Activation of silent information regulator 1 exerts a neuroprotective effect after intracerebral hemorrhage by deacetylating NF-κB/p65.

Nuclear factor (NF)-κB-mediated neuroinflammation is an important mechanism of intracerebral hemorrhage (ICH)-induced neurotoxicity. Silent information regulator 1 (SIRT1) plays a multi-protective effect in a variety of diseases by deacetylating and inhibiting NF-κB/p65. However, the role of SIRT1 in brain damage following ICH remains unclear. We hypothesized that SIRT1 can protect against ICH-induced brain damage by inhibiting neuroinflammation through deacetylating NF-κB/p65. The ICH model was induced in vivo (with collagenase) and in vitro (with hemoglobin). Resveratrol and Ex527 were administered to activate or inhibit SIRT1, respectively. Western blot, immunohistochemistry, and immunofluorescence assays were performed to detect the expression of SIRT1 and p65. Enzyme-linked immunosorbent assays (ELISAs) were used to explore tumor necrosis factor (TNF)-α and interleukin (IL)-1ß release. The neurological score, brain water content, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and brain hemoglobin content were determined to evaluate the neuroprotective effect of SIRT1. SIRT1 expression was decreased, whereas the level of acetylated p65 (Ac-p65) was elevated after ICH in vivo. Moreover, hemoglobin treatment decreased the expression of SIRT1 in vitro. Activation of SIRT1 by resveratrol had a neuroprotective effect, along with decreased levels of Ac-p65, IL-1ß, TNF-α, and apoptosis after ICH. The effect of resveratrol was abolished by the SIRT1 inhibitor Ex527. Our results are consistent with the hypothesis that SIRT1 exerts a neuroprotective effect after ICH by deacetylating p65 to inhibit the NF-κB-dependent inflammatory response.

Expression and cell distribution of SENP3 in the cerebral cortex after experimental subarachnoid hemorrhage in rats: a pilot study.

Subarachnoid hemorrhage (SAH) is one of the life-threatening diseases with high morbidity and mortality rates. Small ubiquitin-like modifier (SUMO)-specific proteases 3 (SENP3), a member of the SUMO-specific protease family, was identified as an isopeptidase that deconjugates SUMOylation (The covalent modification by SUMO) of modified protein substrates. It is reported that SUMO-2/3 conjugation, a member of SUMOylation, presented neuroprotection. The study aimed to evaluate the expression of SENP3 and to explore its role potential role in SAH. A total of 95 Sprague-Dawley rats were randomly divided into sham group and SAH groups at 6, 12, 24, 48 h, day 3, day 5, and day 7. SAH groups suffered experimental SAH by injection with 0.3 ml nonheparinized autoblood into the prechiasmatic cistern. SENP3 expression is surveyed by western blot analysis, real-time polymerase chain reaction, immunohistochemistry, and immunofluorescence. The levels of cleavage caspase-3 were determined by western blot and immunohistochemistry. SENP3 protein expression was significantly up-regulated after SAH which peaked at 24 h; however, the mRNA expression of SENP3 remained unchanged. Meanwhile, the level of cleaved caspase-3 was also increased after SAH. There is a highly positive correlation between cleavage caspase-3 and SENP3 in protein level. Immunofluorescent results showed that the expression of SENP3 was increased in neurons, rather than astrocytes nor microglia. Our findings indicated a possible role of SENP3 in the pathogenesis of early brain injury mediated by apoptosis following SAH.

Expression of Cytoplasmic Gelsolin in Rat Brain After Experimental Subarachnoid Hemorrhage.

Convincing evidence indicates that apoptosis contributes to the unfavorable prognosis of subarachnoid hemorrhage (SAH), a significant cause of morbidity and case fatality throughout the world. Gelsolin (GSN) is a Ca(2+)-dependent actin filament severing, capping, and nucleating protein, as well as multifunctional regulator of cell structure and metabolism, including apoptosis. In the present study, we intended to investigate the expression pattern and cell distribution of GSN in rat brain after experimental SAH. GSN expression was examined in sham group and at 3, 6, 12 h, day 1 (1 day), 2, 3, 5, and 7 days after SAH by Western blot analysis as well as real-time polymerase chain reaction. Immunohistochemistry and immunofluorescence were performed to detect the localization of GSN. The level of GSN protein expression was significantly decreased in SAH group and reached a bottoming point on 1 day after SAH. GSN mRNA level was significantly decreased in SAH groups in comparison with the sham group, and reached a minimum value at 12 h after SAH. Immunohistochemistry showed that GSN was constitutively and obviously expressed in the cortex of the normal rat brain and significantly decreased in the rat cortex after SAH. In addition, immunofluorescence results revealed that GSN expression could be found in both neurons and microglias, as well as in glialfibrillary acidic protein-positive astrocytes. The decreased expression of GSN could mainly be found in neurons and astrocytes as well, and GSN-positive microglias showed different cell morphological characteristics. Interestingly, the protein and gene levels of GSN seemed to be constant in the rat hippocampus of sham and SAH groups. These findings suggested a potential role of GSN in the pathophysiology of the brain at the early stage of SAH.

Tert-butylhydroquinone Ameliorates Early Brain Injury After Experimental Subarachnoid Hemorrhage in Mice by Enhancing Nrf2-Independent Autophagy.

Evidence has shown that the activation of the autophagy pathway after experimental subarachnoid hemorrhage (SAH) protects against neuronal damage. Tert-butylhydroquinone (tBHQ), a commonly used nuclear factor erythroid 2-related factor 2 (Nrf2) activator, was found to significantly enhance autophagy activation. The aim of this study was to explore the effect of tBHQ treatment on early stage brain injury at 24 h after SAH. The results showed that tBHQ treatment failed to stimulate an effective anti-oxidative effect at 24 h after the SAH operation, but succeeded in ameliorating early brain injury, including alleviated brain edema, BBB disruption, neuronal degeneration and neurological deficits. Further exploration found that tBHQ treatment significantly increased the expression of Beclin-1 and the ratio of microtubule-associated protein 1 light chain 3 (LC3)-II to LC3-I, suggesting that autophagy was enhanced after tBHQ treatment. Moreover, tBHQ treatment restored Bcl-2 and Bax expression and reduced caspase-3 cleavage, suggesting the protective effect of tBHQ treatment in ameliorating brain injury after SAH. Furthermore, tBHQ enhanced autophagy activation, decreased neuronal degeneration and improved the neurological score after SAH in Nrf2-deficient mice. Taken together, these findings suggest that tBHQ treatment exerts neuro-protective effects against EBI following SAH by enhancing Nrf2-independent autophagy. Therefore, tBHQ is a promising therapeutic agent against EBI following SAH.

SIRT1 inhibition by sirtinol aggravates brain edema after experimental subarachnoid hemorrhage.

Secondary brain injury following subarachnoid hemorrhage (SAH) is poorly understood. We utilized a rat model of SAH to investigate whether SIRT1 has a protective role against brain edema via the tumor suppressor protein p53 pathway. Experimental SAH was induced in adult male Sprague-Dawley rats by prechiasmatic cistern injection. Brain SIRT1 protein levels were examined in the sham controls and in rats 6, 12, 24, 48, and 72 hr after SAH induction. The SIRT1 inhibitor sirtinol was administered by intracerebroventricular infusion. Neurological functions, blood-brain barrier (BBB) disruption, and brain water content were assessed. Endothelial cell apoptosis, caspase 3 protein expression, p53 acetylation, and matrix metalloproteinase-9 (MMP-9) activity were examined. Compared with the control, SIRT1 protein expression increased remarkably, reaching a maximum at 24 hr after SAH. Sirtinol treatment significantly lowered SIRT1 expression, accompanied by deteriorated neurologic function, BBB disruption, brain edema, increased endothelial cell apoptosis, and increased MMP-9 gelatinase activity compared with the rats treated with vehicle only. Our results suggest that increased expression of endogenous SIRT1 may play a neuroprotective role against brain edema after SAH.

Expression and cell distribution of neuroglobin in the brain tissue after experimental subarachnoid hemorrhage in rats: a pilot study.

Neuroglobin (Ngb) is a member of the globin superfamily expressed mainly in the nervous system and retina of vertebrates. Accumulated evidence has clearly demonstrated that Ngb has a neuro-protective role enhancing cell viability under hypoxia and other types of oxidative stress. It was suggested that oxidant stress could play an important role in neuronal injury after subarachnoid hemorrhage (SAH). The present study aims to examine the expression of Ngb in the temporal cortex and its cellular localization after SAH. We used a prechiasmatic cistern model of SAH. Ngb expression was examined at 3, 6, 12, 24, 48, and 72 h after SAH by western blot analysis and real-time polymerase chain reaction (PCR). Immunohistochemistry and immunofluorescence were performed to detect the localization of Ngb. Real-time PCR demonstrated that Ngb mRNA levels increased from 3 h after SAH, peaked at 6 h. Western blot showed Ngb protein levels were significantly increased in SAH groups in the temporal cortex and reached the peak at 24 h after SAH. The immunohistochemical staining demonstrated that Ngb was weakly expressed in the cortex in the control group while the enhanced expression of Ngb could be detected in the SAH groups. In addition, immunofluorescence results revealed that the over-expressed Ngb was located in the neuronal and microglia cell cytoplasm. These findings indicated that Ngb might play an important neuro-protective effect after SAH.

Astaxanthin offers neuroprotection and reduces neuroinflammation in experimental subarachnoid hemorrhage.

BACKGROUND: Neuroinflammation has been proven to play a crucial role in early brain injury pathogenesis and represents a target for treatment of subarachnoid hemorrhage (SAH). Astaxanthin (ATX), a dietary carotenoid, has been shown to have powerful anti-inflammation property in various models of tissue injury. However, the potential effects of ATX on neuroinflammation in SAH remain uninvestigated. The goal of this study was to investigate the protective effects of ATX on neuroinflammation in a rat prechiasmatic cistern SAH model. METHODS: Rats were randomly distributed into multiple groups undergoing the sham surgery or SAH procedures, and ATX (25 mg/kg or 75 mg/kg) or equal volume of vehicle was given by oral gavage at 30 min after SAH. All rats were sacrificed at 24 h after SAH. Neurologic scores, brain water content, blood-brain barrier permeability, and neuronal cell death were examined. Brain inflammation was evaluated by means of expression changes in myeloperoxidase, cytokines (interleukin-1ß, tumor necrosis factor-α), adhesion molecules (intercellular adhesion molecule-1), and nuclear factor kappa B DNA-binding activity. RESULTS: Our data indicated that post-SAH treatment with high dose of ATX could significantly downregulate the increased nuclear factor kappa B activity and the expression of inflammatory cytokines and intercellular adhesion molecule-1 in both messenger RNA transcription and protein synthesis. Moreover, these beneficial effects lead to the amelioration of the secondary brain injury cascades including cerebral edema, blood-brain barrier disruption, neurological dysfunction, and neuronal degeneration. CONCLUSIONS: These results indicate that ATX treatment is neuroprotective against SAH, possibly through suppression of cerebral inflammation.

Astaxanthin alleviates early brain injury following subarachnoid hemorrhage in rats: possible involvement of Akt/bad signaling.

Apoptosis has been proven to play a crucial role in early brain injury pathogenesis and to represent a target for the treatment of subarachnoid hemorrhage (SAH). Previously, we demonstrated that astaxanthin (ATX) administration markedly reduced neuronal apoptosis in the early period after SAH. However, the underlying molecular mechanisms remain obscure. In the present study, we tried to investigate whether ATX administration is associated with the phosphatidylinositol 3-kinase-Akt (PI3K/Akt) pathway, which can play an important role in the signaling of apoptosis. Our results showed that post-SAH treatment with ATX could cause a significant increase of phosphorylated Akt and Bad levels, along with a significant decrease of cleaved caspase-3 levels in the cortex after SAH. In addition to the reduced neuronal apoptosis, treatment with ATX could also significantly reduce secondary brain injury characterized by neurological dysfunction, cerebral edema and blood-brain barrier disruption. In contrast, the PI3K/Akt inhibitor, LY294002, could partially reverse the neuroprotection of ATX in the early period after SAH by downregulating ATX-induced activation of Akt/Bad and upregulating cleaved caspase-3 levels. These results provided the evidence that ATX could attenuate apoptosis in a rat SAH model, potentially, in part, through modulating the Akt/Bad pathway.

Renal primitive malignant tumor with endocrine activity.

OBJECTIVE: To report a hypertensive and systematically pigmented female with primitive neuroectodermal tumors. CLINICAL PRESENTATION AND INTERVENTION: A female patient presented with a complaint of right flank pain. She had a right renal space-occupying lesion, underwent right radical nephrectomy, and returned to normotensive postoperatively. The pathological examination identified typical primitive neuroectodermal tumor histology. During a 60-month follow-up period, she remained normotensive and demonstrated normal renal and adrenal functions. CONCLUSION: Early diagnosis and definitive surgery led to the patient's long-term survival.

Optimal therapeutic strategies for pineal region lesions.

Background: The removal of pineal region lesions are challenging, and therapeutic strategies for their removal remain controversial. The current study was conducted to identify the characteristics and the optimal therapeutic strategies for pineal region lesions. Methods: This retrospective study reviewed the treatments of 101 patients with pineal region lesions, and different characteristics and therapeutic strategies were observed. Results: There were no statistical differences in the total resection ratio, complications, and prognosis outcomes between the hydrocephalus group and non-hydrocephalus group, except patients in the hydrocephalus group were younger and pediatric patients had an increased level of intracranial infections. Treatments of lesions and hydrocephalus secondary to pineal region lesions were two integral parts to therapeutic strategies. For the management of lesions, germinoma or non-germinoma were diagnosed preoperatively, and resection or diagnostic radiation were chosen to deal with pineal region lesions. Endoscopic-assisted surgery provided a higher total resection rate. For the management of hydrocephalus, endoscopic third ventriculostomy (ETV) had the better therapeutic effect. Additionally, cerebrospinal fluid (CSF) diversion before radiotherapy or resection did not improve prognosis outcome, but it was necessary for patients with severe hydrocephalus. Logistical regression analysis indicated that age, lesion size, reoperation ratio, and intracranial complications were predictors of prognosis outcome. Conclusion: More attention should be paid to intracranial infections in pediatric patients with hydrocephalus secondary to pineal region lesions, and CSF diversion before radiotherapy or resection did not promote prognosis outcome, but it was necessary for patients with severe hydrocephalus. Age, lesion size, reoperation ratio, and intracranial complications may be the predictors of prognosis outcome. Most importantly, the surgical algorithm for pineal region lesions which was based on preoperatively diagnosis (non-germinoma and germinoma) is useful, especially for developing countries.

Andrographolide Inhibits Proliferation and Promotes Apoptosis in Bladder Cancer Cells by Interfering with NF- κ B and PI3K/AKT Signaling In Vitro and In Vivo.

OBJECTIVE: To explore the influences of andrographolide (Andro) on bladder cancer cell lines and a tumor xenograft mouse model bearing 5637 cells. METHODS: For in vitro experiments, T24 cells were stimulated with Andro (0-40 µmol/L) and 5637 cells were stimulated with Andro (0 to 80 µmol/L). Cell growth, migration, and infiltration were assessed using cell counting kit-8, colony formation, wound healing, and transwell assays. Apoptosis rate was examined using flow cytometry. In in vivo study, the antitumor effect of Andro (10 mg/kg) was evaluated by 5637 tumor-bearing mice, and levels of nuclear factor κ B (NF- κ B) and phosphoinositide 3-kinase/AKT related-proteins were determined by immunoblotting. RESULTS: Andro suppressed growth, migration, and infiltraion of bladder cancer cells (P⩽0.05 or P⩽0.01). Additionally, Andro induced intrinsic mitochondria-dependent apoptosis in bladder cancer cell lines. Furthermore, Andro inhibited bladder cancer growth in mice (P⩽0.01). The expression of p65, p-AKT were suppressed by Andro treatment in vitro and in vivo (P⩽0.05 or P⩽0.01). CONCLUSIONS: Andrographolide inhibits proliferation and promotes apoptosis in bladder cancer cells by interfering with NF- κ B and PI3K/AKT signaling in vitro and in vivo.

[Spermatic cord liposarcoma: a case report and review of the literature].

OBJECTIVE: To explore the clinical features and treatment of spermatic cord liposarcoma (SCL). METHODS: We retrospectively analyzed the clinical data of a case of SCL, reviewed the related literature and investigated the diagnosis and treatment of the disease. RESULTS: The patient underwent tumor resection and left inguinal orchidectomy. Postoperative pathology confirmed the case to be s SCL. Neither recurrence nor metastasis was found during the five-month follow-up. CONCLUSION: SCL is a rare medical condition with no specific imaging and laboratory features. Radical orchidectomy with wide local excision of the mass is recommended for its treatment, and adjuvant radiotherapy can be considered in intermediately or highly differentiated tumors and recurrent liposarcomas, while the role of chemotherapy is not well-defined.

A20 Establishes Negative Feedback With TRAF6/NF-κB and Attenuates Early Brain Injury After Experimental Subarachnoid Hemorrhage.

Nuclear factor (NF)-κB-ty -50mediated neuroinflammation plays a crucial role in early brain injury (EBI) after subarachnoid hemorrhage (SAH). As an important negative feedback regulator of NF-κB, A20 is essential for inflammatory homeostasis. Herein, we tested the hypothesis that A20 attenuates EBI by establishing NF-κB-associated negative feedback after experimental SAH. In vivo and in vitro models of SAH were established. TPCA-1 and lentivirus were used for NF-κB inhibition and A20 silencing/overexpression, respectively. Cellular localization of A20 in the brain was determined via immunofluorescence. Western blotting and enzyme-linked immunosorbent assays were applied to observe the expression of members of the A20/tumor necrosis factor receptor-associated factor 6 (TRAF6)/NF-κB pathway and inflammatory cytokines (IL-6, IL-1ß, TNF-α). Evans blue staining, TUNEL staining, Nissl staining, brain water content, and modified Garcia score were performed to evaluate the neuroprotective effect of A20. A20 expression by astrocytes, microglia, and neurons was increased at 24 h after SAH. A20 and inflammatory cytokine levels were decreased while TRAF6 expression was elevated after NF-κB inhibition. TRAF6, NF-κB, and inflammatory cytokine levels were increased after A20 silencing but suppressed with A20 overexpression. Also, Bcl-2, Bax, MMP-9, ZO-1 protein levels; Evans blue, TUNEL, and Nissl staining; brain water content; and modified Garcia score showed that A20 exerted a neuroprotective effect after SAH. A20 expression was regulated by NF-κB. In turn, increased A20 expression inhibited TRAF6 and NF-κB to reduce the subsequent inflammatory response. Our data also suggest that negative feedback regulation mechanism of the A20/TRAF6/NF-κB pathway and the neuroprotective role of A20 to attenuate EBI after SAH.

Prognostic Value of the Number of Lymph Nodes Examined in Patients with Node-Negative Gastric Cancer.

BACKGROUND: Our aim was to evaluate the prognostic value of the number of lymph nodes examined (eLNs) in patients with node-negative gastric cancer (GC) and further to adjust the American Joint Committee on Cancer (AJCC) 8th staging system based on the number of eLNs. METHODS: Node-negative GC patients diagnosed during 1988-2015 from the Surveillance, Epidemiology, and End Results (SEER) database were included. On the basis of a primary cohort of 4159 node-negative GC patients, we built the adjusted AJCC 8th staging system, which was then internally validated by a bootstrap method, and externally validated with an independent cohort of 5565 node-negative GC patients. RESULTS: The median number of eLNs was 10. For the training set, the optimal eLNs thresholds were determined to be 9 for node-negative GC patients. The adjusted AJCC 8th staging system for node-negative GC patients based on the number of eLNs had a significantly higher Harrell's concordance index than the initial AJCC 8th staging system (C-index, 0.635 versus 0.616; P < 0.001). Thus, the adjusted AJCC 8th staging system had superior prognostic stratification. Similar results were found in the validation set. CONCLUSIONS: For node-negative GC patients in the United States, the adjusted AJCC 8th staging system based on the number of eLNs predicted survival more accurately and discriminatively.

Modified American Joint Committee on Cancer Tumor-Node-Metastasis Staging System Based on the Node Ratio Can Further Improve the Capacity of Prognosis Assessment for Gastric Cancer Patients.

Background and Objectives: Our aim was to investigate whether the modified American Joint Committee on Cancer (AJCC) tumor-node-metastasis (TNM) staging system based on the node ratio can further improve the capacity of prognosis assessment for gastric cancer (GC) patients regardless of the number of lymph nodes examined (eLNs). Methods: A total of 17,187 GC patients in the Surveillance, Epidemiology, and End Results (SEER) database were included. On the basis of a training set of 7,660 GC patients, we built the tumor-node ratio-metastasis (TNrM) staging system, which was then externally validated with a validation set of 9,527 GC patients. Results: For the training set, the C-index value of the TNrM staging system was significantly higher than that of the AJCC 8th TNM staging system to predict survival for GC patients (C-index: 0.688 vs. 0.671, P < 0.001). Moreover, the C-index value of the TNrM staging system was significantly higher than that of the 8th TNM staging system to predict survival for GC patients with ≤15 eLNs (C-index: 0.682 vs. 0.673, P < 0.001), as well as for GC patients with >15 eLNs (C-index: 0.700 vs. 0.694, P < 0.001). Similar results were found in the validation set. Conclusions: The TNrM staging system predicted survival more accurately and discriminatively than the AJCC 8th TNM staging system for GC patients regardless of the number of eLNs.

[Diagnosis and treatment of pancreatogenic portal hypertension: analysis of 26 cases].

OBJECTIVE: To investigate the diagnostic and treatment methods of pancreatogenic portal hypertension and to summarize the experience in surgical treatment of these patients, especially in dealing with the complications and sophisticated cases. METHODS: Twenty-six patients with pancreatogenic portal hypertension, 19 males and 7 females, aged 37 (29 - 57), underwent pericardial vessel ligation and splenectomy during the period from January 1990 to November 2006 and were followed up for 8 years (2 - 15 years). The clinical data were analyzed. RESULTS: Seven patients received Roux-en-Y operation for huge pancreatogenic cysts and 3 patients received regional dissection operation of diaphragmatic muscle for severe adhesion. One died of acute myocardial infarction 5 days after the operation, and 25 patients were cured without recurrence during the follow-up. CONCLUSION: Pericardial vessel ligation and splenectomy are rational and reliable methods to treat pancreatogenic portal hypertension. The key issue is how to diagnose pancreatogenic portal hypertension correctly and deal with its complications reasonably.

Biochanin A Reduces Inflammatory Injury and Neuronal Apoptosis following Subarachnoid Hemorrhage via Suppression of the TLRs/TIRAP/MyD88/NF-κB Pathway.

Inflammatory injury and neuronal apoptosis participate in the period of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Suppression of inflammation has recently been shown to reduce neuronal death and neurobehavioral dysfunction post SAH. Biochanin A (BCA), a natural bioactive isoflavonoid, has been confirmed to emerge the anti-inflammatory pharmacological function. This original study was aimed at evaluating and identifying the neuroprotective role of BCA and the underlying molecular mechanism in an experimental Sprague-Dawley rat SAH model. Neurobehavioral function was evaluated via the modified water maze test and modified Garcia neurologic score system. Thus, we confirmed that BCA markedly decreased the activated level of TLRs/TIRAP/MyD88/NF-κB pathway and the production of cytokines. BCA also significantly ameliorated neuronal apoptosis which correlated with the improvement of neurobehavioral dysfunction post SAH. These results indicated that BCA may provide neuroprotection against EBI through the inhibition of inflammatory injury and neuronal apoptosis partially via the TLRs/TIRAP/MyD88/NF-κB signal pathway.

[Diagnosis and treatment of aneurysm in the common trunk of malformed superior mesenteric artery and celiac trunk].

OBJECTIVE: To explore the diagnosis and treatment of the aneurysm in the common trunk of malformed superior mesenteric artery and celiac trunk, especially the approach how to expose and excise such aneurysm. METHODS: The clinical data of 6 patients with aneurysm in the common trunk of malformed superior mesenteric artery and celiac trunk, who were operated on under general anesthesia from 1998 to 2006, were analyzed. At first, the body of pancreas was isolated and retracted, the malformed celiac trunk and its ramification were blocked and ablated, the initial part of the celiac trunk and the distant end of left gastric artery were ligated, and then by-pass operation was operated from infra-renal aorta to the visceral arteries (hepatic, splenic, and superior mesenteric arteries) with artificial blood vessels. Follow-up was conducted for 1 - 8 years. RESULTS: Five cases underwent aneurysm ablation and by-pass from aorta to hepatic, splenic, and superior mesenteric arteries; while 1 case underwent aneurysm ablation and spleen ablation, superior mesenteric artery reconstruction, and by-pass from aorta to hepatic artery simultaneously. All patients were cured without complication and recurrence. No arterial anastomosis stricture or stenosis was found in the 5 patients who received by-pass from aorta to hepatic, splenic, or superior mesenteric artery; however, slight stricture was found at the repaired portion of superior mesenteric artery in another one patient, but without any arterial anastomosis stricture in aorta or hepatic artery. CONCLUSION: It is an effective and safe method to treat the aneurysm common trunk of malformed superior mesenteric artery and celiac trunk by using the artificial blood vessel by-pass from aorta to visceral arteries (hepatic, splenic, and superior mesenteric arteries) after controlling the initial part of common trunk and cutting off the aneurysm there.

Successful treatment of accessory breast cancer with endocrine therapy.

Accessory breast cancers in males are extremely rare, and only a few cases have been reported in the literature. In this paper, an 87-year-old male patient was diagnosed with an accessory breast cancer by means of computed tomography (CT), magnetic resonance imaging (MRI), positron emission tomography-computed tomography (PET-CT), and immunohistochemistry based on needle biopsy, and has undergone successful resection and postoperative adjuvant endocrine therapy. He was the oldest male patient with an accessory breast cancer reported in the Chinese Hospital Knowledge Database and PubMed literature from 1975 to 2015.

Roles of Pannexin-1 Channels in Inflammatory Response through the TLRs/NF-Kappa B Signaling Pathway Following Experimental Subarachnoid Hemorrhage in Rats.

Background: Accumulating evidence suggests that neuroinflammation plays a critical role in early brain injury after subarachnoid hemorrhage (SAH). Pannexin-1 channels, as a member of gap junction proteins located on the plasma membrane, releases ATP, ions, second messengers, neurotransmitters, and molecules up to 1 kD into the extracellular space, when activated. Previous studies identified that the opening of Pannexin-1 channels is essential for cellular migration, apoptosis and especially inflammation, but its effects on inflammatory response in SAH model have not been explored yet. Methods: Adult male Sprague-Dawley rats were divided into six groups: sham group (n = 20), SAH group (n = 20), SAH + LV-Scramble-ShRNA group (n = 20), SAH + LV-ShRNA-Panx1 group (n = 20), SAH + LV-NC group (n = 20), and SAH + LV-Panx1-EGFP group (n = 20). The rat SAH model was induced by injection of 0.3 ml fresh arterial, non-heparinized blood into the prechiasmatic cistern in 20 s. In SAH + LV-ShRNA-Panx1 group and SAH + LV-Panx1-EGFP group, lentivirus was administered via intracerebroventricular injection (i.c.v.) at 72 h before the induction of SAH. The Quantitative real-time polymerase chain reaction, electrophoretic mobility shift assay, enzyme-linked immunosorbent assay, immunofluorescence staining, and western blotting were performed to explore the potential interactive mechanism between Pannexin-1 channels and TLR2/TLR4/NF-κB-mediated signaling pathway. Cognitive and memory changes were investigated by the Morris water maze test. Results: Administration with LV-ShRNA-Panx1 markedly decreased the expression levels of TLR2/4/NF-κB pathway-related agents in the brain cortex and significantly ameliorated neurological cognitive and memory deficits in this SAH model. On the contrary, administration of LV-Panx1-EGFP elevated the expressions of TLR2/4/NF-κB pathway-related agents, which correlated with augmented neuronal apoptosis. Conclusion: Pannexin-1 channels may contribute to inflammatory response and neurobehavioral dysfunction through the TLR2/TLR4/NF-κB-mediated pathway signaling after SAH, suggesting a potential role of Pannexin-1 channels could be a potential therapeutic target for the treatment of SAH.