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Morphine tolerance poses a great challenge for clinicians, whose pathogenesis has a close connection with microglial activation and neuroinflammation. Dihydroartemisinin (DHA) that derives from artemisinin, may serve as a potential anti-inflammatory drug. In this study, the effects as well as the underlying mechanism of DHA on suppressing microglial activation and neuroinflammation were explored. The microglial cell line BV-2 cells were induced by morphine and treated with DHA or minocycline. With the application of CCK-8, the cell viability was detected. Western blot was employed to assess the expressions of Ki67, IBa-1, and TLR4 and quantitative real-time PCR (qRT-PCR) was adopted to evaluate miRNA-16 (miR-16) expression. With the adoption of ELISA kits and qRT-PCR, the release of inflammatory cytokines was evaluated. Besides, luciferase reporter assay was applied to testify the binding relationship between miR-16 and TLR4. NF-κB expression was measured by immunofluorescence. DHA reduced cell viability and decreased protein expression of Ki67 and IBa-1 in morphine-induced BV-2 cells. Additionally, DHA contributed to the declined release of pro-inflammatory cytokines. miR-16 was down-regulated by morphine but was up-regulated by DHA concentration-dependently in BV-2 cells. The inhibition of miR-16 partly abolished the inhibitory effects of DHA on morphine-induced microglial activation and neuroinflammation. Moreover, TLR4 was found to be bound to miR-16, and the inhibitory effect of DHA on TLR4/NF-κB was partly reversed by miR-16 inhibition. In conclusion, DHA remarkably suppressed microglial activation and neuroinflammation through regulating miR-16-mediated TLR4/NF-κB signaling. This study may provide a new solution to improve clinical analgesic efficacy of morphine.

Background Interruption of blood supply will lead to necrosis of body tissues, such as osteonecrosis of femoral head (ONFH). Vascularization has always been regarded as one of the biggest challenges in tissue engineering. In the current study, a novel device was proposed to reconstruct blood supply of necrotic femoral head. Methods Cryo-insult with liquid nitrogen method was adopted to establish the ONFH model. In experimental group, a novel scaffold carrying vascular bundle was implanted into the necrotic femoral head after decompression and the transplanted vascular bundles were anastomosed with the existing blood vessels around the hip. In control group, a traditional porous scaffold was inserted alone without vessels. Feasibility of this strategy was verified by animal experiments. Micro-CT analysis and histological evaluation were performed to investigate its preliminary efficacy. Results Feasibility of this innovative treatment strategy had been successfully verified in animal experiments. In the area of necrosis repair, more bone tissue grew into the scaffold in experimental group than the control group evaluated by Micro-CT (three months: 29.66% VS 20.35%, P＜0.05; six months: 30.47% VS 25.10%, P＜0.05) and histological analysis (24.71% VS 16.45%, P＜0.05 ​at three months; 31.01% VS 20.60%, P＜0.05 ​at six months). Implanted vascular bundles had the potential to branch out many branches in the osteonecrosis repair area to facilitate blood supply reconstruction and bone repair. Conclusions This study proposed a novel device with clinical application prospects in the treatment of ONFH. It has the potential to provide new possibilities for rebuilding the blood supply of femoral head and repairing osteonecrosis. Translational potential statement The novel device proposed in this study has the potential to be applied to the treatment of early femoral head necrosis.

Hypoxic pulmonary hypertension (HPH) is a progressive and irreversible disease that reduces survival. Echinacoside is a phenylethanoid glycoside from Tibetan herbs known for its vasorelaxant effect and for inhibiting the proliferation of rat pulmonary arterial smooth muscle cells. This study aimed to investigate the effect of echinacoside on HPH. Sprague Dawley rats were housed in a hypobaric hypoxia chamber (4500 m) for 28 days to obtain the HPH model. Echinacoside (3.75, 7.5, 15, 30 and 40 mg/kg) was administered by intraperitoneal injection from the 1st to the 28th day. The mean pulmonary artery pressure (mPAP), right ventricular hypertrophy index, hemoglobin, hematocrit, red blood cell concentration and morphological change of pulmonary arteries were evaluated. Vascular perfusion assay was used to assess the pulmonary artery function. Echinacoside reduced mPAP, hemoglobin, hematocrit, right ventricular hypertrophy index and mean wall thickness% of pulmonary arteries in HPH rats. It significantly increased maximum vasoconstriction percentage of pulmonary arteries induced by noradrenaline in a dose-dependent manner. In addition, it improved the responsiveness of pulmonary arteries to acetylcholine and sodium nitroprusside. Therefore, Echinacoside might be an effective treatment against HPH, since it regulated pulmonary artery endothelium and smooth muscle layer function and improved the remodeling of pulmonary artery.

Background: There is obvious difference in individual response to opioids. Many studies have examined the correlation between the μ-opioid receptor 1 (OPRM1) 118A>G genetic variation and opioid requirement in pain treatment, but the conclusion remains elusive. Objectives: To investigate whether the OPRM1 118A>G genetic variation is associated with the opioid requirement. Study Design: Systematic review and meta-analysis. Methods: PubMed, Cochrane library, and EMBASE databases were systematically searched up to May 5, 2018, using the keywords “OPRM1,” “genetic variant,” “opioid,” and “pain” to identify reviews or meta-analyses on this topic. Two independent reviewers performed the data extraction and assessed study quality. The authors investigated the standardized mean difference (SMD) of opioid requirement between AA homozygotes and G allele carriers. The authors also examined the association between the OPRM1 118A>G genetic variation and adverse effects such as nausea and vomiting. Potential bias was assessed using the Egger’s test and the Begg’s test. Results: A total of 530 articles were retrieved from the databases searched, and 36 studies involving 8,609 patients were included in the final analysis. G allele carriers required a higher mean opioid dose (SMD: 0.17; 95% confidence interval [CI]: [0.12, 0.22]; P < 0.001) and displayed less nausea risk difference (RD): –0.04; 95% CI: [–0.06, –0.01]), but the incident rate of vomiting has no relationship with the genetic variant than AA homozygotes in a random-effects meta-analysis. Although there was no evidence of publication bias (Begg’s test: P = 0.333; Egger’s: P = 0.561), heterogeneity was present among studies (I2 = 54.3%). In the subgroup meta-analyses, there was also significance observed in the postoperative pain setting. Limitations: In all of the articles reviewed, postoperative pain and cancer pain were mostly discussed except for one in other pain setting. Conclusions: In this meta-analysis, the results indicate the OPRM1 A118G polymorphism was associated with the opioid requirement and the adverse effects in pain treatment especially in postoperative pain. This may provide valuable information for clinicians to adopt personalized pain management by properly using the opioids in individual patients. Key words: OPRM1, genetic variation, opioid, pain, side effect, review, meta-analysis

Breast cancer type two susceptibility protein (BRCA2) is an essential protein in genome maintenance, homologous recombination (HR), and replication fork protection. Its function includes multiple interaction partners and requires timely localization to relevant sites in the nucleus. We investigated the importance of the highly conserved DNA-binding domain (DBD) and C-terminal domain (CTD) of BRCA2. We generated BRCA2 variants missing one or both domains in mouse embryonic stem (ES) cells and defined their contribution in HR function and dynamic localization in the nucleus, by single-particle tracking of BRCA2 mobility. Changes in molecular architecture of BRCA2 induced by binding partners of purified BRCA2 were determined by scanning force microscopy. BRCA2 mobility and DNA-damage-induced increase in the immobile fraction were largely unaffected by C-terminal deletions. The purified proteins missing CTD and/or DBD were defective in architectural changes correlating with reduced HR function in cells. These results emphasize BRCA2 activity at sites of damage beyond promoting RAD51 delivery.

BRCA2 is an essential protein in genome maintenance, homologous recombination and replication fork protection. Its function includes multiple interaction partners and requires timely localization to relevant sites in the nucleus. We investigated the importance of the highly conserved DNA binding domain (DBD) and C-terminal domain (CTD) of BRCA2. We generated BRCA2 variants missing one or both domains in mouse ES cells and defined their contribution in HR function and dynamic localization in the nucleus, by single particle tracking of BRCA2 mobility. Changes in molecular architecture of BRCA2 induced by binding partners of purified BRCA2 was determined by scanning force microscopy. BRCA2 mobility and DNA damage-induced increase in the immobile fraction was largely unaffected by C- terminal deletions. The purified proteins missing CTD and/or DBD were defective in architectural changes correlating with reduced homologous recombination function in cells. These results emphasize BRCA2 activity at sites of damage beyond promoting RAD51 delivery.

Simple Summary Hyperthermia is a method to expose a tumor to elevated temperatures. Heating of the tumor promotes the effects of various treatment regimens that are based on chemo and radiotherapy. Several aspects, however, limit the efficacy of hyperthermia-based treatments. This review provides an overview of the effects and limitations of hyperthermia and discusses how current drawbacks of the therapy can potentially be counteracted by inhibiting the heat stress response—a mechanism that cells activate to defend themselves against hyperthermia. Abstract Cancer treatments based on mild hyperthermia (39–43 °C, HT) are applied to a widening range of cancer types, but several factors limit their efficacy and slow down more widespread adoption. These factors include difficulties in adequate heat delivery, a short therapeutic window and the acquisition of thermotolerance by cancer cells. Here, we explore the biological effects of HT, the cellular responses to these effects and their clinically-relevant consequences. We then identify the heat stress response—the cellular defense mechanism that detects and counteracts the effects of heat—as one of the major forces limiting the efficacy of HT-based therapies and propose targeting this mechanism as a potentially universal strategy for improving their efficacy.

Pain is accompanied by high morbidity and imposes a substantial economic burden on individuals and society. Unfortunately, few effective therapeutic methods are available for pain relief. Berberine is a natural product that has attracted widespread attention in recent years. Studies have shown that berberine has various pharmacological effects, such as analgesic, anti-inflammatory, anti-bacterial, anti-oxidative stress, anti-thrombotic, anti-tumor, and hypoglycemic activity. According to the literature, berberine exerts its pain-relieving activity by downregulation of transient receptor potential vanilloid (TRPV)-1; suppression of toll-like receptor 4 (TLR4), mitogen-activated protein kinase (MAPK), and nuclear factor kappa-B (NF-κB); and modulation of μ opioid receptors. Moreover, berberine could regulate the dopamine and N-methyl-D-aspartic acid (NMDA) systems and induce the expression of Nrf2 to promote analgesia. The present literature review discusses the analgesic effects of berberine in inflammatory pain, neuropathic pain, cancer pain, chemotherapy pain, and morphine tolerance, and discusses the possible mechanism of berberine in pain regulation.

To assess the safety and efficacy of tranexamic acid (TA) on off-pump coronary artery bypass (OPCAB) surgery.Meta-analysis.Operating room, OPCAB surgery, all surgeries were elective measurements. Searching the following data sources respectively: PubMed/MEDLINE, the Cochrane Library, EMBASE and reference lists of identified articles, we performed a meta-analysis of postoperative 24h blood loss, postoperative allogeneic transfusion, re-operation for massive bleeding, postoperative mortality, and postoperative thrombotic complications.Using electronic databases, we selected 15 randomized control trials (RCTs), carried out between 2003 and 2016, with a total of 1250 patients for our review. TA significantly reduced the postoperative 24h blood loss (mean difference -213.32ml, 95% confidence intervals, -247.20ml to -179.43ml; P0.0001). And, TA also significantly reduced the risk of packed red blood cell (PRBCs) transfusion (risk ratio 0.62; 95% confidence intervals 0.51 to 0.76; P0.0001) and fresh frozen plasma (FFP) transfusion (0.65; 0.52 to 0.81; P0.001). There were no statistical significance on platelet transfusion (risk difference -0.00, 95% confidence interval -0.02 to 0.02; P=0.73) and re-operation (0.00, -0.02 to 0.02; P=1.00). No association was found between TA and morbility (risk difference -0.00, 95% confidence interval -0.02 to 0.02; P=0.99) and thrombotic complications (-0.01, -0.01 to 0.02; P=0.70).TA reduced the probability of receiving a PRBCs and FFP transfusion during OPCAB surgery. And no association with postoperative death and thrombotic events was found. However, further trials with an appropriate sample size are required to confirm TA safety in OPCAB surgery.

Morphine, a highly potent analgesic, is one of the most effective drugs for the treatment of severe pain associated with cancer. It directly acts on the central nervous system to relieve pain, but also cause secondary complications, such as addiction, respiratory depression and constipation due to its activities on peripheral tissues. Besides pain relief, morphine is of great importance on cancer management with its effect on tumor development being the subject of debate for many years with some contradictory findings. Morphine has shown both tumor growth-promoting and growth-inhibiting effects in many published research studies. And various signaling pathways have been suggested to be involved in these effects of morphine. Based on a thorough literature review, we summarized the double-faced effects of morphine in tumor development, including tumor cell growth and apoptosis, metastasis, angiogenesis, immunomodulation and inflammation. And we attempted to optimize morphine administration in cancer patients to attenuate its tumor growth-promoting effects.

P2X4 receptor (P2X4R), a subtype of P2 purinergic receptors, is an ATP-gated receptor through which activity of spinal microglia instigates pain hypersensitivity in various pain conditions. Accumulating evidence indicates that monocyte chemoattractant protein-1 (MCP-1) plays an important role in chronic pain facilitation, and it could stimulate microglia activation and involve in regulating P2X4R expression. However, the mechanism of MCP-1 in regulating the expression of P2X4R in microglia is poorly understood, and whether MCP-1 can aggravate pain via up-regulating spinal P2X4R expression in Cancer-induced Bone Pain (CIBP) remains unclear. In this study, we observed that Iba-1 and P2X4R expression is increased in microglia treated with MCP-1, and blockade with a selective CCR2 antagonist RS-504393 suppressed microglia activation and reduced P2X4R expression in cultured microglia. In response to MCP-1, the expression level of p-Akt was also increased and RS-504393 inhibited the increase. Besides, PI3K inhibitor LY 294002 could attenuate MCP-1-induced P2X4R expression in cultured microglia. MCP-1 was found to be associated with P2X4R expression and mechanical allodynia induced by CIBP in vivo since the expression of MCP-1 was increased in CIBP and RS-504393 alleviated the P2X4R expression and mechanical allodynia in CIBP. Moreover, RS-504393 also reduced the increase of p-Akt induced by CIBP. Inhibition of PI3K/Akt pathway may partly reduce MCP-1/CCR2-induced expression of P2X4R and mechanical allodynia in CIBP rats.

Psoriasis, which is a common chronic inflammatory skin disease, endangers human health and brings about a major economic burden worldwide. To date, treatments for psoriasis remain unsatisfied because of their clinical limitations and various side effects. Thus, developing a safer and more effective therapy for psoriasis is compelling. Previous studies have explicitly shown that psoriasis is an autoimmune disease that is predominantly mediated by T helper 17 (Th17) cells, which express high levels of interleukin-17 (IL-17) in response to interleukin-23 (IL-23). The discovery of the IL-23–Th17–IL-17 axis in the development of psoriasis has led to the paradigm shift of understanding pathogenesis of psoriasis. Although anti-IL-17 antibodies show marked clinical efficacy in treating psoriasis, compared with antibodies targeting IL-17A or IL-17R alone, targeting Th17 cells themselves may have a maximal benefit by affecting multiple proinflammatory cytokines, including IL-17A, IL-17F, IL-22, and granulocyte-macrophage colony-stimulating factor, which likely act synergistically to drive skin inflammation in psoriasis. In this review, we mainly focus on the critical role of Th17 cells in the pathogenesis of psoriasis. Especially, we explore the small molecules that target retinoid-related orphan receptor γt (RORγt), a vital transcription factor for Th17 cells. Given that RORγt is the lineage-defining transcription factor for Th17 cell differentiation, targeting RORγt via small molecular inverse agonists may be a promising strategy for the treatment of Th17-mediated psoriasis.

To evaluate the efficiency of dexmedetomidine on the incidence of delirium in patients after cardiac surgery.Meta-analysis of randomized controlled trials.Operating room and Intensive Care Unit (ICU).Ten trials with a total of 1387 patients undergoing cardiac surgery met the inclusion criteria.Randomized controlled trials (RCTs) comparing the effect of dexmedetomidine versus non-treatment of dexmedetomidine (normal saline (NS), propofol and other anesthetic drugs) on delirium in patients undergoing cardiac surgery were retrieved from PubMed/Medline, Embase, the Cochrane Library and Web of science. The primary outcome was the incidence of delirium. The secondary outcomes were the rate of bradycardia and hypotension, the duration of mechanical ventilation and the length of ICU and hospital stay.Compared with the control group, Dexmedetomidine significantly decreased the incidence of postoperative delirium, (risk ratio 0.46; 95% confidence intervals, 0.34 to 0.62; P 0.00001), while the incidence of bradycardia was increased in dexmedetomidine group (risk ratio 1.86; 95% confidence intervals, 1.16 to 2.99; P = 0.01). There was no significant difference between groups with regarding to the occurrence of hypotension (risk ratio 0.90; 95% confidence intervals, 0.59 to 1.38; P = 0.63), the duration of mechanical ventilation (Mean Difference 0.21; 95% confidence intervals, -0.70 to 1.12; P = 0.65), and the length of ICU (Standard Mean Difference - 0.07; 95% confidence intervals, -0.19 to 0.06; P = 0.3) and hospital stay (Mean Difference - 0.13; 95% confidence intervals, -0.56 to 0.30; P = 0.56).Perioperative dexmedetomidine administration decreased the incidence of delirium in patients after cardiac surgery, but might increase the rate of bradycardia. Furthermore, we did not observe significant differences in the incidence of hypotension, the duration of mechanical ventilation and length of ICU and hospital stay between groups. Future studies are needed to ascertain the effect of dexmedetomidine on the incidence of delirium after coronary artery bypass grafting (CABG) and in patient with cognitive disorder at baseline, whether intraoperative dexmedetomidine infusion could reduce postoperative delirium and the optimal dose of dexmedetomidine.

Chronic pain, including cancer-related pain, is a pain condition often caused by inflammation or dysfunctional nerves. Chronic pain treatment poses a significant health care challenge, where opioids especially morphine are widely used and patients often develop tolerance over time with aggravated pain. microRNA (miRNA) is known to play important roles in regulating gene expressions in the nervous system to affect neuronal network plasticity related to algogenesis and the developing of morphine tolerance. In this article, we reviewed studies conducted in rodent animal models investigating the mechanisms of miRNAs regulation in chronic pain with different phenotypes and morphine tolerance. In addition, the potential of targeting miRNAs for chronic pain and morphine tolerance treatment is also reviewed. Finally, we point out the directions of the future research in chronic pain and morphine tolerance.

Morphine creates a neuroinflammatory response and enhances release of the proinflammatory cytokines like interleukin-1β (IL-1β), which compromises morphine analgesia as well as induces morphine tolerance. In this study, we attempted to investigate the mechanisms of morphine induced IL-1β synthesis and release. Microglial cells were treated with morphine (100 μM) once daily for 3 days. Control groups underwent the same procedure but received sterile saline injection instead of morphine. Toll-like receptor 4 (TLR4) and P2X4 receptor (P2X4R) signaling were analyzed using Western blot; immunofluorescence was used to detect the signaling of CD68; real-time RT-PCR and ELISA kit was used to measure the messenger RNA and protein synthesis and release level of IL-1β. Morphine enhanced IL-1β synthesis and P2X4R protein expression. TLR4 were responsible for morphine-induced IL-1β synthesis, while morphine-induced IL-1β release was via P2X4R. Morphine-induced IL-1β release is mediated by endocytosis of TLR4. These results indicated that TLR4 and P2X4R pathways mediated IL-1β synthesis and release in microglia followed chronic morphine. TLR4 internalization is the main mechanism of morphine-induced microglia activation and IL-1β release.

The purpose of this study was to test the hypothesis that general anesthesia (GA) plus thoracic epidural anesthesia (TEA) has no impact on the outcomes of off-pump coronary artery bypass surgery (OPCABs) compared to GA followed by patient-controlled TEA (PCTEA), while GA plus TEA leads to a higher requirement for vasoactive drug use.Sixty-four patients, American Society of Anesthesiologists physical status II and III, who were scheduled for elective OPCABs, were offered an epidural catheter inserted at the T2-3 interspace and then randomized into 1 of 2 groups according to whether TEA was applied intraoperatively. The TEA(perio) group received GA plus TEA, while the TEA(post) group received GA alone. All groups had postoperative PCTEA. The number of requirements for vasoactive drugs and the extubation times were recorded. The analgesic effect was monitored by visual analog scale (VAS) pain scores. Heart rate, blood pressure, and blood gases were also monitored. The data are presented as mean values ± standard deviation, or medians with quartiles.The proportion of vasoactive drug use was significantly higher in the TEA(perio) group intraoperatively (before or during completion of anastomoses: 59.4 vs. 20.7%, p = 0.004; after completion of anastomoses: 53.1 vs. 17.2%, p = 0.007). There was no statistically significant difference in extubation times or VAS scores between the 2 groups.We conclude that GA plus TEA has no impact on the outcomes of OPCABs, while its use leads to a higher requirement for vasoactive drug use. GA followed by PCTEA facilitates the anesthesia administration, while it does not affect the extubation time and the postoperative analgesic effect.

In a retrospective study, Patel and colleagues [1] claimed that peripheral nerve blocks (PNB) were safe and effective for same day bilateral total knee arthroplasty (TKA) with a significant decrease in perioperative hypotension compared to epidural anesthesia, and that epidural patients requiredmore blood transfusions and greater volumes of fluids. Although the paper did not provide the reasons for hypotension and the measures how to prevent and treat it, we think it is inappropriate to meet the normal blood pressure (BP) with only more fluids and blood transfusions and that as such doctors would have to consider more options. Perioperative hypotension is more likely to happen under epidural anesthesia, especially general anesthesia combined with epidural anesthesia [2]. The primary reason for this hypotensionmay be arterial vasodilation because of residual effects of anesthesia, but not pre-load deficiency or myocardial depression. It is certainly reasonable to support hypotension with a vasopressor (such as phenylephrine). Excess fluid or inotropic therapy is inappropriate, or even harmful for those patients soon after bilateral TKA. Because excess fluid would dilute the blood and reduce the hemoglobin concentration, thereby increase the possibility of iatrogenic blood transfusion. So the epidural group in their study required more blood transfusions and greater volumes of hespan and crystalloid which would cause excessive pre-load once the residual effects of anesthesia gradually disappeared. While inotropic therapy would cause the relatively greater loss of parasympathetic activity which would increase perioperative morbidity [3]. On the other hand, we do not think it is appropriate for all patients in the epidural group to receive laryngeal mask anesthesia since epidural analgesia can provide adequate analgesia for bilateral TKA. IV sedation applying a small dose of propofol or dexmedetomidine might be a better choice.

We read with interest the recent article by Piccioni F et al. [1] stating that epidural analgesia ensures adequate pain relief and is well tolerated by patients after cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC). In their study, a total of 101 consecutive patients received intra- and post-operative thoracic epidural anesthesia (TEA); intraoperative anesthesia was maintained with general anesthesia (GA) plus TEA; 9.9% of patients had hypotensive episodes and 77.2% (78/ 101) of patients received intra-operative red blood cells (RBCs) transfusion. But we do not think GA plus TEA is the best anesthesia regimen for patients undergoing CRS and HIPEC procedures. On the one hand, hypotension is more likely to happen under epidural anesthesia because the epidural administration of local anesthetics leads to functional sympatholysis and TEA has an inherent risk of cardiovascular depression and arterial vasodilation [2]. Furthermore, mean arterial pressure and systemic vascular resistance showed a reduction in patients undergoing CRS and HIPEC which is a very demanding surgery [3]. Those increase the risk of severe intraoperative hypotension, especially in the patients under TEA plus GA. While patient controlled thoracic epidural analgesia (PCTEA) is probably the best option to control pain postoperatively for those patients [4]. So we think GA, instead of TEA combined with GA, followed by PCTEA is the best anesthesiae analgesia regimen in patients undergoing CRS and HIPEC procedures. On the other hand, the main reason for hypotension during epidural anesthesia may be arterial vasodilation, but not pre-load absolute deficiency. It is certainly reasonable to treat hypotension with a vasopressor (such as phenylephrine). Excessive fluid or fresh frozen plasma (FFP) infusion is inappropriate, or even harmful for those patients undergoing CRS þ HIPEC procedures. Because excess fluid or FFP would dilute the blood and reduce the hemoglobin concentration, thereby increase the possibility of iatrogenic RBCs transfusion which is associated with a higher risk of mortality and morbidity in surgical patients [5].

I am very glad to see that Dr Shih et al. reportedmy case of haemomediastinum caused by a ruptured bronchial artery aneurysm [1]. This is one of the bronchial arterial embolisation cases that I performed during October 2006. However, I have to point out a misinterpretation of Fig. 1 of this article [1]. The location the arrow is pointing to is actually the superior vena cava (SVC) with streak artefacts due to highly concentrated contrast injection from the right arm. If we trace that vein carefully upwards, we can see that the noncontrasted blood from the left brachiocephalic vein is draining into this SVC. The small bronchial artery is a branch from the descending thoracic aorta. The bronchial arterial aneurysm is actually showed as a small dot located anterior to the thoracic vertebra in Fig. 1. The angiogram in Fig. 2 will prove that the aneurysm is truly lying anterior to the spine. Due to the rules of ‘Letter to the Editor’, I cannot explain it out in an image or figure with legend; however, the reader may contact me if they want any further explanations and/or would like to see images of the case.

2. Smaka TJ, Cobas M, Velazquez OC, et al: Perioperative management of endovascular abdominal aortic aneurysm repair: Update 2010. J Cardiothorac Vasc Anesth 25:166-176, 2011 3. Scurr JR, Brennan JA, Gilling-Smith GL, et al: Fenestrated endovascular repair for juxtarenal aortic aneurysm. Br J Surg 95:326-332, 2008 4. Gabrielli L, Baudo A, Molinari A, et al: Early complications in endovascular treatment of abdominal aortic aneurysm. Acta Chir Belg 104:519-526, 2004