Spatiotemporal changes in biomass after selective logging in a lowland tropical rainforest in peninsular Malaysia

We studied biomass changes in a lowland tropical rain forest in the Pasoh Forest Reserve of Peninsular Malaysia after selective logging in 1958. A tree census was undertaken every 2 years from 1998 to 2012 in a 6-ha logged forest plot. Total aboveground biomass (AGB) was 72 % of that in a primary forest plot within the same reserve in 1998, but reached 87 % in 2012. AGB regrowth was spatially variable within the logged forest plot and was much less in swampy areas than in upland areas. The overall annual growth rate of AGB in the logged forest throughout the study period was 1.5 % and slowed (to 0.6 %) in a dry period (2004-2006). The biomass of large trees (DBH ≥ 50 cm) increased by 56 % during the study period, but amounted to only 58 % of the biomass of the corresponding size class in the primary forest, suggesting that stand structure is still recovering from logging. Spatiotemporal variation in AGB recovery after logging needs to be taken into account for logging and subsequent management of the tropical lowland forest biome

Genetics of Endometrial Cancers

Endometrial cancers exhibit a different mechanism of tumorigenesis and progression depending on histopathological and clinical types. The most frequently altered gene in estrogen-dependent endometrioid endometrial carcinoma tumors is PTEN. Microsatellite instability is another important genetic event in this type of tumor. In contrast, p53 mutations or Her2/neu overexpression are more frequent in non-endometrioid tumors. On the other hand, it is possible that the clear cell type may arise from a unique pathway which appears similar to the ovarian clear cell carcinoma. K-ras mutations are detected in approximately 15%–30% of endometrioid carcinomas, are unrelated to the existence of endometrial hyperplasia. A β-catenin mutation was detected in about 20% of endometrioid carcinomas, but is rare in serous carcinoma. Telomere shortening is another important type of genomic instability observed in endometrial cancer. Only non-endometrioid endometrial carcinoma tumors were significantly associated with critical telomere shortening in the adjacent morphologically normal epithelium. Lynch syndrome, which is an autosomal dominantly inherited disorder of cancer susceptibility and is characterized by a MSH2/MSH6 protein complex deficiency, is associated with the development of non-endometrioid carcinomas

Selective Anion Sensing By Chiral Macrocyclic Receptors With Multiple Hydrogen-bonding Sites

Chiral macrocycles featuring sulfonamide and/or amide groups as anion-binding sites were synthesized. X-ray crystal structures and DFT calculations have shown that they adopt different conformations that may lead to unique binding behavior. Indeed, various anions could be sensed by their colorimetric and/or fluorescence signal output. The chiral macrocycles showed chiral recognition for chiral anions. Furthermore, a multisensor array with two or four chiral receptors discriminated seven phosphate anions (AMP, ADP, ATP, CMP, GMP, Pi, and PPi) with 100% classification accuracy

Influence of microstructure on fatigue property of ultra high-strength steels

Ultra-high-strength steels (with tensile strength higher than 980 MPa) are widely used in automobile manufacturing owing to their lightweight that contributes to fuel efficiency. The fatigue strength of ultra-high-strength steels with a notch tends to decrease, which is known as the effect of notch sensitivity. In this study, 4-point bending fatigue tests were performed to examine the fatigue strength and notch sensitivity of four steels; namely 590 MPa class steel, 980 MPa class martensitic steel, 980 MPa class bainitic steel, and 980 MPa class precipitation hardening steel plates with three different stress concentration factors. The results indicate that the fatigue strength and notch sensitivity of 980 MPa class steel specimens were higher than those of 590 MPa class steel specimens. The notch sensitivities of tested plate specimens were lower than those reported for cylindrical specimens of bainitic ultra-high-strength steels. Fatigue crack observation revealed that the cracks initiated in 590 MPa class steel, 980 MPa class bainitic, and martensitic steel propagated southward from the lowest bottom of notch. Although similar initial crack propagation pattern was detected in precipitation hardening steel, the crack changed direction when it reached the central part of the specimen

Influence of microstructure on fatigue property of ultra high-strength steels

Ultra-high-strength steels (with tensile strength higher than 980 MPa) are widely used in automobile manufacturing owing to their lightweight that contributes to fuel efficiency. The fatigue strength of ultra-high-strength steels with a notch tends to decrease, which is known as the effect of notch sensitivity. In this study, 4-point bending fatigue tests were performed to examine the fatigue strength and notch sensitivity of four steels; namely 590 MPa class steel, 980 MPa class martensitic steel, 980 MPa class bainitic steel, and 980 MPa class precipitation hardening steel plates with three different stress concentration factors. The results indicate that the fatigue strength and notch sensitivity of 980 MPa class steel specimens were higher than those of 590 MPa class steel specimens. The notch sensitivities of tested plate specimens were lower than those reported for cylindrical specimens of bainitic ultra-high-strength steels. Fatigue crack observation revealed that the cracks initiated in 590 MPa class steel, 980 MPa class bainitic, and martensitic steel propagated vertically from the lowest bottom of notch. Although similar initial crack propagation pattern was detected in precipitation hardening steel, the crack changed direction when it reached the central part of the specimen

Overexpression of DNA Polymerase ζAffects Cisplatin Resistance in Ovarian Cancer: An Immunohistochemical Study

DNA polymerase ζ (Pol ζ) participates in translesional bypass replication. Pol ζ has been shown to be an important contributor to cis-diamminedichloroplatinum (II)(DDP; cisplatin) -induced genomic instability and the subsequent emergence of resistance in vitro. We immunohistochemically examined the expression of Pol ζ in ovarian cancer tissues to determine whether its expression affects the DDP resistance of human ovarian cancers and also to determine whether Pol ζ expression is a prognostic factor for ovarian cancers. We assessed 76 archival, formalin-fixed, paraffin-embedded tissue samples obtained from patients with epithelial ovarian cancers who underwent their first operation between 2003 and 2011. An ovarian cancer tissue array was also used in this study. Immunohistochemical staining of Pol ζ was performed using an anti-human Pol ζ monoclonal rabbit antibody. The strength of expression of Pol ζ was compared with the DDP resistance and clinical features of the study population. The Pol ζ over-expression in ovarian cancer tissue which compared with epithelial cells in normal ovaries was not affected by the histological types, FIGO stage, or patient age, but Pol ζ was significantly more overexpressed in the DDP-resistant group than in the DDP-sensitive group (P = 0.043). Pol ζ over-expression did not significantly affect the survival rate of the ovarian cancer patients; however, the Pol ζ positive group tended to have a poorer long-term prognosis. In conclusion, ovarian carcinoma patients with Pol ζ over-expression are likely to be resistant to DDP, especially in cases of recurrent disease. These results confirm the previous findings in vitro, wherein Pol ζ modulated the cytotoxicity and mutagenicity of DDP

Dysbindin Regulates the Transcriptional Level of Myristoylated Alanine-Rich Protein Kinase C Substrate via the Interaction with NF-YB in Mice Brain

BACKGROUND: An accumulating body of evidence suggests that Dtnbp1 (Dysbindin) is a key susceptibility gene for schizophrenia. Using the yeast-two-hybrid screening system, we examined the candidate proteins interacting with Dysbindin and revealed one of these candidates to be the transcription factor NF-YB. METHODS: We employed an immunoprecipitation (IP) assay to demonstrate the Dysbindin-NF-YB interaction. DNA chips were used to screen for altered expression of genes in cells in which Dysbindin or NF-YB was down regulated, while Chromatin IP and Reporter assays were used to confirm the involvement of these genes in transcription of Myristoylated alanine-rich protein kinase C substrate (MARCKS). The sdy mutant mice with a deletion in Dysbindin, which exhibit behavioral abnormalities, and wild-type DBA2J mice were used to investigate MARCKS expression. RESULTS: We revealed an interaction between Dysbindin and NF-YB. DNA chips showed that MARCKS expression was increased in both Dysbindin knockdown cells and NF-YB knockdown cells, and Chromatin IP revealed interaction of these proteins at the MARCKS promoter region. Reporter assay results suggested functional involvement of the interaction between Dysbindin and NF-YB in MARCKS transcription levels, via the CCAAT motif which is a NF-YB binding sequence. MARCKS expression was increased in sdy mutant mice when compared to wild-type mice. CONCLUSIONS: These findings suggest that abnormal expression of MARCKS via dysfunction of Dysbindin might cause impairment of neural transmission and abnormal synaptogenesis. Our results should provide new insights into the mechanisms of neuronal development and the pathogenesis of schizophrenia

SUMOylation of xeroderma pigmentosum group C protein regulates DNA damage recognition during nucleotide excision repair

The xeroderma pigmentosum group C (XPC) protein complex is a key factor that detects DNA damage and initiates nucleotide excision repair (NER) in mammalian cells. Although biochemical and structural studies have elucidated the interaction of XPC with damaged DNA, the mechanism of its regulation in vivo remains to be understood in more details. Here, we show that the XPC protein undergoes modification by small ubiquitin-related modifier (SUMO) proteins and the lack of this modification compromises the repair of UV-induced DNA photolesions. In the absence of SUMOylation, XPC is normally recruited to the sites with photolesions, but then immobilized profoundly by the UV-damaged DNA-binding protein (UV-DDB) complex. Since the absence of UV-DDB alleviates the NER defect caused by impaired SUMOylation of XPC, we propose that this modification is critical for functional interactions of XPC with UV-DDB, which facilitate the efficient damage handover between the two damage recognition factors and subsequent initiation of NER