Publications by authors named "Jin-Jin Ma"

Microbially-mediated arsenic biotransformation plays a pivotal role in the biogeochemical cycling of arsenic; however, the presence of arsenic biotransformation genes (ABGs) in urban dust remains unclear. To investigate the occurrence and spatiotemporal distributions of ABGs, a total of one hundred and eighteen urban dust samples were collected from different districts of Xiamen city, China in summer and winter. Although inorganic arsenic species, including arsenate [As(V)] and arsenite [As(III)], were found to be predominant, the methylated arsenicals, particularly trimethylarsine oxide [TMAs(V)O] and dimethylarsenate [DMAs(V)], were detected in urban dust.

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Purpose/aim: Bone defects caused by trauma, tumors, congenital malformation, or inflammation are very common in orthopedics. In recent years, mimicking the composition and structure of natural bone tissue has become a hot topic in biomaterial research, with the aim of developing an ideal biomaterial for bone defect transplantation. Here, the feasibility of a biphasic calcium phosphate (BCP)/acylated methacrylate gelatin (GelMA) composite hydrogel to repair bone defects was evaluated in vitro and in rats.

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Objective: The objective is to identify the risk factors for necrotizing enterocolitis (NEC) in neonates by a meta-analysis, and to provide a reference for the prevention of NEC.

Methods: The databases, including Chinese Biomedical Literature Datebase, China National Knowledge Infrastructure, Wanfang database, and Weipu Periodical database, PubMed, Web of Science, Embase, Cochrane Library, were searched for studies on the risk factors for NEC in neonates. The meta-analysis was carried out with the aid of Stata software.

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Community and composition of dust-borne microbes would affect human health and are regulated by microbial community assembly. The dust in kindergarten is always collected to evaluate the microbial exposure of children, yet the microbial assembly, their interactions, and potential pathogens in kindergarten dust remain unclear. Here, we aim to investigate the microbial community assembly and structures, and potential bacterial pathogens in outdoor dust of kindergartens, and reveal the factors influencing the assembly and composition of microbial community.

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Microplastics can act as carriers of heavy metals and may enter humans through ingestion and threaten human health. However, the bioaccessibility of heavy metals associated with microplastics and its implications for human health risk assessments are poorly understood. Therefore, in this study, four typical heavy metals (As(V), Cr(VI), Cd(II), and Pb(II)) and one typical microplastic (polyvinyl chloride, PVC) were chosen to estimate the human health risk of microplastic-associated heavy metals by incorporating bioaccessibility.

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Objective: To observe expression of CD38, a key modulator of nicotinamide dinucleotide (NAD+) metabolism in mice with knee osteoarthritis, and protective effect of CD38 inhibition during the osteoarthritis (OA) development.

Method: The destabilization of the medial meniscus (DMM) model was performed in mice to mimic the process of OA. Immunofluorescence of CD38 was performed to evaluate its response during the OA process.

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Heavy metals in urban dust could pose noticeable human health risks, but there are few studies focusing on comprehensive human health risk assessment with the incorporation of both bioaccessibility and source apportionment in urban dust. Thus, fifty-eight urban dust samples were collected from kindergartens in Xiamen to analyze the bioaccessibility-based, source-specific health risk of heavy metals (V, Co, Ni, As, Mo, Cr, Mn, Cu, Zn, and Pb). Most heavy metals, except for V and Mn, were significantly enriched in urban dust based on their values of geoaccumulation index (I) and may be influenced by human activities.

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Osteoporosis is one of the common clinical orthopedic diseases, which can lead to a variety of complications. There are many pathogenic factors in this disease. The latest research found that ATP6V1H is a new gene leading to the occurrence of osteoporosis, and it is likely to become a new target for the future drug treatment of osteoporosis.

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Article Synopsis
  • Axonal regeneration is crucial for recovery after nervous system damage, but is often limited in mammals; recent research shows that deleting the Klf4 gene can boost this regeneration process.
  • In a mouse model of sciatic nerve injury, reduced Klf4 expression was linked to enhanced healing in sensory neurons, both in lab experiments and live subjects.
  • Additionally, knocking out Klf4 in the cortex improved the regeneration of the corticospinal tract, suggesting that manipulating KLF4 could be a viable approach to support recovery from nerve injuries.
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Traumatic nerve injuries have become a common clinical problem, and axon regeneration is a critical process in the successful functional recovery of the injured nervous system. In this study, we found that peripheral axotomy reduces PTEN expression in adult sensory neurons; however, it did not alter the expression level of PTEN in IB4-positive sensory neurons. Additionally, our results indicate that the artificial inhibition of PTEN markedly promotes adult sensory axon regeneration, including IB4-positive neuronal axon growth.

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In addition to altered gene expression, pathological cytoskeletal dynamics in the axon are another key intrinsic barrier for axon regeneration in the central nervous system (CNS). Here, we show that knocking out myosin IIA and IIB (myosin IIA/B) in retinal ganglion cells alone, either before or after optic nerve crush, induces significant optic nerve regeneration. Combined Lin28a overexpression and myosin IIA/B knockout lead to an additive promoting effect and long-distance axon regeneration.

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The anatomical structure of the mammalian cerebral cortex is the essential foundation for its complex neural activity. This structure is developed by proliferation, differentiation, and migration of neural progenitor cells (NPCs), the fate of which is spatially and temporally regulated by the proper gene. This study was used in utero electroporation and found that the well-known oncogene c-Myc mainly promoted NPCs' proliferation and their transformation into intermediate precursor cells.

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Article Synopsis
  • Recent research identifies a new role for telomerase reverse transcriptase (TERT) in regulating axon regeneration in the mammalian central nervous system (CNS).
  • The study highlights a signaling pathway involving c-Myc, TERT, and p53 that controls sensory axon growth.
  • Overexpressing p53 in sensory neurons and retinal cells can significantly enhance the regeneration of sensory axons and optic nerves, presenting new opportunities for improving CNS healing.
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While axon regeneration is a key determinant of functional recovery of the nervous system after injury, it is often poor in the mature nervous system. Influx of extracellular calcium (Ca ) is one of the first phenomena that occur following axonal injury, and calcium/calmodulin-dependent protein kinase II (CaMKII), a target substrate for calcium ions, regulates the status of cytoskeletal proteins such as F-actin. Herein, we found that peripheral axotomy activates CaMKII in dorsal root ganglion (DRG) sensory neurons, and inhibition of CaMKII impairs axon outgrowth in both the peripheral and central nervous systems (PNS and CNS, respectively).

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The inflammatory response is a critical regulator for the regeneration of axon following nervous system injury. Nuclear factor-kappa B (NF-κB) is characteristically known for its ubiquitous role in the inflammatory response. However, its functional role in adult mammalian axon growth remains elusive.

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Nicotinic acetylcholine receptors (nAChRs) are heteropentameric ligand-gated ion channels that mediate excitatory neurotransmission at the neuromuscular junction (NMJ) and other peripheral and central synapses. At the NMJ, acetylcholine receptors (AChRs) are constantly exposed to mechanical stress resulting from muscle contraction. It is therefore of interest to understand if their function is influenced by mechanical stimuli.

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Background: Postsynaptic enrichment of acetylcholine receptors (AChRs) at the vertebrate neuromuscular junction (NMJ) depends on the activation of the muscle receptor tyrosine MuSK by neural agrin. Agrin-stimulation of MuSK is known to initiate an intracellular signaling cascade that leads to the clustering of AChRs in an actin polymerization-dependent manner, but the molecular steps which link MuSK activation to AChR aggregation remain incompletely defined.

Methodology/principal Findings: In this study we used biochemical, cell biological and molecular assays to investigate a possible role in AChR clustering of cortactin, a protein which is a tyrosine kinase substrate and a regulator of F-actin assembly and which has also been previously localized at AChR clustering sites.

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