Visualization and Analysis of Infectious Disease Research on Nursing Care Based on CiteSpace in China.

Objective: To analyze the relevant research publications on infectious disease nursing in China to understand the current research status of infectious disease in nursing. Methods: Retrieve relevant literature on infectious disease in nursing from the establishment of the Chinese Biomedical Literature Database, China National Knowledge Infrastructure (CNKI), VIP Database, and Wanfang Database until May 10, 2021. Conduct bibliometric analysis using CiteSpace software. Key words were analyzed using cluster analysis. Results: A total of 4693 relevant literature on infectious disease research in nursing care were included in this study. The overall number of publications on infectious disease research in nursing showed an increasing trend, with a peak in 2010. There were 324 papers funded by scientific research funds, mainly from provincial-level fund projects. The core journal with the most published articles was Nursing Research. The research on infectious disease in nursing mainly focused on various aspects of infectious disease in nursing and infection control. CiteSpace cluster analysis of keywords showed that a total of six clusters were formed: infectious diseases, infectious disease care, health education, mental health, infectious disease nurses, and etiology. After 2015, high-mutation keywords included "quality nursing" and "infection control". Conclusion: Chinese research on infectious disease research in nursing closely follows clinical reality and has developed rapidly. Currently, research focuses on infectious disease research in nursing and infection control. Future research trends will further broaden the depth and breadth of the research, enhance research on infection control and quality nursing, and improve the breadth and depth of the research.

[Effect of tillage patterns on the structure of weed communities in oat fields in the cold and arid region of North China].

In order to clarify the effects of tillage patterns on farmland weed community structure and crop production characteristics, based on 10 years location experiment with no-tillage, subsoiling and conventional tillage in the cold and arid region of North China, and supplementary experiment of plowing after 10 years no-tillage and subsoiling, oat was planted in 2 soils under different tillage patterns, and field weed total density, dominant weed types, weed diversity index, field weed biomass and oats yield were measured. The results showed that the regional weed community was dominated by foxtail weed (Setaira viridis); the weed density under long-term no-tillage was 2.20-5.14 times of tillage at different growing stages of oat, but there were no significant differences between conditional tillage and plowing after long-term no-tillage and subsoiling. Field weed Shannon diversity indices were 0.429 and 0.531, respectively, for sandy chestnut soil and loamy meadow soil under no-tillage conditions, and field weed biomass values were 1.35 and 2.26 times of plowing treatment, while the oat biomass values were only 2807.4 kg x hm(-2) and 4053.9 kg x hm(-2), decreased by 22.3% and 46.2%, respectively. The results showed that the weed community characteristics were affected by both tillage patterns and soil types. Long-term no-tillage farmland in the cold and arid region of North China could promote the natural evolution of plant communities by keeping more perennial weeds, and the plowing pattern lowered the annual weed density, eliminated perennial weeds with shallow roots, and stimulated perennial weeds with deep roots.

Oxidative stress in immune-mediated motoneuron destruction.

Experimental autoimmune gray matter disease (EAGMD) is a model of both upper and lower motor neuron degeneration. EAGMD and amyotrophic lateral sclerosis (ALS) possess similar clinical and pathological features. The aim of this study was to find evidence of upper and lower neuronal damage in the EAGMD guinea pigs. The main ultrastructural alterations included abnormal mitochondria and disorganization of neurofilaments in the myelinated nerve fibers of the spinal cord. Swollen mitochondria and dilated endoplasmic reticulum were found in pyramidal cells of the motor cortex. The myelinated fibers in the cerebral peduncle showed atrophied axons and swollen mitochondria. Some motoneurons showed apoptosis-like signs. Pathological changes in the sciatic nerve manifest wallerian-like degeneration. Using immunofluorescence double labeling and confocal laser microscopy, IgG was colocalized with activated microglia in the ventral horn of the spinal cord. We also examined possible evidences of oxidative stress in the EAGMD guinea pig model and the role of p38 mitogen-activated protein kinase (p38MAPK) pathway in motor neuron degeneration. Our findings suggest that nitric oxide and peroxynitrite-mediated oxidative damage may play important roles in the pathogenesis of the neuronal degeneration in the spinal cord. Inflammatory cytokines such as TNF-alpha and IL-1 play important roles in the formation and acceleration of the spinal cord damage. The activation of p38MAPK signal pathway was involved in the development of the motor neuron degeneration of the spinal cord.

Sensory involvement in the SOD1-G93A mouse model of amyotrophic lateral sclerosis.

A subset of patients of amyotrophic lateral sclerosis (ALS) present with mutation of Cu/Zn superoxide dismutase 1 (SOD1), and such mutants caused an ALS- like disorder when expressed in rodents. These findings implicated SOD1 in ALS pathogenesis and made the transgenic animals a widely used ALS model. However, previous studies of these animals have focused largely on motor neuron damage. We report herein that the spinal cords of mice expressing a human SOD1 mutant (hSOD1-G93A), besides showing typical destruction of motor neurons and axons, exhibit significant damage in the sensory system, including Wallerian-like degeneration in axons of dorsal root and dorsal funiculus, and mitochondrial damage in dorsal root ganglia neurons. Thus, hSOD1-G93A mutation causes both motor and sensory neuropathies, and as such the disease developed in the transgenic mice very closely resembles human ALS.

The NADPH oxidase is involved in lipopolysaccharide-mediated motor neuron injury.

Recent evidence indicates that neuroinflammation is a key event in amyotrophic lateral sclerosis (ALS). However, the precise impact of inflammation on motor neurons remains elusive. By using organotypic spinal cord slice cultures, we demonstrate that exposure to lipopolysaccharide (LPS) led to the demise of motor neurons in a dose- and time- dependent manner, whereas interneurons were impaired relatively mildly. The ultrastructure of motor neurons showed extensive vacuolation and swollen mitochondria. Motor neurons lacked the expression of calretinin, and BAPTA-AM, an intracellular calcium chelator, ameliorated motor neuron injury, indicating that the low capacity of calcium buffering may partially account for the vulnerability of motor neurons. NADPH oxidase was activated upon LPS challenge, and apocynin, the selective inhibitor of this enzyme, prevented inflammation-mediated toxicity to motor neurons, suggesting that NADPH oxidase may play a critical role in motor neuron death caused by LPS-induced inflammation.

Ultrastructural evidence of neurofilament involvement in immune-mediated motor neuron injury.

Amyotrophic lateral sclerosis (ALS) is a progressive neurological disorder. A pathologic hallmark of ALS is accumulation of neurofilaments in proximal axons of affected motor neurones. As the neurofilaments involved in immune-mediated spinal cord ventral horn motor neuron degeneration and loss, we developed immune-mediated motor neuron injury animal model by inoculating Lewis rats with swine spinal cord homogenate and investigated the ultrastructural features of neurofilament accumulation using transmission electron microscopy. Our results showed that there was aberrant accumulation of neurofilaments in perikarya and processes of remaining motor neurons in recipient animals, which is similar to those observed in ALS patients. These findings suggest that immune-mediated motor neuron injury may share a common pathogenesis with ALS.

The neuroprotective potential of phase II enzyme inducer on motor neuron survival in traumatic spinal cord injury in vitro.

(1) Phase II enzyme inducer is a kind of compound which can promote the expression of antioxidative enzymes through nuclear factor erythroid 2-related factor 2 (Nrf2) activation. Recently, it has been reported that these compounds show neuroprotective effect via combating oxidative stress. The purpose of this study is to determine whether phase II enzyme inducers have neuroprotective effects on traumatic spinal cord injury. (2) An organotypic spinal cord culture system was used, Phase II enzyme inducers were added to culture medium for 1 week, motor neurons were counted by SMI-32 staining, glutamate, Nrf2, and Heme oxygenase-1(HO-1) mRNA were tested. (3) This study showed motor neuron loss within 1 week in culture. After 1 week in culture, the system was stable. Moreover, Glutamate was increased when in culture 48 h and decreased after 1 week in culture. There was no significant change between 1 and 4 weeks in culture. Necrotic motor neuron and damaged mitochondrial were observed in culture 48 h. Furthermore, phase II enzyme inducers: tert-butyhydroquinone (t-BHQ), 3H-1,2-dithiole-3-thione (D3T), and 5,6-dihydrocyclopenta-1,2-dithiole-3-thione (CPDT) were shown to promote motor neuron survival after dissection, it was due to increasing Nrf2 and HO-1 mRNA expression and protecting mitochondrial not due to decreasing glutamate level. (4) The loss of motor neuron due to dissection can mimic severe traumatic spinal cord injury. These results demonstrate that glutamate excitotoxicity and the damage of mitochondrial is possibly involve in motor neuron death after traumatic spinal cord injury and phase II enzyme inducers show neuroprotective potential on motor neuron survival in traumatic spinal cord injury in vitro.