A New Species of Ganoderma (Ganodermataceae, Polyporales) from Southern China and Optimum Condition for Mycelia Production.

The present study sought to propose Ganoderma guixiense sp. nov. as a new species based on phenotypic and genotypic evidence. Phylogenetic analyses were carried out based on the internal transcribed spacer (ITS), the large subunit of nuclear ribosomal RNA gene (nLSU), and the second subunit of RNA polymerase II (RPB2) sequence data. G. guixiense has been characterized by pileate basidiomata, long stipe, in addition to reddish-black zonate pileal surface. Basidiospores are broadly ellipsoid with one end tapering at maturity, and measuring 9-12.8 × 6.5-9.3 µm. Basidia are oval to subglobose. This study marks the first exploration of the biological characteristics of G. guixiense. The result indicated that the optimal medium of mycelial growth was observed on malt extract agar (MEA) and yeast extract peptone dextrose agar (YPD) while the optimal temperature was found to be 25-30 °C with pH range of 6-7.

Fulvifomes nonggangensis and F. tubogeneratus (Hymenochaetales, Basidiomycota): Two New Species from Southern China Based on Morphological and Molecular Evidences.

Two new species of Fulvifomes are described from specimens collected in rainforests of Nonggang Nature Reserve of southern China, based on morphological characteristics and molecular phylogenetic analysis of the internal transcribed spacer (ITS) and nuclear large subunit ribosomal DNA (nLSU) sequences. Fulvifomes nonggangensis sp. nov. is characterized by perennial, sessile and solitary basidiocarps, applanate pileus, small cystidioles of 9.9-15.4 × 2.9-3.5 µm, large pores of 5-6 per mm, a dimitic hyphal system, and broadly ellipsoid basidiospores of 4.3-5.3 × 3.3-4.2 µm. F. tubogeneratus sp. nov. is characterized by perennial, sessile, and imbricate basidiocarps, a duplex context, small pores of 7-8 per mm, a dimitic hyphal system, and ovoid to subglobose basidiospores of 5.72 × 5.00 µm.

Incremental effect of liraglutide on traditional insulin injections in rats with type 2 diabetes mellitus by maintaining glycolipid metabolism and cardiovascular function.

Type 2 diabetes mellitus (T2DM) is characterized by chronic hyperglycemia, damaged insulin secretion and insulin resistance with high morbidity and mortality. Liraglutide (liragl) and insulin are effective hypoglycemic agents used in T2DM treatment. The potential effect of liragl in combination with insulin on T2DM remains unclear. The aim of the current study was to explore effects of liragl combined with insulin on glycolipid metabolism and cardiovascular function in rats with diabetes. A diabetes model was established in Sprague Dawley rats exposed to a high calorie and high sugar diet in conjunction with intraperitoneal injections of streptozotocin. Results indicated that liragl or insulin used alone decreased glucose and elevated insulin and c-peptide levels. However, their combination revealed greater effects. A significant increase in high-density lipoprotein cholesterol levels along with a decrease in total cholesterol, triglycerides and low-density lipoprotein cholesterol were observed in liragl- and insulin-treated rats compared with STZ-induced diabetes rats. Furthermore, co-administration of liragl and insulin significantly decreased sterol regulatory element-binding protein 1 levels and increased adenosine 5'-monophosphate kinase-α1 and carnitine palmitoyltransferase 1 expression. Combining liragl with insulin reduced myocardial hypertrophy level and gaps between cardiomyocytes compared with liragl or insulin treatment alone. Caspase-3 expression was significantly decreased by combination treatment of liragl and insulin. Oxidative damage was significantly decreased by co-administration of liragl and insulin through enhancing superoxide dismutase expression and reducing malondialdehyde. Furthermore, combination of liragl and insulin significantly reduced myocardial enzyme expression, including myoglobin, creatine kinase-muscle/brain and cardiac troponin I. In summary, the current study demonstrated synergistic effects of liragl and insulin injections on a T2DM rat model by maintaining glycolipid metabolism and cardiovascular function.

Amylosporus sulcatus sp. nov. (Russulales, Basidiomycota) from Southern China.

Amylosporus sulcatus sp. nov. is described from Nonggang Nature Reserve, southern China, on the basis of morphological and molecular data. The morphological description and illustrations for the new species are provided. The species is characterized by pileate and stipitate basidiocarps. The pileus surface is obviously concentrically and radiately sulcate and tomentum, and the pore surface is snow white. Phylogenetic analyses based on sequences of the internal transcribed spacer and nuclear large subunit ribosomal DNA confirmed it to be a new species.

Autophagy-Lysosome Pathway in Renal Tubular Epithelial Cells Is Disrupted by Advanced Glycation End Products in Diabetic Nephropathy.

It has been suggested that autophagy protects renal tubular epithelial cells (TECs) from injury in diabetic nephropathy (DN). However, the manner in which the autophagy-lysosome pathway is changed in this state remains unclear. In this study of DN, we investigated the autophagic activity and lysosomal alterations in vivo and in vitro. We found that autophagic vacuoles and SQSTM1-positive proteins accumulated in TECs from patients with DN and in human renal tubular epithelial cell line (HK-2 cells) treated with advanced glycation end products (AGEs), the important factors that involved in the pathogenesis of DN. In HK-2 cells, exposure to AGEs caused a significant increase in autophagosomes but a marked decrease in autolysosomes, and the lysosomal turnover of LC3-II was not observed, although LC3-II puncta were co-localized with the irregular lysosomal-associated membrane protein1 granules after AGEs treatment. Furthermore, lysosomal membrane permeabilization was triggered by AGEs, which likely resulted in a decrease in the enzymatic activities of cathepsin B and cathepsin L, the defective acidification of lysosomes, and suppression of the lysosomal degradation of DQ-ovalbumin. Oxidative stress evoked by AGEs-receptor for AGE interaction likely played an important role in the lysosomal dysfunction. Additionally, ubiquitinated proteins were co-localized with SQSTM1-positive puncta and accumulated in HK-2 cells after exposure to AGEs, indicating blocked degradation of SQSTM1-positive and ubiquitinated aggregates. Taken together, the results show that lysosomal membrane permeabilization and lysosomal dysfunction are triggered by AGEs, which induce autophagic inactivation in TECs from patients with DN. Disruption of the autophagy-lysosome pathway should be focused when studying the mechanisms underlying DN.

Poly[(µ(3)-quinoline-6-carboxyl-ato-κ(3)N:O:O')silver(I)].

In the title coordination polymer, [Ag(C(10)H(6)NO(2))](n), the Ag(I) cation is coordinated by two O atoms and one N atom from three 6-quinoline-carboxyl-ate anions in a distorted T-shaped AgNO(2) geometry, in which the O-Ag-O angle is 160.44 (9)°. The 6-quinoline-carboxyl-ate anion bridges three Ag(+) cations, forming a nearly planar polymeric sheet parallel to (101). The distance between Ag(+) cations bridged by the carboxyl group is 2.9200 (5) Å. In the crystal, π-π stacking is observed between parallel quinoline ring systems, the centroid-centroid distance being 3.7735 (16) Å.

catena-Poly[[silver(I)-µ-1,2-bis-(4,4-dimethyl-4,5-dihydro-1,3-oxazol-2-yl)ethane-κ(2)N:N'] perchlorate hemihydrate].

In the title coordination polymer, {[Ag(C(12)H(20)N(2)O(2))]ClO(4)·0.5H(2)O}(n), the Ag(I) cation is coordinated by two N atoms from two 1,2-bis-(4,4-dimethyl-4,5-dihydro-1,3-oxazol-2-yl)ethane (L) ligands in a nearly linear geometry [N-Ag-N = 171.07 (8)°]. The L ligand bridges adjacent Ag(+) cations, forming a polymeric chain running along the c axis. The lattice water mol-ecule is situated on a twofold rotation axis, and links to the perchlorate anion via an O-H⋯O hydrogen bond. The long Ag⋯O separation of 3.200 (4) Šindicates a weak inter-action between the perchlorate anion and the Ag(I) cation. Weak C-H⋯O hydrogen bonding occurs between the chain and the lattice water mol-ecule and between the chain and perchlorate anions. Both five-membered rings of the L ligand display envelope conformations; in one five-membered ring, the flap C atom is disordered on opposite sides of the ring with occupancies of 0.65 and 0.35.

Tetra-kis[µ-1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene-κN:N']tetra-kis-(µ-methano-lato-κO:O)bis-(µ-perchlorato-κO:O')tetra-copper(II) bis-(perchlorate).

The title tetra-nuclear Cu(II) complex, [Cu(4)(C(12)H(12)N(2)O(2))(4)(CH(3)O)(4)(ClO(4))(2)](ClO(4))(2), is located around an inversion center. Each Cu(II) atom is coordinated by two cis-O atoms from two bridging methano-late anions and two cis-N atoms from two bridging 1,4-bis-(4,5-dihydro-1,3-oxazol-2-yl)benzene (L) ligands in the basal plane, and is further coordinated by one O atom of the bridging perchlorate anion, forming a distorted square-pyramidal geometry. The Cu⋯Cu separations in the recta-ngular core are 2.9878 (11) and 6.974 (1) Å. In the asymmetric unit, there are two L ligands with a syn conformation. In one L ligand, the dihedral angles between the central benzene ring and the terminal 4,5-dihydro-1,3-oxazol-2-yl mean planes are 22.1 (4) and 33.1 (4)°, and in the other L ligand the corresponding dihedral angles are 29.3 (4) and 29.9 (4)°. The uncoordinated perchlorate anion is linked with the complex mol-ecules via weak C-H⋯O hydrogen bonds.

Effects of interleukin 18 on injury and activation of human proximal tubular epithelial cells.

BACKGROUND/AIMS: Injury and activation of tubular proximal epithelial cells (TEC) play central roles in renal tubulointerstitial fibrosis (TIF), but its mechanisms remain obscure. Interleukin 18 (IL-18) is overproduced during chronic kidney diseases (CKD), but how IL-18 affects the biological behaviour of TEC is not clear. The aim of the present study is to reveal the role of IL-18 in renal TIF. METHODS: The expressions of IL-18 and IL-18 receptor in TEC were detected by immunohistochemical staining in vivo and by reverse transcriptase polymerase chain reaction (RT-PCR) in vitro. TEC line (HK-2 cells) were incubated without or with IL-18. Cell proliferation and cell cycle were evaluated by methyl thiazolyl tetrazolium assay and flow cytometric analysis, respectively. Cell apoptosis was assessed by Hoechst 33258 staining. Expression of alpha-smooth muscle actin was evaluated by RT-PCR, immunocytochemical staining and flow cytometric analysis, respectively. Type I collagen, fibronectin, MCP-1 and RANTES in cultured supernatants were measured by enzyme-linked immunosorbent assay. RESULTS: IL-18 expression in TEC increased significantly in CKD state. IL-18 receptor was constitutively expressed in normal proximal TEC, and its expression increased strongly in CKD state. Proliferation and cell cycle of HK-2 cells were not affected by IL-18. Cell apoptosis, alpha-smooth muscle actin expression, type I collagen and fibronectin production as well as MCP-1 secretion were promoted by IL-18 in dosage- and/or time-dependent manners, but RANTES secretion was not affected. CONCLUSION: IL-18 may play a crucial role in the process of TIF by promoting TEC injury and activation, and could be a target of the therapeutic approaches against TIF.