Wansheng Wang

The electronic orders in Hubbard models on a kagome lattice at van Hove filling are of intense current interest and debate. We study this issue using the singular-mode functional renormalization group theory. We discover a rich variety of electronic instabilities under short-range interactions. With increasing on-site repulsion $U$, the system develops successively ferromagnetism, intra-unit-cell antiferromagnetism, and charge bond order. With nearest-neighbor Coulomb interaction $V$ alone ($U=0$), the system develops intra-unit-cell charge density wave order for small $V$, $s$-wave superconductivity for moderate $V$, and the charge density wave order appears again for even larger $V$. With both $U$ and $V$, we also find spin bond order and chiral ${d}_{{x}^{2}\ensuremath{-}{y}^{2}}+i{d}_{xy}$ superconductivity in some particular regimes of the phase diagram. We find that the $s$-wave superconductivity is a result of charge density wave fluctuations and the squared logarithmic divergence in the pairing susceptibility. On the other hand, the $d$-wave superconductivity follows from bond order fluctuations that avoid the matrix element effect. The phase diagram is vastly different from that in honeycomb lattices because of the geometrical frustration in the kagome lattice.

Tailored synthesis of well-defined anatase TiO2 nanocrystals with a high percentage of reactive facets has attracted widespread attention due to the scientific and technological importance. Here, high-quality nanosized anatase ultrathin TiO2 nanosheets, mainly dominated by {001} facets, were grown on graphene nanosheets by a simple one-pot solvothermal synthetic route. The obtained samples were characterized by X-ray diffraction (XRD), transmission electron microscopy (TEM), high-resolution transmission electron microscopy (HRTEM), ultraviolet–visible (UV–vis) diffuse reflectance spectroscopy, and X-ray photoelectron spectroscopy (XPS). The photocatalytic activity of as-prepared TiO2/graphene composites for degradation of methylene blue (MB) under visible-light irradiation at λ ≥ 400 nm was investigated. The results show that TiO2/graphene nanocomposites have a higher photocatalytic activity than pure TiO2 and P25. This enhanced photocatalytic activity suggests that the photoinduced electrons in TiO2 prefer transferring to the graphene efficiently. As a consequence, the electron transfer via Ti–O–C between TiO2 and C interaction greatly retards the recombination of photoinduced charge carriers and prolongs the carrier lifetime, thus contributing to the enhancement of photocatalytic performance. The amount of graphene is an important factor affecting the photocatalytic activity of TiO2/graphene nanocomposites. The optimum amount of graphene is ca. 1 wt %, at which the TiO2/graphene sample displays the highest reactivity. Furthermore, the photodegradation rate does not show an obvious decrease during five successive cycles, indicating that our TiO2/graphene nanocomposites are stable visible-light photocatalysts.

Extensive studies have demonstrated that transforming growth factor-beta (TGF-beta) plays an important role in the progression of renal diseases. TGF-beta exerts its biological functions mainly through its downstream signalling molecules, Smad2 and Smad3. It is now clear that Smad3 is critical for TGF-beta's pro-fibrotic effect, whereas the functions of Smad2 in fibrosis in response to TGF-beta still need to be determined. Our recent studies have demonstrated that Smad signalling is also a critical pathway for renal fibrosis induced by other pro-fibrotic factors, such as angiotensin II and advanced glycation end products (AGE). These pro-fibrotic factors can activate Smads directly and independently of TGF-beta. They can also cause renal fibrosis via the ERK/p38 MAP kinase-Smad signalling cross-talk pathway. In contrast, blockade of Smad2/3 activation by overexpression of an inhibitory Smad7 prevents collagen matrix production induced by TGF-beta, angiotensin II, high glucose and AGE and attenuates renal fibrosis in various animal models including rat obstructive kidney, remnant kidney and diabetic kidney diseases. Results from these studies indicate that Smad signalling is a key and final common pathway of renal fibrosis. In addition, TGF-beta has anti-inflammatory and immune-regulatory properties. Our most recent studies demonstrated that TGF-beta transgenic mice are protected against renal inflammation in mouse obstructive and diabetic models. Upregulation of renal Smad7, thereby blocking NF.kappaB activation via induction of IkappaBalpha, is a central mechanism by which TGF-beta inhibits renal inflammation. In conclusion, TGF-beta signals through Smad2/3 to mediate renal fibrosis, whereas induction of Smad7 inhibits renal fibrosis and inflammation. Thus, targeting Smad signalling by overexpression of Smad7 may have great therapeutic potential for kidney diseases.

Angiotensin II (Ang II) plays a pivotal role in vascular fibrosis, which leads to serious complications in hypertension and diabetes. However, the underlying signaling mechanisms are largely unclear. In hypertensive patients, we found that arteriosclerosis was associated with the activation of Smad2/3. This observation was further investigated in vitro by stimulating mouse primary aorta vascular smooth muscle cells (VSMCs) with Ang II. There were several novel findings. First, Ang II was able to activate an early Smad signaling pathway directly at 15 to 30 minutes. This was extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) dependent but transforming growth factor-beta (TGF-beta) independent because Ang II-induced Smad signaling was blocked by addition of ERK1/2 inhibitor and by dominant-negative (DN) ERK1/2 but not by DN-TGF-beta receptor II (TbetaRII) or conditional deletion of TbetaRII. Second, Ang II was also able to activate the late Smad2/3 signaling pathway at 24 hours, which was TGF-beta dependent because it was blocked by the anti-TGF-beta antibody and DN-TbetaRII. Finally, activation of Smad3 but not Smad2 was a key and necessary mechanism of Ang II-induced vascular fibrosis because Ang II induced Smad3/4 promoter activities and collagen matrix expression was abolished in VSMCs null for Smad3 but not Smad2. Thus, we concluded that Ang II induces vascular fibrosis via both TGF-beta-dependent and ERK1/2 MAPK-dependent Smad signaling pathways. Activation of Smad3 but not Smad2 is a key mechanism by which Ang II mediates arteriosclerosis.