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A novel magnetic Fe 3 O 4 @SiO 2 @BiFeO 3 /rGO composite was successfully fabricated via a facile hydrothermal method. This composite consisted of flower-like core-shell structured Fe 3 O 4 @SiO 2 @BiFeO 3 microspheres mounting on reduced graphene oxide (rGO) nanosheets. The specific surface areas, magnetization saturation value (M s), and band gap energy (E g) of Fe 3 O 4 @SiO 2 @BiFeO 3 /rGO (x = 0.15 g) were 139.26 m2/g, 20.3 emu/g, and 1.91 eV, respectively. Fe 3 O 4 @SiO 2 @BiFeO 3 /rGO (x = 0.15 g) exhibited remarkable ability to photocatalytically degrade ciprofloxacin (CIP), tetracycline hydrochloride (TC-H), methylene blue (MB), and decolorize a mixed solution of MB, methyl orange (MO), and rhodamine B (Rh B); CIP, TC-H, and MB degradation by Fe 3 O 4 @SiO 2 @BiFeO 3 /rGO conformed to a first-order kinetic reaction, and the corresponding k app values by Fe 3 O 4 @SiO 2 @BiFeO 3 /rGO (x = 0.15 g) were 0.04211, 0.02792, and 0.05967 min−1, respectively. Excellent magnetic separation performance, recyclability, and stability were also observed. A suitable amount of rGO to the as-prepared photocatalyst could decrease the E g , accelerate the transfer of photogenerated electrons (e−), suppress the recombination of photo-generated e−–hole (h+) pairs, and enhance the visible-light response of the catalyst. The •OH is the dominant active species during photocatalysis. This work suggests a promising strategy to synthesize photocatalysts with enhanced ability to catalytically degrade organic pollutant under visible light and excellent recyclability. [ABSTRACT FROM AUTHOR]

Microglia, as the intrinsic immune cells in the brain, are activated following ischemic stroke. Activated microglia participate in the pathological processes after stroke through polarization, autophagy, phagocytosis, pyroptosis, ferroptosis, apoptosis, and necrosis, thereby influencing the injury and repair following stroke. It has been established that polarized M1 and M2 microglia exhibit pro-inflammatory and anti-inflammatory effects, respectively. Autophagy and phagocytosis in microglia following ischemia are dynamic processes, where moderate levels promote cell survival, while excessive responses may exacerbate neurofunctional deficits following stroke. Additionally, pyroptosis and ferroptosis in microglia after ischemic stroke contribute to the release of harmful cytokines, further aggravating the damage to brain tissue due to ischemia. This article discusses the different functional states of microglia in ischemic stroke research, highlighting current research trends and gaps, and provides insights and guidance for further study of ischemic stroke. • Microglia is important in the repair of ischemic stroke. • Microglial polarization is a double-edged sword in ischemic stroke. • Microglial proper autophagy and phagocytosis contribute to functional recovery after ischemic stroke, while excessive activation may worsen the damage. • Microglial pyroptosis, ferroptosis, apoptosis and necrosis in ischemic stroke is in the preliminary stage. [ABSTRACT FROM AUTHOR]

Abstract Background Tamsulosin, an α 1A -adrenergic receptor inhibitor, is prescribed to treat benign prostatic hyperplasia in men >60 years of age, the same demographic most susceptible to abdominal aortic aneurysm. The goal of this study was to investigate the effect of tamsulosin on abdominal aortic aneurysm pathogenesis. Methods Abdominal aortic aneurysms were induced in WT C57BL/6 male mice (n = 9-18/group), using an established topical elastase abdominal aortic aneurysm model. Osmotic pumps were implanted in mice 5 days before operation to create the model, administering either low dose (0.125 µg/day tamsulosin), high dose (0.250µg/day tamsulosin), or vehicle treatments with and without topical application of elastase. Blood pressures were measured preoperatively and on postoperative days 0, 3, 7, and 14. On postoperative day 14, aortic diameter was measured before harvest. Sample aortas were prepared for histology and cytokine analysis. Results Measurements of systolic blood pressure did not differ between groups. Mice treated with the low dose of tamsulosin and with the high dose of tamsulosin showed decreased aortic diameter compared with vehicle-treated control (93% ± 24 versus 94% ± 30 versus 132% ± 24, respectively; P =.0003, P =.0003). Cytokine analysis demonstrated downregulation of pro-inflammatory cytokines in both treatment groups compared with the control (P <.05). Histology exhibited preservation of elastin in both low- and high-dose tamsulosin-treated groups (P =.0041 and P =.0018, respectively). Conclusion Tamsulosin attenuates abdominal aortic aneurysm formation with increased preservation of elastin and decreased production of pro-inflammatory cytokines. Further studies are necessary to elucidate the mechanism by which tamsulosin attenuates abdominal aortic aneurysm pathogenesis. [ABSTRACT FROM AUTHOR]

Introduction Given the unknown biologic antecedents before aortic aneurysm rupture, the purpose of this study was to establish a reproducible model of aortic aneurysm rupture. Methods We fed 7-week-old apolipoprotein E deficient mice a high-fat diet for 4 weeks and osmotic infusion pumps containing Angiotensin II were implanted. Angiotensin II was delivered continuously for 4 weeks at either 1,000 ng/kg/min (n = 25) or 2,000 ng/kg/min (n = 29). A third group (n = 14) were given Angiotensin II at 2,000 ng/kg/min and 0.2% β-aminopropionitrile dissolved in drinking water. Surviving mice were killed 28 days after pump placement, aortic diameters were measured, and molecular analyses were performed. Results Survival at 28 days was significantly different among groups with 80% survival in the 1,000 ng/kg/min group, 52% in the 2,000 ng/kg/min group, and only 14% in the Angiotensin II/β-aminopropionitrile group ( P  = .0001). Concordantly, rupture rates were statistically different among groups (8% versus 38% versus 79%, P  < .0001). Rates of abdominal aortic aneurysm were 48%, 55%, and 93%, respectively, with statistically higher rates in the Angiotensin II/β-aminopropionitrile group compared with both the 1,000 ng and 2,000 ng Angiotensin II groups ( P  = .006 and P  = .0165, respectively). Rates of thoracic aortic aneurysm formation were 12%, 52%, and 79% in the 3 groups with a statistically higher rate in the Angiotensin II/β-aminopropionitrile group compared with 1,000 ng group ( P  < .0001). Conclusions A reproducible model of aortic aneurysm rupture was developed with a high incidence of abdominal and thoracic aortic aneurysm. This model should enable further studies investigating the pathogenesis of aortic rupture, as well as allow for targeted strategies to prevent human aortic aneurysm rupture. [ABSTRACT FROM AUTHOR]

Arthritis is a common chronic disease, and is a major cause of disability and chronic pain in adults. Considering inflammatory responses is closely related with trace elements (TEs), the role of TEs in arthritis has attracted much attention. This study aimed to assess the association between TEs and arthritis. Concentrations of TEs in whole blood [cadmium (Cd), lead (Pb), mercury (Hg), selenium (Se), and manganese (Mn)] and serum [copper (Cu) and zinc (Zn)] were measured in adults who participated in the US National Health and Nutrition Examination Survey. Logistic regression model and Bayesian kernel machine regression model were used to explore the association between TEs and arthritis. The levels of five TEs (Pb, Hg, Cd, Se, and Cu) in the arthritis group changed significantly. Three TEs were found to be associated with an increased risk of arthritis: Pb [OR (95% CI): 2.96 (2.18, 4.03), p-value for trend (P -t) < 0.001], Cd [OR (95% CI): 2.28 (1.68, 3.11), P -t < 0.001], Cu [OR (95% CI): 2.05 (1.53, 2.76), P -t < 0.001]. The Relative Excess Risk of Interaction was 0.35 (95% CI: 0.06–0.65) and 0.38 (95% CI: 0.11–0.64), respectively, suggesting that Hg ions and Se ions have positive additional interactions with alcohol consumption, which reduced the risk of arthritis. Subgroup analysis showed that Pb ions and Cd ions were significantly correlated with osteoarthritis and rheumatoid arthritis. Elevated concentrations of Pb, Cd, and Cu were associated with increased risk of arthritis. Drinking with high levels of Hg or Se may be a protective factor for arthritis. Future studies are warranted to validate these findings in prospective studies. • The concentrations of Pb, Hg, Cd, Se and Cu were significantly different in arthritis patients as compare to healthy controls. • Significantly positive association between the level of Pb, Cd and Cu on arthritis risk. • Alcohol consumption reduces the risk of arthritis at higher concentrations of Hg and Se. [ABSTRACT FROM AUTHOR]

Abstract: We have studied the ground state and thermodynamic properties of the anisotropic 3-state Potts model on square lattice by means of the tensor network-based numerical method. The phase diagrams of this model in the ground state and at finite temperature are identified. The singular behavior at the critical endpoint along the phase boundary is carefully investigated. It is discovered that the sharp peaks appear in the second-order derivative of the field as well as the first-order derivative of the magnetization with respect to temperature on the phase boundary. Our numerical results confirm the prediction of Fisher et al. about the critical endpoint. [Copyright &y& Elsevier]

T-carbon is a novel carbon allotrope with many appealing properties. Since the proposal of T-carbon, there has been a lot of intensive studies devoted to its physical, chemical, optical, magnetic, thermoelectrical and topological properties and possible applications in diverse areas in recent years. In this review, we provide a comprehensive review on the advances of the experiments, intriguing properties and various potential applications of T-carbon in energy storage, optoelectronics, thermoelectrics, topological states, etc. As intercalation and doping are effective methods to modify the electronic structure of materials or even to convert into sparkly different new structures or phases, we also discuss different atom doped T-carbon, which exhibit more intriguing properties and lead to promising potential applications in solar cells, photocatalysis, magnetism, superconductivity and so on. In addition, it is interesting to mention that the hydrogenated T-carbon molecules were found to be possibly related to the physical origin of the UV extinction feature in interstellar medium that has been the half-century long unsolved puzzle. A number of novel derivative structures either derived or inspired from T-carbon are included as well. Finally, we give prospects and outlook for future directions of study on T-carbon and related structures. • T-carbon has been successfully synthesized in two independent experiments. • T-carbon displays excellent mechanical, thermoelectrical and topological properties. • T-carbon has potential applications in energy storage, superconductor, etc. • Many novel structures with rich properties were derived or inspired from T-carbon. • There are still many new research fields and directions to explore for T-carbon. [ABSTRACT FROM AUTHOR]

Abstract: Nitration of asymmetric hydrazones with nitric oxide occurred stereoselectively at C1′-atom, giving mono-nitrated trans isomer as a major outcome. The ratio of trans to cis was up to >99. Higher isolated yields of nitrated products and higher trans/cis ratios of isomers suggest that this procedure offers advantages for synthesizing asymmetry nitro compounds. [Copyright &y& Elsevier]

Neoadjuvant immunotherapy with the combination of intratumoral IL-12 and TNF-α encapsulated in poly-lactic acid microspheres (PLAM) generate a greater systemic immune response than either cytokine alone. We sought to examine the effector cells responsible for this synergy using the poorly immunogenic B16 melanoma and MCA205 sarcoma cell lines. Splenocytes from MCA205 bearing mice treated with IL-12 and TNF-α PLAM contained significantly more tumor-specific IFN-γ secreting cells than IL-12 alone. Adoptive transfer of lymphocytes from mice treated by the combination mediated significant tumor regression in mice bearing established pulmonary metastases. In mice bearing bilateral tumors, treatment of the primary with IL-12 and TNF-α PLAM, resulted in suppression of contralateral tumor growth. Both the local and distant effects were absent in mice depleted of CD8+ T-cells. In B16 bearing mice with established pulmonary disease, only the combination of intratumoral IL-12 and TNF-α resulted in a significant reduction of lung nodules. Both the local and distant effects were eradicated in mice depleted of either CD8+ T-cells or NK cells. The local and sustained release of IL-12 and TNF-α using PLAM synergistically activate both a cytotoxic T-cell and NK cell response, although their impact varies with MHC class I expression. [Copyright &y& Elsevier]

Abstract: Objective: To explore the role and mechanism of myeloid differentiation factor88 (MyD88) in HSP60 signal transduction in dendritic cells. Methods: Mouse DCs were cultured from murine bone marrow cells. The DC marker CD11c was detected by flow cytometry, then DCs were divided into control group, HSP60 groupand RNA interference group. Control group was cultured under normal condition, and HSP60 group was cultured with 10 μg/ml of HSP60. RNA interference group was first cultured with MyD88 siRNA for12 hours and then HSP60 was added into the culture mixture. All groups were cultured for 48 hours. Immuno-chemistry was used to detect the concentration of MyD88 and NF-κB. Western blot was used to detect the concentration of MyD88. Flow cytometry and mixed lymphocyte reaction (MLR) were used to detect the phenotype and functional properties of DCs. ELISA was used to detect the concentration of TNF-α, IFN-γ and IL-12 in the supernatant. Results: The expression of CD11c in murine bone marrow DCs was 88.76%. HSP60 stimulation increased the expression of CD80, CD86, MHC-II in DCs and TNF-α, IFN-γ, IL-12 secretion in the supernatant. HSP60 stimulation also increased the level of MyD88 in the cytoplasm and promoted the shift of NF-κB to karyon and the proliferation of allogeneic T cells. MyD88 siRNA could decrease MyD88 and inhibit these effects induced by HSP60. Conclusion: HSP60 activates DCs through MyD88-dependent pathway. MyD88 plays a critical role in HSP60 signal transduction. Inhibition of MyD88 may be a novel way for treating disease correlated with HSP60. [Copyright &y& Elsevier]

The electronic structures of haloform intercalated molecular solids C60·2CHX3 (X=Cl,Br) at low temperature are investigated by a first-principle calculation. It is found that the density of states of these solids at the Fermi level are quite low, and a phenomenon of hole doping induced insulator–metal transition in these systems is observed at low temperature. [Copyright &y& Elsevier]

We have investigated the current-induced spin transfer torque of a ferromagnet–insulator–ferromagnet tunnel junction by taking the spin-flip scatterings into account. It is found that the spin-flip scattering can induce an additional spin torque, enhancing the maximum of the spin torque and giving rise to an angular shift compared to the case when the spin-flip scatterings are neglected. The effects of the molecular fields of the left and right ferromagnets on the spin torque are also studied. It is found that τRx/Ie (τRx is the spin-transfer torque acting on the right ferromagnet and Ie is the tunneling electrical current) does vary with the molecular fields. At two certain angles, τRx/Ie is independent of the molecular field of the right ferromagnet, resulting in two crossing points in the curve of τRx/Ie versus the relevant orientation for different molecular fields. [Copyright &y& Elsevier]

By means of the nonequilibrium Green function technique, the effect of spin-flip scatterings on the spin-dependent electrical transport in ferromagnet–insulator–ferromagnet (FM–I–FM) tunnel junctions is investigated. It is shown that Jullie&grave;re's formula for the tunnel conductance must be modified when including the contribution from the spin-flip scatterings. It is found that the spin-flip scatterings could lead to an angular shift of the tunnel conductance, giving rise to the junction resistance not being the largest when the orientations of magnetizations in the two FM electrodes are antiparallel, which may offer an alternative explanation for such a phenomenon observed previously in experiments in some FM–I–FM junctions. The spin-flip assisted tunneling is also observed. [Copyright &y& Elsevier]

Air pollution has a significant weakening effect on solar radiation. Therefore, it is important for the development and utilization of solar energy to establish a solar radiation model under the influence of fog and haze. Based on the analysis of existing layer-by-layer weakening solar radiation models, the discontinuous meteorological data provided by MODIS satellite are replaced by continuous measured data from meteorological stations. The beam solar radiation model and diffuse solar radiation model are modified by using relative humidity (φ) and air quality index (AQI). The results show that the correction effects of these modified models are better. The R value of beam solar radiation models have increased by 5.74%, the R value of diffuse solar radiation models have increased by 41.27%, and other statistical parameters (RSE, RMSE and NSE) have also been improved to a certain extent. The calculated value of the modified models is closer to the measured data. In addition, the order of correction parameters also has an effect on the results. The research shows that the best correction effect is to use relative humidity first and then AQI. According to this method, the layer-by-layer weakening solar radiation models can be more accurate and reliable. • Smog is considered to modify the layer-by-layer weakening solar radiation models. • The data measured on the ground instead of MODIS are used to build new models. • Two new variables are added to the layer-by-layer weakening solar radiation models. • The accuracy of the modified solar radiation models has been. [ABSTRACT FROM AUTHOR]

Abstract: By comparing the recently obtained superconducting energy gaps from the scanning tunneling microscopy (STM) and the angle-resolved photoemission spectroscopy (ARPES) for underdoped superconductor Bi2Sr2CaCu2O8+ δ , significant distinctions were observed. By properly taking the effect of quasiparticle spectral weight in the STM spectra into account, good consistency between both energy gaps obtained by STM and ARPES is unveiled. [Copyright &y& Elsevier]

Few large-animal models exist for the study of aortic aneurysms. β-Aminopropionitrile (BAPN) is a compound known to cause aortic aneurysms by inhibiting lysyl oxidase, a collagen cross-linking enzyme. It is hypothesized that BAPN plus aneurysm induction surgery would result in significant aneurysm formation in swine with biologic properties similar to human disease. Initial experiments were performed in uncastrated male swine not treated with BAPN (surgery alone). Subsequently, uncastrated male swine were fed BAPN (0.15 g/kg) for 7 days before undergoing surgery; the infrarenal aorta was circumferentially dissected and measured, balloon dilated, and perfused with elastase (500 units) and type I collagenase (8000 units), with extraluminal elastase application. In the BAPN groups, daily BAPN feedings continued until swine harvest at postoperative days 7, 14, and 28. Swine undergoing surgery alone (n = 12) had significantly less dilation at 28 days compared with BAPN + surgery swine (51.9% ± 29.2% [0%-100%] vs 113.5% ± 30.2% [52.9%-146.2%]; P <.0003). Mean aortic dilation in animals undergoing treatment with surgery and BAPN was 86.9% ± 47.4% (range, 55.6%-157.1%), 105.4% ± 58.1% (50%-133.3%), and 113.5% ± 30.2% (52.9%-146.2%) at 7, 14, and 28 days, respectively. In the BAPN + surgery group, significant elastolysis was present at all time points, whereas aortic wall collagen content was not significantly different. Smooth muscle cells were significantly depleted at 14 and 28 days, and M1 macrophages were increased at 14 and 28 days (P <.05, all). Matrix metalloproteinase 2 was elevated at 7 days (P <.05). Multiple proinflammatory cytokines were elevated within the aortic wall of BAPN + surgery swine. BAPN plus surgery resulted in significantly larger aortic aneurysms than surgery alone and was critical to aneurysm formation in this novel swine model. Hallmarks of human disease, such as elastin fragmentation, smooth muscle cell depletion, macrophage infiltration, matrix metalloproteinase activation, and proinflammatory cytokine expression, were observed in BAPN-treated swine. This model better parallels many of the characteristics of human AAAs and may be suitable for prehuman drug trials. Translation of abdominal aortic aneurysm (AAA) models from small animals to large animals is critical for device development and further elucidation of AAA pathogenesis mechanisms. We have developed a reproducible large-animal model of AAA disease with >100% dilation in swine. The swine AAA have a histology and inflammatory milieu similar to human, and it is hoped that further work using this model will expand our understanding of this disease. [ABSTRACT FROM AUTHOR]

Objective The purpose of this study was to establish a reliable, chronic model of abdominal aortic aneurysm (AAA). Methods Wild-type 8-week-old C56BL/6 male mice (n = 120) were equally divided into three groups: (1) BAPN group: 0.2% 3-aminopropionitrile fumarate salt (BAPN) drinking water was provided to mice 2 days before surgery until the end of study. Sham aneurysm induction surgery was performed using 5 μL of heat deactivated elastase. (2) Elastase group: mice were given regular drinking water without BAPN. During aneurysm induction surgery, 5 μL of the active form of elastase (10.3 mg protein/mL, 5.9 U/mg protein) was applied on top of the infrarenal abdominal aorta adventitia for 5 minutes. (3) BAPN+elastase group: mice were given BAPN drinking water and the active form of elastase application, as above. On postoperative days 7, 14, 21, 28, and 100, aortic samples were collected for histology, cytokine array, and gelatin zymography after aortic diameter measurement. Results Compared with the elastase group, the BAPN+elastase group had a higher AAA formation rate (93% vs 65%; P < .01) with more advanced AAAs (25 of 42 vs 1 of 40 for stage II and III; P < .001). Aneurysms from the BAPN+elastase group demonstrated persistent long-term growth (221.5% ± 36.6%, 285.8% ± 78.6%, and 801% ± 160% on days 21, 28, and 100, respectively; P < .001), with considerable thrombus formation (54%) and rupture (31%) at the advanced stages of AAA development. Cytokine levels (pro-matrix metalloproteinase 9, interleukin-1β, interleukin-6, chemokine [C-C motif] ligand 5, triggering receptor expressed on myeloid cells 1, monocyte chemotactic protein 1, and tissue inhibitor of metalloproteinase 1) in the BAPN+elastase group were higher than in the elastase group on day 7. After day 7, cytokine levels returned to baseline, with the exception of elevated matrix metalloproteinase 2 activity. By histology, CD3-positive T cells in the BAPN+elastase group were elevated on days 28 and 100. Conclusions A combination of oral BAPN administration and periaortic elastase application induced a chronic, advanced-stage AAA with characteristics of persistent aneurysm growth, thrombus formation, and spontaneous rupture. Future studies should use this model, especially for examining tissue remodeling during the late stages of aneurysm development. [ABSTRACT FROM AUTHOR]

Background Testosterone is theorized to play a major role in the pathophysiology of abdominal aortic aneurysms (AAAs) because this disease occurs primarily in men. The role of the androgen receptor (AR) in the formation of AAAs has not been well elucidated, and therefore, it is hypothesized that androgen blockade will attenuate experimental aortic aneurysm formation. Methods Aortas of 8- to 12-week-old male C57Bl/6 wild-type (WT) mice or male AR knockout (AR −/− ) mice were perfused with purified porcine pancreatic elastase (0.35 U/mL) to induce AAA formation. Two groups of WT male mice were treated with the AR blockers flutamide (50 mg/kg) or ketoconazole (150 mg/kg) twice daily by intraperitoneal injection. Aortas were harvested on day 14 after video micrometry was used to measure AAA diameter. Cytokine arrays and histologic analysis were performed on aortic tissue. Groups were compared using an analysis of variance and a Tukey post hoc test. Results Flutamide and ketoconazole treatment (mean ± standard error of the mean) attenuated AAA formation in WT mice (84.2% ± 22.8% [ P = .009] and 91.5% ± 18.2% [ P = .037]) compared with WT elastase (121% ± 5.23%). In addition, AR −/− mice showed attenuation of AAA growth (64.4% ± 22.7%; P < .0001) compared with WT elastase. Cytokine arrays of aortic tissue revealed decreased levels of proinflammatory cytokines interleukin (IL)-α, IL-6, and IL-17 in flutamide-treated and AR −/− groups compared with controls. Conclusions Pharmacologic and genetic AR blockade cause attenuation of AAA formation. Therapies for AR blockade used in prostate cancer may provide medical treatment to halt progression of AAAs in humans. [ABSTRACT FROM AUTHOR]

Objective The protective effects of female gender on the development of abdominal aortic aneurysms (AAAs) have been attributed to anti-inflammatory effects of estrogen. Estrogen synthesis is dependent on the enzyme aromatase, which is located both centrally in the ovaries and peripherally in adipose tissue, bone, and vascular smooth muscle cells. It is hypothesized that deletion of aromatase in both ovarian and peripheral tissues would diminish the protective effect of female gender and would be associated with increased aortic diameter in female mice. Methods Male and female 8- to 10-week-old mice with aromatase (wild type: WT) and without aromatase (ArKO) underwent elastase aortic perfusion with aortic harvest 14 days following. For the contribution of central and peripheral estrogen conversion to be evaluated, female WT mice were compared with female WT and ArKO mice that had undergone ovariectomy (ovx) at 6 weeks followed by elastase perfusion at 8 to 10 weeks. At aortic harvest, maximal aortic dilation was measured and samples were collected for immunohistochemistry and protein analysis. Serum was collected for serum estradiol concentrations. Groups were compared with analysis of variance. Human and mouse AAA cross sections were analyzed with confocal immunohistochemistry for aromatase, smooth muscle markers, and macrophage markers. Results Female WT mice had significant reduction in aortic dilation compared with male WT mice (F WT, 51.5% ± 15.1% vs M WT, 78.7% ± 14.9%; P < .005). The protective effects of female gender were completely eliminated with deletion of aromatase (F ArKO, 82.6% ± 13.8%; P < .05 vs F WT). Ovariectomy increased aortic dilation in WT mice (F WT ovx, 70.6% ± 11.7%; P < .05 vs F WT). Aromatase deletion with ovariectomy further increased aortic dilation compared with WT ovx mice (F ArKO ovx, 87.3% ± 14.7%, P < .001 vs F WT and P < .05 vs F WT ovx). Accordingly, female ArKO ovx mice had significantly higher levels of the proinflammatory cytokines monocyte chemoattractant protein 1 and interleukin-1β and were associated with increased macrophage staining and decreased elastin staining. Regarding serum hormone levels, decreasing estradiol levels correlated with increasing aortic diameter ( R = −0.565; P < .01). By confocal immunohistochemistry, both human and mouse AAA smooth muscle cells (smooth muscle α-actin positive) and macrophages (CD68 positive or Mac-2 positive) expressed aromatase. Conclusions The protective effect of female gender on AAAs is due to estrogen synthesis and requires the presence of both ovarian and extragonadal/peripheral aromatase. Peripheral estrogen synthesis accounts for roughly half of the protective effect of female gender. If peripheral aromatase could be targeted, high levels of local estrogen could be produced and may avoid the side effects of systemic estrogen. [ABSTRACT FROM AUTHOR]

Abstract Spin caloritronics brings us new spin-thermal related effects, such as spin Seebeck effect, spin Nernst effect and their inverse effects. It is time to revisit the thermoelectric effects in ferromagnets by considering them. In this paper, a generalized Fourier law is derived and an anomalous Righi–Leduc effect is proposed for a ferromagnet when a temperature gradient is applied. A full description including particle current, spin current and heat current is necessarily taken into account and gives rise to novel contributions to the Righi–Leduc coefficient. This may shed more light on the spin caloritronics in ferromagnets. Highlights • A generalized Fourier law is derived. • The particle, spin and heat currents are taken into account fully. • Anomalous Righi–Leduc effect is studied for ferromagnets. • Spin caloritronic effects induce extra new terms to the Righi–Leduc coefficient. [ABSTRACT FROM AUTHOR]