1.7 µm figure-9 Tm-doped ultrafast fiber laser.

The evolution of multiphoton microscopy is critically dependent on the development of ultrafast laser technologies. The ultrashort pulse laser source at 1.7 µm waveband is attractive for in-depth three-photon imaging owing to the reduced scattering and absorption effects in biological tissues. Herein, we report on a 1.7 µm passively mode-locked figure-9 Tm-doped fiber laser. The nonreciprocal phase shifter that consists of two quarter-wave plates and a Faraday rotator introduces phase bias between the counter-propagating beams in the nonlinear amplifying loop mirror. The cavity dispersion is compensated to be slightly positive, enabling the proposed 1.7 µm ultrafast fiber laser to deliver the dissipative soliton with a 3-dB bandwidth of 20 nm. Moreover, the mode-locked spectral bandwidth could be flexibly tuned with different phase biases by rotating the wave plates. The demonstration of figure-9 Tm-doped ultrafast fiber laser would pave the way to develop the robust 1.7 µm ultrashort pulse laser sources, which could find important application for three-photon deep-tissue imaging.

Pulsating dynamics in a pure-quartic soliton fiber laser.

We numerically investigate the pulsating dynamics of pure-quartic solitons (PQSs) in a passively mode-locked fiber laser. The bifurcation diagrams show that the PQS can alternate between the stable single soliton and pulsating regimes multiple times before transiting into the chaotic state. This multi-alternation behavior can be attributed to energy redistribution across the central part and the oscillating tails of the PQS, which is caused by an imperfect counterbalance between self-phase modulation (SPM)-induced and fourth-order dispersion (FOD)-induced phase shifts. Soliton creeping behavior can be observed during the pulsating process, accompanied by periodic asymmetric temporal profiles and central wavelength shifts of the PQS. These findings give new insights into the dynamics of PQSs in fiber lasers.

1.7 µm Tm-fiber chirped pulse amplification system with dissipative soliton seed laser.

We report on a 1.7 µm Tm-fiber chirped pulse amplification (CPA) system by virtue of a broadband dissipative soliton seed laser. The seed oscillator delivers the dissipative soliton with 10 dB spectral bandwidth of 23 nm and an average power of 4 mW. The duration of the seed pulse is directly stretched to ∼60ps by a segment of 50 m normal dispersion fiber. Using a two-stage fiber amplifier, the average power of the pulse is amplified to 1.95 W with a slope efficiency of 40.3%. The amplified pulse is then compressed to 348 fs by a pair of fused silica transmission gratings. The compressed average power of 1.3 W and peak power of 155 kW are achieved. These experimental results would pave the way to achieve a high-power femtosecond laser source at 1.7 µm, which could find important applications in fields such as three-photon deep-tissue imaging and material processing.

Mutually induced soliton polarization instability in a bidirectional ultrafast fiber laser.

The bidirectional ultrafast fiber laser is a promising light source for dual-comb applications. The counter-propagating geometry could lead to soliton interaction through gain sharing, as well as the possible outcome of polarization instability. However, the polarization dynamics hidden behind the soliton interaction process in bidirectional fiber lasers were rarely investigated. Herein, we report on the polarization instability induced by the mutual soliton interactions through fiber gain in a bidirectional mode-locked fiber laser. Depending on the adjustment of the intracavity birefringence, the polarization states of two counter-propagating solitons can exhibit similar periodical polarization switching behaviors with a polarization-rotating transition state. The successive interactions of the bidirectional solitons mediated by the polarization cross-saturation effect of gain fiber could be responsible for the soliton polarization instability. These findings, in addition to the fundamental interest of the soliton nonlinear dynamics in dissipative optical systems, also open up new possibilities for creating dynamical control of the soliton polarization state and performance improvement in bidirectional ultrafast fiber lasers.

Molecular mechanisms of heavy metals resistance of Stenotrophomonas rhizophila JC1 by whole genome sequencing.

In this study, a higher metal ions-resistant bacterium, Stenotrophomonas rhizophila JC1 was isolated from contaminated soil in Jinchang city, Gansu Province, China. The Pb2+ (120 mg/L) and Cu2+ (80 mg/L) removal rate of the strain reached at 76.9% and 83.4%, respectively. The genome comprises 4268161 bp in a circular chromosome with 67.52% G + C content and encodes 3719 proteins. The genome function analysis showed czc operon, mer operon, cop operon, arsenic detoxification system in strain JC1 were contributed to the removal of heavy metals. Three efflux systems (i.e., RND, CDF, and P-ATPase) on strain JC1 genome could trigger the removal of divalent cations from cells. cAMP pathway and ABC transporter pathway might be involved in the transport and metabolism of heavy metals. The homology analysis exhibited multi-gene families such as ABC transporters, heavy metal-associated domain, copper resistance protein, carbohydrate-binding domain were distributed across 410 orthologous groups. In addition, heavy metal-responsive transcription regulator, thioredoxin, heavy metal transport/detoxification protein, divalent-cation resistance protein CutA, arsenate reductase also played important roles in the heavy metals adsorption and detoxification process. The complete genome data provides insight into the exploration of the interaction mechanism between microorganisms and heavy metals.

Tre2 (USP6NL) promotes colorectal cancer cell proliferation via Wnt/ß-catenin pathway.

BACKGROUND: Most colorectal cancer (CRC) patients are diagnosed at an advanced or metastatic stage with poor prognosis. Ubiquitin-specific protease 6 N-terminal-like protein (USP6NL) with high expression in CRC tissues regulates CRC cell proliferation via Wnt/ß-catenin pathway. We hypothesized that USP6NL impacts CRC growth and inhibition of USP6NL may be a novel treatment strategy to improve CRC therapy. METHODS: USP6NL level in human CRC tissues and its association with tumor growth and metastasis were examined. Its roles and potential mechanisms in regulating tumor growth were studied by genetic and pharmacological manipulation of CRC cells in vitro and in vivo. RESULTS: Herein, we found that USP6NL was up-regulated in tumorous tissues of CRC patients. Our data suggested that knockdown of USP6NL in human CRC cell lines (HCT116 and LOVO cells) inhibited cell proliferation, induced G0/G1 cell cycle arrest, and prevented the tumorigenicity of HCT116 cells in nude mice, and which was associated with the prevention of Wnt/ß-catenin pathway. On the contrary, USP6NL overexpression in human CRC cells (SW480) showed the opposite result. Our data suggested that the promoted cell proliferation, G1/S cell cycle progression, and the enhanced expression of ß-catenin Cyclin D1 and C-myc while reduced P27 induced by the overexpression of USP6NL were significantly reversed by additional treatment of XAV939, indicating that activating Wnt/ß-catenin pathway was the mechanism, by which USP6NL exerted carcinogenesis in CRC in vitro. Besides, our data suggested that knockdown of USP6NL increased the ubiquitination of ß-catenin, indicating that USP6NL may serve as a deubiquitinase that regulated ß-catenin accumulation in this process. Furthermore, 10058-F4 down-regulated USP6NL, inhibited CRC cell proliferation and induced cell cycle arrest. The result demonstrated a possible feedback loop between USP6NL, ß-catenin and C-myc in regulating CRC cell growth. CONCLUSION: USP6NL was an oncogene in CRC, and it may be a potential target for the treatment of CRC.

Prognostic value of neutrophil to lymphocyte ratio in acute ischemic stroke after reperfusion therapy.

The purpose of this study was to investigate whether baseline neutrophil to lymphocyte ratio (NLR) was an independent predictor for early symptomatic intracranial hemorrhage (sICH), poor functional outcome and mortality at 3 months after reperfusion therapy in acute ischemic stroke (AIS) patients. Using PubMed and EMBASE, we searched for literature published before January 19th, 2019. Two reviewers independently confirmed each study's eligibility, assessed risk of bias, and extracted data. One reviewer combined studies using random effects meta-analysis. 9 studies with 3651 patients were pooled in the meta-analysis. Overall, baseline NLR levels were greater in patients with poor outcome. The standardized mean difference (SMD) in the NLR levels between patients with poor functional outcome (mRS > 2) and good functional outcome (mRS ≤ 2) was 0.54 units (95% credible interval [CI] [0.38, 0.70]). Heterogeneity test showed that there were significant differences between individual studies (p = 0.02; I2 = 72.8%). The NLR levels were associated with sICH in four included studies (n = 2003, SMD = 0.78, 95% [CI] [0.18, 1.38], I2 = 73.9%). Higher NLR levels were positively correlated with 3-month mortality (n = 1389, ES = 1.71, 95% CI [1.01,2.42], p < 0.01, I2 = 0%) when data were used as categorical variables. Our meta-analysis suggests that increased NLR levels are positively associated with greater risk of sICH, 3-month poor functional outcome and 3-month mortality in AIS patients undergoing reperfusion treatments. Although there are some deficits in this study, it may be feasible to predict the prognosis of reperfusion therapy in AIS patients with NLR levels.

Targeting NLRP3 inflammasome improved the neurogenesis and post-stroke cognition in a mouse model of photothrombotic stroke.

Post-stroke cognitive impairment (PSCI) severely affects the quality of a survivor's life, but its neurophysiological basis remains unknown. Neuroinflammation has been considered as an important contributor to PSCI, which could be induced or exacerbated by system inflammation. NACHT-LRR- and pyrin-domain-containing protein 3 (NLRP3) inflammasome is the most widely studied in the initiation of inflammation. Here, using a mouse model of photothrombotic stroke, we demonstrated that NLRP3 activation plays a critical role in PSCI. Intraperitoneal injection of the lipopolysaccharide-activated NLRP3 inflammasome, exacerbated the microglial activation and decreased the number of neurons, impaired the hippocampal neurogenesis, eventually aggravated PSCI. Intraperitoneal injection of MCC950 inhibited the NLRP3 activation, decreased the number of microglia, increased the number of neurons and promoted the hippocampal neurogenesis, eventually improved PSCI. Our results identified NLRP3 inflammasome as an important modifier of neuropathology in PSCI, which could be a could be a potential therapeutic target for PSCI treatment.

Genetic variants on chromosome 9p21 confer risks of cerebral infarction in the Chinese population: a meta-analysis.

Ischemic stroke (IS) is the leading cause of disability. Researchers have demonstrated that IS is more a multifactorial disorder than a single-factor disease. At present, no consistent conclusions have been reached on susceptibility loci for IS on chromosome 9p21. We conducted this meta-analysis to verify whether genetic loci on chromosome 9p21 reported domestically and abroad could be responsible for IS in Chinese populations. We analyzed data from eight studies that covered a total of 9756 individuals with Chinese ancestry comprising 4254 cases and 5502 controls. Each of the four reported susceptibility loci (rs2383206, rs2383207, rs10757274, and rs10757278) was analyzed separately. The odds ratios (ORs) of rs2383206 and rs10757274 were 1.09 (95% confidence interval (CI): 1.02-1.06, P = 0.01) and 1.09 (95% CI: 1.01-1.17, P = 0.03), respectively. For rs2383207, OR value was 0.91 (95% CI: 0.84-0.98, P = 0.01). No statistical association was identified for rs10757278. We have verified previous associations for IS in Chinese populations on chromosome 9p21. Loci rs2383206 and rs10757274 may increase susceptibility to IS. Mutation at locus rs2383207 may be beneficial. However, we are unable to identify any association between rs10757278 and IS.

G-protein-signaling modulator 2 expression and role in a CD133+ pancreatic cancer stem cell subset.

BACKGROUND: To investigate the expression and role of G-protein-signaling modulator 2 (GPSM2) in a CD133+ pancreatic stem cell subset. MATERIALS AND METHODS: Pancreatic cancer stem cells (PCSCs) from the cell line PANC-1 were sorted into CD133+ and CD133- subsets by flow cytometry. The tumorigenic potential of the subsets was assessed by subcutaneous tumor formation experiments in nude mice. Differential expression of GPSM2 was examined by real-time quantitative-PCR (qPCR) and Western blotting. To silence GPSM2 expression, a shRNA lentiviral vector targeting GPSM2 was constructed and stably transfected into CD133+ PCSCs. The inhibitory efficiency of the GPSM2 gene was verified by qPCR and Western blotting. The proliferation, colony formation, and migration abilities of the transfected CD133+ pancreatic cancer cells were assessed by MTT, soft agar colony formation, and Transwell assays. RESULTS: CD133+ and CD133- cell subsets were successfully isolated from PANC-1 cells. The CD133+ subset subcutaneously formed tumors in nude mice that were significantly bigger (343.05±57.59 mm3 vs 176.86±32.58 mm3, P<0.01) and denser (4.13±0.37 g vs 1.07±0.21 g, P<0.01) than those of the CD133- group. The GPSM2 mRNA and protein expression was significantly higher in CD133+ cells than in CD133- cells. Stable downregulation of GPSM2 expression reduced the proliferation, colony formation, and migration abilities of CD133+ PANC-1 cells (P<0.05). CONCLUSION: The CD133+PANC-1 cells have obvious stem cell characteristics and increased GPSM2 expression. Downregulation of GPSM2 significantly reduces the proliferation and migration ability of the cells. Therefore, GPSM2 may provide an important target for regulating PCSCs.

[Effect of Carfilzomib on Proliferation and Apoptosis of Mantle Cell Lymphoma Cells].

OBJECTIVE: To investigate the effect of Carfilzomib on mantle cell lymphoma (MCL), and to compare with effect of Bortezomib. METHODS: The Jeko-1 cells and primary MCL cells were treated with Carfilzomib for 24, 48 and 72 h, then the inhibitory rate was detected using CCK-8. Lymphocytes derived from healthy volunteer were served as cell controls. Bortezomib and Cyclophosphamide (CTX) were served as medicinal controls. At the same time, the apoptosis of cells treated with different drugs was detected using flow cytometry. RESULTS: The inhibitory effect of Carfilzomib on Jeko-1 cells and primary MCL cells was exhibited with time-dependent and concentration-dependent manners (P＜0.01, rJ=0.393, r=0.650, rJJ=0.473, r=0.417), but the effect on lymphocytes derived from healthy volunteer only showed time-dependence (P＜0.01, r=0.928). Under the same concentration, Carfilzomib exhibited the proliferation Jeko-1 cells stronger than Bortezomib (P＜0.01), but the same inhibition on primary MCL cells was not significantly different from that on lymphocytes derived from healthy volunteer (P＞0.05). Under clinical recommended concentration, Carfilzomib had a stronger inhibitory effect on primary MCL cells than that of Bortezomib (P＜0.01). Cell apoptosis assay showed that under the same concentration the ability of Carfilzomib to induce cell apoptosis was significantly stronger than that of Bortezomib (P＜0.05). CONCLUSION: Carfilzomib can inhibit the growth of MCL cells, its inhibitory rate on the MCL cells is higher than that of Bortezomib.

Clinical and pathological analysis of solitary fibrous tumors with portal vein widening: A case report.

RATIONALE: Solitary fibrous tumors (SFTs) are rare soft-tissue tumors characterized with spindle-cell, which occur more common in the chest and rarely seen in the abdomen. So far as we knew, SFTs accompanied with venopathy of portal vein has rarely been reported. PATIENT CONCERNS: A 36-year-old male presented with left-sided abdominal mass and portal vein expansion on ultrasound. DIAGNOSES: The post-operative histopathology confirmed the diagnosis of Solitary fibrous tumor. INTERVENTIONS: Laparotomy was performed and the mass was completely removed. OUTCOMES: Patients had no symptoms, recovered well without recurrence; the portal vein and splenic vein dilatation were alleviated and the symptoms of portal hypertension were relieved. LESSONS: SFTs presents with few symptoms in the early stage of the disease. A rich arteriovenous shunt is beneficial to the diagnosis of SFTs by B-ultrasound and computed tomography (CT) examinations. However, the diagnosis of SFTs must depend on histopathology.

PLK1 as a potential prognostic marker of gastric cancer through MEK-ERK pathway on PDTX models.

BACKGROUND: PLK1 has been identified as having a great effect on cell division and maintaining genomic stability in mitosis, spindle assembly, and DNA damage response by current studies. MATERIALS AND METHODS: We assessed PLK1 expression in cervical cancer tissues and cells. We have also evaluated the effects of PLK1 on gastric cancer cell proliferation, migration, and apoptosis both in vitro and in vivo. RESULTS: Our results show that PLK1 is overexpressed in gastric cancer tissues and cells. Inhibition of PLK1 contributes cell cycle G2-phase arrest and inhibits the proliferation, migration, and apoptosis of gastric cancer (GC) cells, whereas its overexpression promotes proliferation, migration, and apoptosis in these cells. Moreover, PLK1 inhibition reduces expression of pMEK and pERK. More importantly, in vivo by analyzing tumorigenesis in patient-derived tumor xenograft (PDTX) models, the inhibition of PLK1 activity by BI6727 significantly decreased the volume and weight of the tumors compared with control group (P<0.01). CONCLUSION: Our results found that PLK1 has a significant impact on the survival of GC cells; it may become a prognostic judge, a potential therapeutic target, and a preventative biomarker of GC.

Isolation of Photobacterium damselae subsp. piscicida from diseased tongue sole (Cynoglossus semilaevis Gunther) in China.

During the summer of 2006, an epizootic occurred among cultured tongue sole (Cynoglossus semilaevis Gunther) in a fish farm in Qingdao, China. The diseased tongue sole exhibited haemorrhaging of the basal fin, yellowed kidney and ulceration of the body surface. A Gram-negative,rod shaped bacterium (designated strain WY06) was isolated from the gall bladder of diseased fish. Pathogenicity assays revealed that WY06 was virulent to tongue sole and zebrafish (Danio rerio) by intraperitoneal injection challenge, with the LD50 being calculated as 5.5 x 10(3) cfu/g of fish (5.2 x 10(5) cfu/fish) and 1.9 x 10(3) cfu/g of fish (8.9 x 10(2) cfu/fish) respectively. The 16S rRNA gene sequence of strain WY06 demonstrated high similarity (99%) with Photobacterium damselae subsp. piscicida. Phylogenetic analysis showed a clear association of strain WY06 with P. damselae subsp. piscicida. Additional evidence of the identification included in morphological, physiological and biochemical data. The pathogen was sensitive to cifuroxime (30 microg) and ceftriaxone sodium (30 microg). Present study describes P. damselae subsp. piscicida from diseased fish for the first time in China.

Genes encoding the Vibrio harveyi haemolysin (VHH)/thermolabile haemolysin (TLH) are widespread in vibrios.

V. harveyi VHH haemolysin, which shows high homology to the TLH haemolysin (the identities of their deduced amino acid sequences are up to 85.6%), is a putative virulence factor to marine cultured fish. A VHH probe, which is specific to V. harveyi vhhA haemolysin gene, was used to screen EcoR I digests of total DNA from 57 vibrio strains, including 26 vibrio type strains, 20 V. harveyi isolates and 11 V. parahaemolyticus isolates. As a result, 1 strong hybridisation band was detected in 13 type strains, including 2 of Vibrio alginolyticus, 2 of V. harveyi, and 1 strain each of Grimontia hollisae, V. campbellii, V. cincinnatiensis, V. fischeri, V. mimicus, V. natriegens, V. parahaemolyticus, V. proteolyticus and V. logei. Also, 1 weak band was detected in 6 type strains, including V. anguillarum, V. aestuarianus, Photobacterium damselae subsp. damselae, V. fluvialis, V. furnissii and V. vulnificus. There was not any hybridization signal in other type strains. Also, vhh/tlh was present in all isolates of V. harveyi and V. parahaemolyticus. Moreover, 3 isolates of V. harveyi, i.e. VIB 645, VIB 648 and SF1, had duplicated vhh genes. The data indicates that vhh/tlh is widespread in vibrios, especially in V. harveyi related species and V. fischeri related species. To support this conclusion, the vhh/tlh homologue genes in V. anguillarum VIB 72, V. campbellii VIB 285, V. natriegens VIB 299 and V. harveyi VIB 647 were cloned and sequenced, and the deduced amino acid sequences showed high degree of identities to VHH (67% - 99%) and TLH haemolysin (69% - 91%). This study will help us to identify the role of vhh/tlh haemolysin gene in the pathogenicity of vibrios.

Giant mucinous adenocarcinoma of the appendix: a case report.

BACKGROUND: Appendiceal mucinous adenocarcinoma is an extremely rare disease in clinical practice. Here, we report a case of unprecedented size that occupied the entire abdomen of a man. CASE PRESENTATION: A 49-year-old Chinese Han man presented with symptoms of abdominal distension. During a computed tomography imaging examination, a cystic-solid mass that occupied his entire abdominal cavity was detected. During exploratory laparotomy, an appendiceal tumor in his abdominal-pelvic cavity measuring 27.6 × 14.2 cm was found, and he underwent tumor resection. The pathology of the tumor identified a well-differentiated appendiceal mucinous adenocarcinoma with mucin infiltrating into the soft tissue of the lump edge and omentum tissue. After surgery, our patient accepted intraperitoneal infusion chemotherapy. At present, he has had no recurrence for 15 months. CONCLUSIONS: To the best of our knowledge, the present case is the largest appendiceal mucinous adenocarcinoma reported. Surgical tumor resection is the preferred treatment for appendiceal mucinous adenocarcinoma. This is supplemented by chemotherapy which can further prolong survival.

IRF5 regulates lung macrophages M2 polarization during severe acute pancreatitis in vitro.

AIM: To investigate the role of interferon regulatory factor 5 (IRF5) in reversing polarization of lung macrophages during severe acute pancreatitis (SAP) in vitro. METHODS: A mouse SAP model was established by intraperitoneal (ip) injections of 20 µg/kg body weight caerulein. Pathological changes in the lung were observed by hematoxylin and eosin staining. Lung macrophages were isolated from bronchoalveolar lavage fluid. The quantity and purity of lung macrophages were detected by fluorescence-activated cell sorting and evaluated by real-time polymerase chain reaction (RT-PCR). They were treated with IL-4/IRF5 specific siRNA (IRF5 siRNA) to reverse their polarization and were evaluated by detecting markers expression of M1/M2 using RT-PCR. RESULTS: SAP associated acute lung injury (ALI) was induced successfully by ip injections of caerulein, which was confirmed by histopathology. Lung macrophages expressed high levels of IRF5 as M1 phenotype during the early acute pancreatitis stages. Reduction of IRF5 expression by IRF5 siRNA reversed the action of macrophages from M1 to M2 phenotype in vitro. The expressions of M1 markers, including IRF5 (S + IRF5 siRNA vs S + PBS, 0.013 ± 0.01 vs 0.054 ± 0.047, P < 0.01), TNF-α (S + IRF5 siRNA vs S + PBS, 0.0003 ± 0.0002 vs 0.019 ± 0.018, P < 0.001), iNOS (S + IRF5 siRNA vs S + PBS, 0.0003 ± 0.0002 vs 0.026 ± 0.018, P < 0.001) and IL-12 (S + IRF5 siRNA vs S + PBS, 0.000005 ± 0.00004 vs 0.024 ± 0.016, P < 0.001), were decreased. In contrast, the expressions of M2 markers, including IL-10 (S + IRF5 siRNA vs S + PBS, 0.060 ± 0.055 vs 0.0230 ± 0.018, P < 0.01) and Arg-1 (S + IRF5 siRNA vs S + PBS, 0.910 ± 0.788 vs 0.0036 ± 0.0025, P < 0.001), were increased. IRF5 siRNA could reverse the lung macrophage polarization more effectively than IL-4. CONCLUSION: Treatment with IRF5 siRNA can reverse the pancreatitis-induced activation of lung macrophages from M1 phenotype to M2 phenotype in SAP associated with ALI.

Characterization of rhizosphere and endophytic bacterial communities from leaves, stems and roots of medicinal Stellera chamaejasme L.

A diverse array of bacteria that inhabit the rhizosphere and different plant organs play a crucial role in plant health and growth. Therefore, a general understanding of these bacterial communities and their diversity is necessary. Using the 16S rRNA gene clone library technique, the bacterial community structure and diversity of the rhizosphere and endophytic bacteria in Stellera chamaejasme compartments were compared and clarified for the first time. Grouping of the sequences obtained showed that members of the Proteobacteria (43.2%), Firmicutes (36.5%) and Actinobacteria (14.1%) were dominant in both samples. Other groups that were consistently found, albeit at lower abundance, were Bacteroidetes (2.1%), Chloroflexi (1.9%), and Cyanobacteria (1.7%). The habitats (rhizosphere vs endophytes) and organs (leaf, stem and root) structured the community, since the Wilcoxon signed rank test indicated that more varied bacteria inhabited the rhizosphere compared to the organs of the plant. In addition, correspondence analysis also showed that differences were apparent in the bacterial communities associated with these distinct habitats. Moreover, principal component analysis revealed that the profiles obtained from the rhizosphere and roots were similar, whereas leaf and stem samples clustered together on the opposite side of the plot from the rhizosphere and roots. Taken together, these results suggested that, although the communities associated with the rhizosphere and organs shared some bacterial species, the associated communities differed in structure and diversity.

Protective effects of edaravone against cobalt chloride-induced apoptosis in PC12 cells.

OBJECTIVE: To investigate the neuroprotective effects of edaravone (Eda) on cobalt chloride (CoCl2)-induced oxidative stress and apoptosis in cultured PC12 cells as well as the underlying mechanisms. METHODS: PC12 cells impaired by CoCl2 were used as the cell model of hypoxia. MTT (methyl thiazolyl tetrazolium) was used to assay the viability of the PC12 cells exposed to Eda with gradient concentrations; Hochest 33258 stain assay was used to analyze the apoptosis ratio of the PC12 cells; Bcl-2 and Bax protein levels in PC12 cells were examined by western blotting. ROS level, the mitochondrial transmembrane potential and caspase-3 activity in each group were detected by spectrofluorometer. RESULTS: CoCl2 treatment caused the loss of cell viability in PC12 cells, which was associated with the elevation of apoptotic rate, the formation of ROS and the disruption of mitochondrial transmembrane potential. CoCl2 also significantly induced the upregulation of Bax/Bcl-2 ratio and the activation of caspase-3. In contrast, Eda significantly reversed these phenotypes, with its maximum protective effect at 0.1 micromol/L. CONCLUSION: These results indicated that Eda could protect PC12 cells from CoCl2-induced cytotoxicity, and this protection might be ascribed to its anti-oxidative and anti-apoptotic activities.

Gilvimarinus chinensis gen. nov., sp. nov., an agar-digesting marine bacterium within the class Gammaproteobacteria isolated from coastal seawater in Qingdao, China.

A taxonomic study was performed on strain QM42(T), which was isolated from coastal seawater from an aquaculture site near Qingdao, China. Phylogenetic analysis based on 16S rRNA gene sequences showed that strain QM42(T) was a member of the class Gammaproteobacteria. Cells of strain QM42(T) were Gram-negative, yellow, aerobic and rod-shaped. The strain formed a distinct phyletic line with less than 91 % 16S rRNA gene sequence similarity to its closest relatives with validly published names within the class Gammaproteobacteria. The genomic DNA G+C content was 51.9 mol%. The major fatty acids were C(16 : 1)omega7c/iso-C(15 : 0) 2-OH, C(18 : 1)omega7c and C(16 : 0). Based on data from a polyphasic chemotaxonomic, physiological and biochemical study, strain QM42(T) is considered to represent a novel genus and species, for which the name Gilvimarinus chinensis gen. nov., sp. nov., is proposed. The type strain is QM42(T) (=CGMCC 1.7008(T)=DSM 19667(T)).