Volume 139  ·   Issue 14  ·  2026

Plastic surgery, a vital branch of medicine, has undergone rapid growth in China. With rising social and economic standards, alongside an increasing emphasis on aesthetic enhancement, the demand for plastic surgeons has grown considerably. The professional and personal circumstances of practitioners influence the sustainable development of plastic and cosmetic surgery. However, comprehensive research regarding the professional practices and living conditions of plastic surgeons remains limited, particularly in areas, namely, burnout, work-life balance, marital status, reproductive choices, health conditions, and career development. Furthermore, distinctions between male and female surgeons employed in public and private hospitals have not been thoroughly investigated. In nations with advanced plastic surgery sectors, such investigative studies are prioritized.^{[1,2,3,4,5,6]}However, a comprehensive study of this scale has not been conducted domestically. To this end, the Plastic and Aesthetic Surgery Professional Committee of China Medical Women’s Association (CMWA) conducted an extensive survey to investigate the personal and professional situations of Chinese plastic surgeons. To promote enhanced professional fulfillment among medical practitioners, the current study intends to elucidate the working environment of these surgeons and to provide empirical evidence that may guide policy formulation.

In 1932, theChinese Medical Journal(CMJ) was officially established through the merger ofThe China Medical Journaland the English section ofThe National Medical Journal of China, marking a decisive transfer of China’s modern medical discursive authority from foreign missionary physicians to Chinese medical scholars. Measured by journal lineage, this transition had taken nearly half a century to complete; if anchored in Peter Parker’s medical practice in Guangdong beginning in 1835, it spans nearly one century; and if tracing back to the introduction of Western medical knowledge, it would deepen into even longer horizons of over three centuries. Notably, the lineage of theCMJcan be traced toChina Medical Missionary Journal(CMMJ), launched in 1887, and retitled theChina Medical Journalin 1907—an influential conduit for Western medical knowledge and practice in China. Meanwhile,The National Medical Journal of China, inaugurated in 1915 by the newly established National Medical Association of China (later the Chinese Medical Association, CMA), published in both Chinese and English, signaling the Chinese medical community’s entry into the mainstream trajectory of modern medical development. Prior to their formal merger, the two journals maintained close collaboration, and served as key academic platforms for advancing modern medical research and diagnosis and therapeutic practice nationwide.

Parkinson’s disease (PD) is the second most common neurodegenerative disorder. The pathological hallmark of PD is the degeneration of dopaminergic neurons in the substantia nigra, accompanied by abnormal accumulation of α-synuclein.^[1]Levodopa responsiveness plays an important role in the diagnosis and treatment of PD. The acute levodopa challenge test (ALCT) serves as an easy and quantifiable procedure to assess dopaminergic responsiveness and has been widely used in clinical practice. To ensure consistency and standardize the indications, protocols, and interpretation in the clinical use of the ALCT, this expert consensus was developed on the basis of a comprehensive review of the literature and expert discussion, providing practical guidance for neurologists and other health care professionals involved in the care of patients with PD.

Primary immune thrombocytopenia (ITP) is an acquired autoimmune disorder causing isolated thrombocytopenia. Driven by the rapid emergence of novel therapies and new clinical evidence, the Thrombosis and Hemostasis Group of the Chinese Society of Hematology has released the 2025 edition of its guideline for adult ITP.^[1]This update incorporates major advances, including new roles for thrombopoietin receptor agonists (TPO-RAs) and the introduction of spleen tyrosine kinase (SYK) inhibitors, Bruton’s tyrosine kinase (BTK) inhibitors, and neonatal Fc receptor (FcRn) antagonists. The key recommendations emphasize a shift toward individualized, goal-directed therapy aimed at achieving sustained, treatment-free remission.

To the Editor: Hypertriglyceridemia-associated acute pancreatitis (HTG-AP) is the second most common cause of acute pancreatitis (AP) in China, characterized by more complications, higher intensive care unit (ICU) admissions, prolonged hospital stays, and increased recurrence rates (16.0-49.2%) compared with other etiologies.^[1]Recurrent HTG-AP (HTG-RAP) imposes a substantial disease burden, including multiple hospitalizations, diminished quality of life, and an elevated risk of chronic pancreatitis (CP) and pancreatic cancer. Therefore, identifying the key risk factors for HTG-RAP is clinically essential. Hypertriglyceridemia (HTG) is a major risk factor for HTG-RAP recurrence and is caused by genetic and environmental factors. Genetic mutations in genes such as lipoprotein lipase (LPL) and apolipoprotein C-II (APOC2) have been shown to correlate with higher recurrence rates of HTG-RAP in Caucasian populations. However, the genetic predisposition contributing to the risk and recurrence of AP in patients with HTG, particularly in Asian populations, remains poorly understood. This study aimed to identify genetic risk factors for HTG-RAP and investigate their association with recurrence and severity using whole-exome sequencing.

To the Editor: Coronavirus disease 2019 (COVID-19) continues to spread globally. An excessive inflammatory response in severe COVID-19 may cause a cytokine storm that induces multiple organ failure, acute respiratory distress syndrome, and a worse prognosis. Therefore, antiviral monotherapy for severely ill patients with COVID-19 might be insufficient, and the importance of combining immunomodulators is evident. The RECOVERY trial^[1]and subsequent studies have proved that dexamethasone was effective among patients hospitalized with COVID-19 who had hypoxemia.

To the Editor:PSEN1,PSEN2, andAPPhave been verified as causative genes for familial Alzheimer’s disease (AD). Meta-analysis suggests that patients with AD causative mutations may develop symptoms at a younger age (average age of onset at 46.2 years).^[1]However, some cases are late-onset or sporadic. Therefore, studies confined to early-onset or familial AD populations are incomprehensive, leading to an incomplete description of the genetic AD spectrum. In the pathogenesis of AD, amyloid beta (Aβ) is derived from amyloid precursor protein (APP) through proteolysis via the β-secretase and γ-secretase complex, whereas presenilin-1 (PS1) and presenilin-2 (PS2) are critical components of γ-secretase complex.^[2]Previous research on transgenic animal models or transfected cells indicated that mutations could increase the level of Aβ (especially Aβ42) or Aβ42/Aβ40 ratio. This study aimed to screen for pathogenic mutations in a large sample of Chinese population with dementia (Peking Union Medical College Hospital [PUMCH] dementia cohort) and determine the functional effect of the identified mutation byin vitrostudy.

To the Editor: Resting-state functional magnetic resonance imaging (rsfMRI) enables the evaluation of spontaneous neural activity and has revealed intrinsic brain networks essential for emotion regulation, cognitive control, and systemic homeostasis.^[1]Increasing evidence suggests that brain functional connectivity may influence peripheral physiological processes, including immune surveillance and endocrine function—both of which are implicated in cancer development. Meanwhile, cancer remains a major public health challenge, with multifactorial etiologies and largely unexplored neurobiological determinants. Although previous observational studies have hinted at associations between brain function and cancer risk, their conclusions are often limited by confounding and reverse causality. Thus, the potential causal link between intrinsic brain network activity and cancer susceptibility remains unclear and requires rigorous investigation.

To the Editor: The efficacy of anti-programmed death 1 (anti-PD-1) antibodies in treating advanced hepatocellular carcinoma (HCC) is well established. Given that the hepatitis B virus (HBV) is a major cause of HCC and that evidence regarding the interaction between anti-PD-1 antibodies and HBV is limited, we explored the changes in HBV following treatment with finotonlimab, an anti-PD-1 antibody, in patients with HCC. We demonstrated that finotonlimab suppressed HBV replication and maintained viral stability, potentially correlating with improved clinical outcomes. This analysis, involving a relatively large sample size, underscores the dual benefit of anti-PD-1 antibodies in treating patients with HCC and concurrent HBV infection. These findings support further research on the effects and mechanisms of PD-1 antibodies in HBV treatment, potentially contributing to the development of new therapeutic strategies for chronic hepatitis and HCC.

The authors declare that in the correspondence "Keratin 17 enhances the chemotaxis of neutrophils through regulating CXCL1 secretion in keratinocytes via PI3K/AKT/NF-κB pathway in psoriasis" ,^[1]which was published in Vol.139, Issue 5, pages 782-784 of theChinese Medical Journal, the picture of the control mouse inFigure 1Owas incorrect. The corrected Figures are shown below. The error does not affect the results and conclusions of the article. The authors sincerely apologize for the errors.