model of preterm diffuse WMI rather than cystic periventricular leukomalacia was successfully achieved by ligating one of the common carotid arteries on P3 followed by 90 min of hypoxia in a mixture of 10%±0.2% oxygen-nitrogen. The attempt provides an adequate translational animal model for elucidating the underlying mechanism.

Galectin-3 administration drives remyelination after hypoxic-ischemic induced perinatal white matter injury.

Hypoxic-ischemic (HI) induced perinatal white matter injury (PWMI) is a major cause of neurologic disabilities characterized by selective oligodendroglial death and myelin disruption. Galectin-3 (Gal-3) modulates postnatal subventricular zone gliogenesis and attenuates ischemic injury. However, the association between Gal-3 and myelin formation still remains unclear. In this study, we first perform Gal-3 knockdown (KD) to identify the importance of Gal-3 on myelin formation. Our results show impeded myelin formation, manifested by Olig2/CC1 (+) mature oligodendrocytes number, expression of oligodendroglial maturation-associated markers (MBP and CNPase), and myelin thickness and integrity. Then we perform recombinant Gal-3 (rGal-3) administration by intracerebroventricular injection. Notably, although rGal-3 administration shows no beneficial effect on oligodendrogenesis and myelin formation under normal condition, our results show that rGal-3 administration attenuates cognitive deficits and drives remyelination after PWMI, which are coupled to signs of enhanced myelin resiliency and cognition. Also, our results indicates that the significant increases in substrates for remyelination of rGal-3 administration are accompanied by enhanced Iba-1 (microglia marker)/ Mrc1 (M2 marker) (+) microglia and decreased Iba-1/ iNOS (M1 marker) (+) microglia. Altogether, our data in this research confirm the association between Gal-3 and myelin formation, underscore its position for the capacity for remyelination and restoration of function, and unveils the efficacy of rGal-3 administration with anti-inflammatory phenotype microglia (M2 microglia) activation. Thus, the findings suggest that Gal-3 plays a significant role in myelin formation and remyelination restoration.

Effects of delayed HIF-1α expression in astrocytes on myelination following hypoxia-ischaemia white matter injury in immature rats.

BACKGROUND: The underlying cause of neurological sequelae after immature cerebral hypoxia-ischaemia (HI) white matter injury is impaired myelination. Previous studies have indicated that astrocyte activation is closely related to impaired myelination. However, the mechanism of reactive gliosis in white matter injury post-HI remains poorly understood. METHODS: Studies using adult ischaemic animal models demonstrated that hypoxia inducible factor-1α (HIF-1α) expression was involved in the formation of reactive astrocytes. Here, we investigated the temporal expression of HIF-1α and its impact on reactive gliosis and further myelination using a perinatal HI white matter injury model induced in rats at postnatal day 3. The temporal pattern of HIF-1α expression post-HI injury was tested by western blotting and immunofluorescence. Rats were treated with a HIF-1α inhibitor at 72 hours post-HI injury. Reactive gliosis and myelination were assessed with western blotting, immunofluorescence and electron microscopy, and neurological functions were examined by behavioural testing. RESULTS: Our results showed that the expression of HIF-1α was upregulated in neurons at 24 hours and in astrocytes at 7 days post-HI. Inhibiting delayed HIF-1α expression post-HI injury could restrain reactive gliosis, ameliorate hypomyelination, and improve the performance of rats in the Morris water maze test. CONCLUSIONS: Our findings suggest that a delayed increase in HIF-1α in astrocytes is involved in glial scar formation and leads to arrested oligodendrocyte maturation, impaired myelination, and long-term neurological function after experimental white matter injury in immature rats.

Selective Interventricular Septal Radiofrequency Ablation in Patients With Hypertrophic Obstructive Cardiomyopathy: Who Can Benefit?

Introduction: Septal mass reduction is beneficial for hypertrophic obstructive cardiomyopathy (HOCM) patients with severe left ventricular outflow (LVOT) gradient and symptoms, with surgical myectomy or alcohol septal ablation (ASA) currently recommended in selected patients. Radiofrequency (RF) ablation of hypertrophied septum has been published as a novel method to alleviate LVOT obstruction in small populations. This study aims to investigate factors influencing clinical outcomes of radiofrequency septum ablation. Methods and Results: In this study, 20 patients with HOCM who underwent endocardial ablation were included. Echocardiography and cardiac MRI (CMR) data was collected and analyzed pre- and (or) post- procedure. Nineteen patients underwent ablation successfully, while ablation was aborted in one patient with prior RBBB due to transient complete atrioventricular block (AVB). After 6 months of follow-up, NYHA heart functional class improved from III (2 - 3) to II (1 - 2) (p < 0.001), and resting LVOT gradient was significantly reduced (87.6 ± 29.5 mmHg vs. 48.1 ± 29.7, p < 0.001). LVOT gradient reduction was significantly higher in patients with limited basal septal hypertrophy (60.9 ± 8.3 vs. 27.9 ± 7.1, p = 0.01), shorter anterior mitral leaflet (56.1 ± 6.4 vs. 20.4 ± 5.0, p < 0.01), and normally positioned papillary muscle (36.9 ± 7.1 vs. 75.0 ± 6.3, p < 0.05). Conclusions: Endocardial septal ablation appears to be a safe and effective procedure for alleviating LVOT gradient in patients with HOCM, especially in those with limited basal septal hypertrophy, shorter anterior mitral leaflet, and normal positioned papillary muscle.

Spatiotemporal expression patterns of Galectin-3 in perinatal rat hypoxic-ischemic brain injury model.

In this research, we intended to evaluate the expression pattern, distribution and sources of Galectin-3 (Gal-3) in perinatal hypoxic-ischemic brain injury rat model. Postnatal day 3 Sprague-Dawley rat pups were subjected to right carotid artery ligation followed by 2.5 h of hypoxia (6% oxygen). Expression and distribution of Gal-3 were evaluated by western blotting and immunofluorescence. Sources of Gal-3 were evaluated by double staining with neuronic, oligodendrocytic, astrocytic, microglial and endotheliocytic markers. Our results indicated Gal-3 significantly upregulated from 12 h and maintained an increasing tendency within 72 h post injury. Although the relative expression of Gal-3 decreased after 72 h, we detected significant differences until 14d. We found Gal-3 started to distribute in cortex and thalamus area and maintained an increasing tendency. Gal-3 could be detected in cortex, thalamus, corpus callosum and hippocampus area at 72 h post injury. After that, expression of Gal-3 in cortex and thalamus area downregulated, the expression in corpus callosum and hippocampus area vanished. We found astrocyte, microglia, neuron and endotheliocyte were sources of Gal-3 in cortex area; astrocyte, microglia and endotheliocyte were sources of Gal-3 in thalamus area; oligodendrocyte precursor cell and endotheliocyte were sources of Gal-3 in corpus callosum; neuron, microglia and endotheliocyte were sources of Gal-3 in hippocampus. In conclusion, we demonstrated spatiotemporal expression patterns of Galectin-3 post perinatal hypoxic-ischemic brain injury in this research.

Minimization of the perianal infection rate of hematological malignancies with agranulocytosis by quality control circle activity and patient-hospital-student win-win concept.

Objective The agranulocytosis-associated perianal infection (PI) rate ranges from 60% to 100% among patients with hematopoietic malignancies. In this study, we assessed the efficacy of a quality control circle (QCC) to minimize the PI rate. Methods Among 274 patients with severe immunodeficiency (agranulocytosis of ≥2 weeks) in our bone marrow transplantation center, the PI rate was 17.20%. A QCC was established following the 10 steps of the plan-do-check-act (PDCA) model; this was scientifically supported by culturing the bacterial colony from patients' perianal skin to determine the sanitization effect and interval time. Because a warm aqueous solution of potassium permanganate is recommended for sanitization, the bacterial colony culture was also used to determine the proper drug concentration, water temperature, and soaking time. All procedures were standardized. Patients, hospital staff, and medical students were enrolled into the QCC team based on the patient-hospital-student (PHS) win-win concept. Results After establishment of the PDCA model, the PI rate among 253 patients decreased from 17.20% to 5.93% and remained at 5.25% during the following year. The medical expenses and length of hospital stay consequently decreased. Conclusion The QCC and PHS win-win concept can reduce the PI rate and promote medical quality.

CqToll participates in antiviral response against white spot syndrome virus via induction of anti-lipopolysaccharide factor in red claw crayfish Cherax quadricarinatus.

It is well known that Tolls/Toll like receptors (TLRs), a family of pattern recognition receptors, play important roles in immune responses. Previously, we found that a Toll transcript was increased in a transcriptome library of haematopoietic tissue (Hpt) cells from the red claw crayfish Cherax quadricarinatus post white spot syndrome virus infection. In the present study, a full-length cDNA sequence of Toll receptor (named as CqToll) was identified with 3482 bp which contained an open reading frame of 3021 bp encoding 1006 amino acids. The predicted structure of CqToll protein was composed of three domains, including an extracellular domain of 19 leucine-rich repeats residues, a transmembrane domain and an intracellular domain of 138 amino acids. Tissue distribution analysis revealed that CqToll was expressed widely in various tissues determined from red claw crayfish with highest expression in haemocyte but lowest expression in eyestalk. Importantly, significant lower expression of the anti-lipopolysacchride factor (CqALF), an antiviral antimicrobial peptide (AMP) in crustaceans, but not CqCrustin was observed after gene silencing of CqToll in crayfish Hpt cell cultures, indicating that the CqALF was likely to be positively regulated via Toll pathway in red claw crayfish. Furthermore, the transcription of both an immediate early gene and a late envelope protein gene VP28 of WSSV were clearly enhanced in Hpt cells if silenced with CqToll, suggesting that the increase of WSSV replication was likely to be caused by the lower expression of the CqALF resulted from the loss-of-function of CqToll. Taken together, these data implied that CqToll might play a key role in anti-WSSV response via induction of CqALF in a crustacean C. quadricarinatus.