Radiation-induced brain injury is a common complication after radiotherapy for head and neck tumors. It can occur at any time after radiotherapy. The common sites are closely related to the radiotherapy regimen and are more frequently seen in areas receiving the highest radiotherapy dose. Early symptoms include fatigue, dizziness and headaches. In the later stage, epileptic seizures, personality changes and progressive decline in neurocognitive function may occur. Brain computed tomography (CT) often shows focal low-density images, and brain magnetic resonance imaging (MRI) presents with “finger-like” edema in the white matter of the brain during the edema stage. The use of multimodal MRI, positron emission tomography (PET) and other imaging techniques can help to make early diagnosis and differential diagnosis of radiation-induced brain injury. The treatment options include medication, hyperbaric oxygen therapy, surgery and mesenchymal stem cell transplantation. Commonly used drugs in clinical practice include bevacizumab, dexamethasone, citicoline and gangliosides. With the increasing attention paid to radiation-induced brain injury, the research on related mechanisms has been continuously deepened and the corresponding therapeutic drugs have achieved good therapeutic effects. However, effective prevention is more important than treatment. As the brain has complicated structure and functions, damage to functional areas can lead to disability or even death. Optimizing radiotherapy techniques can achieve precise irradiation of tumors and reduce the volume of normal brain tissue exposed to radiation. Radiotherapy plans should be formulated based on factors such as the patient’s age, underlying diseases, and tumor location to avoid excessive exposure to radiation-sensitive areas. Using hippocampal protective radiotherapy to reduce the radiation dose to the hippocampal region can significantly decrease the risk of memory decline and allow the reasonable control of the radiotherapy. The diagnosis and treatment of radiation-induced brain injury is a multidisciplinary collaborative process. It is necessary to strengthen the full life cycle management of patients with head and neck tumors undergoing radiotherapy. Through technological innovation and individualized treatment, the incidence and harm of brain injury should be further reduced.

In recent years, immune checkpoint inhibitor (ICI) has achieved remarkable success in cancer therapy. However, the occurrence of immune-related adverse event (irAE) has increasingly attracted attention. Among them, neurologic immune-related adverse event (n-irAE) is relatively uncommon, but can cause severe outcomes. n-irAE can involve multiple regions of the nervous system, including the peripheral nerves, neuromuscular junction, and central nervous system (CNS), and lead to myositis, myasthenia gravis, encephalitis, myelitis, and other disorders. The diagnosis of n-irAE requires a combination of evaluating the time correlation between symptoms and ICI medication, neurological localization assessments (neuroimaging, cerebrospinal fluid analysis, and electrophysiological studies), and the exclusion of alternative etiologies such as metastatic disease or infection. n-irAE is graded and treated based on clinical severity, and the common therapeutic approaches include corticosteroids, intravenous immunoglobulin, and plasma exchange. Multidisciplinary collaboration and early intervention are crucial for improving patient outcomes. Future efforts should focus on optimizing risk prediction models to achieve individualized management of n-irAE.

Objective This study aims to investigate the impact of clinical characteristics, antibody types, timing of treatment, and tumor comorbidities on the efficacy and prognosis of patients with autoimmune encephalitis (AE), aiming to provide a reference for clinical management. Methods A retrospective analysis was conducted on the medical records of 203 AE patients admitted to the Department of Neurology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, from January 2020 to June 2025. Statistical analysis was performed on patients’ gender, age, disease course, antibody types, and tumor screening results to evaluate their impact on treatment efficacy. Additionally, the clinical assessment scale for autoimmune encephalitis (CASE) scoring system was used to assess treatment outcomes. Results A total of 203 AE patients were included in the study, in which 56.2% cases were male, a median age was 50 years, and most of the disease course was subacute (64.0%). The antibody profiles showed high heterogeneity, with N-methyl-D-aspartate receptor (NMDAR) antibodies being the most common (24.1%). Treatment outcomes revealed that an overall improvement rate is 79.8%, but the significant improvement rate was only 11.3%. The tumor comorbidity rate was 15.3%, and the efficacy of treatment in patients with tumors was slightly lower than that of the non-tumor group. Conclusions The efficacy of AE treatment is influenced by multiple factors, including antibody characteristics, timing of treatment, disease severity, and tumor comorbidities. Timely immunotherapy significantly impacts prognosis, and early diagnosis and treatment can improve clinical outcomes. Precise antibody testing and systematic tumor screening are crucial strategies for promoting the prognosis of AE patients. Future clinical management should strengthen comprehensive assessment of the above factors to achieve optimal treatment outcomes and enhance long-term prognosis.

Objective To explore the reducing serum uric acid (SUA) effects of dapagliflozin, a sodium-glucose linked transporter 2 (SGLT2) inhibitor in patients with type 2 diabetes mellitus (T2DM) with early nephropathy and hyperuricemia. Methods Sixty-five patients with early T2 diabetic nephropathy and hyperuricemia admitted to our hospital from June 2020 to June 2023 were enrolled. After 4 weeks of treatment with dapagliflozin, a paired-sample T-test was used to analyze the changes in SUA, glycosylated hemoglobin (HbA_1c), fasting plasma glucose (FPG), serum creatinine (SCr), total cholesterol (TC), triglyceride (TG), urine albumin-to-creatinine ratio (UACR), body weight and other clinical indexes. Linear regression analysis was performed to determine the relationship between the changes of SUA before (baseline) and after treatment. Results In this group of 65 T2DM patients with early nephropathy and hyperuricemia, 4 weeks of dapagliflozin reduced SUA [(436.1±39.5)vs (392.2±32.2) μmol/L,P<0.001], FPG [(7.66±2.23)vs (6.40±1.06) mmol/L,P<0.001], UACR [(211.3±73.2)vs (177.8±88.3) mg/g,P=0.005], and body weight [(63.1±9.7)vs (62.7±9.3) kg,P=0.038] significantly. Systolic blood pressure, diastolic blood pressure, HbA_1c, TC, TG, SCr, estimated glomerular filtration rate (eGFR), and other levels were not changed (P>0.05). Linear regression analysis showed that the decreased levels of SUA positively correlated with the baseline levels of SUA (β=0.634,R²=0.401,P<0.001). Conclusions SGLT2 could effectively decrease blood glucose levels in patients with early T2DM nephropathy, and significantly reduce serum uric acid and urinary microalbumin.

Objective To evaluate the nutritional risk in hospitalized patients with cirrhosis and explore the relationship between nutritional risk and clinical prognosis. Methods A total of 401 patients with cirrhosis admitted to the infectious diseases department of a grade-Ⅲ hospital in Shanghai from June 2020 to June 2022 were selected as study subjects. The nutritional risk assessment was performed using the Royal Free Hospital-nutrition prioritizing tool (RFH-NPT), and the general information, disease status, laboratory indicators, and clinical prognosis of cirrhosis patients with different nutritional risks were compared. Results In 401 patients, 86 (21.45%) cases had moderate nutritional risk, and 122 (30.42%) cases had high nutritional risk. There were differences in etiological classification, model for end-stage liver disease (MELD) score, Child-Pugh grade, abdominal water volume and laboratory indexes of serum albumin, prealbumin, triglyceride and hemoglobin among patients with different nutritional risks (P < 0.05). With the increase of nutritional risk grade, the incidence of infection, upper gastrointestinal bleeding and electrolyte disturbance increased, and the score of activity of daily living decreased (P < 0.05). Conclusions Cirrhosis patients with moderate to high nutritional risk have severer liver function impairment, high complication rate and poor clinical prognosis compared to those at lower risk.

Anti-dipeptidyl-peptidase-like protein 6 (DPPX) antibody-associated encephalitis is a rare autoimmune encephalitis. This case report describes an elderly male patient with acute onset, whose main symptoms included slurred speech, limb numbness, dizziness, and unsteady gait. The patient had a clear history of preceding infection. Anti-DPPX antibodies were positive in both serum and cerebrospinal fluid, with concurrent seropositivity for anti-ganglioside GQ1b (GQ1b) antibodies. Brain magnetic resonance imaging showed no evidence of acute cerebrovascular disease, tumors, or related lesions. Screening of other systemic organs and lymph nodes revealed no associated malignancies. Without immunotherapy, the patient’s symptoms gradually improved. This case enriches the clinical, diagnostic, and prognostic data on anti-DPPX antibody-associated encephalitis.

Restless legs syndrome (RLS) is a neurological disorder characterized by discomfortable sensations in the lower limbs during sleep. It is often idiopathic, but can also be secondary to various diseases such as peripheral neuropathy. Familial amyloid polyneuropathy (FAP) is an autosomal dominant genetic disorder, and as a rare cause, its early RLS-like manifestations are easily overlooked. This article reports a case of FAP presenting with RLS as initial symptom, and genetic testing shows aTTR gene Y114C mutation. It introduces the diagnosis, treatment and follow-up of the case, and discusses the clinical features based on relevant literature, aiming to remind clinicians to perform genetic screening for FAP in RLS patients with a clear family history and concomitant peripheral neuropathy.

With the rapid development of tumor immunotherapy, the widespread clinical application of immune checkpoint inhibitor (ICI) and chimeric antigen receptor T-cell (CAR-T) therapy has raised concerns about their associated neurotoxicity, which is known as neurologic immune-related adverse event (n-irAE). Immunotherapy significantly improves long-term survival rate of some patients by enhancing the host immune system’s ability to recognize and eliminate tumor cells. However, overactivation of the immune system can also lead to a range of immune-related adverse event (irAE) affecting non-tumor organs. Although neurological involvement is relatively uncommon, it is highly heterogeneous and can cause severe consequences. Peripheral neuropathy (PN) is one of the most important and potentially disabling manifestations. The clinical presentations of PN are diverse, including polyneuropathy, Guillain-Barré syndrome, radiculopathy, and sensory disturbances. The underlying pathogenesis is not fully understood but may involve immune dysregulation, autoantibodies, inflammatory cytokines, and individual genetic susceptibility. This review summarizes recent advances in the clinical features, pathogenesis, diagnosis, and treatment of PN associated with cancer immunotherapy, aiming to provide insights for early clinical recognition and intervention.

Oxaliplatin-induced peripheral neuropathy (OIPN) is a common dose-limiting toxic reaction in chemotherapy for gastrointestinal malignancies such as colorectal and gastric cancers, is characterized by sensory abnormalities and pain that substantially impair treatment efficacy and quality of life. This article provides a systematic review of the pathogenesis, diagnostic criteria, contributing factors, and therapeutic strategies of OIPN, aiming to raise clinician’s attention to OIPN and provide a reference for future clinical management in oncological practice.

Parkinson disease (PD) is a chronic neurodegenerative disease, and the pathgenesis is mainly related to neuronal degeneration and abnormal accumulation of αSyn. Some studies have shown that patients with PD are more likely to suffer from type 2 diabetes mellitus. Hypoglycemic drugs regulate blood glucose through modulating glucose metabolism and improving insulin sensitivity. Some of hypoglycemic drugs also have neuroprotective or antioxidant effect, and their mechanisms of action in neurodegenerative diseases have been extensively studied in recent years. This article reviews the pathological basis and related pathogenesis of PD, exploring the effect of hypoglycemic drugs on the progression of PD.

The gut microbes are crucial for maintaining human health. Intestinal microorganisms and their metabolites participate in the occurrence and development of rheumatic immune diseases by regulating inflammatory factors and immune cells. More studies show that intestinal microbial imbalance is closely related to the pathogenesis of rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis and other rheumatic immune diseases. Recently, transplantation of probiotics and fecal microbiota as emerging therapeutic approaches has shown preliminary efficacy. With the rapid development of metagenomics, in-depth study on gut microbes will provide new perspective and potential intervention strategies for the diagnosis, treatment and prevention of rheumatic immune diseases. This article reviews the role and potential therapeutic effects of gut microbes in rheumatic immune diseases.

Rheumatic autoimmune diseases are characterized by the involvement of multiple systems and organs, and the kidney is a common and critical target. The clinical manifestations of kidney diseases caused by different rheumatic diseases are diverse, ranging from asymptomatic hematuria and proteinuria to rapidly progressive glomerulonephritis and renal failure, and vary in severity. The treatment strategies and prognosis differ depending on the specific clinical manifestation. This article reviews relevant domestic and international literature, summarizing the renal manifestations associated with common rheumatic diseases. The aim is to improve clinicians’ understanding of the diseases, enabling them to intervene early to improve patient outcomes.

Chronic obstructive pulmonary disease (COPD) is one of the most common chronic diseases of the respiratory tract, with a high mortality and disability rate. Sarcopenia is an important extrapulmonary manifestation in COPD patients, and its incidence rate is not low. The pathogenesis of COPD complicated with sarcopenia involves oxidative stress, systemic inflammatory response, autophagy, malnutrition and decreased physical activity, etc. Current research has shown that exercise intervention, nutritional support, and medication treatment can improve patients’ muscle strength and physical mobility, thereby enhancing patient prognosis. This article comprehensively reviews the pathogenesis and treatment of COPD complicated with sarcopenia, aiming to provide a valuable reference for disease research, diagnosis and treatment.

Pyroptosis is a new type of programmed cell death discovered and confirmed in recent years. It is accompanied by changes in intracellular and extracellular osmotic pressure, cell rupture, and the leakage of pro-inflammatory substances, thereby leading to severe inflammatory reactions. In recent years, increased evidence has shown that pyroptosis is closely related to lung diseases, such as lung cancer, bronchial asthma, chronic obstructive pulmonary disease, lung injury, pulmonary arterial hypertension, etc. This article aims to review the role of pyroptosis and its pathophysiological relationship with lung diseases.

The diagnosis and treatment of rare neurological diseases are challenging and impose heavy burdens on patients, thus providing an important opportunity for medical humanities education. This paper explores strategies and methods for integrating medical humanistic spirit into the teaching of rare neurological diseases, aiming to cultivate medical students’ empathy and social responsibility through patient narratives, interdisciplinary collaboration, and ethical practices, thereby promoting patient-centered medical care. The teaching emphasizes the principle of “patient value first”, and guide students to understand the individual dilemmas behind diseases through real clinical cases and health policy analysis, deepen their appreciation for life dignity, and inspire motivation to commit to scientific research and innovation. By integrating humanities and professional expertise, we can enhance the compassion and depth of medical education, providing support for the development of a more compassionate rare disease healthcare system.