Reversible Switching Between Microwave Absorption and EMI Shielding of VO2 Composite Foam.

Developing lightweight composite with reversible switching between microwave (MW) absorption and electromagnetic interference (EMI) shielding is promising yet remains highly challenging due to the completely inconsistent attenuation mechanism for electromagnetic (EM) radiation. Here, a lightweight vanadium dioxide/expanded polymer microsphere composites foam (VO2/EPM) is designed and fabricated with porous structures and 3D VO2 interconnection, which possesses reversible switching function between MW absorption and EMI shielding under thermal stimulation. The VO2/EPM exhibits MW absorption with a broad effective absorption bandwidth of 3.25 GHz at room temperature (25 °C), while provides EMI shielding of 23.1 dB at moderately high temperature (100 °C). This reversible switching performance relies on the porous structure and tunability of electrical conductivity, complex permittivity, and impedance matching, which are substantially induced by the convertible crystal structure and electronic structure of VO2. Finite element simulation is employed to qualitatively investigate the change in interaction between EM waves and VO2/EPM before and after the phase transition. Moreover, the application of VO2/EPM is demonstrated with a reversible switching function in controlling wireless transmission on/off, showcasing its excellent cycling stability. This kind of smart material with a reversible switching function shows great potential in next-generation electronic devices.

Circular RNA circ-RELL1 regulates inflammatory response by miR-6873-3p/MyD88/NF-κB axis in endothelial cells.

Endothelial inflammation is an important contributor to the pathology of atherosclerotic cardiovascular disease (ASCVD). Circular RNAs (circRNAs) function and role in endothelium inflammation still unknown. In our present study, we firstly identified that circ-RELL1 plays a proinflammatory role in ox-LDL-induced HUVECs through high-throughput circRNA microarray assays. Knockdown circ-RELL1 can reduce the expression of ICAM1 and VCAM1 in ox-LDL induced endothelium inflammation. Mechanistically, circ-RELL1 directly bound to miR-6873-3p in cytoplasm. Subsequently miR-6873-3p reduced MyD88 (myeloid differentiation primary response 88) protein expression and alleviated MyD88 medicated NF-κB activation. Furthermore, circ-RELL1 can abolish the inhibition of inflammation response by miR-6873-3p. Our findings illustrate a novel regulatory pathway that circ-RELL1 modulate inflammatory response by miR-6873-3p/MyD88/NF-κB axis in ox-LDL induced endothelial cells, which provides a potential therapeutic candidate for endothelium inflammation in atherosclerotic cardiovascular disease.

Predictive value of admission D-dimer for contrast-induced acute kidney injury and poor outcomes after primary percutaneous coronary intervention.

BACKGROUND: DD was found to be associated with acute myocardial infarction (AMI) and renal insufficiency. However, it is uncertain whether DD is an independent risk factor of CI-AKI in patients undergoing pPCI. METHODS: We prospectively enrolled 550 consecutive patients with STEMI undergoing pPCI between January 2012 and December 2016. The predictive value of admission DD for CI-AKI was assessed by receiver operating characteristic (ROC) and multivariable logistic regression analysis. CI-AKI was defined as an absolute serum creatinine increase ≥0.3 mg/dl or a relative increase in serum creatinine ≥50% within 48 h of contrast medium exposure. RESULTS: Overall, the incidence of CI-AKI was 13.1%. The ROC analysis showed that the cutoff point of DD was 0.69 µg/ml for predicting CI-AKI with a sensitivity of 77.8% and a specificity of 57.3%. The predictive value of DD was similar to the Mehran score for CI-AKI (AUCDD = 0.729 vs AUCMehran = 0.722; p = 0.8298). Multivariate logistic regression analysis indicated that DD > 0.69 µg/ml was an independent predictor of CI-AKI (odds ratio [OR] = 3.37,95% CI:1.80-6.33, p < 0.0001). Furthermore, DD > 0.69 µg/ml was associated with an increased risk of long-term mortality during a mean follow-up period of 16 months (hazard ratio = 3.41, 95%CI:1.4-8.03, p = 0.005). CONCLUSION: Admission DD > 0.69 µg/ml was a significant and independent predictor of CI-AKI and long-term mortality in patients undergoing pPCI.

TGFß1 and HGF regulate CTGF expression in human atrial fibroblasts and are involved in atrial remodelling in patients with rheumatic heart disease.

OBJECTIVE: This study aimed to investigate the effects of transforming growth factor ß1 (TGF ß1) and hepatocyte growth factor (HGF) on the expression of connective tissue growth factor (CTGF) in human atrial fibroblasts, and to explore the relationship of these factors in atrial fibrosis and atrial anatomical remodelling (AAR) of patients with atrial fibrillation (AF). METHODS: Fresh right auricular appendix tissue of 20 patients with rheumatic heart disease undergoing valve replacement surgery was collected during surgeries, 10 patients had sinus rhythm(SR), and 10 patients had chronic atrial fibrillation (CAF). Atrial fibroblasts were then cultured from the tissues with differential attachment technique and treated with either TGFß1 (10 ng/mL) or HGF (100 ng/mL). CTGF mRNA levels were measured by RT-PCR, and CTGF protein content was determined using immunofluorescence and Western blotting assays. RESULTS: CAF group had higher left atrial diameters (LADs) and higher CTGF mRNA expression in atrial fibroblasts compared with SR group. The CTGF protein content in CAF group was higher than that of SR group and positively correlated with LAD and AF duration. After CAF group was treated with TGFß1, CTGF mRNA and protein expression were significantly down-regulated, whereas when treated with HGF, expression was up-regulated compared with SR group. CONCLUSIONS: Increased CTGF expression was associated with enlarged LAD, atrial fibrosis and AAR in patients with AF. TGFß1 and HGF regulate CTGF expression in human atrial fibroblasts with up-regulation of mRNA and down-regulation of protein, therefore, either promote or inhibit atrial fibrosis, which could be related to the incidence and persistence of AF.

Negative association between free triiodothyronine level and contrast-induced acute kidney injury in patients undergoing primary percutaneous coronary intervention.

BACKGROUND: A low FT3 level is significantly associated with a variety of kidney disease and acute myocardial infarction (AMI). However, it remains unclear whether low FT3 is associated with CI-AKI in patients who underwent pPCI. METHODS: Single-center retrospective study evaluated 363 STEMI patients undergoing pPCI. Patients were classfied into 2 groups, low FT3 group (FT3 < 3.1 pmol/L) and normal FT3 group (FT3 ≥ 3.1 pmol/L);CI-AKI was defined as an increase in the serum creatinine levels of ≥50% or 0.3 mg/dL above the baseline level within 48 h after contrast medium exposure. RESULTS: Overall, 80(22.0%) patients had low FT3, and 59(16.3%) patients developed CI-AKI. The incidence of CI-AKI and in-hospital mortality was significantly higher in patients with low FT3 than normal (31.3% vs 12.0%; 15.0% vs 3.2%, respectively, both p < 0.0001). Multivariate logistic regression analysis indicated that low FT3 was an independent predictor of CI-AKI (odds ratio [OR] = 2.62, 95%CI:1.35-5.07, p < 0.05). In addition, low FT3 was associated with an increased risk of all-cause mortality during a mean follow-up period of 20 months (hazard ratio [HR] = 2.54, 95%CI:1.15-5.60, p < 0.05). CONCLUSION: Low FT3 was associated with CI-AKI, short- and long-term mortality in STEMI patients after pPCI.

Anticorrosive, Ultralight, and Flexible Carbon-Wrapped Metallic Nanowire Hybrid Sponges for Highly Efficient Electromagnetic Interference Shielding.

Metal-based materials with exceptional intrinsic conductivity own excellent electromagnetic interference (EMI) shielding performance. However, high density, corrosion susceptibility, and poor flexibility of the metal severely restrict their further applications in the areas of aircraft/aerospace, portable and wearable smart electronics. Herein, a lightweight, flexible, and anticorrosive silver nanowire wrapped carbon hybrid sponge (Ag@C) is fabricated and employed as ultrahigh efficiency EMI shielding material. The interconnected Ag@C hybrid sponges provide an effective way for electron transport, leading to a remarkable conductivity of 363.1 S m-1 and superb EMI shielding effectiveness of around 70.1 dB in the frequency range of 8.2-18 GHz, while the density is as low as 0.00382 g cm-3 , which are among the best performances for electrically conductive sponges/aerogels/foams by far. More importantly, the Ag@C sponge surprisingly exhibits super-hydrophobicity and strong corrosion resistance. In addition, the hybrid sponges possess excellent mechanical resilience even with a large strain (90% reversible compressibility) and an outstanding cycling stability, which is far better than the bare metallic aerogels, such as silver nanowire aerogels and copper nanowire foams. This strategy provides a facile methodology to fabricate lightweight, flexible, and anticorrosive metal-based sponge for highly efficient EMI shielding applications.

Pre-Procedural N-Terminal Pro-B Type Natriuretic Peptide Predicts Contrast-Induced Acute Kidney Injury and Long-Term Outcome in Elderly Patients After Elective Percutaneous Coronary Intervention.

The aim of the study is to evaluate the association of pre-procedural N-terminal pro-B type natriuretic peptide (NT-proBNP) with contrast-induced acute kidney injury (CI-AKI) and long-term outcomes in elderly patients undergoing elective percutaneous coronary intervention (PCI).A total of 540 patients aged ≥ 75 years who had undergone elective PCI between January 2012 and December 2015 were enrolled in this study. Admission NT-proBNP levels were measured before PCI. CI-AKI was defined as a relative increase in serum creatinine (SCr) of ≥50%, or an absolute increase of ≥ 0.3 mg/dL, occurring within 48 hours after contrast medium exposure. The predictive value of NT-proBNP for predicting CI-AKI was assessed by receiver operating characteristic (ROC) and multivariable logistic regression analysis.A total of 54 (10.0%) patients developed CI-AKI. The best cutoff value of NT-pro-BNP for detecting CI-AKI was 1133 pg/mL with 66.7% sensitivity and 70.8% specificity according to the ROC analysis (C statistic = 0.719; 95% CI, 0.679-0.756). Multivariable analysis demonstrated that Lg-NT-proBNP is significantly related to CI-AKI (odds ratio [OR] = 3.892; 95% CI, 1.996-7.590; P < 0.001). Cox regression analysis showed that Lg-NT-proBNP is associated with long-term mortality (adjusted hazard ratio [HR] = 2.158; 95% CI, 1.246-3.740; P = 0.006) during follow-up.Pre-procedural NT-proBNP is a significant and independent predictor of CI-AKI and long-term mortality in elderly patients following elective PCI, and the best cutoff point for predicting CI-AKI was 1133 pg/mL.

Effect of hesperidin on TGF-beta1/Smad signaling pathway in HSC.

Liver fibrosis is a common pathological process for chronic liver injury caused by multiple etiological factors and an inevitable phase leading to liver cirrhosis. According to the previous studies, hesperidin (HDN) shows a very good protective effect on CCl4-induced chemical hepatic fibrosis in rats. In this experiment, based on the findings of the previous studies, a platelet-derived growth factor (PDGF)-induced HSC-T6 model was established to observe the inhibitory effect of HDN on HSC-T6 proliferation. The ELISA method was adopted to detect the content of collagen I in HSC-T6 supernatant. Transforming growth factor (TGF)-beta1, Smad2, Smad3, Smad7 and connective tissue growth factor (CTGF) mRNA expressions were measured by RT-PCR; TGF-beta1 and CT-GF protein expressions in HSC-T6 were determined by Western blot, in order to study HDN's effect on TGF-beta1 signaling pathway in HSC and its potential action mechanism. The results demonstrated that HDN could notably improve HSC-T6 proliferation, Collagen I growth and TGF-beta1, Smad2, Smad3 and CTGF mRNA.expressions. After being intervened with HDN, it could notably inhibit HSC-T6 proliferation and Collagen I growth, reduce TGF-beta1, Smad2, Smad3 and CTGF mRNA and TGF-beta1, CTGF protein expressions and increase Smad7 mRNA expression. HDN's antihepatic fibrosis effect may be related to the inhibition of HSC proliferation and activation by modulating TGF-beta/Smad signaling pathway.

Enhancing the Interaction of Carbon Nanotubes by Metal-Organic Decomposition with Improved Mechanical Strength and Ultra-Broadband EMI Shielding Performance.

The remarkable properties of carbon nanotubes (CNTs) have led to promising applications in the field of electromagnetic interference (EMI) shielding. However, for macroscopic CNT assemblies, such as CNT film, achieving high electrical and mechanical properties remains challenging, which heavily depends on the tube-tube interactions of CNTs. Herein, we develop a novel strategy based on metal-organic decomposition (MOD) to fabricate a flexible silver-carbon nanotube (Ag-CNT) film. The Ag particles are introduced in situ into the CNT film through annealing of MOD, leading to enhanced tube-tube interactions. As a result, the electrical conductivity of Ag-CNT film is up to 6.82 × 105 S m-1, and the EMI shielding effectiveness of Ag-CNT film with a thickness of ~ 7.8 µm exceeds 66 dB in the ultra-broad frequency range (3-40 GHz). The tensile strength and Young's modulus of Ag-CNT film increase from 30.09 ± 3.14 to 76.06 ± 6.20 MPa (~ 253%) and from 1.12 ± 0.33 to 8.90 ± 0.97 GPa (~ 795%), respectively. Moreover, the Ag-CNT film exhibits excellent near-field shielding performance, which can effectively block wireless transmission. This innovative approach provides an effective route to further apply macroscopic CNT assemblies to future portable and wearable electronic devices.

[The relationship between association of microalbuminuria and retinal vessel diameter in population with essential hypertension].

OBJECTIVE: To investigate the association of urinary albumin-to-creatinine ratio (UACR) and the diameter of retinal vessel in population with essential hypertension in Fujian coastal area. METHODS: Central retinal artery and vein equivalents (CRAE and CRVE) were measured from the avoiding mydriatic digitized photographs and semi-automatic fundus analysis software, as well as albumin and urine creatinine. RESULTS: There were significant differences in CRAE levels among the normal control group, normoalbuminuria with essential hypertension group and microalbuminuria with essential hypertension group [(135.68 ± 10.10) µm, (129.79 ± 10.48) µm, (125.29 ± 11.17) µm, all P values < 0.01]. The CRAE levels were significantly negative correlated with UACR (r = -0.29, P < 0.01). Linear regression analysis showed CRAE was associated with UACR in the patients with hypertension(ß = -5.0, P < 0.01). Logistic regression analysis showed, systolic blood pressure (ß = 1.08, P = 0.02) was risk factor for CRAE abnormality. The CRAE abnormality was increased in turn in the normal control group, normoalbuminuria with the essential hypertension group and microalbuminuria with essential hypertension group (P < 0.01). CONCLUSION: The reduction of central retinal artery diameter are associated with the hypertensive renal damage. UACR and CRAE could be used to evaluate the microvascular lesions and be used as an indicator to assess the target organs damage in essential hypertension patients.

[Cardiovascular disease risk and vascular damage status in pre- and hypertension population in coastal areas of Fujian province].

OBJECTIVE: To observe the cardiovascular risk factors and vascular damage status of pre- and hypertensive population in the coastal areas of Fujian province. METHODS: This cross-sectional study surved 3344 Fujian coastal people aged older than 30 years. Glycolipids, uric acid, urine, microalbumin, brachial-ankle pulse wave velocity(baPWV) and central retinal arteriolar equivalent(CRAE) measurements were performed. Variance analysis and binary logistic regression were applied to evaluate cardiovascular risk factors and vascular damage of prehypertensive as well as hypertensive population. RESULTS: (1) The morbidity of prehypertension as well as hypertension was 30.0% in coastal population of Fujian Province, there were more than 3 cardiovascular risk factors in 65.5% (909/1388) of the hypertensive population and 37.5% of the prehypertensive population.(2) The abnormal rates of creatinine ratio(UACR), baPWV, and CRAE in hypertensive [25.7% (357/1388) , 84.2% (1169/1388) , 29.5% (409/1388) ] and prehypertensive population [20.0% (176/880) , 29.1% (256/880) , 25.6% (225/880)] were significantly higher than those of normotensive individuals [8.5% (91/1076), 8.9% (96/1076), 18.8% (202/1076), all P < 0.05].(3) Prehypertension and hypertension served as independent risk factors of UACR, baPWV and CRAE according to logistic regression analysis. The odds ratios (OR) value and 95% confidence intervals were 1.496 (1.095-2.044) , 2.477 (1.815-3.381) , 0.700 (0.549-0.891) in prehypertensive population, and 1.976 (1.454-2.686) , 7.707 (12.938-24.235) , 0.591 (0.474-0.736) in hypertensive population. CONCLUSION: Multiple cardiovascular risk factors coexist in prehypertensive and hypertensive population in the coastal area of coastal areas of Fujian province and there is more morbidity of vascular damage in prehypertensive and hypertensive individuals compared to normotensive subjects in these areas.

Enhancing the Chemical Stability of MXene Through Synergy of Hydrogen Bond and Coordination Bond in Aqueous Solution.

MXenes with unique physicochemical properties have shown substantial potential in electromagnetic interference (EMI) shielding. However, the chemical instability and mechanical fragility of MXenes has become a major hurdle for their application. Abundant strategies have been dedicated to improving the oxidation stability of colloidal solution or mechanical properties of films, which always come at the expense of electrical conductivity and chemical compatibility. Here, hydrogen bond (H-bond) and coordination bond are employed to achieve chemical and colloidal stability of MXenes (0.1 mg mL-1 ) by occupying the reaction sites of Ti3 C2 Tx attacking of water and oxygen molecules. Compared to the Ti3 C2 Tx , the Ti3 C2 Tx modified with alanine via H-bond shows significantly improved oxidation stability (at room temperature over 35 days), while the Ti3 C2 Tx modified with cysteine by synergy of H-bond and coordination bond can be maintained even after 120 days. Simulation and experimental results verify the formation of H-bond and Ti-S bond by a Lewis acid-base interaction between Ti3 C2 Tx and cysteine. Furthermore, the synergy strategy significantly improves the mechanical strength of the assembled film (up to 78.1 ± 7.9 MPa), corresponding the increment of 203% compared to untreated one, almost without compromising the electrical conductivity and EMI shielding performance.

Human tissue kallikrein 1 gene delivery inhibits PDGF-BB-induced vascular smooth muscle cells proliferation and upregulates the expressions of p27Kip1 and p2lCip1.

Tissue kallikrein 1 cleaves kininogen substrate to produce vasoactive kinin peptides that have been implicated in inhibiting neointimal hyperplasia in rat carotid arteries after balloon injury. However, its effects on the proliferation, cell cycle and its mechanisms, for example, cyclin-dependent kinase inhibitors, p27(Kip1) and p2l(Cip1) in vascular biology are poorly understood. The objective of this study was to explore the effects of human tissue kallikrein 1 (hTK1) mediated by recombinant adenovirus (Ad-hTK1) on proliferation and cell cycle of vascular smooth muscle cells (VSMCs) derived from spontaneously hypertensive rats induced by platelet-derived growth factor-BB (PDGF-BB) in vitro. The results showed that, within a given multiplicity of infection (MOI) and time, the hTK1 gene delivery inhibited PDGF-BB-stimulating VSMCs growth in a concentration-dependent (20-100 MOI) and time-dependent (2-5 days) manner by cell counting, with a peak inhibition rate at 36.3% at 72 h (P < 0.01). In addition, hTK1 gene delivery significantly suppressed PDGF-BB-induced proliferation of VSMCs by methyl thiazolyl tetrazoliuin assay, and decreased the percentage of cells in the S phase and in DNA synthesis by flow cytometry, with a peak inhibition rate at 30.2 and 36.4%, respectively (P < 0.01). Western blot assay showed that the protein levels of p27(Kip1) and p2l(Cip1) in cells infected with Ad-hTK1 were much more abundant than those in cells only induced by PDGF-BB, with up-modulating rates at 51.8 and 58.7%, respectively (P < 0.001). We also observed that the effects of hTK1 gene delivery in inhibiting VSMCs proliferation, arresting cell cycling in G(0)/G(1) phase and up-regulating the expression of p27(Kip1) and p2l(Cip1) could be blocked by icatibant (Hoe 140), a specific bradykinin B(2) receptor antagonist. Taken together, these results demonstrated that hTK1 overexpressed by recombinant adenovirus potently inhibits VSMCs proliferation that is required for neointimal hyperplasia and restenosis, and may activate p27(Kip1) and p2l(Cip1) signaling pathways via bradykinin B(2) receptor.

Metallized Skeleton of Polymer Foam Based on Metal-Organic Decomposition for High-Performance EMI Shielding.

Highly conductive polymer foam with light weight, flexibility, and high-performance electromagnetic interference (EMI) shielding is highly desired in the fields of aerospace, communication, and high-power electronic equipment, especially in the board-level packaging. However, traditional technology for preparing conductive polymer foam such as electroless plating and electroplating involves serious pollution, a complex fabrication process, and high cost. It is urgent to develop a facile method for the fabrication of highly conductive polymer foam. Herein, we demonstrated a lightweight and flexible silver-wrapped melamine foam (Ag@ME) via in situ sintering of metal-organic decomposition (MOD) at a low temperature (200 °C) on the ME skeleton modified with poly(ethylene imine). The Ag@ME with a continuous 3D conductive network exhibits good compressibility, an excellent conductivity of 158.4 S/m, and a remarkable EMI shielding effectiveness of 63 dB in the broad frequency of 8.2-40 GHz covering X-, Ku-, K-, and Ka-bands, while the volume content is only 2.03 vol %. The attenuation mechanism of Ag@ME for EM waves is systematically investigated by both EM simulation and experimental analysis. Moreover, the practical EMI shielding application of Ag@ME in board-level packaging is demonstrated and it shows outstanding near-field shielding performance. This novel strategy for fabrication of highly conductive polymer foam with low cost and non-pollution could potentially promote the practical applications of Ag@ME in the field of EMI shielding.

[Effects of telmisartan and pyridoxamine on abdominal aorta vascular remodeling in spontaneously hypertensive rats].

OBJECTIVE: To investigate the effects of telmisartan and pyridoxamine on vascular smooth muscle cells (VSMCs) proliferation and apoptosis as well as abdominal aorta vascular remodeling in spontaneously hypertensive rats (SHRs). METHODS: SHRs randomly received placebo, telmisartan (6 mg kg(-1) x d(-1)), pyridoxamine (200 mg x kg(-1) x d(-1)) or telmisartan (6 mg x kg(-1) x d(-1)) plus pyridoxamine (200 mg x kg(-1) x d(-1), n = 12 each) for 16 weeks. Wistar-Kyoto (WKY, n = 12) rats serve as normotensive control. The systolic blood pressure (SBP) of rat was measured before and weekly thereafter. The serum advanced glycation end-products (AGEs) were detected by competitive ELISA. The serum super oxide dismutase (SOD) and nitric oxide (NO) were measured. The abdominal aorta were assessed by image analysis in HE stained sections. The VSMCs apoptosis and proliferation in abdominal aorta were detected with in situ end labeling technique and proliferating cell nuclear antigen (PCNA) immunohistochemistry staining respectively. RESULTS: SBP were significantly lower in telmisartan and telmisartan plus pyridoxamine therapy group than in placebo treated hypertensive rats while not affected by pyridoxamine (P > 0.05). Activity of SOD and NO were significantly higher and AGEs significantly lower in telmisartan, pyridoxamine and combination therapy treated SHRs than in placebo treated hypertensive rats (P < 0.01). The telmisartan, pyridoxamine and combination therapy can significantly inhibit the PCNA expression and significantly enhance the apoptosis value in abdominal aorta (P < 0.01). The efficacy of combined treatment was significantly higher than telmisartan and pyridoxamine alone (P < 0.05). CONCLUSION: Telmisartan and pyridoxamine could attenuate abdominal aorta vascular remodeling via reducing oxidative stress and AGEs production as well as restoring the balance of VSMCs proliferation and apoptosis in SHRs abdominal aorta.

[Effects of human tissue kallikrein 1 gene delivery on carotid artery neointima formation after balloon angioplasty in spontaneously hypertensive rats].

OBJECTIVE: To investigate the effects of human tissue kallikrein 1(Ad-hKLK1) gene delivery on the neointima formation in carotid arteries of spontaneously hypertensive rats (SHRs). METHODS: Carotid artery restenosis was induced in male SHR rats by balloon-injury. Rats were randomly assigned into 4 groups: Sham-operated (n = 6); Angioplasty (phosphate buffered solution 50 microl, n = 8); Vector virus (control virus, 1 x 10(9) IU in 50 microl, n = 8) and Ad-hKLK1(Ad-hKLK1, 1 x 10(9) IU in 50 microl, n = 8). Rats were sacrificed 4 weeks later. The wall-to-lumen area ratio and intima/media ratio in carotid artery were assessed by image analysis in HE stained sections. The mRNA bradykinin receptor (B1R and B2R) expressions were detected by RT-PCR. The protein expression of the cycle-independent kinase inhibitors p27Kip1 and p2lCip1 were determined by Western blot analysis. RESULTS: Wall-to-lumen area ratio reduced 35.6% and intima/media ratio reduced 38.8%in Ad-hKLK1 treated SHRs compared to angioplasty group (all P < 0.001). The expression of p27Kip1 and p2lCip1 increased significantly in Ad-hKLK1 treated SHRs compared with angioplasty rats (all P < 0.001). The mRNA expression of B2R was significantly upregulated in angioplasty rats compared with sham-operated rats (P < 0.05) while mRNA expression of B1R was similar between the 2 groups. CONCLUSION: hKLK1 gene delivery may effectively reduce neointimal formation via downregulating bradykinin B2R and up-regulating the expressions of p27Kip1, p2lCip1 signaling pathways in carotid arteries of SHRs after balloon injury.

[Effects of human tissue kallikrein gene delivery on the proliferation of vascular smooth muscle cells].

OBJECTIVE: Tissue kallikrein cleaves kininogen substrate to produce vasoactive kinin peptides that have been implicated in the proliferation of vascular smooth muscle cells. We investigated the effects of adenovirus-mediated human tissue kallikrein (Ad-hKLK1) gene delivery on the proliferation of vascular smooth muscle cells of SHR (VSMCs(SHR)) induced by platelet derived growth factor-BB (PDGF-BB). METHODS: Primary VSMCs(SHR) were isolated and cultured from thoracic aorta of male SHR. The VSMCs(SHR) proliferation induced by PDGF-BB was accessed by cell counting and methyl thiazolyl tetrazolium (MTT). Western blot was used to determine the protein expression of hKLK1, the cycle-independent kinase inhibitors p27(Kip1) and p21(Cip1). The mRNA expressions of bradykinin B1 receptor and B2 receptor were detected by RT-PCR in VSMCs(SHR). RESULTS: Proliferation of VSMCs(SHR) induced by PDGF-BB was significantly inhibited post transfection of Ad-hKLK1 (20-100 MOI) in a MOI-dependent manner. The peak inhibition titer of Ad-hKLK1 was 100 MOI with peak inhibition rate of 39.3% (cell counting, n = 3, P < 0.01), 30.2% (MTT, n = 3, P < 0.01) and 36.4% (peak stunning rate of cell-cycle in phase G(0)/G(1)). The inhibitory effects of proliferation and cell-cycle caused by hKLK1 gene delivery could be abolished by Hoe140, a bradykinin B2 receptor antagonist. The protein expression of p27(Kip1) and p21(Cip1) increased significantly after the hKLK1 gene delivery, whereas Hoe140 nearly completely blocked these effects (n = 3, P < 0.001, respectively). PDGF-BB also significantly upregulated the mRNA expression of B2 receptor but not B1 receptor in VSMCs(SHR). CONCLUSION: The hKLK1 gene delivery could inhibit PDGF-BB induced proliferation in VSMCs(SHR) through Bradykinin B2 receptor and up-regulate expression of p27(Kip1) and p2l(Cip1).

Delayed diagnosis of prosopagnosia following a hemorrhagic stroke in an elderly man: A case report.

BACKGROUND: Acquired prosopagnosia is a rare condition characterized by the loss of familiarity with previously known faces and the inability to recognize new ones. It usually occurs after the onset of brain lesions such as in a stroke. The initial identification of prosopagnosia generally relies on a patient's self-report, which can be challenging if it lacks an associated chief complaint. There were few cases of prosopagnosia presenting purely as eye symptoms in the previous literature confirmed by functional magnetic resonance imaging (MRI). CASE SUMMARY: We present a case of delayed diagnosis of prosopagnosia after a right hemisphere stroke in an elderly man whose chief complaint was persistent and progressive "blurred vision" without facial recognition impairment. Ophthalmic tests revealed a homonymous left upper quadrantanopia, with normal visual acuity. He was found by accident to barely recognize familiar faces. The patient showed severe deficit in face recognition and perception tests, and mild memory loss in neuropsychological assessments. Further functional MRI revealed the visual recognition deficits were face-specific. After behavioral intervention, the patient started to rely on other cues to compensate for poor facial recognition. His prosopagnosia showed no obvious improvement eight months after the stroke, which had negative impact on his social network. CONCLUSION: Our case demonstrates that the presentation of prosopagnosia can be atypical, and visual difficulties might be a clinical manifestation solely of prosopagnosia, which emphasizes the importance of routinely considering face recognition impairment among elderly patients with brain lesions.