Objective To explore the value of MRI histogram analysis in the risk assessment of medulloblastoma recur rence.Methods The data of 28 patients pathologically confirmed of medulloblastoma was analyzed retrospectively.All patients were divided into recurrent group and the non recurrent group (each n=14).The ROIs were drawn on the maximum level of enhanced MR sagittal images,and the histogram analysis were performed using the software named Mazda.The statistical analysis was performed on the histogram parameters to find out the different characteristics between the two groups,and the ROC curve was drawn to evaluate its diagnostic efficacy for recurrence of medulloblastoma.Results In all of the 9 parameters which are extracted from histogram,kurtosis had statistical significance between the 2 groups (P=0.018).The area under the ROC curve was 0.776 (P=0.018),and the sensitivity and specificity of kurtosis in the risk assessment of medulloblastoma recurrence were 64.3％ and 71.4％,respectively.Conclusion MRI histogram analysis can be an important method to assess the risk of medulloblastoma recurrence.

BACKGROUND:A great development has been achieved in essential research on tissue engineered cartilage. However, its real application in otolaryngology has been rarely reported. It is faced with the topic to explore the simple and convenient method of repairing laryngeal cartilage by tissue engineering technique. OBJECTIVE:To compare the effect of porous spongy poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) seeded with chondrocytes or using senior tissue engineered cartilage in repairing al ogenic thyroid cartilage defects.METHODS:Chondrocytes at passage 3 were harvested from infant rabbits within 3 days. Porous spongy poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) seeded with chondrocytes composites were made by tissue engineering technique. The chondrocyte-poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) composites were co-cultured in vitro to form junior tissue engineered cartilage. And then respectively used for repairing the thyroid cartilage defects and directly transplanted with junior tissue engineered cartilage (experimental group A, n=5), or firstly the junior tissue engineered cartilage to be implanted subcutaneously for a period of time to further maturity for relative senior tissue engineered cartilage and secondly to be transplanted (experimental group B, n=5) into adult New Zealand white rabbits. Simple poly(3-hydroxybutyrate-co-3-hydroxyhexanoate) sponge scaffold (control group A, n=4) and chondrocyte suspensions(control group B, n=4) were used as reparative materials in defect areas as control groups. Final y, the reparative effect was respectively studied grossly and histological y at 4 weeks (experimental group B) and 8 weeks (experimental group A, control group A and control group B) after transplantation. RESULTS AND CONCLUSION:The cartilage defects were wel repaired in the experimental groups. It was smooth between the reparative area and original cartilage without dents and defects. Both were similar grossly. But few chondrocytes at interfacial region between the reparative area and original cartilage and poor matrices were observed in the experimental group A. A Few chondrocytes and more matrices were observed in the experimental group B. Inflammatory cellinfiltration was not obvious in two experimental groups. Control groups showed soft tissue of dark-red color accompanied with local concave in gross specimens. Histological examination and special staining showed there were no cartilage-like structure and secretion of matrix components. The results showed that it is possible to repair thyroid cartilage defect using junior tissue engineered cartilage directly or junior tissue engineered cartilage after in vitro implantation in al ograft rabbits with immunity, and the immunoreaction is not obvious;in the same period, the repairing effect of mature tissue engineered cartilage is better than that of junior tissue engineered cartilage. However, application of junior tissue engineered cartilage directly can save time, costs, workload and operational link, and avoid the pain from secondary skin surgery, which is one of the more practical approaches.

In this research project, rats were made into animal models of acute focal cerebral ischemia and reperfusion (IR) by occlusion of their middle cerebral artery (MCAO). We observed the effect of endogenous endothelial progenitor cells (EPCs) and serum cytokines on cerebral ischemia rats treated by electro-acupuncture(EA). The results showed: MCAO model had high stability after EA treatment which was delivered via the acupuncture needles inserted into "quchi" and "zusanli" points, the nervous functions of cerebral IR rats recovered faster than those of rats not treated; EPCs in rats' blood increased after acute focal cerebral ischemia and reperfusion; and the growth rate was obvious in IR group. This phenomenon might be related to the inflammation elicited by injury of ischemia and self-repair. Besides, EA treatment could decrease induced nitric oxide synthase (iNOS) activity, alleviate injury after cerebral ischemia, and regulate the quantity of EPCs in blood. The quantity of EPCs in blood increased in IR-24hr. In IR-48 hr, the rise of EPCs quantity was significant (P < 0.01). The level of vascular endothelium growth factor (VEGF) in serum of rats after cerebral ischemia was escalated, which indicated to a certain extent that cerebral ischemia could stimulate stress reaction. EA treatment could raise VEGF level, which suggested that high expression of VEGF could accelerate mobilization, chemotaxis and homing of EPCs. At the same time, the levels of matrix metalloproteinase-9 (MMP-9) and basic fibroblast growth factor (bFGF) also changed. In conclusion, EA treatment could promote neovascularization after cerebral ischemia by mobilizing EPCs, decreasing iNOS activity and increasing VEGF level. This may be one of the ways by which EA could treat cerebral ischemia.
Animals ; Brain Ischemia ; blood ; complications ; pathology ; Cytokines ; blood ; Electroacupuncture ; Endothelial Cells ; cytology ; Infarction, Middle Cerebral Artery ; blood ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; blood ; pathology ; Stem Cells ; cytology

OBJECTIVE: To research the causes of postintubation vocal cord dyskinesia and its contributing factors. METHOD: The causes of vocal cord dyskinesia were confirmed by laryngoscope, three-dimensional spiral CT, stroboscope, and the analysis of therapy. The factors relevant to the causes of vocal cord dyskinesia were analysed based on the following elements: (1) the anatomic or pathological condition of patients or the technical skills of anesthetists. (2) emaciated or obese body and neck. (3) the age of patients. (4) the duration of endotracheal tube retention. (5) the types of operations. (6) anesthesia procedure. RESULT: Among 135 patients, 128 cases (94.81%) manifested arytenoid dislocation, 7 cases (5.19%) vocal cord paralysis. The study showed that the vocal cord dyskinesia associated with anatomic or pathological condition of patients and technical skills of anesthetists (with intubation difficulty) accounted for 76.30%. The patients with relative emaciated body or neck accounted for 90.62% in cases without intubation difficulty. Age had no significant analytical relationship with vocal cord dyskinesia. Prolonged intubation (endotracheal tube retention over 12 hours) was accounted for only 17.64%. The incidence of vocal cord dyskinesia was nearly 0.5% in patients underwent cardio-thoracic surgery, accounting for 59.26% of all the patients. CONCLUSION There are two major causes of vocal cord dyskinesia: arytenoid dislocation and vocal cord paralysis, and the rate of vocal cord dyskinesia could be reduced by the improvement of technical skill of anesthetists and/or sufficient attention to the intubation condition of patients.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Intubation, Intratracheal ; adverse effects ; Laryngoscopes ; adverse effects ; Male ; Middle Aged ; Vocal Cord Paralysis ; etiology ; physiopathology ; Vocal Cords ; physiopathology ; Young Adult

The role of glial scar after intracerebral hemorrhage(ICH)remains unclear.This study aimed to inves-tigate whether microglia-astrocyte interaction affects glial scar formation and explore the specific function of glial scar.We used a pharmacologic approach to induce microglial depletion during different ICH stages and examine how ablating microglia affects astrocytic scar formation.Spatial transcriptomics(ST)analysis was performed to explore the potential ligand-receptor pair in the modulation of microglia-astrocyte interaction and to verify the functional changes of astrocytic scars at different periods.During the early stage,sustained microglial depletion induced disorganized astrocytic scar,enhanced neutrophil infiltration,and impaired tissue repair.ST analysis indicated that microglia-derived insulin like growth factor 1(IGF1)modulated astrocytic scar formation via mechanistic target of rapamycin(mTOR)signaling activation.Moreover,repopulating microglia(RM)more strongly activated mTOR signaling,facilitating a more protective scar formation.The combination of IGF1 and osteopontin(OPN)was necessary and sufficient for RM function,rather than IGF1 or OPN alone.At the chronic stage of ICH,the overall net effect of astrocytic scar changed from protective to destructive and delayed microglial depletion could partly reverse this.The vital insight gleaned from our data is that sustained microglial depletion may not be a reasonable treatment strategy for early-stage ICH.Inversely,early-stage IGF1/OPN treatment combined with late-stage PLX3397 treatment is a promising therapeutic strategy.This prompts us to consider the complex temporal dynamics and overall net effect of microglia and astrocytes,and develop elaborate treatment strategies at precise time points after ICH.