A Gram-stain-negative, wheat, rod-shaped, non-motile, non-spore forming, and facultatively anaerobic bacterium strain, designated as PIT, was isolated from saline silt samples collected in saltern in Yantai, Shandong, China. Growth was observed within the ranges 4–45 °C (optimally at 33 °C), pH 6.0–9.0 (optimally at pH 7.0) and 1.0–11.0% NaCl (optimally at 3.0%, w/v). Strain PIT showed highest 16S rRNA gene sequence similarity to Kangiella sediminilitoris BB-Mw22T (98.3%) and Kangiella taiwanensis KT1T (98.3%). The major cellular fatty acids (>?10% of the total fatty acids) were iso-C15:0 (52.7%) and summed featured 9 (iso-C17:1ω9c/C16:0 10-methyl, 11.8%). The major polar lipids identified were diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylmonomethylethanolamine and phosphatidylglycerol. The major respiratory isoprenoid quinone was Q-8. The G?+?C content of the genomic DNA was 45.8%. Average Nucleotide Identity values between whole genome sequences of strain PIT and next related type strains supported the novel species status. Based on physiological, biochemical, chemotaxonomic characteristics and genomic analysis, strain PIT is considered to represent a novel species within the genus Kangiella, for which the name Kangiella shandongensis sp. nov. is proposed. The type strain is PIT (=?KCTC 82509 T?=?MCCC 1K04352T).
We investigated ATP-binding cassette transporters A1/G1 expression and function in mediating cholesterol efflux by examining the macrophages of cigarette-smoking patients with coronary artery disease (CAD) before and after smoking abstinence. Peripheral blood monocyte cells were collected from nonsmokers (n = 17), non-CAD (NCAD) smokers (n = 35), and CAD smokers (n = 32) before and after 3 months of smoking cessation. We found that the ABCA1 expression level was lower in macrophages from NCAD and CAD smokers than from nonsmokers at baseline. The ABCA1 function of mediating cholesterol efflux was reduced in NCAD and CAD smokers as compared with nonsmokers. After 3 months of smoking cessation, ABCA1 expression and function were improved in CAD smokers. However, ABCG1 expression and function did not change after smoking cessation. Furthermore, ABCA1 expression was inhibited by tar in human acute monocytic leukemia cell line THP-1-derived macrophages through the inhibition of liver X receptors. Nicotine and carbon monoxide did not inhibit ABCA1 expression. Our results indicate that chronic cigarette smoking impaired ABCA1-mediated cholesterol efflux in macrophages and that tobacco abstinence reversed the function and expression of ABCA1, especially in CAD patients. It was tobacco tar, rather than nicotine or carbon monoxide, that played a major role in the tobacco-induced disturbance of cellular cholesterol homeostasis. 相似文献
Although estrogen action is indispensable for normal bone growth in both genders, the roles of estrogen receptors (ERs) in
mediating bone growth are not fully understood. The effects of ER inactivation on bone growth are sex and age dependent, and
may differ between the axial and appendicular regions. In this study, the spatial and temporal expression of ERα and β in
the tibial and spinal growth plates of the female and male rats during postnatal development was examined to explore the possible
mechanisms. The level of mRNA was examined and compared with quantitative real-time PCR. The spatial location was determined
by immunohistochemical analysis. The 1-, 4-, 7-, 12- and 16-week age stages correspond to early life, puberty and early adulthood
after puberty, respectively. Gender- and region-specific differences in ERα and β expression were shown in the growth plates.
Mainly nuclear staining of ERα and β immunoreactivity was demonstrated in the spinal and tibial growth plate chondrocytes
for both genders. Moreover, our study indicated significant effect of gender on temporal ERα and β expression and of region
on temporal ERα/ERβ expression ratio. However, spatial differences of region-related ERα and β expression were not observed.
Gender-related spatial changes were detected only at 16 weeks of both spine and limb growth plates. ERα and β immunoreactivity
was detected in the resting, proliferative and prehypertrophic chondrocytes in the early life stage and during puberty. After
puberty, ERα expression was mainly located in the late proliferative and hypertrophic chondrocytes in female, whereas the
expression still extended from the resting to hypertrophic chondrocytes in males. Gender- and region-specific expression patterns
of ERα and β gene might be one possible reason for differences in sex- and region-related body growth phenotypes. Gender,
age and region differences should be taken into consideration when the roles of ERs in the growth plate are investigated. 相似文献
Intervertebral disc (IVD) degeneration is largely a process of destruction and failure of the extracellular matrix (ECM),
and symptomatic IVD degeneration is thought to be one of the leading causes of morbidity or life quality deterioration in
the elderly. To date, however, the mechanism of IVD degeneration is still not fully understood. Cellular loss from cell death
in the process of IVD degeneration has long been confirmed and considered to contribute to ECM degradation, but the causes
and the manners of IVD cell death remain unclear. Programmed cell death (PCD) is executed by an active cellular process and
is extensively involved in many physiological and pathological processes, including embryonic development and human degenerative
diseases. Thus, the relationship between PCD and IVD degeneration has become a new research focus of interest in recent years.
By reviewing the available literature concentrated on PCD in IVD and discussing the methodology of detecting PCD in IVD cells,
its inducing factors, the relationship of cell death to ECM degradation, and the potential therapy for IVD degeneration by
modulation of PCD, we conclude that IVD cells undergo PCD via different signal transduction pathways in response to different
stimuli, that PCD may play a role in the process of IVD degeneration, and that modulation of PCD might be a potential therapeutic
strategy for IVD degeneration. 相似文献
BackgroundIn the past decade, several countries have seen gradual replacement of endemic multi-resistant healthcare-associated methicillin-resistant Staphylococcus aureus (MRSA) with clones that are more susceptible to antibiotic treatment. One example is Singapore, where MRSA ST239, the dominant clone since molecular profiling of MRSA began in the mid-1980s, has been replaced by ST22 isolates belonging to EMRSA-15, a recently emerged pandemic lineage originating from Europe.ResultsWe investigated the population structure of MRSA in Singaporean hospitals spanning three decades, using whole genome sequencing. Applying Bayesian phylogenetic methods we report that prior to the introduction of ST22, the ST239 MRSA population in Singapore originated from multiple introductions from the surrounding region; it was frequently transferred within the healthcare system resulting in a heterogeneous hospital population. Following the introduction of ST22 around the beginning of the millennium, this clone spread rapidly through Singaporean hospitals, supplanting the endemic ST239 population. Coalescent analysis revealed that although the genetic diversity of ST239 initially decreased as ST22 became more dominant, from 2007 onwards the genetic diversity of ST239 began to increase once more, which was not associated with the emergence of a sub-clone of ST239. Comparative genomic analysis of the accessory genome of the extant ST239 population identified that the Arginine Catabolic Mobile Element arose multiple times, thereby introducing genes associated with enhanced skin colonization into this population.ConclusionsOur results clearly demonstrate that, alongside clinical practice and antibiotic usage, competition between clones also has an important role in driving the evolution of nosocomial pathogen populations.
Electronic supplementary material
The online version of this article (doi:10.1186/s13059-015-0643-z) contains supplementary material, which is available to authorized users. 相似文献
The ubiquitin E3 ligase CUL4A plays important roles in diverse cellular processes including carcinogenesis and proliferation. It has been reported that the expression of CUL4A can be induced by hypoxic-ischemic injury. However, the effect of elevated expression of CUL4A on hypoxia-reoxygenation injury is currently unclear. In this study, human CUL4A (hCUL4A) was expressed in rat pheochromocytoma (PC12) cells using adenoviral vector-mediated gene transfer, and the effects of hCUL4A expression on hypoxia-reoxygenation injury were investigated. In PC12 cells subjected to hypoxia and reoxygenation, we found that hCUL4A suppresses apoptosis and DNA damage by regulating apoptosis-related proteins and cell cycle regulators (Bcl-2, caspase-3, p53 and p27); consequently, hCUL4A promotes cell survival. Taken together, our results reveal the beneficial effects of hCUL4A in PC12 cells upon hypoxia-reoxygenation injury. 相似文献