Organization of an Artificial Multicellular System with a Tunable DNA Patch on a Membrane Surface.

Coordinating multiple artificial cellular compartments into a well-organized artificial multicellular system (AMS) is of great interest in bottom-up synthetic biology. However, developing a facile strategy for fabricating an AMS with a controlled arrangement remains a challenge. Herein, utilizing in situ DNA hybridization chain reaction on the membrane surface, we developed a DNA patch-based strategy to direct the interconnection of vesicles. By tuning the DNA patch that generates heterotrophic adhesion for the attachment of vesicles, we could produce an AMS with higher-order structures straightforwardly and effectively. Furthermore, a hybrid AMS comprising live cells and vesicles was fabricated, and we found the hybrid AMS with higher-order structures arouses efficient molecular transportation from vesicles to living cells. In brief, our work provides a versatile strategy for modulating the self-assembly of AMSs, which could expand our capability to engineer synthetic biological systems and benefit synthetic cell research in programmable manipulation of intercellular communications.

Neuroprotective effect of 1,25­dihydroxyvitamin D3 against hyperoxia­induced brain injury in premature rats.

Studies have shown that vitamin D plays a crucial role in brain development, brain metabolism and neuroprotection. There is little evidence for the neuroprotective effect of 1, 25­dihydroxyvitamin D3 (1,25­(OH)2D3) on various brain injury models. The aim of this study was to investigate the neuroprotection effect of 1,25­(OH)2D3 against hyperoxia­induced brain injury in premature rats. Sprague­Dawley rats were exposed to 95% oxygen or room air for 24 h and treated with 1,25­(OH)2D3 or normal saline for 14 consecutive days. The histopathological changes of optic chiasma tissue were observed by hematoxylin­eosin staining. Immunohistochemistry, qRT­PCR, and western blot were performed to detect the expression of integrin­ß1 and yes­associated protein (YAP) in the organization of the optic chiasm. Histopathological sections of optic chiasma showed visible optic nerve swelling, expanded nerve fiber space, uneven staining, obvious oligodendrocyte proliferation and disordered cell arrangement accompanied by inflammatory cell infiltration and exudation after 7 days and 14 days of hyperoxia exposure. The hyperoxia group treated with 1,25­(OH)2D3 were showed improvement of brain injury with reduced inflammatory exudation, uniform nerve fiber staining and less obvious oligodendrocyte proliferation. Immunohistochemical staining, qRT­PCR and western blot indicated that 1,25­(OH)2D3 treatment upregulated the expression of integrin­ß1 and YAP in the hyperoxia group on day 7. However, the expression of YAP was significantly increased compared with control group and treatment with 1,25­(OH)2D3 reduced the expression of YAP in the hyperoxic group on day 14. 1,25­(OH)2D3 may regulate the expression of integrin­ß1 and YAP to alleviate hyperoxia­induced brain injury in premature rats.

Recent Advances in DNA-Based Cell Surface Engineering for Biological Applications.

Due to its excellent programmability and biocompatibility, DNA molecule has unique advantages in cell surface engineering. Recent progresses provide a reliable and feasible way to engineer cell surfaces with diverse DNA molecules and DNA nanostructures. The abundant form of DNA nanostructures has greatly expanded the toolbox of DNA-based cell surface engineering and gave rise to a variety of novel and fascinating applications. In this review, we summarize recent advances in DNA-based cell surface engineering and its biological applications. We first introduce some widely used methods of immobilizing DNA molecules on cell surfaces and their application features. Then we discuss the approaches of employing DNA nanostructures and dynamic DNA nanotechnology as elements for creating functional cell surfaces. Finally, we review the extensive biological applications of DNA-based cell surface engineering and discuss the challenges and prospects of DNA-based cell surface engineering.

Latent profile analysis on the association of psychological abuse and neglect with mobile phone dependence among adolescences / 中国学校卫生

Objective@#To identity patterns of psychological abuse and neglect among male and female adolescents, and to examine the relationship between psychological abuse and neglect with mobile phone dependence.@*Methods@#A total of 1 070 adolescents from 5 middle schools in Ganzhou and Wuhan were investigated with Child Psychological Abuse and Neglect Scale (CPANS), Mobile Phone Addiction Index Scale (MPAI) and demographic questionnaire. Latent profile analysis (LPA) was used to construct typologies of psychological abuse and neglect involvement in male and female adolescents.@*Results@#Three latent classes were identified for boys: low level psychological abuse and neglect group (56.68%), medium level psychological abuse and neglect group ( 29.80 %), high level psychological abuse and neglect group (13.52%). For girls, four latent classes were identified including low level psychological abuse and neglect group (49.38%), medium level psychological abuse and neglect group (29.01%), high level psychological abuse and neglect group (11.12%); high level psychological abuse group (10.49%). Adolescents who suffered from psychological abuse and neglect were more likely to be dependent on mobile phones. Among them, boys dependence on mobile phones was manifested as out of control, withdrawal, escape and inefficiency[Medium level： B(95%CI )=0.28(0.12-0.44)，0.29(0.11-0.46)，0.35(0.16-0.53)，high level： B(95%CI )=0.37(0.16-0.59)，0.42(0.19-0.65)，0.33(0.07-0.59)，0.50(0.25- 0.74 )， P ＜0.05], while girls showed evasion and inefficiency in high levels of psychological abuse[ B(95%CI )=0.34(0.01-0.67)，0.46(0.14-0.78)， P ＜0.05].@*Conclusion@#There are heterogeneous differences in psychological abuse and neglect between male and female adolescents, and the relationship between each category and mobile phone dependence varies. The results provide suggestions for adolescent mental health intervention.

Rab32 connects ER stress to mitochondrial defects in multiple sclerosis.

BACKGROUND: Endoplasmic reticulum (ER) stress is a hallmark of neurodegenerative diseases such as multiple sclerosis (MS). However, this physiological mechanism has multiple manifestations that range from impaired clearance of unfolded proteins to altered mitochondrial dynamics and apoptosis. While connections between the triggering of the unfolded protein response (UPR) and downstream mitochondrial dysfunction are poorly understood, the membranous contacts between the ER and mitochondria, called the mitochondria-associated membrane (MAM), could provide a functional link between these two mechanisms. Therefore, we investigated whether the guanosine triphosphatase (GTPase) Rab32, a known regulator of the MAM, mitochondrial dynamics, and apoptosis, could be associated with ER stress as well as mitochondrial dysfunction. METHODS: We assessed Rab32 expression in MS patient and experimental autoimmune encephalomyelitis (EAE) tissue, via observation of mitochondria in primary neurons and via monitoring of survival of neuronal cells upon increased Rab32 expression. RESULTS: We found that the induction of Rab32 and other MAM proteins correlates with ER stress proteins in MS brain, as well as in EAE, and occurs in multiple central nervous system (CNS) cell types. We identify Rab32, known to increase in response to acute brain inflammation, as a novel unfolded protein response (UPR) target. High Rab32 expression shortens neurite length, alters mitochondria morphology, and accelerates apoptosis/necroptosis of human primary neurons and cell lines. CONCLUSIONS: ER stress is strongly associated with Rab32 upregulation in the progression of MS, leading to mitochondrial dysfunction and neuronal death.

Superior effect of hypertonic saline over mannitol to attenuate cerebral edema in a rabbit bacterial meningitis model.

OBJECTIVE: Adjunctive therapies that reduce the cerebral edema in bacterial meningitis include osmotic agents. There is a lack of information comparing mannitol vs. hypertonic saline as an osmotic agent for adjunctive therapy of bacterial meningitis. We attempted to elucidate the impact of hypertonic saline in cerebral edema in the setting of bacterial meningitis as well as to explore potential mechanisms of action. DESIGN: Randomized controlled in vivo study. SETTING: University research laboratory. SUBJECTS: Rabbits. INTERVENTIONS: A rabbit model of bacterial meningitis was used comparing 3% hypertonic saline with 20% mannitol as adjunctive therapy. MEASUREMENTS AND MAIN RESULTS: Adjunctive 3% hypertonic saline treatment persistently elevated mean arterial pressure as compared with the model or ampicillin group (p < .01). Although both 20% mannitol and 3% hypertonic saline efficiently elevated serum osmolality for almost 5 hrs (p < .01), 20% mannitol lowered intracranial pressure for only a short time (<2 hrs) and did not elevate cerebral perfusion pressure. Three percent hypertonic saline treatment efficiently lowered intracranial pressure and elevated cerebral perfusion pressure for almost 5 hrs (p < .01). Furthermore, 3% hypertonic saline treatment efficiently elevated serum Na+ concentration for >5 hrs (p < .01). Three percent hypertonic saline treatment was superior to 20% mannitol in lowering leukocyte number and protein content in cerebrospinal fluid (p < .01). Three percent hypertonic saline treatment reduced water content and Evans blue incorporation in the brain (p < .01). Three percent hypertonic saline treatment inhibited aquaporin 4 expression (p < .01) and attenuated pathologic brain damage more efficiently compared with adjuvant 20% mannitol treatment (p < .01). CONCLUSIONS: Adjunctive 3% hypertonic saline treatment significantly elevated mean arterial pressure, reduced intracranial pressure, greatly improved cerebral perfusion pressure, inhibited brain aquaporin 4 expression, reduced cerebral edema, and attenuated brain damage with a superior effect over 20% mannitol in a rabbit bacterial meningitis model.

Glutamate mediates hyperoxia-induced newborn rat lung injury through N-methyl-D-aspartate receptors.

Our laboratory found that the N-methyl-D-aspartate receptor (NMDAR) antagonist, MK-801, was able to decrease hyperoxia-induced lung damage. To further search for direct evidence of glutamate and its NMDARs participating in hyperoxia-induced lung injury, the amount of glutamate in the bronchoalveolar lavage fluid and the expression of NMDAR 2D in lung tissue were tracked in newborn rats that were exposed to 95% oxygen for 1, 3, and 7 days. The protective effect of MK-801 was then observed at different hyperoxia exposure times. As demonstrated by RT-PCR, NMDAR 2D expression was much higher in hyperoxia exposure on the third and the seventh days than in the air control group. The levels of glutamate in the bronchoalveolar lavage fluid on the first and third days of hyperoxia exposure were significantly higher than in the air control group. MK-801 alleviated lung injury and inflammatory reaction induced by 95% O(2) for 3 and 7 days. These results indicate that large amounts of endogenous glutamate from the lungs were released, and its NMDAR were expressed strongly under conditions of high oxygen concentration. We conclude that the endogenous glutamate mediated newborn rat lung damage induced by hyperoxia through NMDARs.