A 21 years old male patient was admitted with a complex trauma of metal penetrating wound in maxillo facial region,neck and chest because of a high falling accident one hour ago. General examination:the vital signs were stable. Specialized examination: metal foreign body penetrated from the front wall of the axilla ,passing left clavicle superficies, through the middle of neck into the posterior pharyngeal wall, then piercing out from the superciliary arch lateral. The patient had apparent tenderness in the right arch,right zygomatic bone and the front of right maxilla. the degree of mouth was about 1. 8cm. X-ray showed the foreign body: from left armpit to right temporal part. The admission diagnosis was : 1. metal penetrating wound in maxillo-facial,neck and chest; 2. right zygomatic maxillary and zygomatic arch fractures. Treatment: the foreign body was removed smoothly through the concurrent operation, and by scendary operation of open reduction and internal fixation of fractures, the finally result of patient was good.
Accidental Falls ; Face ; Facial Bones ; injuries ; Foreign Bodies ; Fracture Fixation, Internal ; Frontal Bone ; Humans ; Male ; Maxilla ; injuries ; Metals ; Neck ; Orthopedic Procedures ; Skull Fractures ; Wounds and Injuries ; Young Adult

Objective To investigate the effects of volatile oil from artemisia dracunculus on myocardial injury caused by viral myocarditis in mice and explore its possible mechanism.Methods Totally 160 adult male BALB/c mice were randomly divided into normal control group (10) and viral myocarditis group (150).Viral myocarditis mice models were reproduced by intraperitoneal inoculation with a solution of coxsackievirus B3 (CVB3),a viral strain with affinity to myocardium,and then randomly divided into model,astragalus group,and low-,medium-,and high-dose volatile oil from artemisia dracunculus groups.After 1 hour of viral infection,normal control group and model group mice were given normal saline by intragastric administration,astragalus group mice were injected with astragalus 0.1 mL in each mouse by intraperitoneal injection,and the mice in other three groups were given low,medium and high dose (2％,5％,10％) 0.3 mL volatile oil from artemisia dracunculus in each mouse by intragastric administration,respectively,once a day for one week consecutively.The mortality,heart/body weight ratio,the activity of natural killer cells (NK cell),virus titer in myocardial homogenate,serum cardiac troponin Ⅰ (cTnI) level and myocardial pathological changes were observed.Results ① Mortality:the mortality of model group was higher than that of the normal control group,astragalus group,low and medium dose volatile oil from artemisia dracunculus groups (60.0％ vs.0％,23.3％,20.0％,28.7％),and the difference in the mortality being of no statistical significance between model group and that of high-dose volatile oil from artemisia dracunculus group (60.0％ vs.47.6％,P ＞ 0.05);the mortality of astragalus group was obviously lower than that of high-dose volatile oil from artemisia dracunculus group (P ＜ 0.01),and the differences in comparisons between the mortalities of astragalus intervention group,and medium-and low-dose volatile oil groups were not statistically significant (all P ＞ 0.05),and the comparison of mortality between low-and medium-dose volatile oil groups were also not statistically significant (P ＞ 0.05).② Immunization parameters:on the 8th day after modeling,the activity of NK cells in the model group was significantly lower than that in the normal control group [(15.91 ± 3.87)％ vs.(38.50 ± 2.32)％],the activities of NK cells in astragalus group,medium-and low-dose volatile oil from artemisia dracunculus groups were significantly higher than that in model group [(19.38 ± 3.27)％,(18.54 ± 3.09)％,(18.36 ± 2.64)％ vs.(15.91 ± 3.87)％,all P ＜ 0.05].None of virus was detected in the myocardial homogenate in the normal control group,and the virus titers in astragalus group,low and medium dose volatile oil from artemisia dracunculus groups were significantly lower than the titer of the model group (10-9/mL:1.96 ± 0.44,1.95 ± 0.46,1.95 ± 0.48 vs.2.41 ± 0.51,all P ＜0.01).③ Myocardial injury parameters:the level of cTnI in the normal control group was less than 0.1 μg/L,obviously lower than that in the model group [(15.84 ± 3.89) μg/L],as well as the ratio of heart/body weight in model group was also significantly higher than that in normal control group (× 10-4:8.3 ± 1.3 vs.4.6 ± 0.1),and the cTnI and the ratio of heart/body weight of astragalus intervention group,low and medium dose volatile oil from artemisia dracunculus groups were markedly lower than those of model group [cTnI (mg/L):10.03 ± 2.35,10.81 ± 2.56,11.10 ± 1.89 vs.15.84 ± 3.89,ratio of heart/body weight (× 10-4):7.2 ± 0.8,7.3 ± 1.0,7.3 ± 0.6 vs.8.3 ± 1.3].In the normal control group,there were no inflammatory cell infiltration and necrosis in myocardial tissue,the scores of myocardial pathological changes were 0.In the model group,the scores of inflammatory cell infiltration (3.25 ± 0.45) and of necrosis (2.91 ± 0.51) were markedly higher than those in the normal control group.And the above scores in astragalus group,low and medium dose volatile oil from artemisia dracunculus groups were significantly lower than those of the model group (infiltration score:2.92 ± 0.39,2.95 ± 0.35,2.95 ± 0.37 vs.3.25 ± 0.45,necrosis score:2.46 ± 0.50,2.50 ± 0.51,2.54 ± 0.50 vs.2.91 ± 0.51,all P ＜0.05).Conclusions Volatile oil from artemisia dracunculus can protect cardiomyocytes by removing the virus and regulating the immune function in the body.But the protective effects of volatile oil from artemisia dracunculus is related to the dosage,and the effects of low and medium dose are better.

Objective:Four cases with NLRP3-related autoinflammatory diseases were reported to summarize the clinical characteristics, genotype, and treatment responses of the disease, and to improve clinical pediatricians' understanding of the disease.Methods:A retrospective analysis was performed on 4 cases with NLRP3-related autoinflammatory diseases diagnosed in Children's Hospital of Anhui Province in 2016—2021, and the clinical features and treatment progress of NLRP3-related autoinflammatory diseases were retrospectively analyzed based on the clinical features, gene reports, and literature review.Results:① All 4 cases were male. Cases 1, 2, and 3 had the disease onset after birth, and case 4 had the disease onset 6 months after birth. All showed periodic fever, repeated urticaria-like rash, protruding forehead, and saddle nose. White blood cells count, erythrocyte sedimentation rate, and C-reactive protein were increased during the attack period, and those in the interval period were normal, and antibiotic treatment was ineffective. ② The genetic test of all these 4 children showed NLRP3 mutation. Children 1, 2, and 3 were heterozygous mutations, and their parents were wild-type. The mutation was located at chromosome Chr1: 247587658, exon c913 (exon3). G>A, the 305th aspartic acid (Asp) of the protein was changed to asparagine (Asn) in child 1. The mutation was located at the chromosomal Chr1: 247588072, the nucleic acid was changed to c1327(exon3)T>C, and the amino acid was changed to p.Y443H in cases 2 and 3. Somatic heterozygous mutation was found in case 4, and the child's parents were wild-type. In this case, the mutation was located at chromosomal Chr1: 247587658, exon3 G>A, and the 305th Asp of the protein was changed to Asn. ③Children in cases 1, 2, and 3 were treated with glucocorticoids and non-steroidal anti-inflammatory drugs at the initial stage, but the effects were limited. After receiving IL-1 antagonist treatment fever, skin rash, joint swelling and pain disappeared, and the inflammatory indexes were returned to normal. The child 4 received non-steroidal anti-inflammatory drugs and methotrexate, but he failed to respond to the treatment. Treatment with tocilizumab was not effective, however, fever, skin rash, or joint pain disappeared after treated with Khanna.Conclusion:①NLRP3-related autoinflammatory diseases can cause periodic fever, urticaria, joint involvement, and severe involvement of the central nervous system and organ amyloidosis. Which are early misdiagnosis is prone to systemic juvenile idiopathic arthritis. ②The disease was an inflammatory disease mediated by interleukin-1. At present, non-steroidal anti-inflammatory drug, glucocorticoid and chronic anti-rheumatic drugs have limited effects. IL-1 antagonists are effective and safe in the treatment of the disease.