ObjectiveTo evaluate the protective effect of Xuebijing injection against renal injury in patients with sepsis, and to explore its possible mechanism.Methods A prospective randomized controlled trial (RCT) was conducted in which 62 severe patients with sepsis and septic shock admitted in Department of Critical Care Medicine of Jiangsu Province Traditional Chinese Medicine Hospital from June 2013 to December 2013 were randomly divided into control group and Xuebijing group, with 31 patients in each group. The patients in both groups received basic treatment for sepsis, and the patients in Xuebijing group were additionally given intravenous injection of Xuebijing 100 mL once a day for 7 days. In both groups, the changes in acute physiology and chronic health evaluationⅡ (APACHEⅡ) score were observed before treatment and 1, 3, 7 days after treatment, and the changes in the levels of interleukins (IL-6, IL-10), prothrombin time (PT), fibrinogen (Fib), activated partial thromboplastin time (APTT), serum creatinine (SCr), and Cystain C (Cys C) were determined before treatment and 1 day and 3 days after treatment.Results There was no statistically significant difference in APACHEⅡ score before treatment between two groups, however, the APACHEⅡ scores were significantly decreased in both groups 3 days and 7 days after treatment compared with those before treatment, and the degree of decrease in Xuebijing group was more obvious 7 days after treatment (13.61±7.62 vs. 16.34±8.70,P< 0.05). Serum concentrations of Cys C, SCr, IL-6, IL-10, PT, APTT, and Fib showed no difference between two groups before treatment (allP> 0.05), while after treatment the degrees of improvement of above indexes in Xuebijing group were obviously superior to those in control group, especially 3 days after treatment[Cys C (mg/L):1.12±0.11 vs. 1.35±0.14, SCr (μmol/L): 115.0±31.0 vs. 135.0±24.0, IL-6 (ng/L): 54.27±28.79 vs. 73.35±31.01,PT (s): 13.50±0.11 vs. 15.71±0.11, APTT (s): 43.66±0.31 vs. 48.03±0.55, Fib (g/L): 1.91±0.51 vs. 1.51±0.52, P< 0.05 orP< 0.01].ConclusionXuebijing injection has certain renal protective effect in patients with sepsis, and its mechanism is possibly related to the regulation and improvement of uncontrolled inflammatory response and coagulation function in sepsis.

Objective To investigate the effect of methylprednisolone on T helper 17 cell (Th17 cells) related cytokines (interleukin (IL)-23,17A,21,22,6,and tansforming growth factor (TGF)-β) in serum and cerebrospinal fluid from patients with relapsing remitting multiple sclerosis and their effects on the pathogenesis.Methods We recruited relapsing remitting multiple sclerosis group (38 patients)and noninflammatory neurological disease group (20 controls),and detected the levels of IL-23,IL-17A,IL-21,IL-22,TGF-β and IL-6 in serum and cerebrospinal fluid (CSF) with ELISA kit in both controls and patients before and after treatment by methylprednisolone.Results After treatment in relapsing remitting multiple sclerosis patients,IL-17A,IL-23,IL-21,and IL-22 levels in cerebrospinal fluid and serum were significantly decreased,however,they were still higher than that in the non-inflammatory neurological disease patients.TGF-β levels was significantly increased (serum:(17.2 ± 5.9) pg/ml vs (34.1 ± 6.5) pg/ml,t =14.351,P =0.000 ; CSF:(26.4 ± 4.7) pg/ml vs (73.2 ± 19.7) pg/ml,t =16.352,P =0.000).The levels of TGF-β in serum and CSF in patients before treatment were lower than those of in non-inflammatory neurological disease patients (serum:(30.2 ± 8.9) pg/ml,t =6.769,P =0.012 ; CSF:(3 1.4 ± 7.5) pg/ml,t =9.368,P =0.017).However,the levels of TGF-β in CSF in patients after treatment were significantly higher than those in non-inflammatory neurological disease patients (t =9.138,P =0.000).Correlation analysis showed that IL-23 and IL-17A were positive correlation in the serum of relapsing remitting multiple sclerosis patients before treatment.Moreover,positive correlations among IL-23,IL-17A and IL-21 were detected in the CSF of relapsing remitting multiple sclerosis patients before treatment.Conclusions Decreased levels of IL-23,IL-17A,IL-21 and IL-22,and elevated levels of TGF-β were detected in serum and CSF of patients with relapsing remitting multiple sclerosis after methylprednisolone treatment.IL-23,IL-17A,IL-21,IL-22 and TGF-β might involve in the pathogenesis of relapsing remitting multiple sclerosis.

In order to explore the pathogenic characters,diagnosis and treatment of canine leptospirosis,a retrospective analysis of the pathogenetic factor,diagnosis and treatment of three dogs were reported which diagnosed as canine leptospirosis in China Agricultural University Teaching Animal Hospital from August to November,2015.The infected dogs showed symptoms of depressed,jaundice,anorexia and vomiting.Two of them had fever history and contacted the water resource outside before getting ill.All three dogs were confirmed anemia,liver and kidney damage by laboratory examination.They were diagnosed with canine leptospirosis according to the positive results of the Leptospira PCR examination base on urine.During the diagnosis and treatment process,one of them was dead,the rest two recovered after antibiotic and symptomatic therapy.In conclusion,dogs which infected with leptospirosis may have a contact with the infected water before.The Leptospira PCR examination base on urine can be used for the diagnosis method of the disease.As to treatment,the use of penicillin and tetracycline drugs such as doxycycline is recommended.

The liver reserve function refers to the compensatory ability to maintain liver function after damage, providing implication for the resection of hepatic malignant tumor. Hepatobiliary scintigraphy imaging can provide quantitative evaluation of liver blood perfusion, and has advantages on the evaluation of liver reserve function and the prediction of postoperative complications. 99Tc m-galactosyl serum albumin (GSA) and 99Tc m-mebrofenin are commonly used imaging agents for hepatobiliary scintigraphy imaging assessment of liver reserve function. This article reviews the application and progress of hepatobiliary scintigraphy in liver reserve function assessment.

Objective To explore the role of interleukin-23 (IL-23) and IL-17 in the pathogenesis of relapsing-remitting multiple sclerosis (RRMS),and determine the effect of methylprednisolone on IL-23 and IL-17 levels.Methods Twenty-nine patients with RRMS (RRMS group) and patients with non-inflammatory neurological diseases (controls),admitted to our hospitals from June 2010 to December 2012 group,were chosen in our study; ELISA was employed to detect the serum and cerebrospinal fluid levels of IL-23 and IL-17 in the two groups before and after methylprednisolone treatment.Results Before treatment,IL-23 and IL-17 levels in serum and cerebrospinal fluid of RRMS group (IL-23:[689.66±111.61] pg/mL and [768.82±70.63] pg/mL; IL-17:[88.15±13.16] pg/mL and [91.51±12.45] pg/mL) were significantly higher than those in the control group (IL-17:[90.94±10.70] pg/mL and [85.71±7.21] pg/mL; IL-23:[17.14±1.55] pg/mL and [17.87±1.61] pg/mL],P＜0.05),and the IL-23 level in cerebrospinal fluid was significantly higher than that in serum (P＜0.05); IL-23 and IL-17 levels in RRMS group after treatment (IL-23:[399.91±61.73] pg/mL and [319.34±91.29] pg/mL; IL-17:[48.01±9.62] pg/mL and [49.08±13.72] pg/mL]) significantly decreased as compared with those before treatment (P＜0.05),but they were still statistically higher than those in the control group (P＜0.05).IL-17 and IL-23 levels had positive correlation in the serum and cerebrospinal fluid of RRMS group (r=0.369,P=0.049; r=0.497,P=0.006).Conclusion IL-23 and IL-17 levels are associated with the pathogenesis of multiple sclerosis; methylprednisolone treatment can decrease the levels of IL-23 and IL-17 in multiple sclerosis.

Objective:To investigate the clinical characteristics, skeletal muscle pathologies and gene variations of chronic progressive external ophthalmoplegia (CPEO).Methods:Sixteen patients with conformed CPEO, admitted to our hospital from January 1997 to December 2021, were chosen. Their clinical data such as onset age and course of diseases and muscle pathological examination results were collected and their gene variation characteristics were analyzed.Results:The initial symptom in all 16 patients was ptosis of varying degrees; 15 patients were with eye movement disorder, 6 with diplopia, 4 with proximal limb weakness, and 3 with dysphagia and dysarthria. Among the 16 patients, electromyography showed myogenic damage in 7 patients, myogenic combined with neurogenic damage in 1 patient, neurogenic damage in 1 patient, and normal in 7 patients. Skeletal muscle biopsies indicated that 14 patients were with ragged red fibers (RRF), 11 patients had cytochrome C oxidase (COX)-negative muscle fibers, 3 patients had a small amount of degenerated and necrotic myofibers with mononuclear phagocytic infiltration. Immunohistochemical staining indicated infiltration of CD8 and CD68 positive lymphocytes. Ten patients accepted genetic test, indicating 6 patients with single large fragment deletion of mitochondrial DNA (mtDNA), 1 patient with mtDNA point mutation, 1 patient with nucleosomal DNA (nDNA) point mutation, and 2 patients without pathogenicity variation clearly associated with clinical phenotype. Electron microscopy in 5 patients showed that abnormal mitochondrial aggregation was noted in 4 patients under the sarcolemma and among the myofibrils.Conclusion:In addition to ptosis and eye movement disorders, a small number of patients with CPEO may be accompanied by dysphagia and limb weakness; and single large fragment deletion of mtDNA is the main mutation form of CPEO.

Objective:To investigate the clinical characteristics, skeletal muscle pathologies and gene variations of chronic progressive external ophthalmoplegia (CPEO).Methods:Sixteen patients with conformed CPEO, admitted to our hospital from January 1997 to December 2021, were chosen. Their clinical data such as onset age and course of diseases and muscle pathological examination results were collected and their gene variation characteristics were analyzed.Results:The initial symptom in all 16 patients was ptosis of varying degrees; 15 patients were with eye movement disorder, 6 with diplopia, 4 with proximal limb weakness, and 3 with dysphagia and dysarthria. Among the 16 patients, electromyography showed myogenic damage in 7 patients, myogenic combined with neurogenic damage in 1 patient, neurogenic damage in 1 patient, and normal in 7 patients. Skeletal muscle biopsies indicated that 14 patients were with ragged red fibers (RRF), 11 patients had cytochrome C oxidase (COX)-negative muscle fibers, 3 patients had a small amount of degenerated and necrotic myofibers with mononuclear phagocytic infiltration. Immunohistochemical staining indicated infiltration of CD8 and CD68 positive lymphocytes. Ten patients accepted genetic test, indicating 6 patients with single large fragment deletion of mitochondrial DNA (mtDNA), 1 patient with mtDNA point mutation, 1 patient with nucleosomal DNA (nDNA) point mutation, and 2 patients without pathogenicity variation clearly associated with clinical phenotype. Electron microscopy in 5 patients showed that abnormal mitochondrial aggregation was noted in 4 patients under the sarcolemma and among the myofibrils.Conclusion:In addition to ptosis and eye movement disorders, a small number of patients with CPEO may be accompanied by dysphagia and limb weakness; and single large fragment deletion of mtDNA is the main mutation form of CPEO.

Objective:To investigate the characteristics of clinical, muscle pathology and gene mutation in patients with nemaline myopathy caused by NEB gene mutation.Methods:The clinical and pathological data of patients with nemaline myopathy caused by NEB gene were collected from Neuromuscular Center of Jiaozuo People′s Hospital from January 1997 to January 2020. The next generation sequencing was preformed to detect NEB gene in all patients, and characteristics of gene mutation were analyzed.Results:Among the 11 patients, there were 8 males and 3 females, and 6 of them came from 2 families. The age of seeing a doctor ranged from 11 to 52 years, the age of onset was from 6 to 23 years, and the course of disease ranged from 5 to 35 years. Neurological examination showed that among the 11 patients, 8 patients had high palatal arch and long face. The muscle tone of both upperlimbs was normal, the tendon reflex was depressed, the proximal muscle strength was grade Ⅲ-Ⅴ, and the distal muscle strength was grade Ⅴ. The muscle tone of both lower extremities was reduced and the tendon reflex was absent. The proximal muscle strength was grade Ⅱ-Ⅳ and the distal muscle strength was grade Ⅲ-Ⅴ. No dysphagia or respiratory muscle involvement was found. Muscle biopsies were performed in 7 of the 11 patients, the pathological changes were muscle fibers of different sizes, circular atrophic muscle fibers and compensatory hypertrophic fibers, and occasionally denatured and necrotic muscle fibers were found. Different degrees of rod aggregation could be seen in all the 7 patients. Electron microscopic examination of 5 patients showed that there was rod aggregation between myofibrils, and most of them were located near the Z band, but no intranuclear rod was found. NEB gene was found in all 11 patients, and a total of 9 different mutation sites were detected, including 8 in exon region and 1 in intron region. Among them, c.21522+3A>G was found in 10 cases, c.1623delT was found in 3 cases and c.17611C>T was found in 3 cases. There was 1 case of c.4417C>T, c.2549delA, c.21065dupA, c.3520G>A, c.20943G>A, c.192G>A respectively.Conclusions:The clinical phenotype of nemaline myopathy caused by NEB gene has great heterogeneity. Muscle pathology shows that rod aggregation is an important basis for the diagnosis of this disease. Mutation c.21522+3A>G in intron is the most common mutation in this group of NEB gene. And the novel mutation sites of NEB gene are respectively c.17611C>T, c.2549delA, c.3520G>A, c.21065dupA, c.20943G>A and c.192G>A.

Objective:To develop an approach for the automatic diagnosis of bone metastasis and to design a parameter of quantitative evaluation for tumor burden on bone scans based on deep learning technology.Methods:A total of 621 cases (389 males, 232 females, age: 12-93 years) of bone scan images from the Department of Nuclear Medicine in Tenth People′s Hospital of Tongji University from March 2018 to July 2019 were retrospectively analyzed. Images were divided into bone metastasis group and non-bone metastasis group. Eighty percent of the cases were randomly extracted from both groups as the training set, and the rest of cases were used as the test set. A deep residual convolutional neural network ResNet34 was used to construct the classification model and the segmentation model. The sensitivity, specificity and accuracy were calculated and the performance differences of the classification model in different age groups (15 cases of <50 years, 75 cases of ≥50 and <70 years, 33 cases of ≥70 years) were analyzed. The regions of metastatic bone lesions were automatically segmented by the segmentation model. The Dice coefficient was used to evaluate the effect of the segmentation model and the manual labeled results. Finally, the bone scans tumor burden index (BSTBI) was calculated to assess the tumor burden of bone metastases.Results:There were 280 cases with bone metastases and 341 cases with non-bone metastases, including 498 in training set and 123 in test set. The classification model could accurately identify bone metastases, with the sensitivity, specificity and accuracy of 92.59%(50/54), 85.51%(59/69) and 88.62%(109/123), respectively, and it performed best in the <50 years group (sensitivity, 2/2; specificity, 12/13; accuracy, 14/15). The specificity in the ≥70 years group (8/12) was the lowest. The Dice coefficient of bone metastatic area and bladder area were 0.739 and 0.925 in the segmentation model, which performed similarly in the three age groups. Preliminary results showed that the value of BSTBI increased with the increase of the number of bone metastatic lesions and the degree of 99Tc m-MDP uptake. The machine learning model in this study took (0.48±0.07) s for the entire analysis process from input to the final BSTBI calculation. Conclusions:The deep learning based on automatic diagnosis framework for bone metastases can automatically and accurately identify segment bone metastases and calculate tumor burden. It provides a new way for the interpretation of bone scans. The proposed BSTBI may be used as a quantitative evaluation indicator in the future to assess the tumor burden of bone metastases based on bone scans.

Objective:To summarize the characteristics of clinical, muscle pathology and gene mutation of late-onset reducing body myopathy caused by FHL1 gene mutation, in order to improve clinicians′ understanding of this disorder. Methods:The clinical, muscle pathology and muscle magnetic resonance imaging data of the proband from a family diagnosed as reducing body myopathy in Jiaozuo People′s Hospital in December 2021 were collected. Genetic tests and pedigree verification were conducted on the proband and her son.Results:The proband was a 59-year-old female with progressive, asymmetrical limb weakness and muscular atrophy. Her mother, sister and brother had similar symptoms. Electromyography showed myogenic and neurogenic damage. Muscle magnetic resonance imaging indicated that the lesion mainly involved the posterior muscles of the thigh and calf, as well as the gluteus maximus. The muscle pathology showed eosinophilic granular inclusion bodies and rimmed vacuoles in the muscle fibers of the lesion. The structure of myofibrils was disordered and abnormal protein deposition was observed. The gene sequencing showed the FHL1 gene p.C150S heterozygous variation. Conclusions:Late-onset reducing body myopathy is characterized by progressive asymmetric proximal limb muscle weakness, partially involving distal limb muscles and gluteus maximus. Muscle pathology shows the characteristic pathological changes of many kinds of myofibrillar myopathies. FHL1 gene mutation is an important basis for diagnosis.