BACKGROUND:The immune response is strongly associated with the pathological development of Parkinson's disease.Studies have shown that the major histocompatibility complex plays a key role in immune response.OBJECTIVE:To summarize the mechanism of major histocompatibility complex regulation of immune response and the effect on the pathological markerα-synuclein of Parkinson's disease.METHODS:"Parkinson's disease,the major histocompatibility complex,innate immunity,adaptive immunity,microglia,T cell,B cell,α-syn,inflammation,MHC-Ⅰ,MHC-Ⅱ"were used as search terms to search the literature in PubMed database.Finally,92 articles were included for reading analysis.RESULTS AND CONCLUSION:(1)Congenital immune response is involved in the occurrence and development of Parkinson's disease,and the change of microglia's pro-inflammatory and anti-inflammatory phenotypes may aggravate the degenerative changes of Parkinson's disease.(2)The phenotype and function of T cells are related to the progression of Parkinson's disease.Regulatory T cells promote the activation of anti-inflammatory microglia and inhibit Th subgroup.B-cell-mediated humoral immunity can clear pathological α-synuclein,and its specific mechanism needs further study.(3)The major histocompatibility complex is closely related to the occurrence of innate and adaptive immunity,and thus affects the inflammation of Parkinson's disease.(4)α-Synuclein can regulate the activation of microglia and the expression of major histocompatibility complex,which leads to inflammatory changes in Parkinson's disease.(5)α-Synuclein is closely related to the immune response of Parkinson's disease and has become an important target for the treatment of Parkinson's disease.

Acute lung injury (ALI) has been a kind of acute and severe disease that is mainly characterized by systemic uncontrolled inflammatory response to the production of huge amounts of reactive oxygen species (ROS) in the lung tissue. Given the critical role of ROS in ALI, a Fe₃O₄ loaded bovine serum albumin (BSA) nanocluster (BF) was developed to act as a nanomedicine for the treatment of ALI. Combining with NIR irradiation, it exhibited excellent ROS scavenging capacity. Significantly, it also displayed the excellent antioxidant and anti-inflammatory functions for lipopolysaccharides (LPS) induced macrophages (RAW264.7), and Sprague Dawley rats via lowering intracellular ROS levels, reducing inflammatory factors expression levels, inducing macrophage M2 polarization, inhibiting NF-κB signaling pathway, increasing CD4⁺/CD8⁺ T cell ratios, as well as upregulating HSP70 and CD31 expression levels to reprogram redox homeostasis, reduce systemic inflammation, activate immunoregulation, and accelerate lung tissue repair, finally achieving the synergistic enhancement of ALI immunotherapy. It finally provides an effective therapeutic strategy of BF + NIR for the management of inflammation related diseases.

BACKGROUND:Currently,the pathogenesis of Parkinson's disease is not clear.Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson's disease.It mainly involves oxidative stress,mitochondrial complex damage,calcium homeostasis,mitochondrial dynamics and mitochondrial quality control.OBJECTIVE:To review the association between α-synuclein and mitochondrial damage in Parkinson's disease.METHODS:The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of"Parkinson's disease,mitochondrial damage and mechanism,α-synuclein"in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of"Parkinson's disease,alpha-synuclein,mitochondria,oxidative stress,calcium homeostasis,mitophagy,mitochondrial dynamics,mitochondrial protein introduction"in English.Finally,70 documents were included for review.RESULTS AND CONCLUSION:Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson's disease,and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson's disease.The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation.The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function,thereby triggering Parkinson's disease.Therefore,the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson's disease.

BACKGROUND:The immune response is strongly associated with the pathological development of Parkinson's disease.Studies have shown that the major histocompatibility complex plays a key role in immune response.OBJECTIVE:To summarize the mechanism of major histocompatibility complex regulation of immune response and the effect on the pathological markerα-synuclein of Parkinson's disease.METHODS:"Parkinson's disease,the major histocompatibility complex,innate immunity,adaptive immunity,microglia,T cell,B cell,α-syn,inflammation,MHC-Ⅰ,MHC-Ⅱ"were used as search terms to search the literature in PubMed database.Finally,92 articles were included for reading analysis.RESULTS AND CONCLUSION:(1)Congenital immune response is involved in the occurrence and development of Parkinson's disease,and the change of microglia's pro-inflammatory and anti-inflammatory phenotypes may aggravate the degenerative changes of Parkinson's disease.(2)The phenotype and function of T cells are related to the progression of Parkinson's disease.Regulatory T cells promote the activation of anti-inflammatory microglia and inhibit Th subgroup.B-cell-mediated humoral immunity can clear pathological α-synuclein,and its specific mechanism needs further study.(3)The major histocompatibility complex is closely related to the occurrence of innate and adaptive immunity,and thus affects the inflammation of Parkinson's disease.(4)α-Synuclein can regulate the activation of microglia and the expression of major histocompatibility complex,which leads to inflammatory changes in Parkinson's disease.(5)α-Synuclein is closely related to the immune response of Parkinson's disease and has become an important target for the treatment of Parkinson's disease.

BACKGROUND:Currently,the pathogenesis of Parkinson's disease is not clear.Relevant studies have shown that α-synuclein and mitochondria are closely related to the pathogenesis of Parkinson's disease.It mainly involves oxidative stress,mitochondrial complex damage,calcium homeostasis,mitochondrial dynamics and mitochondrial quality control.OBJECTIVE:To review the association between α-synuclein and mitochondrial damage in Parkinson's disease.METHODS:The first author searched more than 50 documents from CNKI and WanFang databases from 2010 to 2024 using the keywords of"Parkinson's disease,mitochondrial damage and mechanism,α-synuclein"in Chinese as well as more than 750 documents from PubMed between 2010 and 2024 using the keywords of"Parkinson's disease,alpha-synuclein,mitochondria,oxidative stress,calcium homeostasis,mitophagy,mitochondrial dynamics,mitochondrial protein introduction"in English.Finally,70 documents were included for review.RESULTS AND CONCLUSION:Recent studies have confirmed the important role of mitochondrial dysfunction in the pathophysiology of Parkinson's disease,and the interaction between α-synuclein and mitochondria is a particularly significant factor in the pathogenesis of Parkinson's disease.The cascade of events that begin with naturally unfolded α-synuclein and eventually form mature fibril is collectively known as α-synuclein aggregation.The toxicity of aggregation accumulates in dopaminergic neurons and then disrupts mitochondrial function,thereby triggering Parkinson's disease.Therefore,the underlying mechanism of this bidirectional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of Parkinson's disease.

Thrombocytopenia is one of the common complications of cirrhotic patients, which can induce an increasing bleeding risk and closely correlate with bleeding following invasive procedures. Consequently, how to respond to thrombocytopenia is crucial for improving the prognosis of patients with cirrhosis. This article reviews the main mechanisms of cirrhosis concurrent with thrombocytopenia, as well as the corresponding clinical management strategies.

Objective:To explore the application effect of the milestone evaluation system based on ACGME core competencies in the standardized training of residents in the department of rheumatology and immunology.Methods:A modified Milestone Evaluation Scale was developed for the department of rheumatology and immunology. Self evaluation and mentor evaluation were conducted on 150 residents who received standardized training in grades 1-3 before May 2023. The results were collected and statistically analyzed. One-way analysis of variance and t-test were performed using SPSS 27.0. Results:The self-evaluation and mentor evaluation scores of all residents increased with the training years. Self-evaluation scores were significantly higher than mentor evaluation scores ( P<0.05) for the medical knowledge ( t=2.95, P=0.006), diagnosis and treatment ability ( t=2.57, P=0.015), and learning ability ( t=2.67, P=0.015) of grade 2 residents and the learning ability ( t=2.87, P=0.007) of grade 3 residents. There were no significant differences in the baseline score and ability improvement of residents from different institutions ( P>0.05). Conclusions:The milestone evaluation system is an effective tool for training, assessing, and providing feedback to residents in rheumatology and immunology, and provides essential feedback to resident training bases regarding the training effectiveness. The method is worth promoting.

Parkinson's disease (PD) is one of the hotspots in the research field of neurodegenerative diseases, and its pathogenesis is still controversial. Trace metal elements play an important role in normal growth and development of the human body. Metal ions can cross the blood-brain barrier and enter the brain, leading to α-synapnuclein aggregation, mitochondrial dysfunction, and degeneration of dopaminergic neurons, and then inducing the occurrence of PD. This article mainly reviewed the potential mechanisms of metal elements in PD, discussed the role of metabolic imbalance of common trace metals (copper, iron, manganese, and zinc) in PD, and put forward new insights into the treatment of PD.

Objective:To systematically evaluate the qualitative research on the psychological experience and coping of patients undergoing colonoscopy, so as to provide a basis for understanding the psychological status of patients undergoing colonoscopy and carrying out better psychological nursing.Methods:Chinese and English databases such as PubMed, Embase, Web of Science, CNKI, Wanfang Database and China Biology Medicine disc were searched by computer to collect qualitative studies related to the psychological experience of colonoscopy. The quality of the included studies was evaluated using Australian JBI Evidence-based Health Care Center Qualitative Research Quality Evaluation Standard (2016) , and the research results were integrated through a pooled integration method.Results:A total of 9 studies were included, 33 main results were extracted and summarized into 7 new categories, which were summarized into 3 integrated results, including psychological characteristics of patients undergoing colonoscopy, psychological needs of patients undergoing colonoscopy and coping styles of psychological changes of patients undergoing colonoscopy.Conclusions:Medical staff should pay attention to the psychological characteristics and psychological needs of patients undergoing colonoscopy during the examination, provide a variety of psychological support, improve satisfaction of patients undergoing colonoscopy and reduce the discomfort and negative emotions of patients.

A 74-year-old male patient with hypertension was admitted to hospital because of aphasia and movement disorder of his right limb for 3 hours. He was diagnosed as acute cerebral infarction. Thrombolytic therapy with alteplase (1 mg/ml ) was given 1 hour and 17 minutes after admission. Intravenous injection of alteplase 6.48 mg was given firstly (within 1-2 minutes of completing the injection) and then 58.32 mg was administered intravenously via an infusion pump. About 10 minutes after treatment with alteplase,the patient suddenly developed pallor,drenching sweats,cold limbs,and unconsciousness;his blood pressure dropped from 169/89 mmHg to 112/68 mmHg. Alteplase-induced anaphylaxis was considered. Alteplase was immediately stopped and oxygen inhalation and liquid supplements were given. At the same time,dopamine,diphenhydramine,dexamethasone,and other anti-anaphylactic and anti-shock agents were immediately given. The next morning,the patient developed anemia,RBC 2.12×1012/L,Hb 66 g/L. That night,hematoma appeared in his deep muscle from the right hip (at the injection site)to thigh. The peripheral hematoma was considered to be induced by alteplase. On the 3rd day of admission,the patient developed cerebral palsy and was discharged by his family′s request.