Objective To investigate the effect and the mechanism of parecoxib sodium pretreatment on permeability of blood-brain barrier in a rat model of focal cerebral ischemia-reperfusion injury.Methods Sixty male SD rats weighing 300g were randomly divided into 5 groups (n=12 each):sham operation group (group S);focal cerebral I/R group (group I/R);parecoxib sodium 5 mg/kg pretreatment group (group L);parecoxib sodium7.5mg/kg pretreatment group (group M);parecoxib sodium 10 mg/kg pretreatment group (group H) Middle cerebral artery occlusion models were made by reforming Longa suture method in SD rats.Thirty minutes before ischemia,rats in group L,M and H were injected with 5 mg/kg、7.5 mg/kg and 10 mg/kg parecoxib sodium through the internal jugular vein.Group S and group I/R received equal volume of normal saline.ELISA technique was used to determine the content of S100 β,TNF-α,IL-1 β in Plasma.The changes of cerebral water content and the Evans Blue exudation from brain capillaries were observed.Results Pretreated with parecoxib sodium (5mg/kg、7.5 mg/kg and 10 mg/kg),the content of S100 β,TNF-α,II-1 β in plasma were reduced.The cerebral water content and the EB in brain were reduced.Pretreated with parecoxib sodium 10 mg/kg,Longa scores were reduced.Conclusion Pretreatment with Parecoxib can protect blood-brain barrier against focal cerebral I/R injury by inhibition of the inflammatory reaetion.

A 27-year-old female patient suffering endolymphatic sac tumor with intralabyrinthine hemorrhage was reported. The patient had hearing loss in the left ear with continuous tinnitus, and MRI showed the soft tissue shadow of endolymphatic sac. Considering that the tumor involved semicircular canal and vestibule,endolymphatic cyst tumor resection was performed by labyrinth route. After surgery, there was no cerebrospinal fluid leakage and facial nerve function was normal. More importantly, enhanced MRI of temporal bone showed no tumor recurrence 1 year after surgery.
Female ; Humans ; Adult ; Endolymphatic Sac/surgery* ; Neoplasm Recurrence, Local/pathology* ; Labyrinth Diseases ; Tinnitus ; Ear Neoplasms/pathology* ; Bone Neoplasms ; Hemorrhage

Humans ; Neurofibrosarcoma ; Adrenal Glands

The background of abdominal computed tomography (CT) images is complex, and kidney tumors have different shapes, sizes and unclear edges. Consequently, the segmentation methods applying to the whole CT images are often unable to effectively segment the kidney tumors. To solve these problems, this paper proposes a multi-scale network based on cascaded 3D U-Net and DeepLabV3+ for kidney tumor segmentation, which uses atrous convolution feature pyramid to adaptively control receptive field. Through the fusion of high-level and low-level features, the segmented edges of large tumors and the segmentation accuracies of small tumors are effectively improved. A total of 210 CT data published by Kits2019 were used for five-fold cross validation, and 30 CT volume data collected from Suzhou Science and Technology Town Hospital were independently tested by trained segmentation models. The results of five-fold cross validation experiments showed that the Dice coefficient, sensitivity and precision were 0.796 2 ± 0.274 1, 0.824 5 ± 0.276 3, and 0.805 1 ± 0.284 0, respectively. On the external test set, the Dice coefficient, sensitivity and precision were 0.817 2 ± 0.110 0, 0.829 6 ± 0.150 7, and 0.831 8 ± 0.116 8, respectively. The results show a great improvement in the segmentation accuracy compared with other semantic segmentation methods.
Humans ; Kidney Neoplasms/diagnostic imaging* ; Neural Networks, Computer ; Specimen Handling ; Tomography, X-Ray Computed

Many human genetic diseases, including Hutchinson-Gilford progeria syndrome (HGPS), are caused by single point mutations. HGPS is a rare disorder that causes premature aging and is usually caused by a de novo point mutation in the LMNA gene. Base editors (BEs) composed of a cytidine deaminase fused to CRISPR/Cas9 nickase are highly efficient at inducing C to T base conversions in a programmable manner and can be used to generate animal disease models with single amino-acid substitutions. Here, we generated the first HGPS monkey model by delivering a BE mRNA and guide RNA (gRNA) targeting the LMNA gene via microinjection into monkey zygotes. Five out of six newborn monkeys carried the mutation specifically at the target site. HGPS monkeys expressed the toxic form of lamin A, progerin, and recapitulated the typical HGPS phenotypes including growth retardation, bone alterations, and vascular abnormalities. Thus, this monkey model genetically and clinically mimics HGPS in humans, demonstrating that the BE system can efficiently and accurately generate patient-specific disease models in non-human primates.
Animals ; Disease Models, Animal ; Female ; Gene Editing ; Humans ; Lamin Type A/metabolism* ; Macaca fascicularis ; Progeria/pathology*