Combined use of CLP290 and bumetanide alleviates neuropathic pain and its mechanism after spinal cord injury in rats.

AIM: We aimed to explore whether the combination of CLP290 and bumetanide maximally improves neuropathic pain following spinal cord injury (SCI) and its possible molecular mechanism. METHODS: Rats were randomly divided into five groups: Sham, SCI + vehicle, SCI + CLP290, SCI + bumetanide, and SCI + combination (CLP290 + bumetanide). Drug administration commenced on the 7th day post-injury (7 dpi) and continued for 14 days. All rats underwent behavioral assessments for 56 days to comprehensively evaluate the effects of interventions on mechanical pain, thermal pain, cold pain, motor function, and other relevant parameters. Electrophysiological assessments, immunoblotting, and immunofluorescence detection were performed at different timepoints post-injury, with a specific focus on the expression and changes of KCC2 and NKCC1 proteins in the lumbar enlargement of the spinal cord. RESULTS: CLP290 and bumetanide alleviated SCI-associated hypersensitivity and locomotor function, with the combination providing enhanced recovery. The combined treatment group exhibited the most significant improvement in restoring Rate-Dependent Depression (RDD) levels. In the combined treatment group and the two individual drug administration groups, the upregulation of potassium chloride cotransporter 2 (K+-Cl-cotransporter 2, KCC2) expression and downregulation of sodium potassium chloride cotransporter 1 (Na+-K+-Cl-cotransporter 1, NKCC1) expression in the lumbar enlargement area resulted in a significant increase in the KCC2/NKCC1 ratio compared to the SCI + vehicle group, with the most pronounced improvement seen in the combined treatment group. Compared to the SCI + vehicle group, the SCI + bumetanide group showed no significant paw withdrawal thermal latency (PWTL) improvement at 21 and 35 dpi, but a notable enhancement at 56 dpi. In contrast, the SCI + CLP290 group significantly improved PWTL at 21 days, with non-significant changes at 35 and 56 days. At 21 dpi, KCC2 expression was marginally higher in monotherapy groups versus SCI + vehicle, but not significantly. At 56 dpi, only the SCI + bumetanide group showed a significant difference in KCC2 expression compared to the control group. CONCLUSION: Combined application of CLP290 and bumetanide effectively increases the ratio of KCC2/NKCC1, restores RDD levels, enhances GABAA receptor-mediated inhibitory function in the spinal cord, and relieves neuropathic pain in SCI; Bumetanide significantly improves neuropathic pain in the long term, whereas CLP290 demonstrates a notable short-term effect.

Coordination Between Respiration and Swallowing in Patients With Dysphagia After Cervical Spinal Cord Injury: An Observational Case-Control Study.

PURPOSE: The purpose of the present study was to characterize the differences between respiration and swallowing in patients with dysphagia after cervical spinal cord injury (CSCI) and to explore the underlying physiological changes. METHOD: A total of 95 participants were recruited for bedside swallowing evaluation followed by a flexible endoscopic evaluation of swallowing and surface electromyography with a thermocouple nasal airflow sensor examination: 32 with dysphagia, 33 without dysphagia, and 30 healthy controls. The differences in respiratory patterns, swallowing apnea duration (SAD), inspiratory-expiratory ratio, and swallowing efficiency were observed among healthy adults, CSCI patients with and without dysphagia after CSCI. RESULTS: Compared with those of healthy controls and patients without dysphagia after CSCI, the postswallow respiratory pattern of patients with dysphagia after CSCI was an inspiratory pattern, and the SAD was significantly shorter in patients with dysphagia after CSCI (p < .001). Additionally, the expiratory time in patients with dysphagia was significantly shorter than the inspiratory time, and the swallowing efficiency was reduced, requiring multiple swallows. Moreover, the index of SAD was statistically significant for predicting the development of dysphagia in patients with CSCI (p < .001). CONCLUSION: Patients with CSCI have an inspiratory pattern after swallowing, and the SAD is significantly reduced; SAD can be used as the predictor of dysphagia in patients after CSCI; the pattern of coordination between respiration and swallowing in patients with dysphagia after CSCI is different from that of healthy controls and patients without dysphagia after CSCI. SUPPLEMENTAL MATERIAL: https://doi.org/10.23641/asha.26524717.

Neuronal repair after spinal cord injury by in vivo astrocyte reprogramming mediated by the overexpression of NeuroD1 and Neurogenin-2.

BACKGROUND: As a common disabling disease, irreversible neuronal death due to spinal cord injury (SCI) is the root cause of functional impairment; however, the capacity for neuronal regeneration in the developing spinal cord tissue is limited. Therefore, there is an urgent need to investigate how defective neurons can be replenished and functionally integrated by neural regeneration; the reprogramming of intrinsic cells into functional neurons may represent an ideal solution. METHODS: A mouse model of transection SCI was prepared by forceps clamping, and an adeno-associated virus (AAV) carrying the transcription factors NeuroD1 and Neurogenin-2(Ngn2) was injected in situ into the spinal cord to specifically overexpress these transcription factors in astrocytes close to the injury site. 5-bromo-2´-deoxyuridine (BrdU) was subsequently injected intraperitoneally to continuously track cell regeneration, neuroblasts and immature neurons marker expression, neuronal regeneration, and glial scar regeneration. In addition, immunoprotein blotting was used to measure the levels of transforming growth factor-ß (TGF-ß) pathway-related protein expression. We also evaluated motor function, sensory function, and the integrity of the blood-spinal cord barrier(BSCB). RESULTS: The in situ overexpression of NeuroD1 and Ngn2 in the spinal cord was achieved by specific AAV vectors. This intervention led to a significant increase in cell regeneration and the proportion of cells with neuroblasts and immature neurons cell properties at the injury site(p < 0.0001). Immunofluorescence staining identified astrocytes with neuroblasts and immature neurons cell properties at the site of injury while neuronal marker-specific staining revealed an increased number of mature astrocytes at the injury site. Behavioral assessments showed that the intervention did not improve The BMS (Basso mouse scale) score (p = 0.0726) and gait (p > 0.05), although the treated mice had more sensory sensitivity and greater voluntary motor ability in open field than the non-intervention mice. We observed significant repair of the BSCB at the center of the injury site (p < 0.0001) and a significant improvement in glial scar proliferation. Electrophysiological assessments revealed a significant improvement in spinal nerve conduction (p < 0.0001) while immunostaining revealed that the levels of TGF-ß protein at the site of injury in the intervention group were lower than control group (p = 0.0034); in addition, P70 s6 and PP2A related to the TGF-ß pathway showed ascending trend (p = 0.0036, p = 0.0152 respectively). CONCLUSIONS: The in situ overexpression of NeuroD1 and Ngn2 in the spinal cord after spinal cord injury can reprogram astrocytes into neurons and significantly enhance cell regeneration at the injury site. The reprogramming of astrocytes can lead to tissue repair, thus improving the reduced threshold and increasing voluntary movements. This strategy can also improve the integrity of the blood-spinal cord barrier and enhance nerve conduction function. However, the simple reprogramming of astrocytes cannot lead to significant improvements in the striding function of the lower limbs.

Acute non-traffic traumatic spinal cord injury in the aging population: Analysis of the National Inpatient Sample 2005-2018.

BACKGROUND: This study aimed to determine risk factors for poor in-hospital outcomes in a large cohort of older adult patients with acute non-traffic traumatic spinal cord injury (tSCI). METHODS: This is a population-based, retrospective, observational study. Data of older adults ≥65 years with a primary discharge diagnosis of acute non-traffic tSCI were extracted from the US National Inpatient Sample (NIS) database 2005-2018. Traffic-related tSCI admissions or patients lacking complete data on age, sex and outcomes of interest were excluded. Univariate and multivariate logistic regression analysis was used to determine associations between variables and in-hospital outcomes. RESULTS: Data of 49,449 older patients (representing 246,939 persons in the US) were analyzed. The mean age was 79.9 years. Multivariable analyses revealed that severe International Classification of Disease (ICD)-based injury severity score (ICISS) (adjusted odds ratio [aOR] = 3.14, 95% confidence interval [CI]: 2.77-3.57), quadriplegia (aOR = 2.79, 95%CI: 2.34-3.32), paraplegia (aOR = 2.60, 95%CI:1.89-3.58), cervical injury with vertebral fracture (aOR = 2.19, 95%CI: 1.90-2.52), and severe liver disease (aOR = 2.33, 95%CI: 1.34-4.04) were all strong independent predictors of in-hospital mortality. In addition, malnutrition (aOR = 3.19, 95% CI: 2.93-3.48) was the strongest predictors of prolonged length of stay (LOS). CONCLUSIONS: Several critical factors for in-hospital mortality, unfavorable discharge, and prolonged LOS among US older adults with acute non-traffic tSCI were identified. In addition to the factors associated with initial severity, the presence of severe liver disease and malnutrition emerged as strong predictors of unfavorable outcomes, highlighting the need for special attention for these patient subgroups.

A smartphone-based diagnostic analyzer for point-of-care milk somatic cell counting.

BACKGROUND: Mastitis, a pervasive and detrimental disease in dairy farming, poses a significant challenge to the global dairy industry. Monitoring the milk somatic cell count (SCC) is vital for assessing the incidence of mastitis and the quality of raw cow's milk. However, existing SCC detection methods typically require large-scale instruments and specialized operators, limiting their application in resource-constrained settings such as dairy farms and small-scale labs. To address these limitations, this study introduces a novel, smartphone-based, on-site SCC testing method that leverages smartphone capabilities for milk somatic cell identification and enumeration, offering a portable and user-friendly testing platform. RESULTS: The central findings of our study demonstrate the effectiveness of the proposed method for counting milk somatic cells. Its on-site applicability, facilitated by the microfluidic chip, optical system, and smartphone integration, heralds a paradigm shift in point-of-care testing (POCT) for dairy farms and smaller laboratories. This approach bypasses complex processing and presents a user-friendly solution for real-time SCC monitoring in resource-limited settings. This device boasts several unique features: small size, low cost (<$1,000 total manufacturing cost and <$1 per test), and high accuracy. Remarkably, it delivers test results within just 2 min. Actual-sample testing confirmed its consistency with results from the commercial Bentley FTS/FCM cytometer, affirming the reliability of the proposed method. Overall, these results underscore the potential for transformative change in dairy farm management and laboratory testing practices. SIGNIFICANCE: In summary, this study concludes that the proposed smartphone-based method significantly contributes to the accessibility and ease of SCC testing in resource-limited environments. By fostering the use of POCT technology in food safety control, particularly in the dairy industry, this innovative approach has the potential to revolutionize the monitoring and management of mastitis, ultimately benefiting the global dairy sector.

Inhibition of phospholipase D promotes neurological function recovery and reduces neuroinflammation after spinal cord injury in mice.

Introduction: Spinal cord injury (SCI) is a severely disabling disease. Hyperactivation of neuroinflammation is one of the main pathophysiological features of secondary SCI, with phospholipid metabolism playing an important role in regulating inflammation. Phospholipase D (PLD), a critical lipid-signaling molecule, is known to be involved in various physiological processes, including the regulation of inflammation. Despite this knowledge, the specific role of PLD in SCI remains unclear. Methods: In this study, we constructed mouse models of SCI and administered PLD inhibitor (FIPI) treatment to investigate the efficacy of PLD. Additionally, transcriptome sequencing and protein microarray analysis of spinal cord tissues were conducted to further elucidate its mechanism of action. Results: The results showed that PLD expression increased after SCI, and inhibition of PLD significantly improved the locomotor ability, reduced glial scarring, and decreased the damage of spinal cord tissues in mice with SCI. Transcriptome sequencing analysis showed that inhibition of PLD altered gene expression in inflammation regulation. Subsequently, the protein microarray analysis of spinal cord tissues revealed variations in numerous inflammatory factors. Biosignature analysis pointed to an association with immunity, thus confirming the results obtained from transcriptome sequencing. Discussion: Collectively, these observations furnish compelling evidence supporting the anti-inflammatory effect of FIPI in the context of SCI, while also offering important insights into the PLD function which may be a potential therapeutic target for SCI.

The role of foam cells in spinal cord injury: challenges and opportunities for intervention.

Spinal cord injury (SCI) results in a large amount of tissue cell debris in the lesion site, which interacts with various cytokines, including inflammatory factors, and the intrinsic glial environment of the central nervous system (CNS) to form an inhibitory microenvironment that impedes nerve regeneration. The efficient clearance of tissue debris is crucial for the resolution of the inhibitory microenvironment after SCI. Macrophages are the main cells responsible for tissue debris removal after SCI. However, the high lipid content in tissue debris and the dysregulation of lipid metabolism within macrophages lead to their transformation into foamy macrophages during the phagocytic process. This phenotypic shift is associated with a further pro-inflammatory polarization that may aggravate neurological deterioration and hamper nerve repair. In this review, we summarize the phenotype and metabolism of macrophages under inflammatory conditions, as well as the mechanisms and consequences of foam cell formation after SCI. Moreover, we discuss two strategies for foam cell modulation and several potential therapeutic targets that may enhance the treatment of SCI.

Impact of inflammation and Treg cell regulation on neuropathic pain in spinal cord injury: mechanisms and therapeutic prospects.

Spinal cord injury is a severe neurological trauma that can frequently lead to neuropathic pain. During the initial stages following spinal cord injury, inflammation plays a critical role; however, excessive inflammation can exacerbate pain. Regulatory T cells (Treg cells) have a crucial function in regulating inflammation and alleviating neuropathic pain. Treg cells release suppressor cytokines and modulate the function of other immune cells to suppress the inflammatory response. Simultaneously, inflammation impedes Treg cell activity, further intensifying neuropathic pain. Therefore, suppressing the inflammatory response while enhancing Treg cell regulatory function may provide novel therapeutic avenues for treating neuropathic pain resulting from spinal cord injury. This review comprehensively describes the mechanisms underlying the inflammatory response and Treg cell regulation subsequent to spinal cord injury, with a specific focus on exploring the potential mechanisms through which Treg cells regulate neuropathic pain following spinal cord injury. The insights gained from this review aim to provide new concepts and a rationale for the therapeutic prospects and direction of cell therapy in spinal cord injury-related conditions.

Impact of Frailty on Inpatient Outcomes of Acute Traumatic Spinal Cord Injury: Evidence From US National Inpatient Sample.

OBJECTIVES: Spinal cord injury (SCI) is any spinal cord injury or affliction that results in temporary or permanent impairment of motor or sensory function. This study determined the prevalence of frailty and its impact on in-hospital outcomes of patients admitted with acute traumatic SCI (TSCI). METHODS: This retrospective study extracted data of adults 18 to 85 years with acute TSCI from the US Nationwide Inpatient Sample (NIS) 2016 to 2018. Frailty status were assessed by the 11-factor modified Frailty Index (mFI-11) through claim codes. Patients with an mFI ≥3 were classified as frail. Associations between study variables and in-hospital mortality, discharge status, prolonged length of stay, severe infection, and hospital costs were determined by univariate and multivariable regression analyses. RESULTS: A total of 52,263 TSCI patients were identified, where 12,203 (23.3%) patients were frail. After adjusting for relevant confounders, frailty was independently associated with increased risk for in-hospital mortality [adjusted odds ratio (aOR) = 1.25, 95% CI:1.04-1.49], unfavorable discharge (aOR =1.15, 95% CI: 1.09-1.22), prolonged length of stay (aOR =1.32, 95% CI: 1.24-1.40), and severe infection (aOR =2.52, 95% CI: 2.24-2.83), but not hospital cost. Stratified analyses revealed frailty was associated with higher unfavorable discharge and severe infection regardless of age, Charlson Comorbidity Index, and injury level. CONCLUSIONS: In acute TSCI, frailty is independently associated with increased risk for adverse inpatient outcomes in terms of in-hospital mortality, prolonged hospital stays, unfavorable discharge, and particularly severe infection.

Spinal cord injury-induced gut dysbiosis influences neurological recovery partly through short-chain fatty acids.

Spinal cord injury (SCI) can reshape gut microbial composition, significantly affecting clinical outcomes in SCI patients. However, mechanisms regarding gut-brain interactions and their clinical implications have not been elucidated. We hypothesized that short-chain fatty acids (SCFAs), intestinal microbial bioactive metabolites, may significantly affect the gut-brain axis and enhance functional recovery in a mouse model of SCI. We enrolled 59 SCI patients and 27 healthy control subjects and collected samples. Thereafter, gut microbiota and SCFAs were analyzed using 16 S rDNA sequencing and gas chromatography-mass spectrometry, respectively. We observed an increase in Actinobacteriota abundance and a decrease in Firmicutes abundance. Particularly, the SCFA-producing genera, such as Faecalibacterium, Megamonas, and Agathobacter were significantly downregulated among SCI patients compared to healthy controls. Moreover, SCI induced downregulation of acetic acid (AA), propionic acid (PA), and butyric acid (BA) in the SCI group. Fecal SCFA contents were altered in SCI patients with different injury course and injury segments. Main SCFAs (AA, BA, and PA) were administered in combination to treat SCI mice. SCFA supplementation significantly improved locomotor recovery in SCI mice, enhanced neuronal survival, promoted axonal formation, reduced astrogliosis, and suppressed microglial activation. Furthermore, SCFA supplementation downregulated NF-κB signaling while upregulating neurotrophin-3 expression following SCI. Microbial sequencing and metabolomics analysis showed that SCI patients exhibited a lower level of certain SCFAs and related bacterial strains than healthy controls. SCFA supplementation can reduce inflammation and enhance nourishing elements, facilitating the restoration of neurological tissues and the improvement of functional recuperation. Trial registration: This study was registered in the China Clinical Trial Registry ( www.chictr.org.cn ) on February 13, 2017 (ChiCTR-RPC-17010621).

The identification of new roles for nicotinamide mononucleotide after spinal cord injury in mice: an RNA-seq and global gene expression study.

Background: Nicotinamide mononucleotide (NMN), an important transforming precursor of nicotinamide adenine dinucleotide (NAD+). Numerous studies have confirmed the neuroprotective effects of NMN in nervous system diseases. However, its role in spinal cord injury (SCI) and the molecular mechanisms involved have yet to be fully elucidated. Methods: We established a moderate-to-severe model of SCI by contusion (70 kdyn) using a spinal cord impactor. The drug was administered immediately after surgery, and mice were intraperitoneally injected with either NMN (500 mg NMN/kg body weight per day) or an equivalent volume of saline for seven days. The central area of the spinal cord was harvested seven days after injury for the systematic analysis of global gene expression by RNA Sequencing (RNA-seq) and finally validated using qRT-PCR. Results: NMN supplementation restored NAD+ levels after SCI, promoted motor function recovery, and alleviated pain. This could potentially be associated with alterations in NAD+ dependent enzyme levels. RNA sequencing (RNA-seq) revealed that NMN can inhibit inflammation and potentially regulate signaling pathways, including interleukin-17 (IL-17), tumor necrosis factor (TNF), toll-like receptor, nod-like receptor, and chemokine signaling pathways. In addition, the construction of a protein-protein interaction (PPI) network and the screening of core genes showed that interleukin 1ß (IL-1ß), interferon regulatory factor 7 (IRF 7), C-X-C motif chemokine ligand 10 (Cxcl10), and other inflammationrelated factors, changed significantly after NMN treatment. qRT-PCR confirmed the inhibitory effect of NMN on inflammatory factors (IL-1ß, TNF-α, IL-17A, IRF7) and chemokines (chemokine ligand 3, Cxcl10) in mice following SCI. Conclusion: The reduction of NAD+ levels after SCI can be compensated by NMN supplementation, which can significantly restore motor function and relieve pain in a mouse model. RNA-seq and qRT-PCR systematically revealed that NMN affected inflammation-related signaling pathways, including the IL-17, TNF, Toll-like receptor, NOD-like receptor and chemokine signaling pathways, by down-regulating the expression of inflammatory factors and chemokines.

The Effect of Glycine and N-Acetylcysteine on Oxidative Stress in the Spinal Cord and Skeletal Muscle After Spinal Cord Injury.

Oxidative stress is a frequently occurring pathophysiological feature of spinal cord injury (SCI) and can result in secondary injury to the spinal cord and skeletal muscle atrophy. Studies have reported that glycine and N-acetylcysteine (GlyNAC) have anti-aging and anti-oxidative stress properties; however, to date, no study has assessed the effect of GlyNAC in the treatment of SCI. In the present work, we established a rat model of SCI and then administered GlyNAC to the animals by gavage at a dose of 200 mg/kg for four consecutive weeks. The BBB scores of the rats were significantly elevated from the first to the eighth week after GlyNAC intervention, suggesting that GlyNAC promoted the recovery of motor function; it also promoted the significant recovery of body weight of the rats. Meanwhile, the 4-week heat pain results also suggested that GlyNAC intervention could promote the recovery of sensory function in rats to some extent. Additionally, after 4 weeks, the levels of glutathione and superoxide dismutase in spinal cord tissues were significantly elevated, whereas that of malondialdehyde was significantly decreased in GlyNAC-treated animals. The gastrocnemius wet weight ratio and total antioxidant capacity were also significantly increased. After 8 weeks, the malondialdehyde level had decreased significantly in spinal cord tissue, while reactive oxygen species accumulation in skeletal muscle had decreased. These findings suggested that GlyNAC can protect spinal cord tissue, delay skeletal muscle atrophy, and promote functional recovery in rats after SCI.

Glycine and N-Acetylcysteine (GlyNAC) Combined with Body Weight Support Treadmill Training Improved Spinal Cord and Skeletal Muscle Structure and Function in Rats with Spinal Cord Injury.

Skeletal muscle atrophy is a frequent complication after spinal cord injury (SCI) and can influence the recovery of motor function and metabolism in affected patients. Delaying skeletal muscle atrophy can promote functional recovery in SCI rats. In the present study, we investigated whether a combination of body weight support treadmill training (BWSTT) and glycine and N-acetylcysteine (GlyNAC) could exert neuroprotective effects, promote motor function recovery, and delay skeletal muscle atrophy in rats with SCI, and we assessed the therapeutic effects of the double intervention from both a structural and functional viewpoint. We found that, after SCI, rats given GlyNAC alone showed an improvement in Basso-Beattie-Bresnahan (BBB) scores, gait symmetry, and results in the open field test, indicative of improved motor function, while GlyNAC combined with BWSTT was more effective than either treatment alone at ameliorating voluntary motor function in injured rats. Meanwhile, the results of the skeletal muscle myofiber cross-sectional area (CSA), hindlimb grip strength, and acetylcholinesterase (AChE) immunostaining analysis demonstrated that GlyNAC improved the structure and function of the skeletal muscle in rats with SCI and delayed the atrophication of skeletal muscle.

Clinical characteristics and proposed mechanism of pediatric spinal cord injury resulting from backbend practice.

Objective: Pediatric spinal cord injury without radiographic abnormality (SCIWORA) caused by backbend practice is increasing. This study proposed an underlying 'combined injury mechanism' related to the spinal cord and femoral nerve overstretching. Methods: Pediatric patients diagnosed with backbend-associated SCIWORA at the China Rehabilitation Research Center during 2017-2021 were recruited. Clinical and imaging data were collected, and each patient's clinical course and prognosis were determined. Healthy dancers were recruited to simulate the backbend, obtain images, and estimate the spinal cord and femoral nerve stretch ratio. A model for the 'combined injury mechanism' was established using 4-week-old SD rats. Results: Forty-two SCIWORA female patients with an average age of 6 (SD 1) years and an average hospitalization time of 91 (SD 43) days were assessed. The primary initial symptom was pain in the back and/or lower extremities (33, 79%). The average time from injury onset to severe paralysis was 2.0 (SD 0.6) hours. Most patients had complete paraplegia (32, 76%), and neurological levels were distributed mainly in thoracic segments (38, 91%). Patients with elicited tendon reflexes on admission tended to have an incomplete spinal cord injury (p = 0.001) and improved motor recovery (p = 0.018). After one year, the most common complications were scoliosis (31, 74%) and abnormal hips (14, 33%). Injury of the caudal spinal cord torn by nerve roots was confirmed by surgical exploration in a case. The thoracic spinal cord and femoral nerves were overstretched by 148.8 ± 3.6% and111.7 ± 4.0%, respectively, in a full backbend posture. The 'combined injury mechanism' was partially replicated in the animal model. Conclusion: Spinal overstretch and transient dislocation are considered the primary mechanisms by which SCIWORA occurs in children. Overstretching the femoral nerve aggravates spinal cord injuries caused by backbend practice.

Healthy Eating for All? The Challenge of Adhering to Dietary Guidelines for Low-Income Groups in China.

The Chinese Dietary Guidelines propose a balanced diet for healthy living, but the affordability of this diet needs to be considered, especially for low-income households. To investigate the affordability of a healthy diet, this study analyzes the daily retail prices of 46 food items in 36 Chinese cities from 2016 to 2021. This study compares expenditure, diet composition, and nutritional status in two scenarios aligned with the guidelines. The results show that the mean minimum cost of a balanced diet exceeds the current per capita food expenditure for at least 182.85 million urban households. This suggests that low-income people would need to increase their expenditure by at least 20-121% to achieve the recommended diets. This study also identifies affordable and nutrient-dense foods such as standard flour, eggs, black beans, and cabbage, which policymakers should focus on when monitoring food prices. The findings recommend a combination of social and food system policies to reduce prices and make healthy diets accessible. This study identifies the gaps in the Chinese Dietary Guidelines for ensuring accessibility for vulnerable groups and provides a template for policymakers and researchers to track diet affordability using available food price data in China, contributing to China's 2030 Health Plan and the UN's Sustainable Development Goals.

Effects of Policy Intervention on Food System Resilience to Emergency Risk Shock: Experience from China during COVID-19 Pandemic.

Achieving the goal of zero hunger within the goal of sustainable development requires improving the resilience of food systems to various types of risk shocks; food systems have shown significant vulnerability to COVID-19 outbreaks and transmission. By analyzing the impact of China's lockdown policy and food security emergency policy in 2020 on food prices during the COVID-19 pandemic, we can clarify the role of policy intervention in enhancing the resilience of the food system, which can provide guidance, using China's experience, for dealing with global food safety emergencies in the future. Firstly, we selected Beijing, Shanghai and Guangdong as food-consuming areas, and Shandong, Henan, and Hubei as food-producing areas. We also collected food security emergency policy data from the Chinese government website during the COVID-19 pandemic. Secondly, a difference-in-difference method was used to observe that Chinese cabbage and pork prices in the main food-producing areas and food-consuming areas rose more obviously after the adoption of lockdown policy, and Chinese cabbage and pork prices in the food-consuming areas increased more obviously than those in food-producing areas. However, staple food prices have not risen significantly. Thirdly, the response of four kinds of food prices to the food security emergency policy is analyzed quantitatively and graphically using the food price volatility index and food price increase rate; we observed that the response of food prices to the food security emergency policy is related to the food types and regions. For food types, the fluctuation degree and increase in Chinese cabbage and pork prices decreased significantly after the adoption of the food security emergency policy. For regions, when the food security emergency policy was adopted, the food prices in the main food-consuming areas fluctuated more obviously than those in food-producing areas. Finally, we found that the implementation of the transport policy and the joint supply emergency policy in the main producing and consuming areas has played a very significant and positive role in stabilizing food prices.

Case Report: Upper Thoracic Esophageal Paralysis Accompanying a Type 1 Leprosy Reaction.

Type 1 leprosy reactions (T1LRs) occur mainly in patients with borderline leprosy and an unstable immune status. The main symptoms of T1LRs include aggravated skin lesions and nerve damage. Nerve damage involving the glossopharyngeal and vagus nerves causes dysfunction of the nose, pharynx, larynx, and even the esophagus, which are innervated by these nerves. Here, we report a case of upper thoracic esophageal paralysis caused by vagus nerve involvement in a patient with T1LRs. Although infrequent, this serious emergency merits attention.

Successful application of ALA-PDT in rare cutaneous infection of Mycobacterium parascrofulaceum.

Skin infections caused by Mycobacterium parascrofulaceum (MP) are extremely rare in clinical practice. In view of its potential hazard of spreading to systemic infection, correct diagnosis and effective treatment are extremely important. Due to the highly similar appearance of lymphangitic sporotrichosis (LS) and swimming pool granuloma (SPG) caused by Mycobacterium marinum (MM), MP infection is easily misdiagnosed as the above two skin diseases. Here, we report successful application of 5-aminolevulinic acid photodynamic therapy (ALA-PDT) in the treatment of a rare case of upper limb skin MP infection, providing reference for more safe and efficient disposal of such cases in clinic.

Mechanism of skeletal muscle atrophy after spinal cord injury: A narrative review.

Spinal cord injury leads to loss of innervation of skeletal muscle, decreased motor function, and significantly reduced load on skeletal muscle, resulting in atrophy. Factors such as braking, hormone level fluctuation, inflammation, and oxidative stress damage accelerate skeletal muscle atrophy. The atrophy process can result in skeletal muscle cell apoptosis, protein degradation, fat deposition, and other pathophysiological changes. Skeletal muscle atrophy not only hinders the recovery of motor function but is also closely related to many systemic dysfunctions, affecting the prognosis of patients with spinal cord injury. Extensive research on the mechanism of skeletal muscle atrophy and intervention at the molecular level has shown that inflammation and oxidative stress injury are the main mechanisms of skeletal muscle atrophy after spinal cord injury and that multiple pathways are involved. These may become targets of future clinical intervention. However, most of the experimental studies are still at the basic research stage and still have some limitations in clinical application, and most of the clinical treatments are focused on rehabilitation training, so how to develop more efficient interventions in clinical treatment still needs to be further explored. Therefore, this review focuses mainly on the mechanisms of skeletal muscle atrophy after spinal cord injury and summarizes the cytokines and signaling pathways associated with skeletal muscle atrophy in recent studies, hoping to provide new therapeutic ideas for future clinical work.

MicroRNAs in spinal cord injury: A narrative review.

Spinal cord injury (SCI) is a global medical problem with high disability and mortality rates. At present, the diagnosis and treatment of SCI are still lacking. Spinal cord injury has a complex etiology, lack of diagnostic methods, poor treatment effect and other problems, which lead to the difficulty of spinal cord regeneration and repair, and poor functional recovery. Recent studies have shown that gene expression plays an important role in the regulation of SCI repair. MicroRNAs (miRNAs) are non-coding RNA molecules that target mRNA expression in order to silence, translate, or interfere with protein synthesis. Secondary damage, such as oxidative stress, apoptosis, autophagy, and inflammation, occurs after SCI, and differentially expressed miRNAs contribute to these events. This article reviews the pathophysiological mechanism of miRNAs in secondary injury after SCI, focusing on the mechanism of miRNAs in secondary neuroinflammation after SCI, so as to provide new ideas and basis for the clinical diagnosis and treatment of miRNAs in SCI. The mechanisms of miRNAs in neurological diseases may also make them potential biomarkers and therapeutic targets for spinal cord injuries.