A wireless physiological parameter monitoring system with a treatment feedback function during neonatal phototherapy.

Objective. Neonatal jaundice is a common condition in the early stages of newborns, and phototherapy is a fast, safe and effective method that is used to treat it. However, recent studies have shown that phototherapy may elicit side effects in infants, such as hypothermia, hyperthermia and dehydration. To improve the quality of phototherapy and the prognosis of patients, the changes in neonatal physiological parameters during phototherapy should be monitored to give better feedback to pediatricians or the phototherapy system. However, the current standard of clinical care during neonatal phototherapy with hard-wired devices limits this realization.Approach. Here, we developed a prototype of a neonatal wearable device, which can wirelessly potentially monitor the jaundice value, transepidermal water loss, skin wettedness factor and body orientation during phototherapy, and conducted prototype validation experiments. We also set up user-friendly interfaces and an analysis system on custom software, all designed to make the future addition of data interfaces for treatment feedback functions easier.Main results. The preliminaryin vitroexperiment demonstrated the effectiveness of simultaneous monitoring of the required physiological parameters. And further suggestions and specific operations are discussed in terms of optimization of the treatment of neonatal jaundice.Significance. It is believed that the established system has the potential to provide a basis for future phototherapy nursing guidelines and physiological monitoring standards.

Epigallocatechin gallate attenuates mitochondrial DNA-induced inflammatory damage in the development of ventilator-induced lung injury.

OBJECTIVE: We aim to investigate the role of mitochondrial DNA (mtDNA), a novel endogenous pro-inflammatory cytokine, in the development of ventilator-induced lung injury (VILI). Moreover, the protective effect of epigallocatechin gallate (EGCG) on VILI through inhibiting local mtDNA release was examined. METHODS: From March 2015 to March 2016, bronchoalveolar lavage fluid (BALF) from 36 patients with VILI and well-matched 36 patients without VILI after major surgery were consecutively collected. The expression levels of mtDNA and inflammatory cytokines in BALF were tested. SD rats were divided into five groups: control, low tidal volume (7 ml/kg) group, high tidal volume (HTV, 40 ml/kg) group, HTV+low dose EGCG and HTV+high dose EGCG groups. BALF were collected to examine the expression levels of mtDNA and several inflammatory cytokines and the lung tissue was harvested for pathological examinations. In addition, cyclic stretch cell culture was used and culture media was collected to analyze expressions of inflammatory cytokines. Administration of mtDNA in a rat model and in vitro cell culturing were used to confirm its pro-inflammatory properties in the development of inflammatory lung injury. RESULTS: A Significant elevation of mtDNA was detected in BALF from patients with VILI (581 ±â€¯193 vs. 311 ±â€¯137, p < 0.05) and also in rats ventilated with HTV. EGCG could significantly inhibit HTV-induced local mtDNA release and attenuate the level of inflammatory lung injuries (reduced infiltration of local inflammatory cells, lower lung wet/dry ratio and expression levels of inflammatory cytokines). The beneficial effects of EGCG on preventing inflammatory lung injuries were in a concentration-dependent manner. Meanwhile, higher expression levels of mtDNA and inflammatory cytokines were observed in the media of cyclic stretched cell culture compared to those in the control group (p < 0.05). Furthermore, intra-tracheal administration of mtDNA in rats could lead to a marked increase of local inflammatory cytokines and subsequent inflammatory lung injuries (p < 0.05). And by adding mtDNA into the cell culture, higher level of inflammatory cytokines in the media was detected (p < 0.05). EGCG also showed preventive effects on inflammatory responses on a concentration-dependent manner (p < 0.05). CONCLUSION: The increased expression level of mtDNA and subsequent inflammatory cytokines overproduction may play an important role in the development of VILI. EGCG may be a potential novel therapeutic candidate for protection against VILI by inhibiting the local release of mtDNA.