分子生物学: オープンアクセス

Pasteurella multocida is a non-motile coccobacillus pathogenic Gram-negative bacterium and belongs to Pasteurellaceae family. Pasteurella multocida causes diseases in economically important animals and birds in developing and developed countries. Haemorrhagic septicaemia in cattle and buffaloes and other diseases like fowl cholera (turkey, chicken, and duck), Septicaemic pasteurellosis (sheep, pig, and goat) and Snuffles (rabbit) are caused by Pasteurella multocida. In this analysis we have taken three outer membrane proteins (vacJ, ompW and skp) from P. multocida which are involved in infectious diseases of animals and birds. The literature shows that all three outer membrane proteins are infectious in nature. This is supported by multiple sequence alignment and analysis of physicochemical properties of protein sequences encoded by vacJ, ompW and skp outer membrane protein families. The studied proteins are similar with respect to number of positively and negatively charged amino acids, molecular weight, Theoretical pI, instability index and grand average of hydropathicity (GRAVY) in the proteins from P. multocida strains infecting different genera. The domains, transmembrane helices, twin arginine signal peptides and ß-barrels are also broadly similar. This suggests common mechanism of action of these proteins across host genera.

Centromere protein A (CENP-A) is a centromere-specific histone H3 variant present in prekinetochores in nuclei and kinetochores of mitotic chromosomes. The proliferating cell nuclear antigen (PCNA) forms replication foci in S phase but diffuses in nuclei except for nucleoli in other phases. Here to elucidate the molecular behavior of CENP-A and PCNA throughout the cell cycle, we performed a prolong time-lapse imaging of HT-1080 cell line stably expressing mKO-CENP-A and EGFP-PCNA with a highly sensitive EM-CCD camera. We followed the mKO-CENP-A dots in interphase nuclei from G1 through to G2 phase, monitoring the cell cycle progression by the appearance of replication foci of EGFP-PCNA in S phase.

Improvements in the care of patients with cardiovascular disease have led to improved survival but also a burgeoning population of patients with advanced heart disease. Cardiac stem cells (CSC) continue to promise opportunities to repair damaged cardiac tissue. However, precisely how stem cells accomplish cardiac repair, especially after ischemic damage, remains controversial. It has been postulated that the clinical benefit of adult stem cells for cardiovascular disease results from the release of cytokines and growth factors by the transplanted cells, stimulation of new blood vessel growth, enhancing tissue perfusion, and via preservation or even regeneration of myocardial tissue, leading to improvements in cardiac performance after myocardial infarction and in patients with advanced heart failure, reducing inflammation, and scar formation, as well as protecting cardiomyocytes from apoptosis. In addition, reducing fibrosis these factors might also stimulate endogenous repair by activating cardiac stem cells. Interestingly, stem cells discovered to be resident in the heart appear to be functionally superior to extra-cardiac adult stem cells when transplanted for cardiac repair and regeneration. Stem cells are the seeds of tissue repair and regeneration and a promising source for novel therapies. However, apart from hematopoietic stem cell (HSC) transplantation, all other stem cell treatments yet remain experimental. Mounting hopes have encouraged numerous clinical trials, but it has been difficult to obtain unequivocal evidence for robust clinical benefit. This review provides a historic framework and an abridgment of how the theories of CSC origin and potential evolved from early times to the present day. The development of more effective cardiac therapies may thus require targeting this important cell population. Here, we summarize and offer some thoughts on the state of the field of cell therapy for ischemic heart diseases and the therapeutic potential of cardiac stem cells.

Disease therapy based on genetic materials is now a reality. The technique of gene silencing also called as RNA interference (RNAi) keeps our hopes alive. RNAi based drugs have now advanced steps closer towards clinical trials. The powerful in-vivo RNAi machinery and its delicate factors apprehend that RNAi-dependent therapies might create a billion dollar business against the pathogenic organisms and diseases for which treatment options are currently restricted conventionally. Recent years have highlighted both the promises and challenges in the delivery of different RNAi therapeutics. Apart from the delivery, the design, stability and degradation of RNAi based effective molecules appear to be the major lime light to challenge the conventional drug safety concerns and ensures to be the most powerful gene recovery in future which may execute a billion dollar business hope.

The genotypes of Mycobacterium tuberculosis (M. tuberculosis) have been found to differ in their resistance to different drugs. Although there is a high incidence of tuberculosis (TB) in Jiangxi, knowledge of the genotypes of M. tuberculosis in this province is limited in recent years. In this study, we investigated the relationship between genetic diversity and drug resistance in M. tuberculosis isolates collected from Jiangxi during January to October, 2014. A total of 133 M. tuberculosis isolates collected from the Jiangxi Chest Hospital were genotyped using both spacer oligonucleotide typing (spoligotyping) and 24-locus mycobacterial interspersed repetitive units-variable number of tandem repeats (MIRU-VNTR). The resistance of these isolates to four first-line, and four second-line, anti-TB drugs, namely, isoniazid, rifampicin, ethambutol, streptomycin, capreomycin, amikacin, levofloxacin and protionamide, was then tested. The results indicate that the Beijing family was the most prevalent genotype (75.94%), followed by the T1 family (13.53%), the MANU2 family (1.50%), the T2 family (0.75%) and the Beijing-like genotype (0.75%). We also found nine new genotypes that did not match those in the Spoldb4.0 database. The 24-locus MIRU-VNTR method had a low clustering rate (10.53%) and a high HGDI (0.9723), and proved a high resolution method for genotyping M. tuberculosis isolates. More than half of the M. tuberculosis isolates collected in the present study were resistant to anti-TB drugs (56.39%, 75/133), and the majority of these were resistant to more than one drug (81.33%, 61/75). The Beijing family is the most prevalent TB strain in Jiangxi province, China. More than half the M. tuberculosis isolates collected were resistant to anti-TB drugs, and the majority was resistant to more than one drug. There was, however, no relationship between genetic diversity and drug resistance. Moreover, our results suggest that treatment history can lead to the development of drug resistance (P < 0.05), which supports the more moderate use of medication in the treatment of TB.