Search

Heat stress decreases milk yield and deleteriously alters milk composition. Reduced feed intake partially explains some of the consequences of heat stress, but metabolic changes in the mammary tissue and liver associated with milk synthesis have not been thoroughly evaluated. In the current study, changes of protein abundance in the mammary tissue and liver between heat-stressed cows with ad libitum intake and pair-fed thermal neutral cows were investigated using the iTRAQ proteomic approach. Most of the differentially expressed proteins from mammary tissue and liver between heat-stressed and pair-fed cows were involved in Gene Ontology category of protein metabolic process. Pathway analysis indicated that differentially expressed proteins in the mammary tissue were related to pyruvate, glyoxylate and dicarboxylate metabolism pathways, while those in the liver participated in oxidative phosphorylation and antigen processing and presentation pathways. Several heat shock proteins directly interact with each other and were considered as central "hubs" in the protein interaction network. These findings provide new insights to understand the turnover of protein biosynthesis pathways within hepatic and mammary tissue that likely contribute to changes in milk composition from heat-stressed cows.

The harmful algal bloom (HAB)-forming dinoflagellate Karenia mikimotoi was exposed to different nitrogen (N) conditions, in order to study the population growth, temporary cyst production and cellular biochemical compositions in laboratory. The results indicated the population growth of K. mikimotoi was inhibited by different levels of N starvation but showed similar fast recovery after the resupplement of N, and temporary cysts were induced in the period of N starvation. K. mikimotoi grew well in inorganic (NO3-, NO2- and NH4+) and organic (urea) nitrogen sources, but the growth parameters (K, Tp, r) showed differences when simulated by Logistic model regressions. When the cellular organic compounds were measured simultaneously, K. mikimotoi cultured in urea produced more short-chained fatty acids while K. mikimotoi cultured in NH4+ produced more non-fatty acids compounds, indicating the potential change of toxins production cultured by various N sources. We concluded that K. mikimotoi could adapt to fluctuating N environments typical of coastal environments including total N concentration (deficiency or recovery) and relative compositions (different N sources).

The frequent emergence of drug-resistant bacteria has created an urgent demand for new antimicrobial agents. Traditional methods of novel antibiotic development are almost obsolete. Antimicrobial peptides (AMPs) are now regarded as a potential solution to revive the traditional methods of antibiotic development, although, until now, many AMPs have failed in clinical trials. A comprehensive database of AMPs with information about their antimicrobial activity and cytotoxicity will help promote the process of finding novel AMPs with improved antimicrobial activity and reduced cytotoxicity and eventually accelerate the speed of translating the discovery of new AMPs into clinical or preclinical trials. LAMP, a database linking AMPs, serves as a tool to aid the discovery and design of AMPs as new antimicrobial agents. The current version of LAMP has 5,547 entries, comprising 3,904 natural AMPs and 1,643 synthetic peptides. The database can be queried using either simply keywords or combinatorial conditions searches. Equipped with the detailed antimicrobial activity and cytotoxicity data, the cross-linking and top similar AMPs functions implemented in LAMP will help enhance our current understanding of AMPs and this may speed up the development of new AMPs for medical applications. LAMP is freely available at: http://biotechlab.fudan.edu.cn/database/lamp.

As one of the most widespread protein post-translational modifications, phosphorylation is involved in many biological processes such as cell cycle, apoptosis. Identification of phosphorylated substrates and their corresponding sites will facilitate the understanding of the molecular mechanism of phosphorylation. Comparing with the labor-intensive and time-consuming experiment approaches, computational prediction of phosphorylation sites is much desirable due to their convenience and fast speed. In this paper, a new bioinformatics tool named CKSAAP_PhSite was developed that ignored the kinase information and only used the primary sequence information to predict protein phosphorylation sites. The highlight of CKSAAP_PhSite was to utilize the composition of k-spaced amino acid pairs as the encoding scheme, and then the support vector machine was used as the predictor. The performance of CKSAAP_PhSite was measured with a sensitivity of 84.81%, a specificity of 86.07% and an accuracy of 85.43% for serine, a sensitivity of 78.59%, a specificity of 82.26% and an accuracy of 80.31% for threonine as well as a sensitivity of 74.44%, a specificity of 78.03% and an accuracy of 76.21% for tyrosine. Experimental results obtained from cross validation and independent benchmark suggested that our method was very promising to predict phosphorylation sites and can be served as a useful supplement tool to the community. For public access, CKSAAP_PhSite is available at http://59.73.198.144/cksaap_phsite/.

Pulmonary vascular medial hypertrophy in hypoxic pulmonary arterial hypertension (PAH) is caused in part by decreased apoptosis in pulmonary artery smooth muscle cells (PASMCs). Puerarin, an isoflavone purified from the Chinese medicinal herb kudzu, ameliorates chronic hypoxic PAH in animal models. Here we investigated the effects of puerarin on apoptosis of hypoxic human PASMCs (HPASMCs), and to determine the possible underlying mechanisms.HPASMCs were cultured for 24 h in normoxia or hypoxia (5% O₂) conditions with and without puerarin. Cell number and viability were determined with a hemacytometer or a cell counting kit. Apoptosis was detected with a TUNEL test, rhodamine-123 (R-123) fluorescence, a colorimetric assay, western blots, immunohistochemical staining and RT-PCR. Hypoxia inhibited mitochondria-dependent apoptosis and promoted HPASMC growth. In contrast, after puerarin (50 µM or more) intervention, cell growth was inhibited and apoptosis was observed. Puerarin-induced apoptosis in hypoxic HPASMCs was accompanied by reduced mitochondrial membrane potential, cytochrome c release from the mitochondria, caspase-9 activation, and Bcl-2 down-regulation with concurrent Bax up-regulation.Puerarin promoted apoptosis in hypoxic HPASMCs by acting on the mitochondria-dependent pathway. These results suggest a new mechanism of puerarin relevant to the management of clinical hypoxic pulmonary hypertension.