Microfluidic Platform for In Vitro Study on the Development of Cell Therapy

Cell therapy has emerged as a treatment of many endocrine disorders. Microfluidics has been developed for a myriad of biological applications and the intrinsic capability of controlling and interrogating the cellular microenvironment with unrivalled precision. Development of microfluidic technologies has potentials to address cell-relevant biological phenomena, and aligns capabilities with translational challenges and goals. Human islet transplantation is a promising cell-based therapy for Type I diabetes mellitus (TIDM). We developed a pumpless liquid delivery system driven by surface tension to significantly simplify the microfluidic operation for islet in vitro study. With the new device, an improvement can be achieved with lower material consumption, increased assay sensitivity, accuracy, and higher spatiotemporal resolution. Hypoparathyroidism is an uncommon condition associated with abnormally low levels of parathyroid hormone (PTH), leading to low calcium levels in blood and bones and to an increase of serum phosphorus. Allotransplantation of encapsulated parathyroid cells is an alternative treatment without immunosuppressants, while avoiding complications of supplemental therapy. We are able to manipulate the flow in microfluidic channels of our new microencapsulator device and efficiently generate the micro-encapsulated cells (with the size of <100 µm), which can be the answer to the future cell therapy of hypoparathyroidism. Furthermore, cell therapy treatment strategies also include isolation and transfer of specific stem cell populations, administration of effector cells, induction of mature cells to become pluripotent cells, and reprogramming of mature cells. To acquire the sufficient information of cell reprogramming, understand the cell physiological mechanisms, and test the function of potential cellular products, we designed a new perfusion chamber device allowing us to perform the efficient perfusion at the single cell level

Additional file 2: of Community health education improves child health care in Rural Western China

Interview guide. (DOC 212 kb

Additional file 1: of Community health education improves child health care in Rural Western China

The questionnaire. (DOC 313 kb

sj-docx-1-cre-10.1177_02692155241235336 - Supplemental material for Transcranial direct current stimulation for upper extremity motor dysfunction in poststroke patients: A systematic review and meta-analysis

Supplemental material, sj-docx-1-cre-10.1177_02692155241235336 for Transcranial direct current stimulation for upper extremity motor dysfunction in poststroke patients: A systematic review and meta-analysis by Xian Tang, Nan Zhang, Zhiyuan Shen, Xin Guo, Jun Xing, Shujuan Tian and Yuan Xing in Clinical Rehabilitation</p

Ginsenoside Rd improves rat cardiac function after 30 minutes ischemia and 3 hours reperfusion.

<p>Values presented are mean ± SEM. Abbreviations: LVSP, left ventricular systolic pressure; LVEDP, left ventricular end diastolic pressure; ±LVd<i>P</i>/d<i>t</i>_max, the instantaneous first derivation of left ventricle pressure; MI/R, myocardial ischemia/reperfusion (30 minutes/3 hours). n = 8/group. **<i>P</i><0.01 vs. Sham, ^#<i>P</i><0.05, ^##<i>P</i><0.01 vs. MI/R.</p

Ginsenoside Rd inhibits mitochondrial-mediated apoptosis in NRCs subjected to SI/R.

<p>(<b>A</b>) Representative western blot for cytochrome c release. SI/R increased cytosolic translocation of mitochondrial cytochrome c. Densitometric analysis demonstrates 10 μM GSRd inhibited mitochondrial cytochrome c release. (<b>B</b>) Representative western blot for Bcl-2 and Bax expression after various experimental treatments. Densitometric analysis demonstrates SI/R reduced the Bcl-2/Bax ratio, but GSRd increased the Bcl-2/Bax ratio. (<b>C</b>) Representative western blot for SI/R-induced casepase-3 and caspase-9 activation. Densitometric analysis demonstrates 10 μM GSRd reduced expression of cleaved caspase-9 and caspase-3. All values presented are mean±SEM. n = 6; **<i>P</i><0.01 vs. Control, ^#<i>P</i><0.05, ^##<i>P</i><0.01 vs. SI/R.</p

Schematic diagram depicting protective signaling of GSRd in MI/R-induced apoptosis.

<p>GSRd inhibits the apoptotic signaling cascades initiated by MI/R-generated ROS. Arrows (→) indicate activation or induction, and segments ending with a (⊢) indicate inhibition/blockade. Solid lines (—) indicate mechanisms strongly supported by the current study, and dotted lines (--) indicate hypothesized connections requiring further investigations.</p

Ginsenoside Rd increases mitochondrial membrane potential (MMP) in NRCs subjected to SI/R.

<p>MMP was measured with fluorescent dye JC-1. 10 μM GSRd was administered 30 minutes prior to SI/R. Fluorescent intensity of JC-1 was determined at excitation wavelength 488 nm and emission wavelength 530 nm via flow cytometry. Values presented are mean ± SEM. **<i>P</i><0.01 vs. Control, ^##<i>P</i><0.01 vs. SI/R. These experiments were performed in triplicate with similar results.</p

Ginsenoside Rd increases phosphorylation of Akt and GSK-3β in NRCs subjected to SI/R.

<p>Densitometric analysis demonstrates GSRd increased the ratio of P-Akt/Akt and P-GSK-3β/GSK-3β, which was significantly blocked by Akt-inhibitor LY294002. Values presented are mean±SEM. n = 6; ^#<i>P</i><0.05, ^##<i>P</i><0.01 vs. SI/R, ^&&<i>P</i><0.01 vs. SI/R+GSRd.</p

Ginsenoside Rd reduces intracellular ROS generation in NRCs subjected to SI/R.

<p>Intracellular ROS accumulation was measured via fluorescence probe DCFH-DA. Fluorescent intensity was determined at excitation wavelength 488 nm and emission wavelength 525 nm via flow cytometry. Values presented are mean ± SEM. **<i>P</i><0.01 vs. Control, ^#<i>P</i><0.05 vs. SI/R. These experiments were performed in triplicate with similar results.</p