20 research outputs found
Transmission of new CRF07_BC Strains with 7 amino acid deletion in Gag p6
A 7 amino acid deletion in Gag p6 (P6delta7) emerged in Chinese prevalent HIV-1 strain CRF07_BC from different epidemic regions. It is important to determine whether this mutation could be transmitted and spread. In this study, HIV-1 Gag sequences from 5 different epidemic regions in China were collected to trace the transmission linkage and to analyze genetic evolution of P6delta7 strains. The sequence analysis demonstrated that P6delta7 is a CRF07_BC specific deletion, different P6delta7 strains could be originated from different parental CRF07_BC recombinants in different epidemic regions, and the transmission of P6delta7 strain has occurred in IDU populations. This is for the first time to identify the transmission linkage for P6delta7 strains and serves as a wake-up call for further monitoring in the future; In addition, P6delta7 deletion may represent an evolutionary feature which might exert influence on the fitness of CRF07_BC strain
Chronic Kidney Disease Increases Atrial Fibrillation Inducibility: Involvement of Inflammation, Atrial Fibrosis, and Connexins
Chronic kidney disease (CKD) causes atrial structural remodeling and subsequently increases the incidence of atrial fibrillation (AF). Atrial connexins and inflammatory responses may be involved in this remodeling process. In this study, nephrectomy was used to produce the CKD rat model. Three months post-nephrectomy, cardiac structure, function and AF vulnerability were quantified using echocardiography and electrophysiology methods. The left atrial tissue was tested for quantification of fibrosis and inflammation, and for the distribution and expression of connexin (Cx) 40 and Cx43. An echocardiography showed that CKD resulted in the left atrial enlargement and left ventricular hypertrophy, but had no functional changes. CKD caused a significant increase in the AF inducible rate (91.11% in CKD group vs. 6.67% in sham group, P < 0.001) and the AF duration [107 (0â770) s in CKD vs. 0 (0â70) s in sham, P < 0.001] with prolonged P-wave duration. CKD induced severe interstitial fibrosis, activated the transforming growth factor-ÎČ1/Smad2/3 pathway with a massive extracellular matrix deposition of collagen type I and α-smooth muscle actin, and matured the NLR (nucleotide-binding domain leucine-rich repeat-containing receptor) pyrin domain-containing protein 3 (NLRP3) inflammasome with an inflammatory cascade response. CKD resulted in an increase in non-phosphorylated-Cx43, a decrease in Cx40 and phosphorylated-Cx43, and lateralized the distribution of Cx40 and Cx43 proteins with upregulations of Rac-1, connective tissue growth factor and N-cadherin. These findings implicate the transforming growth factor-ÎČ1/Smad2/3, the NLRP3 inflammasome and the connexins as potential mediators of increased AF vulnerability in CKD
Comparison of two large earthquakes in China: the 2008 Sichuan Wenchuan Earthquake and the 2013 Sichuan Lushan Earthquake
Increased vulnerability to atrial and ventricular arrhythmias caused by different types of inhaled tobacco or marijuana products
GW26-e1435 Tanshinone IIA Reduces Atrial Fibrillation by Inhibiting Left Atrial Fibrosis Via MMP-9 / TIMP-1 Pathway in Isoproterenol-Induced Myocardial Infarction Rats
FineâTuning XâRay Sensitivity in OrganicâInorganic Hybrids via an Unprecedented MixedâLigand Strategy
Abstract Crystalline organicâinorganic hybrids, which exhibit colorimetric responses to ionizing radiation, have recently been recognized as promising alternatives to conventional Xâray dosimeters. However, Xârayâresponsive organicâinorganic hybrids are scarce and the strategy to fineâtune their detection sensitivity remains elusive. Herein, an unprecedented mixedâligand strategy is reported to modulate the Xâray detection efficacy of organicâinorganic hybrids. Deliberately blending the stimuliâresponsive terpyridine carboxylate ligand (tpcâ) and the auxiliary pbaâ group with different ratios gives rise to two OD thoriumâbearing clusters (Thâ102 and Thâ103) and a 1D coordination polymer (Thâ104). Notably, distinct Xâray sensitivity is evident as a function of molar ratio of the tpcâ ligand, following the trend of Thâ102 > Thâ103 > Thâ104. Moreover, Thâ102, which is exclusively built from the tpcâ ligands with the highest degree of ÏâÏ interactions, exhibits the most sensitive radiochromic and fluorochromic responses toward Xâray with the lowest detection limit of 1.5 mGy. The study anticipates that this mixedâligand strategy will be a versatile approach to tune the Xâray sensing efficacy of organicâinorganic hybrids
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Impairment of Endothelial Function by Cigarette Smoke Is Not Caused by a Specific Smoke Constituent, but by Vagal Input From the Airway.
BACKGROUND: Exposure to tobacco or marijuana smoke, or e-cigarette aerosols, causes vascular endothelial dysfunction in humans and rats. We aimed to determine what constituent, or class of constituents, of smoke is responsible for endothelial functional impairment. METHODS: We investigated several smoke constituents that we hypothesized to mediate this effect by exposing rats and measuring arterial flow-mediated dilation (FMD) pre- and post-exposure. We measured FMD before and after inhalation of sidestream smoke from research cigarettes containing normal and reduced nicotine level with and without menthol, as well as 2 of the main aldehyde gases found in both smoke and e-cigarette aerosol (acrolein and acetaldehyde), and inert carbon nanoparticles. RESULTS: FMD was reduced by all 4 kinds of research cigarettes, with extent of reduction ranging from 20% to 46% depending on the cigarette type. While nicotine was not required for the impairment, higher nicotine levels in smoke were associated with a greater percent reduction of FMD (41.1±4.5% reduction versus 19.2±9.5%; P=0.047). Lower menthol levels were also associated with a greater percent reduction of FMD (18.5±9.8% versus 40.5±4.8%; P=0.048). Inhalation of acrolein or acetaldehyde gases at smoke-relevant concentrations impaired FMD by roughly 50% (P=0.001). However, inhalation of inert carbon nanoparticles at smoke-relevant concentrations with no gas phase also impaired FMD by a comparable amount (P<0.001). Bilateral cervical vagotomy blocked the impairment of FMD by tobacco smoke. CONCLUSIONS: There is no single constituent or class of constituents responsible for acute impairment of endothelial function by smoke; rather, we propose that acute endothelial dysfunction by disparate inhaled products is caused by vagus nerve signaling initiated by airway irritation