Transcriptomic analysis of epicardial adipose tissue reveals the potential crosstalk genes and immune relationship between type 2 diabetes mellitus and atrial fibrillation.

BACKGROUND: The complex relationship between atrial fibrillation (AF) and type 2 diabetes mellitus (T2DM) suggests a potential role for epicardial adipose tissue (EAT) that requires further investigation. This study employs bioinformatics and experimental approaches to clarify EAT's role in linking T2DM and AF, aiming to unravel the biological mechanisms involved. METHOD: Bioinformatics analysis initially identified common differentially expressed genes (DEGs) in EAT from T2DM and AF datasets. Pathway enrichment and network analyses were then performed to determine the biological significance and network connections of these DEGs. Hub genes were identified through six CytoHubba algorithms and subsequently validated biologically, with further in-depth analyses confirming their roles and interactions. Experimentally, db/db mice were utilized to establish a T2DM model. AF induction was executed via programmed transesophageal electrical stimulation and burst pacing, focusing on comparing the incidence and duration of AF. Frozen sections and Hematoxylin and Eosin (H&E) staining illuminated the structures of the heart and EAT. Moreover, quantitative PCR (qPCR) measured the expression of hub genes. RESULTS: The study identified 106 DEGs in EAT from T2DM and AF datasets, underscoring significant pathways in energy metabolism and immune regulation. Three hub genes, CEBPZ, PAK1IP1, and BCCIP, emerged as pivotal in this context. In db/db mice, a marked predisposition towards AF induction and extended duration was observed, with HE staining verifying the presence of EAT. Additionally, qPCR validated significant changes in hub genes expression in db/db mice EAT. In-depth analysis identified 299 miRNAs and 33 TFs as potential regulators, notably GRHL1 and MYC. GeneMANIA analysis highlighted the hub genes' critical roles in stress responses and leukocyte differentiation, while immune profile correlations highlighted their impact on mast cells and neutrophils, emphasizing the genes' significant influence on immune regulation within the context of T2DM and AF. CONCLUSION: This investigation reveals the molecular links between T2DM and AF with a focus on EAT. Targeting these pathways, especially EAT-related ones, may enable personalized treatments and improved outcomes.

Neuroprotective mechanism of L-cysteine after subarachnoid hemorrhage.

Hydrogen sulfide, which can be generated in the central nervous system from the sulfhydryl-containing amino acid, L-cysteine, by cystathionine-ß-synthase, may exert protective effects in experimental subarachnoid hemorrhage; however, the mechanism underlying this effect is unknown. This study explored the mechanism using a subarachnoid hemorrhage rat model induced by an endovascular perforation technique. Rats were treated with an intraperitoneal injection of 100 mM L-cysteine (30 µL) 30 minutes after subarachnoid hemorrhage. At 48 hours after subarachnoid hemorrhage, hematoxylin-eosin staining was used to detect changes in prefrontal cortex cells. L-cysteine significantly reduced cell edema. Neurological function was assessed using a modified Garcia score. Brain water content was measured by the wet-dry method. L-cysteine significantly reduced neurological deficits and cerebral edema after subarachnoid hemorrhage. Immunofluorescence was used to detect the number of activated microglia. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the levels of interleukin 1ß and CD86 mRNA in the prefrontal cortex. L-cysteine inhibited microglial activation in the prefrontal cortex and reduced the mRNA levels of interleukin 1ß and CD86. RT-PCR and western blot analysis of the complement system showed that L-cysteine reduced expression of the complement factors, C1q, C3α and its receptor C3aR1, and the deposition of C1q in the prefrontal cortex. Dihydroethidium staining was applied to detect changes in reactive oxygen species, and immunohistochemistry was used to detect the number of NRF2- and HO-1-positive cells. L-cysteine reduced the level of reactive oxygen species in the prefrontal cortex and the number of NRF2- and HO-1-positive cells. Western blot assays and immunohistochemistry were used to detect the protein levels of CHOP and GRP78 in the prefrontal cortex and the number of CHOP- and GRP78-positive cells. L-cysteine reduced CHOP and GRP78 levels and the number of CHOP- and GRP78-positive cells. The cystathionine-ß-synthase inhibitor, aminooxyacetic acid, significantly reversed the above neuroprotective effects of L-cysteine. Taken together, L-cysteine can play a neuroprotective role by regulating neuroinflammation, complement deposition, oxidative stress and endoplasmic reticulum stress. The study was approved by the Animals Ethics Committee of Shandong University, China on February 22, 2016 (approval No. LL-201602022).

Resveratrol reduces brain injury after subarachnoid hemorrhage by inhibiting oxidative stress and endoplasmic reticulum stress.

Previous studies have shown that resveratrol, a bioactive substance found in many plants, can reduce early brain injury after subarachnoid hemorrhage, but how it acts is still unclear. This study explored the mechanism using the experimental subarachnoid hemorrhage rat model established by injecting autologous blood into the cerebellomedullary cistern. Rat models were treated with an intraperitoneal injection of 60 mg/kg resveratrol 2, 6, 24 and 46 hours after injury. At 48 hours after injury, their neurological function was assessed using a modified Garcia score. Brain edema was measured by the wet-dry method. Neuronal apoptosis in the prefrontal cortex was detected by terminal deoxyribonucleotidyl transferase-mediated biotin-16-dUTP nick-end labeling assay. Levels of reactive oxygen species and malondialdehyde in the prefrontal cortex were determined by colorimetry. CHOP, glucose-regulated protein 78, nuclear factor-erythroid 2-related factor 2 and heme oxygenase-1 mRNA expression levels in the prefrontal cortex were measured by reverse transcription polymerase chain reaction. Tumor necrosis factor-alpha content in the prefrontal cortex was detected by enzyme linked immunosorbent assay. Immunohistochemical staining was used to detect the number of positive cells of nuclear factor-erythroid 2-related factor 2, heme oxygenase 1, glucose-regulated protein 78, CHOP and glial fibrillary acidic protein. Western blot assay was utilized to analyze the expression levels of nuclear factor-erythroid 2-related factor 2, heme oxygenase 1, glucose-regulated protein 78 and CHOP protein expression levels in the prefrontal cortex. The results showed that resveratrol treatment markedly alleviated neurological deficits and brain edema in experimental subarachnoid hemorrhage rats, and reduced neuronal apoptosis in the prefrontal cortex. Resveratrol reduced the levels of reactive oxygen species and malondialdehyde, and increased the expression of nuclear factor-erythroid 2-related factor 2, heme oxygenase-1 mRNA and protein in the prefrontal cortex. Resveratrol decreased glucose-regulated protein 78, CHOP mRNA and protein expression and tumor necrosis factor-alpha level. It also activated astrocytes. The results suggest that resveratrol exerted neuroprotective effect on subarachnoid hemorrhage by reducing oxidative damage, endoplasmic reticulum stress and neuroinflammation. The study was approved by the Animals Ethics Committee of Shandong University, China on February 22, 2016 (approval No. LL-201602022).

8.2 kW high beam quality quasi-continuous-wave face-pumped Nd:YAG slab amplifier.

An 8 kW level quasi-continuous-wave (QCW) face-pumped 1064 nm slab laser with high beam quality was developed by a master oscillator power amplifier (MOPA) system. A single-mode fiber seed laser was amplified by two-stage single-pass Nd:YAG rod preamplifiers and four face-pumped Nd:YAG slab amplifiers. The slab amplifiers were well designed with uniform pumping and uniform cooling for well-distributed thermal and stress. A dynamically feedbacked optical aberration compensation device was employed to correct low-order optical aberration, and the residue high-order optical aberration was corrected by an adaptive optics system. The QCW MOPA delivered up to an average power of 8.2 kW with a pulse duration of 200 µs at a repetition rate of 400 Hz. The beam quality factor was measured to be ß=3.5.

Electrophysiological characteristics of paroxysmal atrial fibrillation originating from superior vena cava: a clinical analysis of 30 cases.

To analyze characteristics of electrocardiogram (ECG), electrophysiological intracardiac mapping and radiofrequency ablation (RF) of paroxysmal atrial fibrillation (PAF) originating from superior vena cava (SVC), aiming to investigate electrophysiological characteristics of PAF with SVC origin. Clinical data of 30 subjects (18 men and 12 women, aged, 58.6 ± 15.5 years) with PAF of SVC origin were retrospectively analyzed; All patients underwent RF during 2006.9-2012.7. ECG of AF and atrial premature contractions (APCs), procedure and fluoroscopic time, numbers of ablation sites within SVC, complications and success rate were studied. Compared with P wave of sinus rhythm (SR), APCs of SVC origin exhibited higher amplitude in lead II (0.23 ± 0.11 vs. 0.15 ± 0.06 mv), III (0.19 ± 0.09 vs. 0.13 ± 0.08 mv), AVF (0.21 ± 0.13 vs. 0.14 ± 0.10 mv), V2 (0.24 ± 0.07 vs. 0.15 ± 0.09 mv) and V3 (0.21 ± 0.09 vs. 0.12 ± 0.05 mv) (P < 0.05), as well as more biphasic polarity in lead V1 (80.0% vs. 26.6%, P < 0.05) and isoelectric in AVL (60.0% vs. 6.7%, P < 0.05). In terms of left pulmonary vein (LPV) and right pulmonary vein (RPV) electrical isolation, procedure time (14.3 ± 11.5 vs. 33.7 ± 14.2, 28.1 ± 6.8 min, P < 0.05), fluoroscopic time (9.6 ± 3.8 vs. 21.1 ± 9.3, 19.4 ± 9.7 min, P < 0.05), ablation sites (11.2 ± 3.1 vs. 37.1 ± 13.7, 31.4 ± 10.4 points, P < 0.05) of SVC isolation (SVCI) remarkably decreased compared with that of mean LPV and RPV. After the procedure, 9 patients still presented paroxymal rapid firing within the SVC in the setting of SR restoration, 2 patients developed paroxysmal atrial flutter within 1 month after completion of ablation and were controlled by antiarrhythmic drugs. The APCs and AF of SVC origin manifested distinctive ECG features, which could be helpful to distinguish SVC from other foci before ablation, the completion of SVCI required shorter procedure and fluoroscopic time, as well as less ablation points, and meanwhile, the success rate was high with less complication.

Role of inflammation in the initiation and maintenance of atrial fibrillation and the protective effect of atorvastatin in a goat model of aseptic pericarditis.

The present study was designed to determine the association between atrial fibrillation (AF) and inflammation in a goat sterile pericarditis model and to assess the effect of atorvastatin, a cholesterol­reducing drug, on AF. A total of 15 adult male goats were randomly divided into control, untreated pericarditis and atorvastatin­treated pericarditis groups. Pericarditis was induced via thoracotomy and atorvastatin was administered orally (60 mg/day) to the goats in the latter group for the duration of the study, commencing 1 week prior to surgery. The levels of high­sensitivity C­reactive protein (hs­CRP), interleukin(IL)­6 and tumor necrosis factor­α (TNF­α) were significantly elevated following surgery in the untreated pericarditis and atorvastatin groups compared with the control group (P<0.05). However, lower levels of hs­CRP, IL­6 and TNF­α were observed in the atorvastatin group compared with the untreated pericarditis group (P<0.05). Additionally, the animals in the atorvastatin­treated pericarditis group had a longer effective refractory period (ERP) and a higher rate adaptation of the ERP compared with those in the untreated pericarditis group (P<0.05). There was a significant negative correlation between the levels of ERP and hs­CRP in the untreated pericarditis group. The inducibility of AF in the left atrium and the duration of AF in the untreated pericarditis and atorvastatin­treated groups increased significantly following surgery (P<0.05). The pericarditis group, however, had a longer duration of AF compared with the atorvastatin group (P<0.05). Thus, inflammation may promote AF by shortening atrial ERP and by reducing the rate adaptation of ERP. These results suggested that atorvastatin can attenuate AF by inhibiting inflammation and may assist in preventing the occurrence and recurrence of AF following cardiac surgery.

Impact of body mass index on the development of pocket hematoma: A retrospective study in Chinese people.

BACKGROUND: Pocket hematoma is one of the major complications associated with cardiovascular implantable electronic devices (CIEDs) implantation. The aim of this study is to evaluate the impact of body mass index (BMI) on the occurrence of pocket hematoma after CIEDs implantation. METHODS: The study is a retrospective review of 972 patients receiving CIEDs implantation between 2008 and 2012 in a tertiary hospital. RESULTS: Twenty two patients (2.2%) developed severe pocket hematoma requiring re-intervention. The hematoma rate (4.6%, n = 15) of patients with a BMI of < 23 kg/m(2) was significantly higher compared with that of patients with a BMI of ≥ 23 kg/m(2) (1.1%, n = 7, P < 0.001). In multivariate regression analysis, a BMI < 23.0 kg/m(2) may be associated with the development of severe pocket hematoma. An increase of 1.0 kg/m(2) in BMI was associated with lower incidence of hematoma formation (OR: 0.84; 95% CI: 0.74-0.95; P = 0.006). CONCLUSION: BMI < 23 kg/m(2) was associated with a higher incidence of pocket hematoma, requiring re-intervention. The data support that great care must be taken when patients were with a lower BMI received CIEDs implantation.

[Study on spectral property of phase transition of PcNi-VO2 films].

Highly oriented VO2 thin films were deposited on sapphire substrate and [C8H17O]8 PcNi thin films were spin-coated onto VO2 thin films. The microstructure of VO2 thin films was studied with XRD. The phase transition was observed and the change in the optical properties of the PcNi/VO2 multilayer-films were investigated with infrared spectrometer. It was found that the mid-infrared transmittance of the complex films in the wavelength range 1.5 to 5.5 mm raised with PcNi coating. The thermochromism of PcNi/VO2 films did not changed compared with VO2 films and the transition temperature was the same as that of VO2. It can be anticipated that the optical limiting property of PcNi/VO2 films will be superior to that of VO2 thin films or PcNi thin films.

[Research on optical property of phase transition VO2 films].

Optical transmission spectra of VO2 films on glass, fused silica, and sapphire were recorded and analyzed during heating process. Thermally induced phase transition of VO2 films occurred at a certain temperature, associated with abrupt changes in optical properties. The transition temperature and the contrast of the optical properties depended on the substrate and the deposit method used. The change in transmittance delta T at 5 microns of VO2 films deposited on sapphire by RF magnetron sputtering was 70%, and the corresponding relative change delta T/TRT was 94%. For the VO2 films deposited on glass by RF magnetron sputtering, delta T at 2.5 microns was 64.2%, and delta T/TRT was as high as 98%.