Minimally invasive surgical approaches for spontaneous intracranial hemorrhage in neonates aged 0-3 months.

OBJECTIVE: The aim of this study is to assess the clinical efficacy of minimally invasive surgical interventions in addressing spontaneous intracranial hemorrhage among neonates aged 0-3 months. METHODS: A retrospective analysis was conducted on a cohort of 30 neonates diagnosed with spontaneous intracranial hemorrhage, who underwent minimally invasive cranial trepanation and drainage procedures at our department between 2011 and 2015. RESULTS: A comprehensive follow-up, spanning a duration of 1-5 years, was conducted for all 30 neonates, revealing a 100% survival rate among the pediatric cohort. CONCLUSION: The findings suggest that minimally invasive cranial trepanation and drainage exhibit efficacy in neonates aged 0-3 months experiencing spontaneous intracranial hemorrhage, leading to a reduction in both mortality and disability rates. It is recommended that surgery be promptly performed upon definitive diagnosis and identification of operation indications to prevent severe brain damage resulting from prolonged intracranial hypertension and potential fatal outcomes in neonates. Furthermore, the surgical procedure is characterized by its simplicity, involving minimal trauma.

Effect of replacing inorganic trace minerals at lower organic levels on growth performance, blood parameters, antioxidant status, immune indexes, and fecal mineral excretion in weaned piglets.

Organic trace minerals (OTMs) have the potential to replace inorganic trace minerals (ITMs), but the degree to which the dietary levels can be reduced is not well defined. This study aimed to investigate the effect of replacing of ITMs with lower levels of OTMs on growth performance, blood parameters, antioxidant status, and immune indexes in weaned piglets. The experiment was conducted in a subtropical city in Guangdong Province in South China (subtropical climate) from July to September 2018. A total of 600 pigs with an average initial BW of 8.90 kg were allotted by gender and weight to 5 treatments with 6 replicate pens per treatment. Experimental treatments: (A) Control group (a basal diet with iron, copper, manganese, and zinc from sulfates and sodium selenite providing commercially utilized levels in China of 150, 25, 40, 150, and 0.5 mg/kg, respectively). (B) 1/2 ITM group (inorganic trace minerals providing 1/2 control group levels). (C) 1/2 OTM group (1/2 control group trace mineral levels with manganese, iron, zinc, and selenium from Sel-Plex® and Cu from Bioplex®). (D) 1/3 ITM group (1/3 control group trace mineral levels from inorganic forms). (E) 1/3 OTM group (1/3 control group trace mineral levels from organic forms). The results suggest no significant effects of trace mineral sources or levels, on average daily gain (ADG) and average daily feed intake (ADFI) among different treatments during the entire experiment. The level of zinc in serum was significantly decreased in the 1/3 ITM group. The 1/3 OTM group had a significantly higher (P < 0.05) immunoglobulin G (IgG) level in serum. Fecal mineral excretion decreased significantly (P < 0.05) when decreased dietary levels of trace minerals were included at 1/2 and 1/3 levels regardless of sources. Fecal concentrations of zinc excretion were lower (P < 0.05) with 1/2 OTM supplementation than 1/2 ITMs. The present study shows that replacing high doses of ITMs with low concentrations (1/3) of OTMs does not adversely affect the growth performance of piglets. At low levels, total replacement of ITMs with OTMs improved IgG and reduced fecal excretion of copper, zinc, iron, and manganese, thereby mitigating environmental pollution.

Melatonin enhances autophagy and decreases apoptosis induced by nanosilica in RAW264.7 cells.

Melatonin is one of the main hormones that regulate biological rhythms and have immunomodulation, anti-inflammatory, and antioxidation functions. In this study, we aimed to explore the effect of melatonin on the autophagy, apoptosis, and inflammatory reaction of macrophages (RAW264.7 cells) stimulated by nanosilica. SiO2 (100 mg/mL, 10-20 nm) was used to stimulate RAW264.7 cells at different time points (0, 2, 4, 8, 12, and 24 hr). Melatonin (200 µM) was added to SiO2 -stimulated macrophages at 12 hr. Beclin-1, LC3, Bax, Bcl-2, and Caspase-3 were examined with western blotting. Flow cytometry was used to detect apoptosis. The levels of TNF-α, IL-1ß, and IL-18 were detected by ELISA. The level of TNF-α in the supernatant of SiO2 -stimulated cells gradually increased with time but decreased following melatonin administration. In contrast, the expression of IL-1ß and IL-18 increased after melatonin treatment. LC3 and Bax signaling pathways were activated in SiO2 -stimulated RAW264.7 cells, showing elevated expression of LC3 and reduced expression of Bax in the melatonin-treated cells. GFP-LC3 puncta were significantly increased in SiO2 -stimulated RAW264.7 cells and decreased in melatonin-treated cells. The apoptotic rate in SiO2 -stimulated RAW264.7 cells increased with time and decreased after melatonin treatment, and the number of phagosomes increased with the stimulation of nanosilica and the treatment of melatonin. Melatonin might promote autophagy and inhibit apoptosis as well as inflammatory responses of RAW264.7 cells stimulated by nanosilica. © 2019 IUBMB Life, 2019.

Effect of pad-fan cooling and dietary organic acid supplementation during late gestation and lactation on reproductive performance and antioxidant status of multiparous sows in hot weather.

A 2 × 2 factorial arrangement (rearing room with or without pad-fan cooling × diet with or without 2.5 kg/t organic acid) was used to evaluate the effect of pad-fan cooling and dietary organic acid supplementation during perinatal period on reproductive performance and antioxidant status of sows in hot weather. This study was conducted in a subtropical city in Guangdong Province in South China between August and October, 2015. At day 85 of gestation, a total of 112 sows were randomly assigned to the four treatments with 28 sows per treatment, and maintained until day 21 of lactation, and the feeding trial lasted for 51 days. During the experimental period, room temperature and humidity were recorded hourly. The lactation feed intake of sows (P = 0.109) and stillbirths (P < 0.05) increased when the sows were reared in the room with the pad-fan cooling against the room without pad-fan cooling. The number of weak newborns per litter and the malondialdehyde content in days 14 and 21 milk decreased (P < 0.05), while the lactation feed intake of sows, weaned litter weights, and individual pig weights increased when the sows were fed the organic acid (P < 0.05). In conclusion, pad-fan cooling in rearing room improved the lactation feed intake of sows, and dietary organic acid supplementation improved reproductive performance and milk antioxidant status of sows. Pad-fan cooling is recommended in farrowing room, but not in gestating room.

Ketamine promotes inflammation through increasing TLR4 expression in RAW264.7 cells.

SUMMERY: Ketamine (KTM), a N-methyl-D-aspartate (NMDA) receptor antagonist, was found to has an anti-inflammatory effect, but some patients suffered from exacerbated pro-inflammatory reactions after anesthesia with KTM. The present study was aimed to examine the underlying mechanism of pro-inflammatory effects of KTM. In this study, RAW264.7 cells were exposed to KTM and NMDA alone or combined for 30 min before lipopolysaccharide (LPS) stimulation. The expression levels of IL-6 and TNF-α were detected by RT-PCR and ELISA, and those of NMDA receptors by RT-PCR in RAW264.7 cells. Additionally, the TLR4 expression was determined by RT-PCR and flow cytometry, respectively. The results showed that in RAW264.7 cells, KTM alone promoted the TLR4 expression, but did not increase the expression of IL-6 or TNF-α. In the presence of LPS, KTM caused a significantly higher expression of IL-6 and TNF-α than LPS alone. NMDA could neither alter the IL-6 and TNF-α mRNA expression, nor reverse the enhanced expression of IL-6 and TNF-α mRNA by KTM in LPS-challenged cells. After TLR4-siRNA transfection, RAW264.7 cells pretreated with KTM no longer promoted the IL-6 and TNF-α expression in the presence of LPS. In conclusion, KTM accelerated LPS-induced inflammation in RAW264.7 cells by promoting TLR4 expression, independent of NMDA receptor.

Volatile anesthetics inhibit the activity of calmodulin by interacting with its hydrophobic site.

BACKGROUND: Volatile anesthetics (VAs) may affect varied and complex physiology processes by manipulating Ca(2+)-calmodulin (CaM). However, the detailed mechanism about the action of VAs on CaM has not been elucidated. This study was undertaken to examine the effects of VAs on the conformational change, hydrophobic site, and downstream signaling pathway of CaM, to explore the possible mechanism of anesthetic action of VAs. METHODS: Real-time second-harmonic generation (SHG) was performed to monitor the conformational change of CaM in the presence of VAs, each plus 100 µmol/L Ca(2+). A hydrophobic fluorescence indicator, 8-anilinonaphthalene-1-sulfonate (ANS), was utilized to define whether the VAs would interact with CaM at the hydrophobic site or not. High-performance liquid chromatography (HPLC) was carried out to analyze the activity of CaM-dependent phosphodiesterase (PDE1) in the presence of VAs. The VAs studied were ether, enflurane, isoflurane, and sevoflurane, with their aqueous concentrations 7.6, 9.5, 11.4 mmol/L; 0.42, 0.52, 0.62 mmol/L; 0.25, 0.31, 0.37 mmol/L and 0.47, 0.59, 0.71 mmol/L respectively, each were equivalent to their 0.8, 1.0 and 1.2 concentration for 50% of maximal effect (EC50) for general anesthesia. RESULTS: The second-harmonic radiation of CaM in the presence of Ca(2+) was largely inhibited by the VAs. The fluorescence intensity of ANS, generated by binding of Ca(2+) to CaM, was reversed by the VAs. HPLC results also showed that AMP, the product of the hydrolysis of cAMP by CaM-dependent PDE1, was reduced by the VAs. CONCLUSIONS: Our findings demonstrate that the above VAs interact with the hydrophobic core of Ca(2+)-CaM and the interaction results in the inhibition of the conformational change and activity of CaM. This in vitro study may provide us insight into the possible mechanism of anesthetic action of VAs in vivo.

Adenovirus-delivered angiopoietin 1 accelerates the resolution of inflammation of acute endotoxic lung injury in mice.

BACKGROUND: The immune system plays a key role in protecting the organism from infection. Timely resolution of the inflammatory response to infection plays a vital role in returning homeostasis and maintaining normal organ function. Angiopoietin1 prevents endothelial activation, part of the inflammatory response to a pathogen, and has an anti-inflammatory effect in acute lung injury. We designed this study to investigate whether increasing serum production of angiopoietin1 by IV administration of adenoviral-delivered angiopoietin1 could accelerate the resolution of inflammation in endotoxin-induced acute lung injury in mice. METHODS: Lipopolysaccharide was intratracheally instilled to induce acute lung injury in animals pretreated for 24 hours with adenoviral-GFP vector or adenoviral-GFP-angiopoietin1, respectively. An additional 6 mice in each pretreatment group were killed before lipopolysaccharide instillation to serve as controls. Indices of resolution of inflammation were analyzed. Apoptotic polymorphonuclear leukocytes and their phagocytosis by macrophages were determined by fluorescent activated cell sorter. The expression of angiopoietin1 in tissues and granulocyte macrophage colony-stimulating factor in the bronchoalveolar lavage fluid were measured. RESULTS: Lipopolysaccharide induced leukocyte infiltration into air spaces, with maximal infiltration 48 hours after lipopolysaccharide instillation. Pretreatment with adenovirus-GFP-angiopoietin1 markedly increased angiopoietin1 expression, reduced leukocyte, and neutrophil infiltration and shortened the duration of inflammation. Adenovirus-GFP-angiopoietin1 pretreatment augmented the magnitude without altering the time course of granulocyte macrophage colony-stimulating factor. CONCLUSIONS: Our results suggest that angiopoietin1 pretreatment promotes resolution of inflammation in endotoxin-induced acute lung injury in mice by accelerating the apoptosis of neutrophils and their phagocytosis by macrophages.

Enhanced expression of the decoy receptor IL-13Ralpha2 in macrophages of Schistosoma japonicum-infected mice.

BACKGROUND: Type 2 cytokine interleukin (IL)-13 and its decoy receptor, IL-13 receptor (R) alpha2 appear to play a major role in tissue fibrosis of schistosomiasis and asthma. IL-13 is a key regulator of the extracellular matrix (ECM). It is known to signal to cells by binding to the IL-13Ralpha1, which then heterodimerizes with IL-4Ralpha. In contrast, IL-13Ralpha2 binds IL-13 with high affinity but does not signal. IL-13Ralpha2 is known to down-regulate granulomatous inflammation and prolong host survival in Schistosoma mansoni (S. mansoni) infection, but little is known about the location and expression level of IL-13Ralpha2 in the context of S. japonicum infection. METHODS: We established S. japonicum-infected mouse models. Kinetic serum levels of IL-13Ralpha2 were examined with ELISA. IL-13Ralpha2 mRNA and protein of liver tissues were determined by PCR and immunoblotting analysis, respectively. Detection of IL-13Ralpha2 expression and location in macrophages was performed by TaqMan PCR and fluorescent immunocytochemistry technique, respectively. RESULTS: A marked elevation of mRNA and protein expression of IL-13Ralpha2 was observed in mice during S. japonicum infection. An enhanced expression of IL-13Ralpha2 was further demonstrated in primary macrophages of murine schistosomiasis. CONCLUSIONS: IL-13Ralpha2 in macrophages may be a critical contributor to pathogenesis of schistosomiasis. The data highlight the potential importance of cell signaling and antifibrotic gene therapeutics in T helper 2 cell (Th2)-mediated diseases.