scholarly journals A zero-flow microfluidics for long-term cell culture and detection

AIP Advances ◽  
2015 ◽  
Vol 5 (4) ◽  
pp. 041310 ◽  
Author(s):  
Shengbo Sang ◽  
Xiaoliang Tang ◽  
Qiliang Feng ◽  
Aoqun Jian ◽  
Wendong Zhang
Keyword(s):  
2008 ◽  
Vol 101 (1) ◽  
pp. 190-195 ◽  
Author(s):  
Chunxiong Luo ◽  
Xuejun Zhu ◽  
Tao Yu ◽  
Xianjia Luo ◽  
Qi Ouyang ◽  
...  

2011 ◽  
Vol 14 (1) ◽  
pp. 145-152 ◽  
Author(s):  
Hasan E. Abaci ◽  
Raghavendra Devendra ◽  
Quinton Smith ◽  
Sharon Gerecht ◽  
German Drazer

1977 ◽  
Vol 5 (3-4) ◽  
pp. 153-157 ◽  
Author(s):  
Ellen Rieske ◽  
Georg W. Kreutzberg

2015 ◽  
Vol 3 (2) ◽  
pp. 383-390 ◽  
Author(s):  
Yon Jin Chuah ◽  
Shreyas Kuddannaya ◽  
Min Hui Adeline Lee ◽  
Yilei Zhang ◽  
Yuejun Kang

Surface silanization with 3-aminopropyl triethoxy silane (APTES) ± glutaraldehyde (GA) enhanced the biocompatibility of poly(dimethylsiloxane) surfaces for long term cell culture investigation.


2012 ◽  
Vol 78 (8) ◽  
pp. 3010-3013 ◽  
Author(s):  
Kim Heylen ◽  
Katharina Ettwig ◽  
Ziye Hu ◽  
Mike Jetten ◽  
Boran Kartal

ABSTRACTA quick and simple protocol for long-term cryopreservation of anaerobic ammonium-oxidizing bacteria (anammox bacteria) was developed. After 29 weeks of preservation at −80°C, activity recovery for all tested cultures under at least one of the applied sets of preservation conditions was observed. Growth recovery was also demonstrated for a single-cell culture of “CandidatusKuenenia stuttgartiensis.”


2018 ◽  
Vol 92 (17) ◽  
Author(s):  
Janis A. Müller ◽  
Anna Glöckle ◽  
Ali Gawanbacht ◽  
Matthias Geyer ◽  
Jan Münch ◽  
...  

ABSTRACTVIRIP has been identified as natural HIV-1 inhibitor targeting the gp41 fusion peptide. An optimized analogue (VIR-576) was effective in a phase I/II clinical trial and initial studies showed that HIV-1 resistance to VIRIP-based inhibitors has a high genetic barrier. Partially resistant CXCR4 (X4)-tropic HIV-1 NL4-3 variants could be obtained, however, after more than 15 months of passaging in MT-4 cells in the presence of another derivative (VIR-353). Sequence analyses identified the accumulation of seven mutations across the HIV-1 envelope glycoprotein but outside the gp41 fusion peptide. The authors suggested that the three initial alterations conferred resistance, while subsequent changes restored viral fitness. Here, we introduced these mutations individually and in combination into X4- and CCR5 (R5)-tropic HIV-1 constructs and determined their impact on VIR-353 and VIR-576 susceptibility, viral infectivity, replication fitness, and fusogenicity. We found that essentially all seven mutations contribute to reduced susceptibility to VIRIP-based inhibitors. HIV-1 constructs containing ≥4 changes were substantially more resistant to both VIRIP-based inhibitors and the VRC34.01 antibody targeting the fusion peptide. However, they were also much less infectious and fusogenic than those harboring only the three initial alterations. Furthermore, the additional changes attenuated rather than rescued HIV-1 replication in primary human cells. Thus, the genetic barrier to HIV-1 resistance against VIRIP-based inhibitors is higher than previously suggested, and mutations reducing viral susceptibility come at a severe fitness cost that was not rescued during long-term cell culture passage.IMPORTANCEMany viral pathogens are critically dependent on fusion peptides (FPs) that are inserted into the cellular membrane for infection. Initially, it was thought that FPs cannot be targeted for therapy because they are hardly accessible. However, an optimized derivative (VIR-576) of an endogenous fragment of α1-antitrypsin, named VIRIP, targeting the gp41 FP reduced viral loads in HIV-1-infected individuals. Characterization of HIV-1 variants selected during long-term cell-culture passage in the presence of a VIRIP derivative suggested that just three mutations in the HIV-1 Env protein might be sufficient for VIRIP resistance and that four subsequent changes restored viral fitness. Here, we show that all seven mutations contribute to reduced viral susceptibility to VIRIP-based inhibitors and demonstrate that the additional changes strongly impair rather than rescue HIV-1 infectivity, fusogenicity, and replication fitness. High genetic barrier to resistance and severe fitness cost support further clinical development of this class of antiviral agents.


2019 ◽  
Vol 165 (2) ◽  
pp. 331-343 ◽  
Author(s):  
Nobuyuki Kato ◽  
Youki Ueda ◽  
Hiroe Sejima ◽  
Weilin Gu ◽  
Shinya Satoh ◽  
...  

Talanta ◽  
2021 ◽  
Vol 223 ◽  
pp. 121738
Author(s):  
Meng-Meng Liu ◽  
Hui Liu ◽  
Shan-Hong Li ◽  
Yu Zhong ◽  
Yao Chen ◽  
...  

1996 ◽  
Vol 76 (4) ◽  
pp. 2635-2643 ◽  
Author(s):  
J. C. Poyer ◽  
M. J. Zoran

1. The role of activity-dependent mechanisms in target-mediated induction of secretory properties was investigated at regenerating neuromuscular synapses of the American pond snail, Helisoma trivolvis, in cell culture. 2. Identified motoneurons were isolated into cell culture conditions that promoted neurite outgrowth. Buccal neurons 19 (B19) were cultured alone for 2 days, at which time dissociated muscle fibers were manipulated into contact with newly formed neurites. 3. Immediately before the plating of muscle fibers, the sodium channel blocker, tetrodotoxin (TTX), or the acetylcholine receptor antagonist, d-tubocurarine chloride (curare), was added to the culture dish. After 48 h of exposure, the inhibitors were removed by repeated dilution of the culture medium and electrophysiological analyses were performed. 4. Cholinoceptive assay cells were manipulated into contact with the presynaptic neurons to assess secretory properties along neuronal processes. Assay cells were used to control for variations in postsynaptic sensitivity that could result from long-term exposure to activity inhibitors. 5. These analyses demonstrated that inhibition of TTX-sensitive presynaptic activity and inhibition of curare-sensitive postsynaptic activation both blocked the induction of excitation-secretion coupling typically induced in these motoneurons by appropriate target contact. Neuron B5, which rapidly acquires functional synaptic properties in vitro, was unaffected in its secretory function by 48 h of activity inhibition. 6. Acquisition of secretory competence was not suppressed due to a reduction in the viability or long-term changes in excitability of the activity-inhibited neurons, as indicated by analyses of electrophysiological properties. 7. Although target-contact and activity both participated in the induction of secretory modifications in neuron B19, target-mediated changes did not involve retrograde effects on presynaptic neuronal excitability. 8. We hypothesize that contact-mediated mechanisms govern the initiation of presynaptic modifications in B19, however, our data indicate that the acquisition of functional excitation-secretion coupling also involves activity-dependent mechanisms. Although the mechanistic role of activity remains undefined, our results suggest that the activation of the target muscle plays a critical role in a retrograde signaling pathway underlying maturation of a functional secretory apparatus in target-contacted neuronal processes.


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