Pulmonary Vein: Embryology, Anatomy, Function and Disease

Four pulmonary veins come from respective lung lobes drain oxygen-rich blood back to the left atrium. Failure of incorporation with the left atrium can lead to a condition, called Cor triatriatum sinister, that the left atrium is separated into two chambers by an abortive fibrous tissue. The venous system of lung and whole body communicate with each other in the earlier time and they will be disconnected in the following developmental process. Total or partial anomalous pulmonary venous connection refers to that there is/are some degree of the communication exists after birth, which can occur in different sites. In the veterinary field, retrospective studies and several case reports have been published to describe these rare congenital cardiovascular diseases in several species. More cases are need for better understanding their clinical manifestation, treatment options and outcomes

Effect of Porosity Gradient in Gas Diffusion Layer on Cell Performance with Thin-Film Agglomerate Model in Cathode Catalyst Layer of a PEM Fuel Cell

ABSTRACT A one-dimensional, steady-state, two-phase, isothermal numerical simulations were performed to investigate the effect on cell performance of a PEM fuel cell under non-uniform porosity of gas diffusion layer. In the simulation, the non-uniform porosity of gas diffusion layer was taken into account to analyze the transport phenomena of water flooding and mass transport in the gas diffusion layer. The porosity of the gas diffusion layer is treated as a linear function. Furthermore, the structure of the catalyst layer is considered to be a cylindrical thin-film agglomerate. Regarding the distribution analysis of liquid water saturation, oxygen concentration and water concentration depend on the porosity of gas diffusion layer. In the simulation, the ε CG and ε GC represent the porosity of the interfaces between the channel and gas diffusion layer and the gas diffusion layer and the catalyst layer, respectively. The simulation results indicate that when the (ε CG , ε GC ) = (0.8, 0.4), higher liquid water saturation appears in the gas diffusion layer and the catalyst layer. On the contrary, when the (ε CG , ε GC ) = (0.4, 0.4), lower liquid water saturation appears. Once the liquid water produced by the electrochemical reaction and condensate of vapor water may accumulate in the open pores of the gas diffusion layer and reduced the oxygen transport to the catalyst sites. This research attempts to use a thin-film agglomerate model, which analyze the significant transport phenomena of water flooding and mass transport under linear porosity gradient of gas diffusion layer in the cathode of a PEM fuel cell

Genetic polymorphisms in glutathione S-transferase (GST) superfamily and risk of arsenic-induced urothelial carcinoma in residents of southwestern Taiwan

<p>Abstract</p> <p>Background</p> <p>Arsenic exposure is an important public health issue worldwide. Dose-response relationship between arsenic exposure and risk of urothelial carcinoma (UC) is consistently observed. Inorganic arsenic is methylated to form the metabolites monomethylarsonic acid and dimethylarsinic acid while ingested. Variations in capacity of xenobiotic detoxification and arsenic methylation might explain individual variation in susceptibility to arsenic-induced cancers.</p> <p>Methods</p> <p>To estimate individual susceptibility to arsenic-induced UC, 764 DNA specimens from our long-term follow-up cohort in Southwestern Taiwan were used and the genetic polymorphisms in GSTM1, GSTT1, GSTP1 and arsenic methylation enzymes including GSTO1 and GSTO2 were genotyped.</p> <p>Results</p> <p>The GSTT1 null was marginally associated with increased urothelial carcinoma (UC) risk (HR, 1.91, 95% CI, 1.00-3.65), while the association was not observed for other GSTs. Among the subjects with cumulative arsenic exposure (CAE) ≥ 20 mg/L*year, the GSTT1 null genotype conferred a significantly increased cancer risk (RR, 3.25, 95% CI, 1.20-8.80). The gene-environment interaction between the GSTT1 and high arsenic exposure with respect to cancer risk was statistically significant (multiplicative model, <it>p </it>= 0.0151) and etiologic fraction was as high as 0.86 (95% CI, 0.51-1.22). The genetic effects of GSTO1/GSTO2 were largely confined to high arsenic level (CAE ≥ 20). Diplotype analysis showed that among subjects exposed to high levels of arsenic, the AGG/AGG variant of GSTO1 Ala140Asp, GSTO2 5'UTR (-183)A/G, and GSTO2 Asn142Asp was associated with an increased cancer risk (HRs, 4.91, 95% CI, 1.02-23.74) when compared to the all-wildtype reference, respectively.</p> <p>Conclusions</p> <p>The GSTs do not play a critical role in arsenic-induced urothelial carcinogenesis. The genetic effects of GSTT1 and GSTO1 on arsenic-induced urothelial carcinogenesis are largely confined to very high exposure level.</p

GT-repeat polymorphism in the heme oxygenase-1 gene promoter and the risk of carotid atherosclerosis related to arsenic exposure

<p>Abstract</p> <p>Background</p> <p>Arsenic is a strong stimulus of heme oxygenase (HO)-1 expression in experimental studies in response to oxidative stress caused by a stimulus. A functional GT-repeat polymorphism in the HO-1 gene promoter was inversely correlated to the development of coronary artery disease in diabetics and development of restenosis following angioplasty in patients. The role of this potential vascular protective factor in carotid atherosclerosis remains unclear. We previously reported a graded association of arsenic exposure in drinking water with an increased risk of carotid atherosclerosis. In this study, we investigated the relationship between HO-1 genetic polymorphism and the risk of atherosclerosis related to arsenic.</p> <p>Methods</p> <p>Three-hundred and sixty-seven participants with an indication of carotid atherosclerosis and an additional 420 participants without the indication, which served as the controls, from two arsenic exposure areas in Taiwan, a low arsenic-exposed Lanyang cohort and a high arsenic-exposed LMN cohort, were studied. Carotid atherosclerosis was evaluated using a duplex ultrasonographic assessment of the extracranial carotid arteries. Allelic variants of (GT)n repeats in the 5'-flanking region of the HO-1 gene were identified and grouped into a short (S) allele (< 27 repeats) and long (L) allele (≥ 27 repeats). The association of atherosclerosis and the HO-1 genetic variants was assessed by a logistic regression analysis, adjusted for cardiovascular risk factors.</p> <p>Results</p> <p>Analysis results showed that arsenic's effect on carotid atherosclerosis differed between carriers of the class S allele (OR 1.39; 95% CI 0.86-2.25; <it>p </it>= 0.181) and non-carriers (OR 2.65; 95% CI 1.03-6.82; <it>p </it>= 0.044) in the high-exposure LMN cohort. At arsenic exposure levels exceeding 750 μg/L, difference in OR estimates between class S allele carriers and non-carriers was borderline significant (<it>p </it>= 0.051). In contrast, no such results were found in the low-exposure Lanyang cohort.</p> <p>Conclusions</p> <p>This exploratory study suggests that at a relatively high level of arsenic exposure, carriers of the short (GT)n allele (< 27 repeats) in the HO-1 gene promoter had a lower probability of developing carotid atherosclerosis than non-carriers of the allele after long-term arsenic exposure via ground water. The short (GT)n repeat in the HO-1 gene promoter may provide protective effects against carotid atherosclerosis in individuals with a high level of arsenic exposure.</p

Detection of SARS-associated Coronavirus in Throat Wash and Saliva in Early Diagnosis

Early detection of SARS-CoV in throat wash and saliva suggests that these specimens are ideal for SARS diagnosis

Serum lipid level is not associated with symptomatic intracerebral hemorrhage after intravenous thrombolysis for acute ischemic stroke

Background This study assessed whether serum lipid levels are associated with the risk of symptomatic intracerebral hemorrhage (sICH) and functional outcomes in patients with acute ischemic stroke after receiving intravenous thrombolysis. Methods We retrospectively analyzed consecutive ischemic stroke patients who were treated with intravenous tissue plasminogen activator between January 2007 and January 2017. Lipid levels on admission, including total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglyceride levels, as well as potential predictors of sICH were tested using univariate and multivariate analyses. Results Of the 229 enrolled patients (100 women, aged 68 ± 13 years), 14 developed sICH and 103 (45%) had favorable functional outcomes at 3 months. The patients with sICH more often had diabetes mellitus (71% vs. 26%, P = 0.01) and had more severe stroke (mean National Institutes of Health Stroke Scale [NIHSS] score of 16 vs. 13, P = 0.045). Regarding lipid subtype, total cholesterol, LDL-C, HDL-C, and triglyceride levels were not associated with sICH or functional outcomes. According to the results of multivariate analysis, the frequency of sICH was independently associated with diabetes mellitus (odds ratio [OR] = 6.04; 95% CI [1.31–27.95]; P = 0.02) and the NIHSS score (OR = 1.12; 95% CI [1.02–1.22]; P = 0.01). A higher NIHSS score was independently associated with unfavorable functional outcomes (OR = 0.86; 95% CI [0.81–0.91]; P < 0.001). Conclusions Serum lipid levels on admission, including total cholesterol, LDL-C, HDL-C, and triglyceride levels, were not associated with sICH or 3-month functional outcomes after intravenous thrombolysis for acute ischemic stroke

Dengue-1 Envelope Protein Domain III along with PELC and CpG Oligodeoxynucleotides Synergistically Enhances Immune Responses

The major weaknesses of subunit vaccines are their low immunogenicity and poor efficacy. Adjuvants can help to overcome some of these inherent defects with subunit vaccines. Here, we evaluated the efficacy of the newly developed water-in-oil-in-water multiphase emulsion system, termed PELC, in potentiating the protective capacity of dengue-1 envelope protein domain III. Unlike aluminum phosphate, dengue-1 envelope protein domain III formulated with PELC plus CpG oligodeoxynucleotides induced neutralizing antibodies against dengue-1 virus and increased the splenocyte secretion of IFN-γ after in vitro re-stimulation. The induced antibodies contained both the IgG1 and IgG2a subclasses. A rapid anamnestic neutralizing antibody response against a live dengue virus challenge was elicited at week 26 after the first immunization. These results demonstrate that PELC plus CpG oligodeoxynucleotides broaden the dengue-1 envelope protein domain III-specific immune responses. PELC plus CpG oligodeoxynucleotides is a promising adjuvant for recombinant protein based vaccination against dengue virus

Type 2 Diabetes Variants Disrupt Function of SLC16A11 through Two Distinct Mechanisms

Type 2 diabetes (T2D) affects Latinos at twice the rate seen in populations of European descent. We recently identified a risk haplotype spanning SLC16A11 that explains ∼20% of the increased T2D prevalence in Mexico. Here, through genetic fine-mapping, we define a set of tightly linked variants likely to contain the causal allele(s). We show that variants on the T2D-associated haplotype have two distinct effects: (1) decreasing SLC16A11 expression in liver and (2) disrupting a key interaction with basigin, thereby reducing cell-surface localization. Both independent mechanisms reduce SLC16A11 function and suggest SLC16A11 is the causal gene at this locus. To gain insight into how SLC16A11 disruption impacts T2D risk, we demonstrate that SLC16A11 is a proton-coupled monocarboxylate transporter and that genetic perturbation of SLC16A11 induces changes in fatty acid and lipid metabolism that are associated with increased T2D risk. Our findings suggest that increasing SLC16A11 function could be therapeutically beneficial for T2D. Video Abstract [Figure presented] Keywords: type 2 diabetes (T2D); genetics; disease mechanism; SLC16A11; MCT11; solute carrier (SLC); monocarboxylates; fatty acid metabolism; lipid metabolism; precision medicin