Objective: To investigate the trends in incidence and mortality of thyroid cancer in Nantong City, Jiangsu Province from 2013 to 2022, so as to provide a basis for optimizing comprehensive regional prevention and control strategies. Methods: Data on incidence and mortality of thyroid cancer in Nantong City from 2013 to 2022 were collected via the Nantong Cancer Registration Reporting System. Crude incidence and mortality were calculated. The Chinese population-standardized incidence and Chinese population-standardized mortality were calculated using the standard age structure from the Fifth National Population Census in 2000. The average annual percent change (AAPC) was used to analyze the trends in incidence and mortality of thyroid cancer across different genders, age groups, and urban-rural areas from 2013 to 2022. Results: The crude incidence and Chinese population-standardized incidence in Nantong City rose from 5.79/100 000 and 4.36/100 000 in 2013 to 34.87/100 000 and 30.40/100 000 in 2022, respectively (AAPC=22.226%, 24.139%, both P<0.05). The crude mortality increased from 0.39/100 000 to 1.07/100 000 (AAPC=10.469%, P<0.05), while the trend for Chinese population-standardized mortality was not statistically significant (P>0.05). The Chinese population-standardized incidence and Chinese population-standardized mortality for females were 20.41/100 000 and 0.30/100 000, respectively, which were 3.28 times and 1.50 times those of males. The Chinese population-standardized incidence showed upward trends for both males and females (AAPC=22.840%, 24.592%, both P<0.05), while the trends for Chinese population-standardized mortality were not statistically significant (both P>0.05). From 2013 to 2022, the crude incidence in the age groups of 15-<45, 45-<65, and 65-<85 years, and the crude mortality in the age group of 65-<85 years showed upward trends (AAPC=27.808%, 21.756%, 13.365%, and 8.030%, all P<0.05), while trends in other age groups were not statistically significant (all P>0.05). The Chinese population-standardized incidence in urban areas was 16.96/105, which was 1.40 times that of rural areas. The Chinese population-standardized mortality in rural areas was 0.27/105, which was 1.29 times that of urban areas. From 2013 to 2022, the Chinese population-standardized incidence in both urban and rural areas and Chinese population-standardized mortality in rural areas showed upward trends (AAPC=17.264%, 27.758%, 6.387%, all P<0.05), while trend in Chinese population-standardized mortality in urban areas was not statistically significant (P>0.05). Conclusions From 2013 to 2022, the crude incidence, Chinese population-standardized incidence, and crude mortality of thyroid cancer in Nantong City all showed upward trends in the total population, males, and females, while the trend in Chinese population-standardized mortality was stable. There were differences in mortality trends between urban and rural areas: the trend in urban areas was stable, whereas the trend in rural areas was upward.

Oral squamous cell carcinoma (OSCC) is a common head and neck malignancy. Approximately 50% to 60% of patients with OSCC are diagnosed at a locally advanced stage (clinical staging III-IVa). Even with comprehensive and sequential treatment primarily based on surgery, the 5-year overall survival rate remains below 50%, and patients often suffer from postoperative functional impairments such as difficulties with speaking and swallowing. Programmed death receptor-1 (PD-1) inhibitors are increasingly used in the neoadjuvant treatment of locally advanced OSCC and have shown encouraging efficacy. However, clinical practice still faces key challenges, including the definition of indications, optimization of combination regimens, and standards for efficacy evaluation. Based on the latest research advances worldwide and the clinical experience of the expert group, this expert consensus systematically evaluates the application of PD-1 inhibitors in the neoadjuvant treatment of locally advanced OSCC, covering combination strategies, treatment cycles and surgical timing, efficacy assessment, use of biomarkers, management of special populations and immune related adverse events, principles for immunotherapy rechallenge, and function preservation strategies. After multiple rounds of panel discussion and through anonymous voting using the Delphi method, the following consensus statements have been formulated: 1) Neoadjuvant therapy with PD-1 inhibitors can be used preoperatively in patients with locally advanced OSCC. The preferred regimen is a PD-1 inhibitor combined with platinum based chemotherapy, administered for 2-3 cycles. 2) During the efficacy evaluation of neoadjuvant therapy, radiographic assessment should follow the dual criteria of Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 and immune RECIST (iRECIST). After surgery, systematic pathological evaluation of both the primary lesion and regional lymph nodes is required. For combination chemotherapy regimens, PD-L1 expression and combined positive score need not be used as mandatory inclusion or exclusion criteria. 3) For special populations such as the elderly (≥ 70 years), individuals with stable HIV viral load, and carriers of chronic HBV/HCV, PD-1 inhibitors may be used cautiously under the guidance of a multidisciplinary team (MDT), with close monitoring for adverse events. 4) For patients with a poor response to neoadjuvant therapy, continuation of the original treatment regimen is not recommended; the subsequent treatment plan should be adjusted promptly after MDT assessment. Organ transplant recipients and patients with active autoimmune diseases are not recommended to receive neoadjuvant PD-1 inhibitor therapy due to the high risk of immune related activation. Rechallenge is generally not advised for patients who have experienced high risk immune related adverse events such as immune mediated myocarditis, neurotoxicity, or pneumonitis. 5) For patients with a good pathological response, individualized de escalation surgery and function preservation strategies can be explored. This consensus aims to promote the standardized, safe, and precise application of neoadjuvant PD-1 inhibitor strategies in the management of locally advanced OSCC patients.

In response to the clinical needs of cancer treatment and rehabilitation, Professor Lin Hongsheng proposed the Wuzhi Wuyang (five treatments and rehabilitation) concept on the basis of years of clinical experience and the Guben Qingyuan (consolidate the foundation and clear the source) theory. Wuzhi Wuyang emphasizes the importance of treatment and rehabilitation and aims to provide personalized and stage-specific treatment and rehabilitation plans by integrating the advantages of traditional Chinese medicine (TCM) and modern medicine to achieve comprehensive life-cycle management for patients with cancer. The proposal of Wuzhi Wuyang has provided new ideas and methods for the treatment, prevention, and rehabilitation of cancer, along with valuable references for clinical practice and academic research. This article summarizes the connotation of Wuzhi Wuyang and its application in the comprehensive management of cancer prevention and treatment with TCM.

ObjectiveBola-like short peptides exhibit novel self-assembly properties due to the formation of peptide dimers via hydrogen bonding interactions between their C-terminals. In this configuration, hydrophilic amino acids are distributed at both terminals, making these peptides behave similarly to Bola peptides. The electrostatic repulsive interactions arising from the hydrophilic amino acids at each terminal can be neutralized, thereby greatly promoting the lateral association of β-sheets. Consequently, assemblies with significantly larger widths are typically the dominant nanostructures for Bola-like peptides. To investigate the effect of hydrophilic amino acids on the self-assembly behavior of Bola-like peptides, the peptides Ac-RI₃-CONH₂ and Ac-HI₃-CONH₂ were designed and synthesized using the Bola-like peptide Ac-KI₃-CONH₂ as a template. Their self-assembly behavior was systematically examined. MethodsAtomic force microscopy (AFM) and transmission electron microscopy (TEM) were employed to characterize the morphology and size of the assemblies. The secondary structures of the assemblies were analyzed using circular dichroism (CD) and Fourier transform infrared (FTIR) spectroscopy. Small-angle neutron scattering (SANS) was used to obtain detailed structural information at a short-length scale. Based on these experimental results, the effects of hydrophilic amino acids on the self-assembly behavior of Bola-like short peptides were systematically analyzed, and the underlying formation mechanism was explored. ResultsThe aggregation process primarily involved three steps. First, peptide dimers were formed through hydrogen bonding interactions between their C-terminals. Within these dimers, the hydrophilic amino acids K, R, and H were positioned at both terminals, enabling the peptides to self-assemble in a manner similar to Bola peptides. Next, β-sheets were formed via hydrogen bonding interactions along the peptide backbone. Finally, self-assemblies were generated through the lateral association of β-sheets. The results demonstrated that both Ac-KI₃-CONH₂ and Ac-RI₃-CONH₂ could self-assemble into double-layer nanotubes with diameters of approximately 200 nm. These nanotubes were formed by the edge fusion of helical ribbons, which initially emerged from twisted ribbons. Notably, the primary assemblies of these peptides exhibited opposite chirality: nanofibers formed by Ac-KI₃-CONH₂ displayed left-handed chirality, whereas those formed by Ac-RI₃-CONH₂ exhibited right-handed chirality. This reversal in torsional direction was primarily attributed to the different abilities of K and R to form hydrogen bonds with water. In contrast, Ac-HI₃-CONH₂ formed narrower twisted ribbons with a significantly reduced width of approximately 30 nm, which was attributed to the strong steric hindrance caused by the imidazole rings. The multilayer height of these ribbons was mainly due to the unique structure of the imidazole rings, which can function as both hydrogen bond donors and acceptors, thereby promoting aggregate growth in the vertical direction. ConclusionThe final morphology of the self-assemblies resulted from a delicate balance of various non-covalent interactions. By altering the types of hydrophilic amino acid residues in Bola-like short peptides, the relative strength of non-covalent interactions that drive assembly formation can be effectively regulated, allowing precise control over the morphology and chirality of the assemblies. This study provides a simple and effective approach for constructing diverse self-assemblies and lays a theoretical foundation for the development of functional biomaterials.

Stroke is one of the leading causes of death and disability worldwide， ranking as the second leading cause of mortality globally and the primary cause of adult disability. Its pathological process involves complex cascade mechanisms， with high incidence and disability rates， posing a major threat to human health. According to statistics from the World Health Organization， more than 13 million new cases of stroke occur globally each year， resulting in direct medical costs and socioeconomic burdens amounting to hundreds of billions of dollars. In recent years， breakthroughs in the study of programmed cell death mechanisms have provided new insights into stroke treatment. Among them， ferroptosis， a novel form of cell death driven by iron-dependent lipid peroxidation， has attracted widespread attention in the pathological process of stroke. Ferroptosis is closely associated with iron metabolism disorders， oxidative stress， and lipid peroxidation， and exhibits unique regulatory effects in key pathological processes of stroke， such as ischemia-reperfusion injury， disruption of the blood-brain barrier， and neuronal apoptosis. It plays an important role in post-stroke neurological damage. Chinese medicine， as an essential component of traditional Chinese medicine （TCM）， has demonstrated advantages in modulating ferroptosis and exerting neuroprotective effects. This review systematically summarizes current research on the neuroprotective mechanisms of Chinese medicine compound formulas and monomers through the regulation of ferroptosis pathways in post-stroke conditions， aiming to provide a basis for optimizing clinical treatment strategies and exploring new therapeutic approaches， and to offer new strategies and approaches for stroke treatment.

[Objective] To investigate the infection status and characteristics of HEV among voluntary blood donors in Ningbo, and to provide a basis for improving the blood screening strategy. [Methods] A total of 12 227 blood samples from voluntary blood donors in Ningbo from June 2022 to May 2023 were tested for HEV serology, enzymology, and nucleic acid testing. Furthermore, HEV gene sequencing was performed for genotyping analysis, and donors with reactive nucleic acid testing results were followed up to confirm their infection status. [Results] The reactivity rate of HEV Ag, anti-HEV IgM and anti-HEV IgG was 0.098%, 0.899% and 29.198%, respectively. There was no difference in the reactivity of anti-HEV IgM and anti-HEV IgG between genders, donation frequencies and donation types (P>0.05). The reactivity rate increased significantly with age (P<0.05). The rate of ALT disqualification (ALT>50U/L) was significantly higher than that in non-reactive samples (P<0.05). The HEV Ag reactivity rate (0.098%) was not correlated with gender, donation frequency, donation type or age. One HEV RNA positive case was found, with a positive rate of 0.008%(1/12 227). It was confirmed to be hepatitis E virus genotype 3 by sequencing analysis. Apart from HEV Ag reactivity, all other blood safety screening items were non-reactive, suggesting this case might be in the acute infection phase. The follow-up results showed that all indicators of the donor's previous blood donation were non-reactive. [Conclusion] Pre-donation ALT detection can reduce the risk of transfusion-transmitted HEV (TT-HEV) to a certain extent, and the effective way to prevent TT-HEV is to detect HEV RNA and serology of donor blood.

With the widespread use of antibiotics, drug-resistant bacterial infections have become a significant threat to human health. Finding new antibacterial strategies that can effectively control drug-resistant bacterial infections has become an urgent task. Unlike small molecule drugs that target bacterial proteins, antisense oligonucleotide (ASO) can target genes related to bacterial resistance, pathogenesis, growth, reproduction and biofilm formation. By regulating the expression of these genes, ASO can inhibit or kill bacteria, providing a novel approach for the development of antibacterial drugs. To overcome the challenge of delivering antisense oligonucleotide into bacterial cells, various drug delivery systems have been applied in this field, including cell-penetrating peptides, lipid nanoparticles and inorganic nanoparticles, which have injected new momentum into the development of antisense oligonucleotide in the antibacterial realm. This review summarizes the current development of small nucleic acid drugs, the antibacterial mechanisms, targets, sequences and delivery vectors of antisense oligonucleotide, providing a reference for the research and development of antisense oligonucleotide in the treatment of bacterial infections.

To investigate the incidence of postoperative neuropsychic dysfunction (PND) in Parkinson's disease (PD) patients undergoing deep brain stimulation (DBS) and to analyze its influencing factors.

ObjectiveNeuroinflammation plays a crucial role in both the onset and progression of ischemic stroke, exerting a significant impact on the recovery of the central nervous system. Excessive neuroinflammation can lead to secondary neuronal damage, further exacerbating brain injury and impairing functional recovery. As a result, effectively modulating and reducing neuroinflammation in the brain has become a key therapeutic strategy for improving outcomes in ischemic stroke patients. Among various approaches, targeting immune regulation to control inflammation has gained increasing attention. This study aims to investigate the role of in vitro induced regulatory T cells (Treg cells) in suppressing neuroinflammation after ischemic stroke, as well as their potential therapeutic effects. By exploring the mechanisms through which Tregs exert their immunomodulatory functions, this research is expected to provide new insights into stroke treatment strategies. MethodsNaive CD4⁺ T cells were isolated from mouse spleens using a negative selection method to ensure high purity, and then they were induced in vitro to differentiate into Treg cells by adding specific cytokines. The anti-inflammatory effects and therapeutic potential of Treg cells transplantation in a mouse model of ischemic stroke was evaluated. In the middle cerebral artery occlusion (MCAO) model, after Treg cells transplantation, their ability to successfully migrate to the infarcted brain region and their impact on neuroinflammation levels were examined. To further investigate the role of Treg cells in stroke recovery, the changes in cytokine expression and their effects on immune cell interactions was analyzed. Additionally, infarct size and behavioral scores were measured to assess the neuroprotective effects of Treg cells. By integrating multiple indicators, the comprehensive evaluation of potential benefits of Treg cells in the treatment of ischemic stroke was performed. ResultsTreg cells significantly regulated the expression levels of both pro-inflammatory and anti-inflammatory cytokines in vitro and in vivo, effectively balancing the immune response and suppressing excessive inflammation. Additionally, Treg cells inhibited the activation and activity of inflammatory cells, thereby reducing neuroinflammation. In the MCAO mouse model, Treg cells were observed to accumulate in the infarcted brain region, where they significantly reduced the infarct size, demonstrating their neuroprotective effects. Furthermore, Treg cell therapy notably improved behavioral scores, suggesting its role in promoting functional recovery, and increased the survival rate of ischemic stroke mice, highlighting its potential as a promising therapeutic strategy for stroke treatment. ConclusionIn vitro induced Treg cells can effectively suppress neuroinflammation caused by ischemic stroke, demonstrating promising clinical application potential. By regulating the balance between pro-inflammatory and anti-inflammatory cytokines, Treg cells can inhibit immune responses in the nervous system, thereby reducing neuronal damage. Additionally, they can modulate the immune microenvironment, suppress the activation of inflammatory cells, and promote tissue repair. The therapeutic effects of Treg cells also include enhancing post-stroke recovery, improving behavioral outcomes, and increasing the survival rate of ischemic stroke mice. With their ability to suppress neuroinflammation, Treg cell therapy provides a novel and effective strategy for the treatment of ischemic stroke, offering broad application prospects in clinical immunotherapy and regenerative medicine.

Stroke is one of the leading causes of death and disability worldwide， ranking as the second leading cause of mortality globally and the primary cause of adult disability. Its pathological process involves complex cascade mechanisms， with high incidence and disability rates， posing a major threat to human health. According to statistics from the World Health Organization， more than 13 million new cases of stroke occur globally each year， resulting in direct medical costs and socioeconomic burdens amounting to hundreds of billions of dollars. In recent years， breakthroughs in the study of programmed cell death mechanisms have provided new insights into stroke treatment. Among them， ferroptosis， a novel form of cell death driven by iron-dependent lipid peroxidation， has attracted widespread attention in the pathological process of stroke. Ferroptosis is closely associated with iron metabolism disorders， oxidative stress， and lipid peroxidation， and exhibits unique regulatory effects in key pathological processes of stroke， such as ischemia-reperfusion injury， disruption of the blood-brain barrier， and neuronal apoptosis. It plays an important role in post-stroke neurological damage. Chinese medicine， as an essential component of traditional Chinese medicine （TCM）， has demonstrated advantages in modulating ferroptosis and exerting neuroprotective effects. This review systematically summarizes current research on the neuroprotective mechanisms of Chinese medicine compound formulas and monomers through the regulation of ferroptosis pathways in post-stroke conditions， aiming to provide a basis for optimizing clinical treatment strategies and exploring new therapeutic approaches， and to offer new strategies and approaches for stroke treatment.