[Nutritional support in children with pneumonia on mechanical ventilation by short-peptide enteral nutrition formula].

OBJECTIVE: To observe the incidence of malnutrition and nutritional risk in children with pneumonia on mechanical ventilation in the pediatric intensive care unit (PICU), and to explore the nutritional support effect of short-peptide enteral nutrition formula. METHODS: A total of 68 children with severe pneumonia who were hospitalized in the PICU from October 2017 to October 2018 and required mechanical ventilation were enrolled for a prospective randomized controlled study. The children were randomly divided into a control group and an experimental group. Through the nasogastric feeding tube, the experimental group received the short-peptide enteral nutrition formula, and the control group received the intact-protein enteral nutrition formula. The weight-for-age Z score, STRONGkids nutritional risk score, and pediatric critical illness score of the two groups were evaluated. The serum levels of total protein, albumin, and prealbumin (PA) on admission and before discharge were measured. The gastrointestinal tolerance and clinical outcome indicators of the two groups were observed. RESULTS: Among the 68 mechanically ventilated children, 26 (38%) had malnutrition, including moderate malnutrition (10 cases, 15%) and severe malnutrition (16 cases, 24%); 10 cases (15%) had malnutrition at discharge. Sixty-three children (93%) had nutritional risk, including moderate nutritional risk in 21 cases and high nutritional risk in 42 cases. The moderate and high nutritional risk rates of the critical and extreme critical groups were significantly higher than those of the non-critical group (P<0.05). Compared with the control group, the experimental group had significantly shorter duration of mechanical ventilation and total length of hospital stay, significantly higher serum PA level and weight growth rate, and significantly better gastrointestinal tolerance (P<0.05). There were no significant differences in the incidence of ventilator-associated pneumonia and disease outcome between the two groups (P>0.05). CONCLUSIONS: The detection rates of malnutrition and nutritional risk in children with pneumonia on mechanical ventilation are relatively high. Short-peptide enteral nutrition formula can help improve their treatment outcome and are more suitable for nutritional support in critically ill children on mechanical ventilation.

Tumor-targeted delivery of a C-terminally truncated FADD (N-FADD) significantly suppresses the B16F10 melanoma via enhancing apoptosis.

Fas-associated protein with death domain (FADD), a pivotal adaptor protein transmitting apoptotic signals, is indispensable for the induction of extrinsic apoptosis. However, overexpression of FADD can form large, filamentous aggregates, termed death effector filaments (DEFs) by self-association and initiate apoptosis independent of receptor cross-linking. A mutant of FADD, which is truncated of the C-terminal tail (m-FADD, 182-205 aa) named N-FADD (m-FADD, 1-181 aa), can dramatically up-regulate the strength of FADD self-association and increase apoptosis. In this study, it was found that over-expression of FADD or N-FADD caused apoptosis of B16F10 cells in vitro, even more, N-FADD showed a more potent apoptotic effect than FADD. Meanwhile, Attenuated Salmonella Typhimurium strain VNP20009 was engineered to express FADD or N-FADD under the control of a hypoxia-induced NirB promoter and each named VNP-pN-FADD and VNP-pN-N-FADD. The results showed both VNP-pN-FADD and VNP-pN-N-FADD delayed tumor growth in B16F10 mice model, while VNP-pN-N-FADD suppressed melanoma growth more significantly than VNP-pN-FADD. Additionally, VNP-pN-FADD and VNP-pN-N-FADD induced apoptosis of tumor cells by activating caspase-dependent apoptotic pathway. Our results show that N-FADD is a more potent apoptotic inducer and VNP20009-mediated targeted expression of N-FADD provides a possible cancer gene therapeutic approach for the treatment of melanoma.

Use of 16S rRNA Gene-Targeted Group-Specific Primers for Real-Time PCR Analysis of Predominant Bacteria in Mouse Feces.

Mouse models are widely used for studying gastrointestinal (GI) tract-related diseases. It is necessary and important to develop a new set of primers to monitor the mouse gut microbiota. In this study, 16S rRNA gene-targeted group-specific primers for Firmicutes, Actinobacteria, Bacteroidetes, Deferribacteres, "Candidatus Saccharibacteria," Verrucomicrobia, Tenericutes, and Proteobacteria were designed and validated for quantification of the predominant bacterial species in mouse feces by real-time PCR. After confirmation of their accuracy and specificity by high-throughput sequencing technologies, these primers were applied to quantify the changes in the fecal samples from a trinitrobenzene sulfonic acid-induced colitis mouse model. Our results showed that this approach efficiently predicted the occurrence of colitis, such as spontaneous chronic inflammatory bowel disease in transgenic mice. The set of primers developed in this study provides a simple and affordable method to monitor changes in the intestinal microbiota at the phylum level.

[Expression of stromal cell derived factor-1 and CXC chemokine receptor 4 and the effects of budesonide on their expression in mice with asthma].

OBJECTIVE: To study the expression of stromal cell derived factor-1(SDF-1) and CXC chemokine receptor 4 (CXCR4) in the airway and the effect of budesonide on their expression in mice with asthma. METHODS: Thirty BALB/c male mices were randomly divided into three groups: placebo control, untreated asthma, and budesonide-treated asthma. The asthma group were induced by intraperitoneal injection of 10% ovalbumin (OVA ) on days 1, 8 and 15, and then from days 22 to 34, challenged by inhalation of 2% OVA aerosol every other day. The budesonide-treated asthma group received an inhalation of budesonide (1 mg ) before OVA challenge. The pathological changes of the airway were assessed by hematoxylin and eosin staining. The immunohistochemistry was used to estimate the expression of SDF-1 in the lung. RT-PCR was used to evaluate the expression of CXCR4 in the lung. RESULTS: Compared with the control group, SDF-1 and CXCR4 expression in the lung in the untreated asthma group increased significantly (p<0.05). The budesonide-treated asthma group demonstrated significantly decreased SDF-1 (0.426+/-0.052 vs 0.361+/-0.065; p<0.05) and CXCR4 (0.829+/-0.027 vs 0.723+/-0.094; p<0.05) expression in the lung as compared with the untreated asthma group. Both SDF-1 (r=0.744, p<0.01) and CXCR4 (r=0.553, p<0.01)were positively correlated with the thickness of the airway wall. CONCLUSIONS: SDF-1 and CXCR4 may be associated with airway remodeling in mice with asthma. Budesonide can improve airway remodeling, possibly by decreasing the expression of SDF-1 and CXCR4.