Exploring the potential mechanism of WuFuYin against hypertrophic scar using network pharmacology and molecular docking.

BACKGROUND: Hypertrophic scar (HTS) is dermal fibroproliferative disorder, which may cause physiological and psychological problems. Currently, the potential mechanism of WuFuYin (WFY) in the treatment of HTS remained to be elucidated. AIM: To explore the potential mechanism of WFY in treating HTS. METHODS: Active components and corresponding targets were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. HTS-related genes were obtained from the GeneCards, DisGeNET, and National Center for Biotechnology Information. The function of targets was analyzed by performing Gene Ontology and Kyoto Encyclopaedia of Genes and Genome (KEGG) enrichment analysis. A protein + IBM-protein interaction (PPI) network was developed using STRING database and Cytoscape. To confirm the high affinity between compounds and targets, molecular docking was performed. RESULTS: A total of 65 core genes, which were both related to compounds and HTS, were selected from multiple databases. PPI analysis showed that CKD2, ABCC1, MMP2, MMP9, glycogen synthase kinase 3 beta (GSK3B), PRARG, MMP3, and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma (PIK3CG) were the hub targets and MOL004941, MOL004935, MOL004866, MOL004993, and MOL004989 were the key compounds of WFY against HTS. The results of KEGG enrichment analysis demonstrated that the function of most genes were enriched in the PI3K-Akt pathway. Moreover, by performing molecular docking, we confirmed that GSK3B and 8-prenylated eriodictyol shared the highest affinity. CONCLUSION: The current findings showed that the GSK3B and cyclin dependent kinase 2 were the potential targets and MOL004941, MOL004989, and MOL004993 were the main compounds of WFY in HTS treatment.

Emerging strategies for tissue engineering in vascularized composite allotransplantation: A review.

Vascularized composite allotransplantation (VCA), which can effectively improve quality of life, is a promising therapy for repair and reconstruction after face or body trauma. However, intractable issues are associated with VCA, such as the inevitable multiple immunogenicities of different tissues that cause severe rejection, the limited protocols available for clinical application, and the shortage of donor sources. The existing regimens used to extend the survival of patients receiving VCAs and suppress rejection are generally the lifelong application of immunosuppressive drugs, which have side effects. Consequently, studies aiming at tissue engineering methods for VCA have become a topic. In this review, we summarize the emerging therapeutic strategies for tissue engineering aimed to prolong the survival time of VCA grafts, delay the rejection and promote prevascularization and tissue regeneration to provide new ideas for future research on VCA treatment.

Heme oxygenase-1 induction mitigates burn-associated early acute kidney injury via the TLR4 signaling pathway.

OBJECTIVES: Early acute kidney injury (AKI) after burn contributes to disastrous prognoses for severely burned patients. Burn-induced renal oxidative stress and secondary proinflammatory mediator release contribute to early AKI development, and Toll-like receptor (TLR) 4 regulates inflammation. Heme oxygenase-1 (HO-1) is a stress-responsive enzyme that plays a vital role in protecting against ischemia-induced organ injury via its antioxidant properties and regulation of inflammation. We investigated the potential effect of HO-1 induction in preventing burn-induced early AKI and its related mechanism. METHODS: A classic major-burn rat model was established using a 100 °C water bath, and hemin was injected intraperitoneally immediately after the injury to induce HO-1. Histological staining and blood tests were used to assess AKI progression based on structural changes and function. Renal levels of HO-1, oxidative stress, proinflammatory mediators and TLR4-related signals were detected using ELISA, immunostaining, qRT-PCR, and western blotting. The selective TLR4 inhibitor TAK242 and TLR4 inducer LPS were introduced to determine the roles of HO-1 in burn-related renal inflammation and the TLR4 pathway. RESULTS: Hemin improved burn-induced renal histological damage and dysfunction, and this beneficial effect was related to reduced renal oxidative stress and the release of proinflammatory mediators, such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1ß, IL-6 and intracellular adhesion molecule-1 (ICAM-1). Hemin downregulated the expression of TLR4 and the subsequent phosphorylation of IKKα/ß, IκBα, and NF-κB p65;. TAK242 exerted an effect similar to but weaker than hemin; and LPS reversed the antiinflammatory effect of hemin and the regulation of TLR4 signals. These results suggested that the TLR4 signaling pathway mediated the HO-1-facilitated regulation of renal inflammation after burn. CONCLUSION: The present study demonstrated that HO-1 induction prevented burn-induced early AKI by targeting renal inflammation, which was mediated via regulation of the TLR4/NF-κB signaling pathway.

ASMq protects against early burn wound progression in rats by alleviating oxidative stress and secondary mitochondria­associated apoptosis via the Erk/p90RSK/Bad pathway.

Burn wounds present an evolutionary progression, in which the initial wound tissue deepens and expands following thermal injury. Progressive tissue damage in the zone of stasis may worsen burn injury, which is associated with oxidative stress and secondary apoptosis, and worsen the prognosis of patients with burn wounds. The mitochondrial apoptotic pathway is involved in receiving oxidative signals and regulating tissue apoptosis. Previously, Abnormal Savda Munziq (ASMq), a natural compound of traditional Uyghur Medicine, which includes ten types of herb, has been reported to exhibit a number of effects, including anti­inflammatory, antioxidative and anti­apoptotic activities. The present study demonstrated that ASMq protected against early burn wound progression following thermal injury in rats; this effect may be mediated by its ability to attenuate oxidative stress­induced mitochondria­associated apoptosis. The present study may provide a novel therapeutic method to prevent early burn wound progression following burn injury.

Astaxanthin protects against early acute kidney injury in severely burned rats by inactivating the TLR4/MyD88/NF-κB axis and upregulating heme oxygenase-1.

Early acute kidney injury (AKI) contributes to severe morbidity and mortality in critically burned patients. Renal inflammation plays a vital role in the progression of early AKI, acting as a therapeutic target. Astaxanthin (ATX) is a strong antioxidant widely distributed in marine organisms that exerts many biological effects in trauma and disease. ATX is also suggested to have anti-inflammatory activity. Hence, we attempted to explore the role of ATX in protecting against early postburn AKI via its anti-inflammatory effects and the related mechanisms. A severely burned model was established for histological and biochemical assessments based on adult male rats. We found that oxidative stress-induced tissue inflammation participated in the development of early AKI after burn injury and that the MyD88-dependent TLR4/NF-κB pathway was activated to regulate renal inflammation. The TLR4 and NF-κB inhibitors TAK242 and PDTC showed similar effects in attenuating burn-induced renal inflammation and early AKI. Upon ATX treatment, the release of inflammatory mediators in the kidneys was downregulated, while the TLR4/MyD88/NF-κB axis was inhibited in a dose-related manner. TAK242 and PDTC could enhance the anti-inflammatory effect of high-dose ATX, whereas lipopolysaccharide (LPS) reversed its action. Furthermore, the expression of heme oxygenase (HO)-1 was upregulated by ATX in a dose-related manner. Collectively, the above data suggest that ATX protects against renal inflammation in a dose-related manner by regulating the TLR4/MyD88/NF-κB axis and HO-1 and ultimately prevents early AKI following severe burns.

Locally activated mitophagy contributes to a "built-in" protection against early burn-wound progression in rats.

AIMS: Deep burn-wounds undergo a dynamic progression in the initial or periburn area after insults, and the zone of stasis is the crucial region suffering the deterioration, considered as salvageable. Few studies explored the role of mitochondria in this process. This study is to clarify a possible "built-in" protection of mitophagy. MAIN METHODS: A classic "comb" scald rat model was established. Histological and blood-flow observation were processed based on hematoxylin-eosin staining and laser analysis. Oxidative and apoptotic status were analyzed by commercial kits. Transmission-electron microscope, immunofluorescence staining, and western blot were applied to detect the mitophagy in the zone of stasis and potential regulators. Adenovirus-based gene-silence contributed to determine the role of HIF-1α as a regulatory mediator. KEY FINDINGS: We found that burn-caused typical ischemia and histological deterioration in the zone of stasis, in parallel with increases in oxidative stress and apoptosis. Mitochondrial damage was involved in the aforementioned changes. Furthermore, we detected mitophagy in burn-wounds, which was contradictory to the burn-wound conversion. HIF-1α expression was closely related to the level of mitophagy, while BNIP3 and PARKIN are involved downstream. SIGNIFICANCE: We demonstrate that burn-induced mitochondrial impairment contributes to the mobilization of injurious mechanisms in the zone of stasis and that mitophagy provides a beneficial way to protect against burn-wound progression via the elimination of damaged mitochondria. Our findings offer insights into mitochondrial quality control in burn-wound progression and suggest the novel concept that HIF-1α may be a therapeutic target due to its possible regulation on BNIP3- or PARKIN-mediated mitophagy.

Mitochondrial Fusion and Fission in Neuronal Death Induced by Cerebral Ischemia-Reperfusion and Its Clinical Application: A Mini-Review.

Mitochondria are highly dynamic organelles which are joined by mitochondrial fusion and divided by mitochondrial fission. The balance of mitochondrial fusion and fission plays a critical role in maintaining the normal function of neurons, of which the processes are both mediated by several proteins activated by external stimulation. Cerebral ischemia-reperfusion (I/R) injury can disrupt the balance of mitochondrial fusion and fission through regulating the expression and post-translation modification of fusion- and fission-related proteins, thereby destroying homeostasis of the intracellular environment and causing neuronal death. Furthermore, human intervention in fusion- and fission-related proteins can influence the function of neurons and change the outcomes of cerebral I/R injury. In recent years, researchers have found that mitochondrial dysfunction was one of the main factors involved in I/R, and mitochondria is an attractive target in I/R neuroprotection. Therefore, mitochondrial-targeted therapy of the nervous system for I/R gradually started from basic study to clinical application. In the present review, we highlight recent progress in mitochondria fusion and fission in neuronal death induced by cerebral I/R to help understanding the regulatory factors and signaling networks of aberrant mitochondrial fusion and fission contributing to neuronal death during I/R, as well as the potential neuroprotective therapeutics targeting mitochondrial dynamics, which may help clinical treatment and development of relevant dugs.

Epidemic characteristics of the COVID-19 outbreak in Tianjin, a well-developed city in China.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is already a pandemic. Few studies investigated the epidemic characteristics of the COVID-19 outbreak in the well-developed cities. METHODS: Epidemiological data of 136 confirmed COVID-19 cases were collected from the dataset of COVID-19 in Tianjin. All confirmed cases were categorized according to their potential infection sources. Daily numbers of confirmed cases of each category were plotted by date of onset, and the epidemic form of each category was inferred. RESULTS: Among the 136 confirmed COVID-19 cases, 48 cases were categorized as imported cases and their close contacts, which were the majority of early cases. A total of 43 cases were found an epidemiological link to the Baodi department store, and they were inferred to be a common-source outbreak. Additionally, 35 cases were considered as familial clusters of COVID-19 cases, and 10 cases were sporadic. The 45 cases were inferred to be a propagated epidemic. CONCLUSIONS: Local transmission of COVID-19 mainly occurred within families and a poorly ventilated public place in Tianjin. Besides the imported cases, the pattern of local transmission of COVID-19 was a mixture of the propagated epidemic and the common-source outbreak in Tianjin.

Regeneration of skin appendages and nerves: current status and further challenges.

Tissue-engineered skin (TES), as an analogue of native skin, is promising for wound repair and regeneration. However, a major drawback of TES products is a lack of skin appendages and nerves to enhance skin healing, structural integrity and skin vitality. Skin appendages and nerves are important constituents for fully functional skin. To date, many studies have yielded remarkable results in the field of skin appendages reconstruction and nerve regeneration. However, patients often complain about a loss of skin sensation and even cutaneous chronic pain. Restoration of pain, temperature, and touch perceptions should now be a major challenge to solve in order to improve patients' quality of life. Current strategies to create skin appendages and sensory nerve regeneration are mainly based on different types of seeding cells, scaffold materials, bioactive factors and involved signaling pathways. This article provides a comprehensive overview of different strategies for, and advances in, skin appendages and sensory nerve regeneration, which is an important issue in the field of tissue engineering and regenerative medicine.

Epidemiology of bus fires in mainland China from 2006 to 2015.

OBJECTIVE: This study analyses the epidemiological characteristics of bus fires in mainland China over the past 10 years to develop prevention strategies and emergency procedures for such incidence and the resulting casualties. METHODS: We collected reports on bus fires from the media and news websites and looked up on Medline, PubMed, and Chinese National Knowledge Infrastructure databases for relevant publications in English or Chinese from January 1, 2006 to December 31, 2015. RESULTS: In the past 10 years, there were 382 bus fires in mainland China. The frequency of fires was markedly higher in 2013 and 2014. The vast majority (89.1%) of the fires were caused by spontaneous combustion, followed by arson (5.0%). There were reports of casualties in 41 (10.7%) of the bus fires, including 144 deaths and 567 injuries. The fires leading to casualties resulted from spontaneous combustion in 22 (53.7%) incidents, arson in 12 (29.3%) incidents, and traffic accidents in 7 (17.1%) incidents. Arson caused the most casualties, including 91 deaths and 323 injuries. CONCLUSIONS: This epidemiological study presents characteristic findings related to bus fires in China mainland. The general trend of bus fires showed a gradual increase but with a fluctuation in several years. The regional distribution of bus fires revealed some specific characteristics, and most of bus fires happened in those regions locating in the eastern area of China mainland. The largest number of bus fires were caused by spontaneous combustion. Bus fires caused by arson accounting for only 5% of the total bus fires resulted in the most severe casualties. Most of bus arson occurred in the morning and evening rush hours.

Nrf2/HO-1 mediates the neuroprotective effect of mangiferin on early brain injury after subarachnoid hemorrhage by attenuating mitochondria-related apoptosis and neuroinflammation.

Early brain injury (EBI) is involved in the process of cerebral tissue damage caused by subarachnoid hemorrhage (SAH), and multiple mechanisms, such as apoptosis and inflammation, participate in its development. Mangiferin (MF), a natural C-glucoside xanthone, has been reported to exert beneficial effects against several types of organ injury by influencing various biological progresses. The current study aimed to investigate the potential of MF to protect against EBI following SAH via histological and biological assessments. A rat perforation model of SAH was established, and MF was subsequently administered via intraperitoneal injection at a low and a high dose. High-dose MF significantly lowered the mortality of SAH animals and ameliorated their neurological deficits and brain edema. MF also dose-relatedly attenuated SAH-induced oxidative stress and decreased cortical cell apoptosis by influencing mitochondria-apoptotic proteins. In addition, MF downregulated the activation of the NLRP3 inflammasome and NF-κB as well as the production of inflammatory cytokines, and the expression of Nrf2 and HO-1 was upregulated by MF. The abovementioned findings indicate that MF is neuroprotective against EBI after SAH and Nrf2/HO-1 cascade may play a key role in mediating its effect through regulation of the mitochondrial apoptosis pathway and activation of the NLRP3 inflammasome and NF-κB.

Astaxanthin protects against early burn-wound progression in rats by attenuating oxidative stress-induced inflammation and mitochondria-related apoptosis.

Burn-wound progression can occur in the initial or peri-burn area after a deep burn injury. The stasis zone has a higher risk of deterioration mediated by multiple factors but is also considered salvageable. Astaxanthin (ATX), which is extracted from some marine organisms, is a natural compound with a strong antioxidant effect that has been reported to attenuate organ injuries caused by traumatic injuries. Hence, we investigated the potential effects of ATX on preventing early burn-wound progression. A classic "comb" burn rat model was established in this study for histological and biological assessments, which revealed that ATX, particularly higher doses, alleviated histological deterioration in the stasis zone. Additionally, we observed dose-dependent improvements in oxidative stress and the release of inflammatory mediators after ATX treatment. Furthermore, ATX dose-dependently attenuated burn-induced apoptosis in the wound areas, and this effect was accompanied by increases in Akt and Bad phosphorylation and a downregulation of cytochrome C and caspase expression. In addition, the administration of Ly 294002 further verified the effect of ATX. In summary, we demonstrated that ATX protected against early burn-wound progression in a rat deep-burn model. This protection might be mediated by the attenuation of oxidative stress-induced inflammation and mitochondria-related apoptosis.

Diagnosis and management of tumor-like hypophysitis: A retrospective case series.

Tumor-like hypophysitis is an uncommon sellar condition that presents as inflammatory lesions on the structures of the pituitary gland. The diagnosis and management of hypophysitis poses a significant challenge, as its clinical manifestation and appearance in imaging studies are difficult to distinguish from that of pituitary tumors. The present retrospective study summarizes two rare cases of primary granulomatous hypophysitis, two cases of lymphocytic hypophysitis, and three cases in which a pathological diagnosis was not determined due to the use of hormone replacement therapy only. The mean age of the patients studied was 45.71±22.16 years, and the patients comprised two males and five females. The clinical signs of hypophysitis included headache, fever, gradual decrease in visual acuity, nausea and vomiting. Enhanced magnetic resonance imaging revealed sellar and pituitary stalk lesions, with iso- or hypodense signals on T1-weighted images. Transsphenoidal surgery was performed in three cases. It was challenging to diagnose hypophysitis due to the lack of any significant specific clinical signs. A transsphenoidal biopsy with fast-frozen pathology is able to diagnose hypophysitis. Glucocorticoid therapy may be a potential treatment for hypophysitis, as complete removal of pituitary masses may disable pituitary function.

Polyurethane membrane/knitted mesh-reinforced collagen-chitosan bilayer dermal substitute for the repair of full-thickness skin defects via a two-step procedure.

The advent of dermal substitutes provides a revolutionary strategy for the repair and reconstruction of deep skin defects. Dermal substitutes form a regenerative template that provides the porous structure and mechanical support necessary to guide cell migration, deposition of the extracellular matrix (ECM) and angiogenesis. Commercially available dermal substitutes, particularly collagen-based dermal scaffolds, are widely used in clinical practice. However, the poor mechanical properties of collagen-based dermal scaffolds compromise their biological effects, as well as the repair outcomes. Here, we describe a bilayer dermal substitute prepared by integrating a hybrid dermal scaffold with a polyurethane (PU) membrane to obtain a PU membrane/knitted mesh-reinforced collagen-chitosan bilayer dermal substitute (PU-PLGAm/CCS). The morphology of PU-PLGAm/CCS was investigated and, to characterize the effects of PU-PLGAm/CCS on tissue regeneration, dermal substitutes were transplanted to repair full-thickness skin wounds in Sprague-Dawley rats using a two-step surgical procedure. These results were then compared with those obtained using the PELNAC™ Artificial Dermis. In the weeks after the first operation, wound changes were analysed based on macroscopic observations, and tissue specimens were harvested for histology, immunohistochemistry, immunofluorescence real-time quantitative PCR, and Western blotting analysis. Following the second operation (i.e., transplantation of split-thickness skin grafts), the repair outcomes were investigated based on the mechanical strength and ECM expression. PU-PLGAm/CCS significantly inhibited wound contracture, promoted angiogenesis, and facilitated the ordered arrangement of neotissue, such that the repair outcomes were improved in the PU-PLGAm/CCS group compared with the PELNAC™ group. In conclusion, the favourable microstructure and structural stability of dermal substitutes facilitated tissue regeneration. PU-PLGAm/CCS achieved a balance between porous structure, biocompatibility and mechanical properties for dermal regeneration by integrating the advantages of biological and synthetic biomaterials, which demonstrates its potential for skin tissue engineering.

Effects of hydrogen-rich saline on early acute kidney injury in severely burned rats by suppressing oxidative stress induced apoptosis and inflammation.

BACKGROUND: Early acute kidney injury (AKI) in severely burned patients predicts a high mortality that is multi-factorial. Hydrogen has been reported to alleviate organ injury via selective quenching of reactive oxygen species. This study investigated the potential protective effects of hydrogen against severe burn-induced early AKI in rats. METHODS: Severe burn were induced via immersing the shaved back of rats into a 100°C bath for 15 s. Fifty-six Sprague-Dawley rats were randomly divided into Sham, Burn + saline, and Burn + hydrogen-rich saline (HS) groups, and renal function and the apoptotic index were measured. Kidney histopathology and immunofluorescence staining, quantitative real-time PCR, ELISA and western blotting were performed on the sera or renal tissues of burned rats to explore the underlying effects and mechanisms at varying time points post burn. RESULTS: Renal function and tubular apoptosis were improved by HS treatment. In addition, the oxidation-reduction potential and malondialdehyde levels were markedly reduced with HS treatment, whereas endogenous antioxidant enzyme activities were significantly increased. HS also decreased the myeloperoxidase levels and influenced the release of inflammatory mediators in the sera and renal tissues of the burned rats. The regulatory effects of HS included the inhibition of p38, JNK, ERK and NF-κB activation, and an increase in Akt phosphorylation. CONCLUSION: Hydrogen can attenuate severe burn-induced early AKI; the mechanisms of protection include the inhibition of oxidative stress induced apoptosis and inflammation, which may be mediated by regulation of the MAPKs, Akt and NF-κB signalling pathways.

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death.

Early brain injury (EBI) following aneurysmal subarachnoid haemorrhage (SAH) insults contributes to the poor prognosis and high mortality observed in SAH patients. Topiramate (TPM) is a novel, broad-spectrum, antiepileptic drug with a reported protective effect against several brain injuries. The current study aimed to investigate the potential of TPM for neuroprotection against EBI after SAH and the possible dose-dependency of this effect. An endovascular perforation SAH model was established in rats, and TPM was administered by intraperitoneal injection after surgery at three different doses (20mg/kg, 40mg/kg, and 80mg/kg). The animals' neurological scores and brain water content were evaluated, and ELISA, Western blotting and immunostaining assays were conducted to assess the effect of TPM. The results revealed that TPM lowers the elevated levels of myeloperoxidase and proinflammatory mediators observed after SAH in a dose-related fashion, and the nuclear factor-kappa B (NF-κB) signalling pathway is the target of neuroinflammation regulation. In addition, TPM ameliorated SAH-induced cortical neuronal apoptosis by influencing Bax, Bcl-2 and cleaved caspase-3 protein expression, and the effect of TPM was enhanced in a dose-dependent manner. Various dosages of TPM also upregulated the protein expression of the γ-aminobutyric acid (GABA)-ergic signalling molecules, GABAA receptor (GABAAR) α1, GABAAR γ2, and K(+)-Cl(-) co-transporter 2 (KCC2) together and downregulated Na(+)-K(+)-Cl(-) co-transporter 1 (NKCC1) expression. Thus, TPM may be an effective neuroprotectant in EBI after SAH by regulating neuroinflammation and neuronal cell death.

Astaxanthin attenuates early acute kidney injury following severe burns in rats by ameliorating oxidative stress and mitochondrial-related apoptosis.

Early acute kidney injury (AKI) is a devastating complication in critical burn patients, and it is associated with severe morbidity and mortality. The mechanism of AKI is multifactorial. Astaxanthin (ATX) is a natural compound that is widely distributed in marine organisms; it is a strong antioxidant and exhibits other biological effects that have been well studied in various traumatic injuries and diseases. Hence, we attempted to explore the potential protection of ATX against early post burn AKI and its possible mechanisms of action. The classic severe burn rat model was utilized for the histological and biochemical assessments of the therapeutic value and mechanisms of action of ATX. Upon ATX treatment, renal tubular injury and the levels of serum creatinine and neutrophil gelatinase-associated lipocalin were improved. Furthermore, relief of oxidative stress and tubular apoptosis in rat kidneys post burn was also observed. Additionally, ATX administration increased Akt and Bad phosphorylation and further down-regulated the expression of other downstream pro-apoptotic proteins (cytochrome c and caspase-3/9); these effects were reversed by the PI3K inhibitor LY294002. Moreover, the protective effect of ATX presents a dose-dependent enhancement. The data above suggested that ATX protects against early AKI following severe burns in rats, which was attributed to its ability to ameliorate oxidative stress and inhibit apoptosis by modulating the mitochondrial-apoptotic pathway, regarded as the Akt/Bad/Caspases signalling cascade.

Left type I proatlantal artery with bilateral aberrant vertebral arteries and a ruptured aneurysm: a case report and review of the literature.

Persistent proatlantal artery is one rare kind of persistent primitive anastomoses between carotid and basilar vascular system. This case firstly introduces a type I proatlantal artery with complex vascular anomalies of bilateral vertebral arteries and a ruptured aneurysm, which is extremely uncommon. A 43-year-old female was hospitalised for SAH and ventricular hematocele. The subsequent digital subtraction angiography and computed tomography angiography revealed a type I proatlantal artery which arises from left internal carotid artery, associating with a hypoplastic right vertebral artery, an aplastic left vertebral artery and a ruptured left posterior inferior cerebellar artery aneurysm. An interventional procedure was taken later. The present case raises awareness on the incidence of persistent primitive anastomoses which combined other complex vascular anomalies before surgical or interventional procedures, especially in view of unique blood supply to posterior circulation from the primitive vessel.