Three-dimensional analysis of puncture needle path through safety triangle approach PLD and design of puncture positioning guide plate.

OBJECTIVE: In this study, the three-dimensional relationship between the optimal puncture needle path and the lumbar spinous process was discussed using digital technology. Additionally, the positioning guide plate was designed and 3D printed in order to simulate the surgical puncture of specimens. This plate served as an important reference for the preoperative simulation and clinical application of percutaneous laser decompression (PLD). METHOD: The CT data were imported into the Mimics program, the 3D model was rebuilt, the ideal puncture line N and the associated central axis M were developed, and the required data were measured. All of these steps were completed. A total of five adult specimens were chosen for CT scanning; the data were imported into the Mimics program; positioning guide plates were generated and 3D printed; a simulated surgical puncture of the specimens was carried out; an X-ray inspection was carried out; and an analysis of the puncture accuracy was carried out. RESULTS: (1) The angle between line N and line M was 42°~55°, and the angles between the line M and 3D plane were 1°~2°, 5°~12°, and 78°~84°, respectively; (2) As the level of the lumbar intervertebral disc decreases, the distance from point to line and point to surface changes regularly; (3) The positioning guide was designed with the end of the lumbar spinous process and the posterior superior iliac spine on both sides as supporting points. (4) Five specimens were punctured 40 times by using the guide to simulate surgical puncture, and the success rate was 97.5%. CONCLUSION: By analyzing the three-dimensional relationship between the optimal puncture needle path and the lumbar spinous process, the guide plate was designed to simulate surgical puncture, and the individualized safety positioning of percutaneous puncture was obtained.

A New Method of Biostorage and Biopreservation for Human Amputated Extremities.

OBJECTIVES: We have explored a better method to preserve and store human medically amputated large size samples. The approach involved developing a special embalming solution and procedures for biopreservation and biostorage of a large-sized sample as a whole specimen rather than dissected small parts. Evaluation of the effect of our special embalming solution and procedures on whole human amputated extremities compared with excised small tissues was conducted. Histological and morphological techniques and elemental analyses were utilized to assess the effects of our new method using the special embalming solution. METHODS: Whole remains and excised tissues (skin, muscle, saphenous nerve, and femoral artery) were immersed in a special embalming solution for 6, 12, and 24 months, respectively. Then samples from whole remains and excised tissues were paraffin embedded and Hematoxylin-Eosin staining was performed. Transmission electron microscopy was performed to detect the microstructure of the samples. At the same time, concentrations of chemical elements in the embalming solution from whole remains and excised tissues were separately determined by using inductively coupled plasma atomic emission spectrometry. RESULTS: The morphological structure of tissues was well preserved at 6 and 12 months, and few chemical elements, especially trace elements, leached into the embalming fluid. The macroelements leached into the fluid earlier than the trace elements, but there were some differences in the ultrastructure after preservation for 24 months between tissues excised before and after embalming. Over time, the types and concentrations of chemical elements in the embalming fluid increased. The trace elements in the whole remains were preserved better than those in the removed tissues, and trace elements in muscles and femoral artery were better preserved than those in the skin and saphenous nerve. CONCLUSION: The special embalming fluid can preserve fresh amputated remains well for a short time (less than 24 months), and performs better for the whole remains than excised tissues. This specific embalming fluid should be further studied to achieve higher quality preservation of different tissues for a longer period of time.

Genetic analysis of the forkhead transcriptional factor 2 gene in three Chinese families with blepharophimosis syndrome.

PURPOSE: Clinically, blepharophimosis syndrome (BPES) has been divided into two subsets according to the association of ocular malformation with (type I) or without (type II) premature ovarian failure (POF). BPES is ascribed to mutations in the forkhead transcriptional factor 2 (FOXL2) gene. This study aimed at identifying clinical features and mutations within the FOXL2 gene in three Chinese families with BPES. METHODS: A clinical and molecular genetic investigation was performed in affected and unaffected members from three Chinese families with BPES. Genomic DNA was prepared from leucocytes of peripheral venous blood, the entire coding region of FOXL2 were amplified with PCR, and direct DNA sequencing of the PCR products was performed for mutations in FOXL2. RESULTS: Three mutations in FOXL2 were found in three families, including c.672_701dup30, c.663_692dup30, and c.475dupC. Of the three, the c.475dupC (p.His159fs) was novel in family C and resulted in a frameshift mutation to generate a truncated protein owing to a premature stop codon at codon 238. The new duplication mutation was associated with BPES type II. The c.672_701dup30 (p.Ala224_Ala234dup10) and the c.663_692dup30 (p.Ala221_Ala231dup10) were detected in family A and family B, respectively, leading to expansions of the polyalanine (poly-Ala) tract that is frequently the hot spot of mutations within FOXL2. CONCLUSIONS: Our results expand the spectrum of FOXL2 mutations, and further indicate the association of a novel duplication mutation leading to a truncated protein with BPES type II. The other two known mutations may support the previous hypothesis regarding expansions of the polyalanine tract associated with BPES type II as a mutational hot spot in FOXL2.