Visiting Scholar Recital: Peixi Wang, soprano

Kennesaw State University School of Music presents a visiting scholar recital featuring Peixi Wang, soprano.https://digitalcommons.kennesaw.edu/musicprograms/1393/thumbnail.jp

Melt Electrowriting of Scaffolds with a Porosity Gradient to Mimic the Matrix Structure of the Human Trabecular Meshwork

The permeability of the Human Trabecular Meshwork (HTM) regulates eye pressure via a porosity gradient across its thickness modulated by stacked layers of matrix fibrils and cells. Changes in HTM porosity are associated with increases in intraocular pressure and the progress of diseases like glaucoma. Engineered HTMs could help to understand the structure-function relation in natural tissues, and lead to new regenerative solutions. Here, melt electrowriting (MEW) is explored as a biofabrication technique to produce fibrillar, porous scaffolds that mimic the multilayer, gradient structure of native HTM. Poly(caprolactone) constructs with a height of 125-500 μm and fiber diameters of 10-12 μm are printed. Scaffolds with a tensile modulus between 5.6 and 13 MPa, and a static compression modulus in the range of 6-360 kPa are obtained by varying the scaffolds design, i.e., density and orientation of the fibers and number of stacked layers. Primary HTM cells attach to the scaffolds, proliferate, and form a confluent layer within 8-14 days, depending on the scaffold design. High cell viability and cell morphology close to that in the native tissue are observed. The present work demonstrates the utility of MEW to reconstruct complex morphological features of natural tissues

Melt Electrowriting of Graded Porous Scaffolds to Mimic the Matrix Structure of the Human Trabecular Meshwork

The permeability of the human trabecular meshwork (HTM) regulates eye pressure via a porosity gradient across its thickness modulated by stacked layers of matrix fibrils and cells. Changes in HTM porosity are associated with increases in intraocular pressure and the progress of diseases such as glaucoma. Engineered HTMs could help to understand the structure-function relation in natural tissues and lead to new regenerative solutions. Here, melt electrowriting (MEW) is explored as a biofabrication technique to produce fibrillar, porous scaffolds that mimic the multilayer, gradient structure of native HTM. Poly(caprolactone) constructs with a height of 125-500 μm and fiber diameters of 10-12 μm are printed. Scaffolds with a tensile modulus between 5.6 and 13 MPa and a static compression modulus in the range of 6-360 kPa are obtained by varying the scaffold design, that is, the density and orientation of the fibers and number of stacked layers. Primary HTM cells attach to the scaffolds, proliferate, and form a confluent layer within 8-14 days, depending on the scaffold design. High cell viability and cell morphology close to that in the native tissue are observed. The present work demonstrates the utility of MEW for reconstructing complex morphological features of natural tissues

A Two-Step Strategy for Fabrication of Biocompatible 3D Magnetically Responsive Photonic Crystals

Extremely stable and biocompatible 3D magnetically responsive photonic crystals (MRPCs) are successfully prepared in aqueous solution. Classic hydrothermal synthesis was applied for preparation of the Fe3O4@C core. Modified Stöber method was then employed for synthesis of the different size of Fe3O4@C@SiO2. Unlike the traditional magnetic nanoparticles, the highly negative charged superparamagnetic nanospheres (SMNs), i.e., the double-shell structure Fe3O4@C@SiO2 are capable of rapidly self-assembling into 3D MRPCs with full visible and various colors that can be periodically and reversibly tuned under different kinds of external magnetic fields (EMFs) within 1 s. The assembling behavior and mechanism of the 3D MRPCs under EMF were monitored and analyzed. The preparation is simple and the size of the SMN is easily controllable by adjusting the amount of catalyst. Compared with the previous works, the synthesized 3D MRPCs are hydrophilic, and exhibit extremely high stability after 6-month storage. To conclude, our study provides an effective two-step strategy for fabrication of biocompatible 3D MRPCs and it reveals great potentials in biological fields

Simultaneous and Ultrasensitive Detection of Foodborne Bacteria by Gold Nanoparticles-Amplified Microcantilever Array Biosensor

Foodborne pathogens, especially bacteria, are explicitly threatening public health worldwide. Biosensors represent advances in rapid diagnosis with high sensitivity and selectivity. However, multiplexed analysis and minimal pretreatment are still challenging. We fabricate a gold nanoparticle (Au NP)-amplified microcantilever array biosensor that is capable of determining ultralow concentrations of foodborne bacteria including Escherichia coli O157:H7, Vibrio parahaemolyticus, Salmonella, Staphylococcus aureus, Listeria monocytogenes, Shigella, etc. The method is much faster than using conventional tools without germiculturing and PCR amplification. The six pairs of ssDNA probes (ssDNA1 + ssDNA2 partially complementary to the target gene) that originated from the sequence analysis of the specific gene of the bacteria were developed and validated. The ssDNA1 probes were modified with -S-(CH2)6 at the 5′-end and ready to immobilize on the self-assembled monolayers (SAMs) of the sensing cantilevers in the array and couple with Au NPs, while 6-mercapto-1-hexanol SAM modification was carried out on the reference cantilevers to eliminate the interferences by detecting the deflection from the environment induced by non-specific interactions. For multianalyte sensing, the target gene sequence was captured by the ssDNA2-Au NPs in the solution, and then the Au NPs-ssDNA2-target complex was hybridized with ssNDA1 fixed on the beam of the cantilever sensor, which results in a secondary cascade amplification effect. Integrated with the enrichment of the Au NP platform and the microcantilever array sensor detection, multiple bacteria could be rapidly and accurately determined as low as 1–9 cells/mL, and the working ranges were three to four orders of magnitude. There was virtually no cross-reaction among the various probes with different species. As described herein, it holds great potential for rapid, multiplexed, and ultrasensitive detection in food, environment, clinical, and communal samples

Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury by Inhibiting ROS-Activated ERK1/2 and p38MAPK Signaling Pathways in PC12 Cells

Hydrogen sulfide (H2S) has been proposed as a novel neuromodulator and neuroprotective agent. Cobalt chloride (CoCl2) is a well-known hypoxia mimetic agent. We have demonstrated that H2S protects against CoCl2-induced injuries in PC12 cells. However, whether the members of mitogen-activated protein kinases (MAPK), in particular, extracellular signal-regulated kinase1/2(ERK1/2) and p38MAPK are involved in the neuroprotection of H2S against chemical hypoxia-induced injuries of PC12 cells is not understood. We observed that CoCl2 induced expression of transcriptional factor hypoxia-inducible factor-1 alpha (HIF-1α), decreased cystathionine-β synthase (CBS, a synthase of H2S) expression, and increased generation of reactive oxygen species (ROS), leading to injuries of the cells, evidenced by decrease in cell viability, dissipation of mitochondrial membrane potential (MMP) , caspase-3 activation and apoptosis, which were attenuated by pretreatment with NaHS (a donor of H2S) or N-acetyl-L cystein (NAC), a ROS scavenger. CoCl2 rapidly activated ERK1/2, p38MAPK and C-Jun N-terminal kinase (JNK). Inhibition of ERK1/2 or p38MAPK or JNK with kinase inhibitors (U0126 or SB203580 or SP600125, respectively) or genetic silencing of ERK1/2 or p38MAPK by RNAi (Si-ERK1/2 or Si-p38MAPK) significantly prevented CoCl2-induced injuries. Pretreatment with NaHS or NAC inhibited not only CoCl2-induced ROS production, but also phosphorylation of ERK1/2 and p38MAPK. Thus, we demonstrated that a concurrent activation of ERK1/2, p38MAPK and JNK participates in CoCl2-induced injuries and that H2S protects PC12 cells against chemical hypoxia-induced injuries by inhibition of ROS-activated ERK1/2 and p38MAPK pathways. Our results suggest that inhibitors of ERK1/2, p38MAPK and JNK or antioxidants may be useful for preventing and treating hypoxia-induced neuronal injury