Objective　To analyze the whole genome sequence characteristics of dengue serotype 2 virus (DENV-2) strains isolated from Guangzhou in 2023, providing new foundational data to support local dengue fever prevention and control efforts. Methods　Dengue viruses were isolated from serum samples of dengue fever patients using C6/36 cells. Whole genome sequencing of dengue virus was performed using Nanopore sequencing technology (Nanopore platform). The sequencing data were assembled utilizing IPH-NANO v1.0 software, and homology analysis, phylogenetic analysis, and amino acid site variation analysis of the dengue virus genome sequence were conducted using software such as BioEdit7.0.9.0, MEGA11, and iqTree1.6.12. Results　A total of 13 DENV-2 isolates were obtained from the serum samples of dengue fever patients in Guangzhou in 2023, all of which were derived from locally infected cases. The whole genome sequences obtained by sequencing and splicing ranged from 10 429-10 439 nt in length. The nucleotide (amino acid) homology among the 13 isolates was 99.7%-99.9% (99.6%-9.9%). A genome-wide phylogenetic analysis showed that the genotypes of all 13 Guangzhou isolates were identified as the Cosmopolitan genotype and were grouped in the same evolutionary clade as isolates from Réunion (French overseas territory), Djibouti, Kenya, and other regions. Compared with the reference sequence (NC001474), a total of 26 amino acid site variations were identified in the C/prM/E protein regions of the 13 isolates, including 4 variations in the C protein region, 8 in the prM protein region, and 14 in the E protein region. Conclusion　The DENV-2 strains isolated from Guangzhou in 2023 exhibited high homology, with closely related isolates primarily originating from countries or regions such as Réunion, Djibouti, and Kenya, it highlights the need for further assessment of the risk of dengue fever importation from East Africa, South Asia, and other regions.

With the rapid advancement of synthetic biology, CRISPR-Cas systems have emerged as a powerful tool for gene editing, demonstrating significant potential in various fields, including medicine, agriculture, and industrial biotechnology. This review comprehensively summarizes the significant progress in applying artificial intelligence (AI) technologies to the design, mining, and modification of CRISPR-Cas systems. AI technologies, especially machine learning, have revolutionized sgRNA design by analyzing high-throughput sequencing data, thereby improving the editing efficiency and predicting off-target effects with high accuracy. Furthermore, this paper explores the role of AI in sgRNA design and evaluation, highlighting its contributions to the annotation and mining of CRISPR arrays and Cas proteins, as well as its potential for modifying key proteins involved in gene editing. These advancements have not only improved the efficiency and precision of gene editing but also expanded the horizons of genome engineering, paving the way for intelligent and precise genome editing.
CRISPR-Cas Systems/genetics* ; Artificial Intelligence ; Gene Editing/methods* ; RNA, Guide, CRISPR-Cas Systems/genetics* ; Machine Learning ; Humans ; Genetic Engineering/methods* ; Synthetic Biology

Growth factors (GFs) are a class of peptides that facilitate cell growth by binding to specific receptors on the cell membrane. With unique properties, GFs are widely applied in the repair of injured tissue. To address the limitations associated with natural peptide-based GFs and recombinant GFs, researchers have developed diverse GF mimetics. This article offers a comprehensive review on common types of GFs and their applications in tissue repair and summarizes the features of GF mimetics currently under development. The aim is to provide valuable references for promoting the application of GFs in regenerative medicine.
Intercellular Signaling Peptides and Proteins/therapeutic use* ; Humans ; Tissue Engineering/methods* ; Regenerative Medicine/methods* ; Animals ; Wound Healing/drug effects* ; Biomimetic Materials

Objective:To explore the deubiquitination modification of the deubiquitinase BRCC3 in rats with neuropathic pain (NPP) treated with meridian tuina of Zhuang medicine and its analgesic molecular mechanism.Methods:Rats were divided into normal group, sham-operation group, model group, sham-tuina group, and meridian tuina of Zhuang medicine group using a random number table method, with 9 rats in each group. Except for the normal and sham operation groups, spinal nerve ligation models were prepared in all other groups. On the first day after surgery, intervention was carried out on the meridian tuina of Zhuang medicine and sham-tuina groups for 14 days, while the other three groups were not intervened; the paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) of each group of rats were measured at 0 days before operation, 1, 7, and 14 days after operation. Western blot was used to detect the expressions of BRCC3 and NLRP3 proteins in spinal cord tissue, and ELISA was used to detect the level of IL-1β in serum.Results:On postoperative 7 and 14 d, compared with the model group, the meridian tuina of Zhuang medicine group showed an increase in PWMT and PWTL, a decrease in NLPR3 and BRCC3 expression in spinal cord tissue, and a decrease in serum IL-1β levels ( P<0.05). Compared with the sham-tuina group, the meridian tuina of Zhuang medicine group showed an increase in PWMT and PWTL, a decrease in NLRP3 protein expression in spinal cord tissue, and a decrease in IL-1β levels in serum ( P<0.05). Conclusion:Meridian tuina of Zhuang medicine can alleviate pain sensitivity in SNL model rats, and its mechanism is related to the inhibition of the expression of deubiquitinase BRCC3 by meridian massage of Zhuang medicine, which increases the ubiquitination level of NLRP3 and hinders its activation, thereby blocking the immune inflammatory response mediated by inflammatory factors.

G protein-coupled receptor 120(GPR120)is one of the membrane receptors for long chain free fatty acids and is distributed in alveolus macrophages and airway epithelial Club cells.GPR120 activation alleviates the inflammation of respiratory tract,improves airway hyper-responsiveness,stimulates proliferation of Club cells and promotes the repair of respiratory epithelium,which may attenuate asthma and acute lung injury.

OBJECTIVE To investigate the effect of dioscin on renal injury in septic rats and its possible mechanism. METHODS The septic rat model was induced by using cecal ligation and puncture. Sixty model rats were randomly divided into model group （0.5% sodium carboxymethyl cellulose solution）， dioscin low-dose， medium-dose and high-dose groups （30， 60， 120 mg/kg） and dexamethasone group （positive control， 10 mg/kg）， with 12 rats per group； another 12 rats were selected as the sham operation group （0.5% sodium carboxymethyl cellulose solution）. After 15 minutes of modeling， rats in each group were injected with medicine/0.5% sodium carboxymethyl cellulose solution via the tail vein. Twenty-four hours after administration， the levels of creatinine （Cr）， blood urea nitrogen （BUN）， neutrophil gelatinase associated lipocalin （NGAL）， kidney injury molecule-1 （KIM- 1）， interleukin 6 （IL-6）， IL-1β and tumor necrosis factor-α （TNF-α） in serum and malondialdehyde （MDA） in renal tissue， superoxide dismutase （SOD） activity and the protein expressions of nuclear factor E2-related factor 2 （Nrf2）， heme oxygenase-1 （HO-1）， NOD-like receptor protein 3 （NLRP3） were detected； renal histomorphology was observed. RESULTS Compared with model group， pathological injury of renal tissue was improved significantly in dioscin low-dose， medium-dose and high-dose groups； the levels of Cr， BUN， NGAL， KIM-1， IL-6， IL-1β and TNF-α in serum， MDA level and protein expression of NLRP3 in renal tissue were decreased significantly （P＜0.05）； SOD activity in renal tissue， protein expressions of Nrf2 and HO-1 were increased significantly （P＜0.05）， in a dose-dependent manner （P＜0.05）. The pathological damage of renal tissue in the dioscin high-dose group was similar to dexamethasone group， and there was no statistically significant difference in the levels of the above indicators （P＞0.05）. CONCLUSIONS Dioscin can activate the Nrf2/HO-1 signaling pathway to inhibit NLRP3 inflammasome， and realize the inhibition of inflammatory factors and oxidative stress， so as to protect the kidney injury in sepsis.

OBJECTIVE To investigate the effect of dioscin on renal injury in septic rats and its possible mechanism. METHODS The septic rat model was induced by using cecal ligation and puncture. Sixty model rats were randomly divided into model group （0.5% sodium carboxymethyl cellulose solution）， dioscin low-dose， medium-dose and high-dose groups （30， 60， 120 mg/kg） and dexamethasone group （positive control， 10 mg/kg）， with 12 rats per group； another 12 rats were selected as the sham operation group （0.5% sodium carboxymethyl cellulose solution）. After 15 minutes of modeling， rats in each group were injected with medicine/0.5% sodium carboxymethyl cellulose solution via the tail vein. Twenty-four hours after administration， the levels of creatinine （Cr）， blood urea nitrogen （BUN）， neutrophil gelatinase associated lipocalin （NGAL）， kidney injury molecule-1 （KIM- 1）， interleukin 6 （IL-6）， IL-1β and tumor necrosis factor-α （TNF-α） in serum and malondialdehyde （MDA） in renal tissue， superoxide dismutase （SOD） activity and the protein expressions of nuclear factor E2-related factor 2 （Nrf2）， heme oxygenase-1 （HO-1）， NOD-like receptor protein 3 （NLRP3） were detected； renal histomorphology was observed. RESULTS Compared with model group， pathological injury of renal tissue was improved significantly in dioscin low-dose， medium-dose and high-dose groups； the levels of Cr， BUN， NGAL， KIM-1， IL-6， IL-1β and TNF-α in serum， MDA level and protein expression of NLRP3 in renal tissue were decreased significantly （P＜0.05）； SOD activity in renal tissue， protein expressions of Nrf2 and HO-1 were increased significantly （P＜0.05）， in a dose-dependent manner （P＜0.05）. The pathological damage of renal tissue in the dioscin high-dose group was similar to dexamethasone group， and there was no statistically significant difference in the levels of the above indicators （P＞0.05）. CONCLUSIONS Dioscin can activate the Nrf2/HO-1 signaling pathway to inhibit NLRP3 inflammasome， and realize the inhibition of inflammatory factors and oxidative stress， so as to protect the kidney injury in sepsis.

True plus-minus lid syndrome is a rare clinical phenomenon characterized by ptosis on one side of the upper eyelid and uncompensated retraction on the other side. The reported cases in the past were all acquired plus-minus lid syndrome cases. This article presented a 26-year-old female patient with true plus-minus lid syndrome, who was in good health with no history of other underlying diseases, surgery or trauma. Her upper eyelid had been asymmetrical since childhood, showing retraction on the right and mild ptosis on the left, and it was left untreated. In March 2022, the patient was admitted to the Department of Plastic Surgery at the Second Hospital of Nanjing, Nanjing University of Chinese Medicine. The levator muscle of the upper eyelid was shortened on the left side, and the levator muscle of the upper eyelid was released and lengthened on the right side by surgery. After a 17-month follow-up, the bilateral corneal exposure rate was basically symmetrical, and the operative effect was satisfactory. The author also discussed the symptoms, signs, and differential diagnosis of true and pseudo plus-minus lid syndrome by reviewing the literature and inferred the pathogenesis of this case, which is helpful for selecting surgical methods.

OBJECTIVE To observe the effect of Qiai(Artemisia argyi Levl.et Van.var.argyi cv.Qiai)essential oil on the healing of infected skin wounds and explore its mechanism.METHODS 30 Kunming mice were randomly divided into five equal groups:blank control group,substrate group,positive control group(3 mL·kg-1 Mupirocin ointment),low-dose group(each patch containing 7.3 mg of Qiai essential oil),and high-dose group(each patch containing 57.6 mg of Qiai essential oil).After anesthe-sia,a 10 mm full-thickness circular skin wound was created on the back of each mouse.Following hemostasis,100 μL of Staphylococ-cus aureus bacterial solution(1.5×108 CFU·mL-1)was applied to the wound.The wounds in each group were treated in the afore-mentioned manner,the dressing was changed daily,and the healing of the skin wound was observed.On the 12th day post-surgery,the mice were euthanized and the skin around the wounds was collected for HE and Masson staining to observe pathological features;qPCR and Western blotting were used to detect the expression of genes related to wound healing(Col1a1,Col3a1,Fn1,VEGFA),in-flammatory factors(IL-1β,IL-6,TNF-α),and the PI3K/Akt signaling pathway in the wound skin tissue.Further,in NIH-3T3 mouse embryonic fibroblasts,the potential impact of Artemisia argyi volatile oil on PI3K/Akt signaling pathway activity was investigated using the PI3K inhibitor PI-103.RESULTS Animal experiments have shown that compared to the blank control group,the relative wound area in both the low-dose and high-dose groups significantly decreased;the infiltration of inflammatory cells in the wound tis-sues reduced,while the expression of collagen fibers increased;qPCR showed that,compared to the blank control group,the expres-sion of VEGFA,Col3a1,and Col1a1 in the low-dose and high-dose groups significantly increased,while the expression of inflamma-tory factors IL-1β and TNF-α decreased;further Western blotting revealed that compared to the blank control group,both the phos-phorylated PI3K/total PI3K ratio and the phosphorylated Akt/total Akt ratio in the low-dose and high-dose groups significantly in-creased in a dose-dependent manner.Cellular experimental results also confirmed that the volatile oil from Artemisia argyi exerts a reg-ulatory effect on the PI3K/Akt signaling pathway in NIH-3T3 cells.CONCLUSION The essential oil of Qiai can promote wound healing,with its mechanism possibly involving the activation of the PI3K/Akt signaling pathway,suppression of inflammatory factor ex-pression,and promotion of collagen expression.

True plus-minus lid syndrome is a rare clinical phenomenon characterized by ptosis on one side of the upper eyelid and uncompensated retraction on the other side. The reported cases in the past were all acquired plus-minus lid syndrome cases. This article presented a 26-year-old female patient with true plus-minus lid syndrome, who was in good health with no history of other underlying diseases, surgery or trauma. Her upper eyelid had been asymmetrical since childhood, showing retraction on the right and mild ptosis on the left, and it was left untreated. In March 2022, the patient was admitted to the Department of Plastic Surgery at the Second Hospital of Nanjing, Nanjing University of Chinese Medicine. The levator muscle of the upper eyelid was shortened on the left side, and the levator muscle of the upper eyelid was released and lengthened on the right side by surgery. After a 17-month follow-up, the bilateral corneal exposure rate was basically symmetrical, and the operative effect was satisfactory. The author also discussed the symptoms, signs, and differential diagnosis of true and pseudo plus-minus lid syndrome by reviewing the literature and inferred the pathogenesis of this case, which is helpful for selecting surgical methods.