The dual role of FSP1 in programmed cell death: resisting ferroptosis in the cell membrane and promoting necroptosis in the nucleus of THP-1 cells.

BACKGROUND: Acute monocytic leukemia-M5 (AML-M5) remains a challenging disease due to its high morbidity and poor prognosis. In addition to the evidence mentioned earlier, several studies have shown that programmed cell death (PCD) serves a critical function in treatment of AML-M5. However, the role and relationship between ferroptosis and necroptosis in AML-M5 remains unclear. METHODS: THP-1 cells were mainly treated with Erastin and IMP-366. The changes of ferroptosis and necroptosis levels were detected by CCK-8, western blot, quantitative real-time PCR, and electron microscopy. Flow cytometry was applied to detect the ROS and lipid ROS levels. MDA, 4-HNE, GSH and GSSG were assessed by ELISA kits. Intracellular distribution of FSP1 was studied by immunofluorescent staining and western blot. RESULTS: The addition of the myristoylation inhibitor IMP-366 to erastin-treated acute monocytic leukemia cell line THP-1 cell not only resulted in greater susceptibility to ferroptosis characterized by lipid peroxidation, glutathione (GSH) depletion and mitochondrial shrinkage, as the FSP1 position on membrane was inhibited, but also increased p-RIPK1 and p-MLKL protein expression, as well as a decrease in caspase-8 expression, and triggered the characteristic necroptosis phenomena, including cytoplasmic translucency, mitochondrial swelling, membranous fractures by FSP1 migration into the nucleus via binding importin α2. It is interesting to note that ferroptosis inhibitor fer-1 reversed necroptosis. CONCLUSION: We demonstrated that inhibition of myristoylation by IMP-366 is capable of switching ferroptosis and ferroptosis-dependent necroptosis in THP-1 cells. In these findings, FSP1-mediated ferroptosis and necroptosis are described as alternative mechanisms of PCD of THP-1 cells, providing potential therapeutic strategies and targets for AML-M5.

Exosome is a Fancy Mobile Sower of Ferroptosis.

Exosomes, nano-sized small extracellular vesicles, have been shown to serve as mediators between intercellular communications by transferring bioactive molecules, such as non-coding RNA, proteins, and lipids from secretory to recipient cells, modulating a variety of physiological and pathophysiological processes. Recent studies have gradually demonstrated that altered exosome charges may represent a key mechanism driving the pathological process of ferroptosis. This review summarizes the potential mechanisms and signal pathways relevant to ferroptosis and then discusses the roles of exosome in ferroptosis. As well as transporting iron, exosomes may also indirectly convey factors related to ferroptosis. Furthermore, ferroptosis may be transmitted to adjacent cells through exosomes, resulting in cascading effects. It is expected that further research on exosomes will be conducted to explore their potential in ferroptosis and will lead to the creation of new therapeutic avenues for clinical diseases.

P53: A Key Target in the Development of Osteoarthritis.

Osteoarthritis (OA), a chronic degenerative disease characterized mainly by damage to the articular cartilage, is increasingly relevant to the pathological processes of senescence, apoptosis, autophagy, proliferation, and differentiation of chondrocytes. Clinical strategies for osteoarthritis can only improve symptoms and even along with side effects due to age, sex, disease, and other factors. Therefore, there is an urgent need to identify new ideas and targets for current clinical treatment. The tumor suppressor gene p53, which has been identified as a potential target for tumor therapeutic intervention, is responsible for the direct induction of the pathological processes involved in OA modulation. Consequently, deciphering the characteristics of p53 in chondrocytes is essential for investigating OA pathogenesis due to p53 regulation in an array of signaling pathways. This review highlights the effects of p53 on senescence, apoptosis, and autophagy of chondrocytes and its role in the development of OA. It also elucidates the underlying mechanism of p53 regulation in OA, which may help provide a novel strategies for the clinical treatment of OA.

The suppression of hyperlipid diet-induced ferroptosis of vascular smooth muscle cells protests against atherosclerosis independent of p53/SCL7A11/GPX4 axis.

Ferroptosis as a novel programmed cell death that involves metabolic dysfunction due to iron-dependent excessive lipid peroxidation has been implicated in atherosclerosis (AS) development characterized by disrupted lipid metabolism, but the atherogenic role of ferroptosis in vascular smooth muscle cells (VSMCs), which are principal components of atherosclerotic plaque fibrous cap, remains unclear. The aim of this study was to determine the effects of ferroptosis on AS induced by lipid overload, and the effects of that on VSMCs ferroptosis. We found intraperitoneal injection of Fer-1, a ferroptosis inhibitor, ameliorated obviously high-fat diet-induced high plasma levels of triglycerides, total cholesterol, low-density lipoprotein, glucose and atherosclerotic lesions in ApoE-/- mice. Moreover, in vivo and in vitro, Fer-1 reduced the iron accumulation of atherosclerotic lesions through affecting the expression of TFR1, FTH, and FTL in VSMCs. Interestingly, Fer-1 did augment nuclear factor E2-related factor 2/ferroptosis suppressor protein 1 to enhance endogenous resistance to lipid peroxidation, but not classic p53/SCL7A11/GPX4. Those observations indicated inhibition of VSMCs ferroptosis can improve AS lesions independent of p53/SLC7A11/GPX4, which preliminarily revealed the potential mechanism of ferroptosis in aortic VSMCs on AS and provided new therapeutic strategies and targets for AS.

Critical roles of FTO-mediated mRNA m6A demethylation in regulating adipogenesis and lipid metabolism: Implications in lipid metabolic disorders.

The goal this review is to clarify the effects of the fat mass and obesity-associated protein (FTO) in lipid metabolism regulation and related underlying mechanisms through the FTO-mediated demethylation of m6A modification. FTO catalyzes the demethylation of m6A to alter the processing, maturation and translation of the mRNAs of lipid-related genes. FTO overexpression in the liver promotes lipogenesis and lipid droplet (LD) enlargement and suppresses CPT-1-mediated fatty acid oxidation via the SREBP1c pathway, promoting excessive lipid storage and nonalcoholic fatty liver diseases (NAFLD). FTO enhances preadipocyte differentiation through the C/EBPß pathway, and facilitates adipogenesis and fat deposition by altering the alternative splicing of RUNX1T1, the expression of PPARγ and ANGPTL4, and the phosphorylation of PLIN1, whereas it inhibits lipolysis by inhibiting IRX3 expression and the leptin pathway, causing the occurrence and development of obesity. Suppression of the PPARß/δ and AMPK pathways by FTO-mediated m6A demethylation damages lipid utilization in skeletal muscles, leading to the occurrence of diabetic hyperlipidemia. m6A demethylation by FTO inhibits macrophage lipid influx by downregulating PPARγ protein expression and accelerates cholesterol efflux by phosphorylating AMPK, thereby impeding foam cell formation and atherosclerosis development. In summary, FTO-mediated m6A demethylation modulates the expression of lipid-related genes to regulate lipid metabolism and lipid disorder diseases.

Focus on ferroptosis, pyroptosis, apoptosis and autophagy of vascular endothelial cells to the strategic targets for the treatment of atherosclerosis.

Vascular endothelial cells (VECs), which are lined up in the inner surface of blood vessels, are in direct contact with the metabolite-related endogenous danger signals in the circulatory system. Moreover, VECs death impairs vasodilation and increases endothelium-dependent permeability, which is strongly correlated with the development of atherosclerosis (AS). Among several forms of cell death, regulatory death of endothelial cells frequently occurs in AS, mainly including ferroptosis, pyroptosis, apoptosis and autophagy. In this review, we summarize regulatory factors and signaling mechanisms of regulatory death in endothelial cells, discussing their effects in the context of the atherosclerotic procession.

Circular RNAs: Rising stars in lipid metabolism and lipid disorders.

The underlying mechanisms of circular RNAs (circRNAs) in lipid metabolism regulation and the pathogenesis of lipid disorder diseases are clarified in this review. circRNAs are produced from host genes by back splicing and are mainly degraded by RNase L. circRNAs act as molecular sponges or scaffolds that bind with microRNAs or proteins and thus affect the intracorporeal processes of lipid metabolism. CircRNA_11897 and circSAMD4A facilitated adipogenesis while circH19 and circRNA_26852 accelerated adipolysis in adipose tissue. CircSAMD4A promoted the differentiation of preadipocytes, but circH19 and circFUT10 inhibited this differentiation. CircFUT10 also promoted the proliferation of preadipocytes. CiRS-133 fostered the browning of white adipose tissue. CircACC1, circRNA_021412, circRNA_0046366, and circRNA_0046367 promoted the mitochondrial ß-oxidation of fatty acids in hepatocytes. CircRNA_021412 suppressed the synthesis of triglycerides in hepatocytes. CircScd1 inhibited hepatic lipid droplet formation. circ_0092317, circ_0003546, circ_0028198, circ_0092317, and circACC1 probably reduced cholesterol efflux from macrophages. circ_0037251 likely promoted lipid accumulation and inhibited lipophagy in macrophages. circRNAs participate in lipid metabolism regulation and affect the development of lipid disorder diseases.

Complicated trafficking behaviors involved in paradoxical regulation of sortilin in lipid metabolism.

This review aims to summarize and discuss the most recent advances in our understanding of the underlying mechanisms of the paradoxical effects of sortilin on lipid metabolism. The vacuolar protein sorting 10 protein (Vps10p) domain in the sortilin protein is responsible for substrate binding. Its cytoplasmic tail interacts with adaptor molecules, and modifications can determine whether sortilin trafficking occurs via the anterograde or retrograde pathway. The complicated trafficking behaviors likely contribute to the paradoxical roles of sortilin in lipid metabolism. The anterograde pathway of sortilin trafficking in hepatocytes, enterocytes, and peripheral cells likely causes an increase in plasma lipid levels, while the retrograde pathway leads to the opposite effect. Hepatocyte sortilin functions via the anterograde or retrograde pathway in a complicated and paradoxical manner to regulate apoB-containing lipoprotein metabolism. Clarifying the regulatory mechanisms underlying the trafficking behaviors of sortilin is necessary and may lead to artificial sortilin intervention as a potential therapeutic strategy for lipid disorder diseases. Conclusively, the paradoxical regulation of sortilin in lipid metabolism is likely due to its complicated trafficking behaviors.

Long-term adenosine A1 receptor activation-induced sortilin expression promotes α-synuclein upregulation in dopaminergic neurons.

Prolonged activation of adenosine A1 receptor likely leads to damage of dopaminergic neurons and subsequent development of neurodegenerative diseases. However, the pathogenesis underlying long-term adenosine A1 receptor activation-induced neurodegeneration remains unclear. In this study, rats were intraperitoneally injected with 5 mg/kg of the adenosine A1 receptor agonist N6-cyclopentyladenosine (CPA) for five weeks. The mobility of rats was evaluated by forced swimming test, while their cognitive capabilities were evaluated by Y-maze test. Expression of sortilin, α-synuclein, p-JUN, and c-JUN proteins in the substantia nigra were detected by western blot analysis. In addition, immunofluorescence staining of sortilin and α-synuclein was performed to detect expression in the substantia nigra. The results showed that, compared with adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (5 mg/kg) + CPA co-treated rats, motor and memory abilities were reduced, surface expression of sortin and α-synuclein in dopaminergic neurons was reduced, and total sortilin and total α-synuclein were increased in CPA-treated rats. MN9D cells were incubated with 500 nM CPA alone or in combination with 10 µM SP600125 (JNK inhibitor) for 48 hours. Quantitative real-time polymerase chain reaction analysis of sortilin and α-synuclein mRNA levels in MN9D cells revealed upregulated sortilin expression in MN9D cells cultured with CPA alone, but the combination of CPA and SP600125 could inhibit this expression. Predictions made using Jasper, PROMO, and Alibaba online databases identified a highly conserved sequence in the sortilin promoter that was predicted to bind JUN in both humans and rodents. A luciferase reporter assay of sortilin promoter plasmid-transfected HEK293T cells confirmed this prediction. After sortilin expression was inhibited by sh-SORT1, expression of p-JUN and c-JUN was detected by western blot analysis. Long-term adenosine A1 receptor activation levels upregulated α-synuclein expression at the post-transcriptional level by affecting sortilin expression. The online tool Raptor-X-Binding and Discovery Studio 4.5 prediction software predicted that sortilin can bind to α-synuclein. Co-immunoprecipitation revealed an interaction between sortilin and α-synuclein in MN9D cells. Our findings indicate that suppression of prolonged adenosine A1 receptor activation potently inhibited sortilin expression and α-synuclein accumulation, and dramatically improved host cognition and kineticism. This study was approved by the University Committee of Animal Care and Supply at the University of Saskatchewan (approval No. AUP#20070090) in March 2007 and the Animals Ethics Committee of University of South China (approval No. LL0387-USC) in June 2017.

eIF2α promotes vascular remodeling via autophagy in monocrotaline-induced pulmonary arterial hypertension rats.

PURPOSE: Eukaryotic initiation factor 2α (eIF2α) plays important roles in the proliferation and survival of pulmonary artery smooth muscle cells (PASMCs) in animal hypoxia-induced pulmonary hypertension models. However, the underlying mechanism remains unknown at large. Autophagy has been reported to play a key role in the vascular remodeling in pulmonary arterial hypertension (PAH). The purposes of this study are to determine the functions of eIF2α and autophagy in the vascular remodeling of the monocrotaline-induced PAH rats and to clarify the correlation between eIF2α and autophagy. METHODS: We established a rat model of monocrotaline-induced PAH, and we established a cell model of platelet derived growth factor (PDGF)-induced PASMCs proliferation. The vascular morphology and the expression of eIF2α, LC3B, and p62 were assessed in the pulmonary arterial tissue of Sprague-Dawleyrats and PDGF-induced PASMCs. RESULTS: Autophagy was significantly active in monocrotaline model group (MCT)-induced PAH rats, which obviously promotes vascular remodeling in MCT-induced PAH rats. Furthermore, the proliferation of PASMCs was induced by PDGF in vitro. The expression of LC3B, eIF2α was increased in the PDGF-induced PASMCs proliferation, and the expression of p62 was reduced in the PDGF-induced PASMCs proliferation. Moreover, eIF2α siRNA downregulated the expression of eIF2α and LC3B, and upregulated the expression of p62 in PDGF-induced PASMCs proliferation. eIF2α siRNA inhibited the PDGF-induced PASMCs proliferation. Finally, chloroquine can upregulate the protein expression of LC3B and p62, it also can inhibit proliferation in PDGF-induced PASMCs. CONCLUSION: Based on these observations, we conclude that eIF2α promotes the proliferation of PASMCs and vascular remodeling in monocrotaline-induced PAH rats through accelerating autophagy pathway.

Sortilin promotes macrophage cholesterol accumulation and aortic atherosclerosis through lysosomal degradation of ATP-binding cassette transporter A1 protein.

Sortilin is closely associated with hyperlipidemia and the risk of atherosclerosis (AS). The role of sortilin and the underlying mechanism in peripheral macrophage are not fully understood. In this study, we investigated the effect of macrophage sortilin on ATP-binding cassette transporter A1 (ABCA1) expression, ABCA1-mediated cholesterol efflux, and aortic AS. Macrophage sortilin expression was upregulated by oxidized low-density lipoproteins (ox-LDLs) in both concentration- and time-dependent manners. Its expression reached the peak level when cells were incubated with 50 µg/ml ox-LDL for 24 h. Overexpression of sortilin in macrophage reduced cholesterol efflux, leading to an increase in intracellular total cholesterol, free cholesterol, and cholesterol ester. Sortilin was found to bind with ABCA1 protein and suppress macrophage ABCA1 expression, resulting in a decrease in cholesterol efflux from macrophages. The inhibitory effect of sortilin in cholesterol efflux was partially reversed by treatment with chloroquine, a lysosomal inhibitor. On the contrary, the ABCA1 protein level and ABCA1-mediated cholesterol efflux is increased by sortilin short hairpin RNA transfection. The fecal and biliary cholesterol 3H-sterol from cholesterol-laden mouse peritoneal macrophage was reduced by sortilin overexpression through lentivirus vector (LV)-sortilin in low-density lipoprotein receptor knockout mice, which was prevented by co-treatment with chloroquine. Treatment with LV-sortilin reduced plasma high-density lipoprotein and increased plasma ox-LDL levels. Accordingly, aortic lipid deposition and plaque area were exacerbated, and ABCA1 expression was reduced in mice in response to infection with LV-sortilin alone. These effects of LV-sortilin were partially reversed by chloroquine. Sortilin enhances lysosomal degradation of ABCA1 protein and suppresses ABCA1-mediated cholesterol efflux from macrophages, leading to foam cell formation and AS development.

The zonal pattern of arterial supply to the brachial plexus and its clinical significance.

PURPOSE: To provide the anatomical basis of blood supply of brachial plexus for the clinical microsurgical treatment of brachial plexus injury. METHODS: Thirteen adult anticorrosive cadaveric specimens (8 males, 5 females) were dissected in this study. 3 fresh cases (2 males, 1 female) were used to observe the zonal pattern of arteries supplying brachial plexus, and 10 cases (6 males, 4 females) were used to observe the source and distribution of the brachial plexus arteries under microscope. RESULTS: The brachial plexus is supplied by branches of the subclavian-axillary axis (SAA), and these branches anastomose each other. According to distribution feature, blood supply of the brachial plexus could be divided into three zones. The first zone was from the nerve roots of intervertebral foramina to its proximal trunks, which was supplied by the vertebral artery and the deep cervical artery. The second zone was from the distal nerve trunks of the brachial plexus, encompassing the divisions to its proximal cords, which was supplied by direct branches of the subclavian artery or by branches originating from the dorsal scapular artery. The third zone was from the distal portion of the cords to terminal branches of the brachial plexus, which was supplied by direct branches of the axillary artery. CONCLUSIONS: The zonal pattern of arterial supply to the brachial plexus is a systematic and comprehensive modality to improve anatomical basis for the clinical microsurgical treatment for brachial plexus injury.

Implications of Sortilin in Lipid Metabolism and Lipid Disorder Diseases.

The present review provides a summary of recent evidence of sortilin expression, function, and regulation and its implications in lipid metabolism and development of lipid disorder diseases. As a member of the vacuolar protein sorting 10 protein (Vps10p) receptor family, sortilin mediates intracellular trafficking of diverse endogenous or exogenous protein substrates between the trans-Golgi network (TGN) and plasma membrane compartments. Recent studies reveal that sortilin regulates the expression of lipid genes, plasma lipid level, and the development of lipid disorder diseases. Sortilin promotes atherogenesis by regulating hepatic very low density lipoprotein (VLDL) secretion and plasma lipid level and subsequently macrophage lipid accumulation. Sortilin deficiency is caused by accelerated proteasome degradation under insulin resistance conditions and is thereby implicated in the hyperlipidemia of type 2 diabetes mellitus (T2DM). Sortilin facilitates hepatic cholesterol accumulation by inhibiting hepatic cholesterol catabolism, which promotes the development of nonalcoholic fatty liver disease (NAFLD). Sortilin plays an important role in lipid metabolism and represents a promising therapeutic target for lipid disorder diseases.

Microanatomy of the brachial plexus roots and its clinical significance.

PURPOSE: To provide the anatomical basis of brachial plexus roots for the diagnosis and treatment of brachial plexus root avulsion injury. METHODS: The morphological features of brachial plexus roots were observed and measured on 15 cervicothoracic spine of adult cadavers. The relationship of brachial plexus nerve roots and the surrounding tissues also were observed, as well as the blood supply of anterior and posterior roots of the brachial plexus. RESULTS: Origination of the nerve roots in the dorsal-ventral direction from the midline was fine-tuned at each level along the spinal cord. The minimum distance of the origin of the nerve root to midline was 2.2 mm at C 5, while the maximum was 3.1 mm at T 1. Inversely, the distance between the origin of the posterior root and the midline of the spinal cord gradually decreased, the maximum being 4.2 mm at C 5 and minimum 2.7 mm at T 1. Meanwhile, there was complicated fibrous connection among posterior roots of the brachial plexus. The C 5-6 nerve roots interlaced with tendons of the scalenus anterior and scalenus medius and fused with the transverse-radicular ligaments in the intervertebral foramina. However, these ligaments were not seen in C 7-8, and T 1. The blood supply of the anterior and posterior roots of the brachial plexus was from the segmental branches of the vertebral artery, deep cervical artery and ascending cervical artery, with a mean outer diameter of 0.61 mm. CONCLUSIONS: The systematic and comprehensive anatomic data of the brachial plexus roots provides the anatomical basis to diagnose and treat the brachial plexus root avulsion injury.

Sortilin: A novel regulator in lipid metabolism and atherogenesis.

Several lines of evidence have shown that SORT1 gene within 1p13.3 locus is an important modulator of the low-density lipoprotein-cholesterol (LDL-C) level and atherosclerosis risk. Here, we summarize the effects of SORT1, which codes for sortilin, on lipid metabolism and development of atherosclerosis and explore the mechanisms underlying sortilin effects on lipid metabolism especially in hepatocytes and macrophages. Recent epidemiological evidence demonstrated that sortilin has been implicated as the causative factor and regulates lipid metabolism in vivo. Hepatic sortilin overexpression leads to both increased and decreased LDL-C levels by several different mechanisms, suggesting the complex roles of sortilin in hepatic lipid metabolism. Macrophage sortilin causes internalization of LDL and probably a reduction in cholesterol efflux, resulting in the intracellular accumulation of excessive lipids. In addition, sortilin deficiency in an atherosclerotic mouse model results in decreased aortic atherosclerotic lesion. Sortilin involves in lipid metabolism, promotes the development of atherosclerosis, and possibly becomes a potential therapeutic target for atherosclerosis treatment.

Applied anatomical study of the vascularized ulnar nerve and its blood supply for cubital tunnel syndrome at the elbow region.

Cubital tunnel syndrome is often accompanied by paresthesia in ulnar nerve sites and hand muscle atrophy. When muscle weakness occurs, or after failure of more conservative treatments, anterior transposition is used. In the present study, the ulnar nerve and its blood vessels were examined in the elbows of 18 adult cadavers, and the external diameter of the nutrient vessels of the ulnar nerve at the point of origin, the distances between the origin of the vessels and the medial epicondyle of the humerus, and the length of the vessels accompanying the ulnar nerve in the superior ulnar collateral artery, the inferior ulnar collateral artery, and the posterior ulnar recurrent artery were measured. Anterior transposition of the vascularized ulnar nerve was performed to treat cubital tunnel syndrome. The most appropriate distance that the vascularized ulnar nerve can be moved to the subcutaneous tissue under tension-free conditions was 1.8 ± 0.6 cm (1.1-2.5 cm), which can be used as a reference value during the treatment of cubital tunnel syndrome with anterior transposition of the vascularized ulnar nerve.

Three-dimensional visualization of the cutaneous angiosome using angiography.

The purpose of this study was to establish the three-dimensional (3D) architecture of the cutaneous angiosome for assessment and design of the perforator flaps. Two fresh cadavers were injected with carboxymethyl cellulose (CMC)/lead oxide and computed tomography (CT) scanned before and after the injection. The various parts of the cutaneous and subcutaneous tissue derived from one of the injected cadavers were also CT scanned. Three-dimensional reconstruction of the cutaneous angiosome and the two flap designs were performed using Materialise's Interactive Medical Image Control System (MIMICS). Both the reconstructed cutaneous angiosomes and the digital flaps can be displayed independently or in conjunction with bones, source arteries, and skin. The 3D architecture of the cutaneous angiosome ensures clear display of the spatial location, distribution range, and anastomoses relationship of the cutaneous perforators. In addition, the caliber, length, and position of a particular source artery are illustrated in the exact spatial location. As a result, the technique provides visualization of the general area and the expandable direction of a respective flap. This technique has the potential to play an important role in assessing perforator blood supply territory and in the design of new flaps.

Anatomical study to the vessels of the lower limb by using CT scan and 3D reconstructions of the injected material.

PURPOSE: To find out the advantages and insufficiency of the 3D reconstruction and traditional anatomy by comparing them with each other. METHODS: 1. Infused with the radio-opaque material from the arteries and veins, respectively, fresh lower extremity specimens were subjected to spiral CT scanning and then 3D reconstruction was conducted to obtain 3D vessels. 2. Anatomizing the specimens to show the vessel system. 3. Comparing the images of 3D reconstruction and photos of the dissected specimens. RESULTS: 3D software could dissect and reconstruct the bones, vessels, skin and muscles, and the reconstructed photos could be shown, respectively or combinedly. On the other hand, the course, distribution, and anastomoses of the vessels could be viewed from different aspects and different layers, but the results were not completely correct, so they were not suitable for data acquisition. While the vessel systems could be observed clearly on the dissected specimens, so could the origin, course, distribution and the anastomoses of any vessel. The data acquisition could be conducted. CONCLUSIONS: The method of angiography with 3D reconstruction is very good and has considerable advantages for observing the 3D state of human blood vessels, and their distribution at different angles and different levels, but it cannot totally represent or replace the traditional dissected specimens.

Measurement and analysis of the perforator arteries in upper extremity for the flap design.

The aim of this study was to provide the anatomical basis for the skin flap pedicled with the nutrient vessels of the cutaneous nerves and cutaneous veins of the upper extremity. Radio-opaque material was injected into the common carotid arteries of five fresh cadavers. The skin and the fascia were meticulously dissected, removed, and radiographed. The Photoshop CS and Scion image 4.02 were used to analyze the cutaneous arteries, the density of vessels, and the vascular territories of the perforator arteries. The results showed that the cutaneous arteries of the upper extremity came from 16 original arteries, and accordingly, the superficial tissue of the upper extremity could be divided into 16 vascular territories. The external diameter and the area of blood supply of each perforator were growing downwards from the proximum to the distal end. But the points at which the perforator arteries came out from the deep tissue were concentrated near the cutaneous nerves and cutaneous veins, and the arteries formed vascular chains. The density of the arteries near the cutaneous nerves and cutaneous veins was much higher than that of other areas. This article discussed the regularity of the nutrient vessels of the cutaneous nerves and veins on the basis of the experimental results.

Demonstration of three injection methods for the analysis of extrinsic and intrinsic blood supply of the peripheral nerve.

BACKGROUND: The use of free vascularized nerve grafts requires an intimate and accurate knowledge of the blood supply of peripheral nerve. This study was designed to compare the advantages and disadvantages of three methods employed to reveal the blood supply of the peripheral nerve, and to provide morphological basis for vascularized nerve grafts. METHODS: The blood supply of brachial plexus and its main branches (ulnar, median, radial, musculocutaneous and axillary nerve) were observed using three vascular injection techniques: three specimens were injected with red latex through the thoracic aorta; two side specimens were injected with a Chinese ink solution, through the subclavian artery, for diaphanization and histology; one fresh cadaver was injected with the gelatin-lead oxide mixture through the femoral artery for radiography. RESULTS: The blood supply of the brachial plexus and its main branches was well examined using the three different vascular injection techniques. Perfusion with red latex exposed the extrinsic blood supply. Diaphanization and histology showed the intrinsic blood supply, while gelatin-lead oxide injection technique interactively displayed both the intrinsic and extrinsic blood supply to the peripheral nerve. CONCLUSION: The standard method for the study of the extrinsic blood supply to the peripheral nerve is the red latex perfusion; diaphanization and histology are very suitable to study the intrinsic blood supply of the peripheral nerve; while gelatin-lead oxide technique is the standard for visualization of the integral topography of the blood supply of the peripheral nerve.