Transcriptomics combined with physiological analysis reveals the mechanism of cadmium uptake and tolerance in Ligusticum chuanxiong Hort. under cadmium treatment.

Introduction: Ligusticum chuanxiong Hort. is a widely used medicinal plant, but its growth and quality can be negatively affected by contamination with the heavy metal cadmium (Cd). Despite the importance of understanding how L. chuanxiong responds to Cd stress, but little is currently known about the underlying mechanisms. Methods: To address this gap, we conducted physiological and transcriptomic analyses on L. chuanxiong plants treated with different concentrations of Cd2+ (0 mg·L-1, 5 mg·L-1, 10 mg·L-1, 20 mg·L-1, and 40 mg·L-1). Results: Our findings revealed that Cd stress inhibited biomass accumulation and root development while activating the antioxidant system in L. chuanxiong. Root tissues were the primary accumulation site for Cd in this plant species, with Cd being predominantly distributed in the soluble fraction and cell wall. Transcriptomic analysis demonstrated the downregulation of differential genes involved in photosynthetic pathways under Cd stress. Conversely, the plant hormone signaling pathway and the antioxidant system exhibited positive responses to Cd regulation. Additionally, the expression of differential genes related to cell wall modification was upregulated, indicating potential enhancements in the root cell wall's ability to sequester Cd. Several differential genes associated with metal transport proteins were also affected by Cd stress, with ATPases, MSR2, and HAM3 playing significant roles in Cd passage from the apoplast to the cell membrane. Furthermore, ABC transport proteins were found to be key players in the intravesicular compartmentalization and efflux of Cd. Discussion: In conclusion, our study provides preliminary insights into the mechanisms underlying Cd accumulation and tolerance in L. chuanxiong, leveraging both physiological and transcriptomic approaches. The decrease in photosynthetic capacity and the regulation of plant hormone levels appear to be major factors contributing to growth inhibition in response to Cd stress. Moreover, the upregulation of differential genes involved in cell wall modification suggests a potential mechanism for enhancing root cell wall capabilities in isolating and sequestering Cd. The involvement of specific metal transport proteins further highlights their importance in Cd movement within the plant.

MicroRNA-155-3p promotes breast cancer progression through down-regulating CADM1.

BACKGROUND/PURPOSE: Cell adhesion molecule 1 (CADM1) functions as a tumor suppressor and has been identified to be frequently inactivated in breast cancer, and closely associated with patients' poor prognosis and advanced TNM stage. However, the mechanisms underlying CADM1 in breast cancer progression remains incompletely clear. miR-155, a predicted modulator of CADM1 was reported to be overexpressed in breast cancer, and its high expression level was closely related to the malignant progression of breast cancer. The present study aimed to explore whether miR-155-3p could modulate CADM1 expression and then involved in the progression of breast cancer. METHODS: The expression patterns of miR-155-3p in breast cancer tissues and cell lines were determined by RT-PCR technology. The relationship between CADM1 and miR-155-3p were determined by the luciferase gene reporter and Western Blot (WB) assays. Cell proliferation, apoptosis rates and tumorigenesis were determined by CCK-8, flow cytometry and in vivo xenotransplanation experiments, respectively. RESULTS: miR-155-3p was up-regulated in breast cancer tissues and cells when compared to the adjacent normal tissues and normal breast MCF 10A cells. The mRNA and protein levels of CADM1 showed opposite expression patterns to that of miR-155-3p expression detected, and miR-155-3p could negatively regulate CADM1 expression in breast cancer MCF-7 cells. Moreover, gain-of function assay showed that overexpression of miR-155-3p promoted cell proliferation, tumorigenesis and repressed cell apoptosis, but these effects were all significantly impaired when the cells were simultaneously transfected with OE-CADM1, the overexpressing vector of CADM1. CONCLUSION: This study revealed that miR-155-3p could accelerate the progression of breast cancer via down-regulation of CADM1 expression.

Guillain-Barré syndrome following bacterial meningitis: a case report and literature review.

BACKGROUND: We reported a case of an adult that presented Guillain-Barré syndrome (GBS) after bacterial meningitis which was secondary to chronic suppurative otitis media (CSOM). To our knowledge, this is the first case involving an adult presenting with GBS following bacterial meningitis. CASE PRESENTATION: A 46-year man with type 2 diabetes and otitis media (OM) suffered with fever, headache, and vomiting for 6 days. The patient's neck stiffness was obvious and the Kernig and Brudzinski signs were produced. The result of cerebrospinal fluid (CSF) analysis and cytological examination of the CSF supported the diagnose of bacterial meningitis. On day 17 the patient felt numbness in both hands and feet, which gradually progressed to weakness of the limbs. Bladder dysfunction occurred, which required catheterization. The patient showed a tetraparesis with emphasis on the legs. The deep tendon reflexes of limbs were absent. The patient had peripheral hypalgesia and deep sensory dysfunction. The symptoms were possibly a result of GBS. Nerve conduction study showed that the F wave latency of the upper and lower limbs was prolonged, particularly the lower limbs. 8 days later the repeated nerve conduction study showed a low compound muscle action potential (3.3 mV) with a normal distal motor latency (14.2 ms) and a low motor nerve conduction velocity (34.3 m/s) in the tibial nerve. The patient still required assistance when walking 3 months after onset. CONCLUSIONS: GBS following bacterial meningitis is rare and limbs weakness in patients with bacterial meningitis was usually considered because of weakness. This case should serve as a reminder for clinical doctors that when a patient with bacterial meningitis complains about limbs numbness or weakness, GBS should be considered, especially when the patient had diabetes mellitus (DM) history.

Development of atherosclerotic-moyamoya syndrome with genetic variant of RNF213 p.R4810K and p.T1727M: A case report.

OBJECTIVE: We report a rare case of atherosclerotic-moyamoya syndrome (A-MMS) in an adult female with genetic variant of both ring finger 213 (RNF213) p.R4810K and p.T1727M. CASE REPORT: A 46-year-old previously healthy, right-handed woman displayed transient slurred speech, which started to worsen four years ago. Initial magnetic resonance angiography (MRA) revealed stenosis in left middle cerebral artery (MCA), bilateral anterior cerebral artery (ACA), and left posterior cerebral artery (PCA). The patient subsequently underwent catheter angiography, which confirmed the formation of moyamoya vessels, with Suzuki's angiographic staging of grade-3 on the left side. Although the patient had been on both anti-platelet and statin therapy at the time, a follow-up examination showed further exacerbation of left MCA stenosis, along with enhanced moyamoya vessel formation. On black-blood imaging using DANTE-SPACE, there were eccentric, evolving lesions in the left MCA. We next screened for potential genetic variants, using genomic DNA samples isolated from both the patient and her immediate family members. The results showed that the patient, along with her mother, sister, and brother, possessed the heterozygous variant of the RNF213 gene, including c.14429G > A (p.R4810K) and c.5180C > T (p.T1727M). The patient's daughter did not have the variant. CONCLUSION: Collectively, we present a unique case of A-MMS with genetic variant of RNF213 p.R4810K and p.T1727M, manifesting as progression. Based on the family tree, these two mutations are on the same RNF213 haplotype. Whether atherosclerosis is the cause of A-MMS or it further exacerbates the injury of MMD to the A-MMS patients with RNF213 gene variant is a question to be investigated.