Barriers for pregnant women living in rural, agricultural villages to accessing antenatal care in Cambodia: A community-based cross-sectional study combined with a geographic information system

Article describes how morbidity and mortality is still a major public health issue in low- and middle-income countries such as Cambodia. This study examines the barriers for pregnant women living in rural, agricultural villages

Lineage -CD34+CD31+ cells that appear in association with severe burn injury are inhibitory on the production of antimicrobial peptides by epidermal keratinocytes.

Antimicrobial peptides are major host defense effectors against Pseudomonas aeruginosa skin infections. Due to the lack of such peptide production, severely burned hosts are greatly susceptible to P. aeruginosa burn wound infection. β-Defensin (HBD) production by normal human epidermal keratinocytes (NHEK) was inhibited by lineage(-)CD34(+) cells isolated from peripheral blood of severely burned patients. Lineage(-)CD34(+) cells obtained from severely burned patients were characterized as CD31(+), while healthy donor lineage(-)CD34(+) cells were shown to be CD31(-) cells. Lineage(-)CD34(+)CD31(-) cells did not show any inhibitory activities on HBD-1 production by NHEK. CCL2 and IL-10 released from lineage(-)CD34(+)CD31(+) cells were shown to be inhibitory on the peptide production by NHEK, while these soluble factors were not produced by lineage(-)CD34(+)CD31(-) cells. After treatment with a mixture of mAbs for CCL2 and IL-10, the culture fluids of lineage(-)CD34(+)CD31(+) cells did not show any inhibitory activities on HBD-1 production by NHEK. Lineage(-)CD34(+)CD31(+) cells that appear in association with burn injuries play a role on the inhibition of antimicrobial peptide production by skin keratinocytes through the production of CCL2 and IL-10

Effect of glycyrrhizin on pseudomonal skin infections in human-mouse chimeras.

In our previous studies, peripheral blood lineage(-)CD34(+)CD31(+) cells (CD31(+) IMC) appearing in severely burned patients have been characterized as inhibitor cells for the production of β-defensins (HBDs) by human epidermal keratinocytes (NHEK). In this study, the effect of glycyrrhizin on pseudomonal skin infections was studied in a chimera model of thermal injury. Two different chimera models were utilized. Patient chimeras were created in murine antimicrobial peptide-depleted NOD-SCID IL-2rγ(null) mice that were grafted with unburned skin tissues of severely burned patients and inoculated with the same patient peripheral blood CD31(+) IMC. Patient chimera substitutes were created in the same mice that were grafted with NHEK and inoculated with experimentally induced CD31(+) IMC. In the results, both groups of chimeras treated with glycyrrhizin resisted a 20 LD50 dose of P. aeruginosa skin infection, while all chimeras in both groups treated with saline died within 3 days of the infection. Human antimicrobial peptides were detected from the grafted site tissues of both groups of chimeras treated with glycyrrhizin, while the peptides were not detected in the same area tissues of controls. HBD-1 was produced by keratinocytes in transwell-cultures performed with CD31(+) IMC and glycyrrhizin. Also, inhibitors (IL-10 and CCL2) of HBD-1 production by keratinocytes were not detected in cultures of patient CD31(+) IMC treated with glycyrrhizin. These results indicate that sepsis stemming from pseudomonal grafted site infections in a chimera model of burn injury is controllable by glycyrrhizin. Impaired antimicrobial peptide production at the infection site of severely burned patients may be restored after treatment with glycyrrhizin

HBD-1 production by patient unburned skin tissues in cultures supplemented with CD31⁺ IMC culture fluids.

<p>Patient #16∼#18 CD31⁺ IMC (1×10⁶ cells/ml) were individually treated with or without glycyrrhizin (100 µg/ml) for 12 hours. After washing with media, these cells were cultured for an additional 36 hours. Culture fluids harvested from the cultures supplemented with or without glycyrrhizin were added (5∼20%, v/v) to cultures of patient unburned skin tissues (0.2×0.2 cm), and cultured for 48 hours. Culture fluids harvested were assayed for HBD-1 by ELISA. *<i>P</i><0.05; **<i>P</i><0.01 vs. cultures without glycyrrhizin.</p

Culture fluids of lineage⁻CD34⁺CD31⁺ cells are inhibitory on HBD-1 production by NHEK. A.

<p>Inhibition of HBD production in NHEK cultures supplemented with culture fluids of lineage⁻CD34⁺CD31⁺ cells. Culture fluids were harvested 48 hours after cultivation of lineage⁻CD34⁺CD31⁺ cells (1×10⁶ cells/ml) derived from burn patients #8, #9, #13, #14 and #15 (open circles). The culture fluids of lineage⁻CD34⁺CD31⁻ cells of healthy donors #1∼#5 (filled circles) were utilized as a control. Five to 40% (v/v) of these culture fluids were added to cultures of NHEK (1×10⁵ cells/ml). Culture fluids harvested from NHEK cultures were assayed for HBD-1 by ELISA. * <i>P</i><0.01 vs control. <b>B–D.</b> Production of IL-10, IL-13 and CCL2 by lineage⁻CD34⁺CD31⁺ cells. Lineage⁻CD34⁺CD31⁺ cells (1×10⁵ cells/ml, open circles) isolated from peripheral blood of burn patients #8, #9, #13, #14 and #15 were cultured for 12 to 48 hours. As controls, peripheral blood lineage⁻CD34⁺CD31⁻ cells of healthy donors #1∼#5 (filled circles) were cultured under the same conditions. Supernatants obtained were assayed for IL-10 (<b>B</b>), IL-13 (<b>C</b>) and CCL2 (<b>D</b>) by ELISA. * <i>P</i><0.05, ** <i>P</i><0.01 vs lineage⁻CD34⁺CD31⁻ cells.</p

Additional file 1 of An assessment of physician assistant student diversity in the United States: a snapshot for the healthcare workforce

Additional file 1: Supplemental Appendix 1. Top PA Performers Ranked by Number of Graduates from 2014-2018