ACSL4 exacerbates ischemic stroke by promoting ferroptosis-induced brain injury and neuroinflammation.

Acyl-CoA synthetase long-chain family member 4 (ACSL4) is an important isozyme for polyunsaturated fatty acids (PUFAs) metabolism that dictates ferroptosis sensitivity. The role of ACSL4 in the progression of ischemic stroke is unclear. Here, we found that ACSL4 expression was suppressed in the early phase of ischemic stroke and this suppression was induced by HIF-1α. Knockdown of ACSL4 protected mice against brain ischemia, whereas, forced overexpression of ACSL4 exacerbated ischemic brain injury. ACSL4 promoted neuronal death via enhancing lipid peroxidation, a marker of ferroptosis. Moreover, knockdown of ACSL4 inhibited proinflammatory cytokine production in microglia. These data identify ACSL4 as a novel regulator of neuronal death and neuroinflammation, and interventions of ACSL4 expression may provide a potential therapeutic target in ischemic stroke.

[Efficacy of splenic artery trunk embolization with detachable balloon for portal hypertension and hypersplenism].

OBJECTIVE: To investigate the efficacy of detachable balloon for splenic artery trunk embolization in patients with cirrhotic portal hypertension and hypersplenism. METHODS: Eight patients with cirrhotic portal hypertension received splenic artery trunk disconnection using detachable balloons under the guidance of digital subtraction angiography. The diameter and blood flow of the portal vein, the superior mesenteric vein, the splenic vein and the hepatic artery were measured by color Doppler ultrasound. Markers of liver function and blood coagulation, and routine blood parameters were assessed. Gastroscopy was used to evaluate to the degree of gastroesophageal varices. All complications experienced during the perioperative period were recorded. RESULTS: The portal vein diameter decreased from 1.55±0.38 cm to 1.55±0.38 cm, and the splenic artery diameter decreased from 1.45±0.10 cm to 1.41±0.09 cm (P < 0.05). The portal vein blood flow was reduced from 971.52±174.77 ml/min to 785.86±100.17 ml/min, and the splenic vein blood flow decreased from 938.01±208.86 ml/min to 644.02±188.15 ml/min, while the hepatic artery blood flow increased from 261.25±65.47 ml/min to 449.32±84.05 ml/min (P < 0.05). The symptoms of splenism were improved effectively, with platelet counts rising from 37.75±10.61*109/L to 138.63±28.22*109/L after the procedure (P < 0.05). There were no episodes of severe complications or death in the perioperative period, and all patients showed remarkable improvement in markers of liver function and coagulation function, and improvement of esophagogastric varices. CONCLUSIONS: The interventional disconnection technique of the splenic artery trunk using detachable balloon for the treatment of portal hypertension and hypersplenism is safe and effective.

Primary balloon angioplasty for chronic occlusion of intracranial internal carotid artery: A case report.

Chronic occlusion of large intracranial arteries is the main cause of ischemic stroke in China. Patients with symptomatic intracranial artery occlusion and hemodynamic impairment are at high risk of recurrent stroke. Chronic occlusion of the intracranial segment of the internal carotid artery is a common type of intracranial artery occlusion. Medical management is regarded as the standard treatment for this disease. With the development of endovascular treatment, some patients with chronic cerebral artery occlusion have achieved satisfactory results with endovascular therapy. We reported a patient with symptomatic chronic occlusion of the ophthalmic segment of the internal carotid artery. Simple balloon angioplasty was performed, and the occluded ophthalmic segment of the internal carotid artery was successfully recanalized without perioperative complications. At 4 months follow-up, the internal carotid artery remained patent and perfusion of the right cerebral hemisphere improved dramatically. In addition, we briefly reviewed the relevant literature.

An efficient conservative treatment modality for cervical pregnancy: angiographic uterine artery embolization followed by immediate curettage.

OBJECTIVE: We sought to evaluate a conservative treatment modality, angiographic uterine artery embolization (UAE) followed by immediate curettage, in the treatment of cervical pregnancy. STUDY DESIGN: Sixteen patients with cervical pregnancy were first treated by UAE to control or prevent vaginal bleeding. Curettage of cervical canal was performed immediately after UAE to remove gestational tissue from the cervix. Clinical outcome assessments include vaginal bleeding, serum ß-human chorionic gonadotropin level, cervical mass, menstruation, fertility, and hospitalization time. RESULTS: Fifteen patients were successfully treated by UAE followed by immediate curettage. One patient at very early gestational age underwent UAE only. Quick regression of serum human chorionic gonadotropin level and cervical mass, fertility preservation, and a short hospital stay were observed. CONCLUSION: UAE followed by immediate curettage is an efficient conservative treatment for cervical pregnancy. This procedure may become a useful alternative to other conservative approaches.

Portal hypertension caused by pancreatic cancer: Multidetector computed tomography diagnosis and multivariate analysis of variceal hemorrhage.

CONTEXT: Pancreatic cancer portal hypertension (PCPH) is a rare cause of gastrointestinal bleeding. This study retrospectively assessed gastrointestinal bleeding risk factors in 57 PCPH patients diagnosed via multidetector computed tomography (MDCT). MATERIALS AND METHODS: The data of patients with pancreatic cancer from January 2008 to January 2018 at Qingdao Municipal Hospital were reviewed. PCPH patients were screened with MDCT and followed up. MDCT findings (e.g., the location of the venous obstruction, type of variceal veins pathway, and splenomegaly) were recorded. Variceal hemorrhage was recorded. The MDCT findings and clinical data of the PCPH patients were used in this analysis to explore the risk factors of variceal hemorrhage using binary logistic regression and multivariate logistic regression model. RESULTS: Fifty-seven of the 182 patients were diagnosed with PCPH. A total of 7 draining routes and 11 types of varices were found. Of these patients, eight experienced variceal hemorrhage. Univariate analysis showed that splenomegaly (odds ratio [OR] = 10.364, P = 0.003) was significantly associated with an increased risk of variceal hemorrhage. Multivariate analysis showed that splenomegaly (OR = 66.491, 95% confidence interval: 2.790-1584.643, P = 0.009) was an independent influencing factor for variceal hemorrhage in PCPH patients. CONCLUSIONS: Patients with pancreatic cancer have high morbidity of PCPH. The splenomegaly is more prone to hemorrhage. Splenomegaly was an independent risk factor of variceal hemorrhage. MDCT can provide insight into the stenosis and occlusion of the portal vein system and the drainage routes of variceal veins and is one of the best ways to diagnose PCPH.

YTHDC1 mitigates ischemic stroke by promoting Akt phosphorylation through destabilizing PTEN mRNA.

YTH Domain Containing 1 (YTHDC1) is one of the m6A readers that is essential for oocyte development and tumor progression. The role of YTHDC1 in neuronal survival and ischemic stroke is unknown. Here, we found that YTHDC1 was unregulated in the early phase of ischemic stroke. Knockdown of YTHDC1 exacerbated ischemic brain injury and overexpression of YTHDC1 protected rats against brain injury. Mechanistically, YTHDC1 promoted PTEN mRNA degradation to increase Akt phosphorylation, thus facilitating neuronal survival in particular after ischemia. These data identify YTHDC1 as a novel regulator of neuronal survival and modulating m6A reader YTHDC1 may provide a potential therapeutic target for ischemic stroke.

Acute liver failure and infarction complicating TIPS placement.

Here in we report a case of acute liver failure with hepatic infarction after transjugular intrahepatic portosystemic shunt (TIPS). An upper gastrointestinal hemorrhage patient with a medical history of alcoholic cirrhosis underwent a TIPS procedure. One day after TIPS, his alanine aminotransferase and aspartate aminotransferase levels increased to 1214 U/L and 1511 U/L, respectively. Two days after TIPS, they peaked at alanine aminotransferase 8389 U/L and aspartate aminotransferase >7500 U/L, respectively. An emergent stent occlusion was performed on the second day. Portography showed that there were no portal vein branches or parenchymal stains on the edge of the right liver lobe. A CT scan demonstrated diffuse hepatic parenchyma, homogeneous hypodense lesion, and bilateral pleural effusion. The patient died of liver failure and multiple organ dysfunction syndrome 6 hours after the stent occlusion.

FoxM1 promotes epithelial-mesenchymal transition of hepatocellular carcinoma by targeting Snai1.

Forkhead box protein M1 (FoxM1) is aberrantly expressed in several types of human malignancy, and serves an important role in tumor metastasis. Epithelial­mesenchymal transition (EMT) of cancer cells has been associated cancer metastasis; however, the implication of FoxM1 in EMT and its putative roles in the regulation of cancer metastasis remain to be elucidated. In the present study, the expression of FoxM1, Snai1 and E­cadherin in hepatocellular carcinoma (HCC) cell lines with various metastatic potentials, and in normal liver cells, was investigated using western blot analysis and reverse transcription­quantitative polymerase chain reaction. The effects of FoxM1 on the invasive and migratory capabilities of HCC cells were evaluated using wound healing and Transwell migration assays. The present results demonstrated that FoxM1 expression was significantly upregulated in HCC cells compared with in normal hepatocytes (P<0.05). In addition, FoxM1 expression was significantly increased in MHCC­LM3 cells, characterized by higher metastatic potential, compared with in SMMC­7721 cells, which have a lower metastatic potential. Furthermore, overexpression of FoxM1 was demonstrated to be negatively correlated with E­cadherin (P<0.05) and positively associated with Snai1 (P<0.05) expression. These observations suggested that FoxM1 may enhance the invasion and migration of cancer cells, and thus promotes their EMT, in a mechanism that may involve the regulation of Snai1. Therefore, it may be hypothesized that FoxM1 has potential as a novel diagnostic marker and therapeutic target for the treatment of patients with HCC.

Extensive calcifications in portal venous system in a patient with hepatocarcinoma.

Calcification of the portal venous system is a rare entity that can be incidentally discovered during computed tomography (CT). We describe a case of extensive calcifications in the portal venous system in a middle-aged male patient with hepatocellular carcinoma (HCC). This patient presented with epigastric pain that had no obvious origin prior to admission. Laboratory examinations were positive for hepatitis B surface antigen and α-fetoprotein, and severe esophageal and gastric varices were detected during gastroscopy. Abdominal X-ray plain film showed well-defined linear and track-like calcification, with irregular margins directed along the course of the portal venous system. CT revealed extensive calcifications along the course of the portal, splenic, superior mesenteric and gastroesophageal veins. He underwent splenectomy 22 years ago due to splenomegaly and partial hepatectomy seven months before because of HCC of low-grade differentiation, confirmed by pathology. Finally, the patient was diagnosed with postoperative recurrent HCC and extensive portal venous system calcification after selective hepatic angiography under digital subtraction angiography.