[Analysis of the necessity of anticoagulation therapy and influencing factors of stent occlusion after transjugular intrahepatic portosystemic shunt].

Objective: To explore the necessity of anticoagulation therapy and influencing factors of stent occlusion after transjugular intrahepatic portosystemic shunt. Methods: The basic information, laboratory test results, preoperative portal venous pressure, postoperative anticoagulation time, postoperative stent stenosis or occlusion, followed-up and other data of all patients who underwent TIPS surgery in Shandong Provincial Hospital from 2010 to 2019 were retrospectively analyzed. Data were analyzed using t-test, χ2 test, and multivariate analysis (logistic regression and Cox-regression-analysis). Results: A total of 280 cases were finally included in the study, of which 110 (39.3%) had stent stenosis or occlusion, and 170 (60.7%) had stent patency. New or worsening ascites were identified in 194 cases during the follow-up period, including 14 (31.1%) cases in the stent stenosis or occlusion group and 19 (12.8%) cases in the stent patency group. Univariate analysis showed that presence or absence of platelet (P=0.037) and total bilirubin (P=0.038) were correlated with stent stenosis or occlusion. Postoperative continuous anticoagulation was correlated with stent blockage (P=0.029) in patients with partial portal vein thrombosis. Postoperative continuous anticoagulation and stent occlusions were not significantly correlated in patients with preoperative portal cavernoma and preoperative portal vein patency (P=0.848; P=0.744). Multivariate analysis results showed that whether long-term anticoagulation (P=0.017), all-cause rebleeding (P<0.001), postoperative significant hepatic encephalopathy (P<0.012), and postoperative new or worsening ascites (P<0.001) was significantly associated with stent occlusion (P<0.05), while platelets (P=0.134), total bilirubin (P=0.229), international normalized ratio (P=0.436), and portal vein pressure (P=0.230) were not significantly associated with stent occlusion after surgery. Conclusion: In patients with partial portal vein thrombosis before surgery, continuous anticoagulation for 30 days post-TIPS therapy can effectively prevent stent stenosis or occlusion; while in patients with portal vein patency, portal cavernoma and complete portal vein blockage before surgery, postoperative anticoagulation has no significant effect on stent stenosis or occlusion.

Impact and clinical significance of Embosphere microsphere artery embolization therapy in serum VEGF expression level of women patients with uterine fibroids.

OBJECTIVE: We aimed to investigate the effect of Embosphere microsphere artery embolization on the serum level of vascular endothelial growth factor (VEGF) in patients with uterine fibroid. PATIENTS AND METHODS: From March 2014 to December 2015, 128 women in child-bearing age with uterine intramural fibroids were enrolled in the patient group. At the same time, 128 healthy cases in child-bearing age were randomly selected and enrolled in the control group. Enzyme-linked immunosorbent assay was used to measure the serum level of VEGF, and immunohistochemical staining method was used to study the expression of VEGF in the uterine fibroids. Embosphere microsphere artery embolization surgery was performed on cases in the patient group. RESULTS: The serum level of VEGF in the patient group was significantly higher than that of the control group. Immunohistochemical staining results showed that in the control group, VEGF expression level in uterine fibroid tissue was significantly higher. Compared with before the treatment, tumor diameter in the patient group reduced significantly 3 months after the treatment. Erythrocyte count, hemoglobin, and menstrual blood volume increased significantly 6 months after treatment. CONCLUSIONS: Serum VEGF level can be considered as a marker for uterine fibroid, and by using VEGF as a marker we can increase the probability of early diagnosis. We showed that, compared with hysterectomy, Embosphere microsphere embolization had an evident advantage and might be an excellent candidate to replace hysterectomy.

Predictors of acid suppression success in patients with chronic laryngitis.

BACKGROUND: Up to 50% of the patients suspected of reflux laryngitis syndrome failed to respond to acid suppression therapy. However, predictors of acid suppression success have not been determined. METHODS: Consecutive patients with chronic laryngitis were enrolled prospectively. All the patients underwent laryngoscopy, esophagogastroduodenoscopy and 24-h multichannel intraluminal impedance and pH (MII-pH) monitoring before receiving rabeprazole 10 mg b.i.d. for 3 months. Patient was considered as a responder to acid suppression if the chief laryngeal complaint score during the last week since last interview had decreased by at least 50% after the start of therapy compared with baseline. Cox regression analysis was used to determine the independent predictors of acid suppression success. KEY RESULTS: Of 92 patients (age 42.4 ± 14.3 years, 50 women), 42 (45.7%) responded to acid suppression after 3 months. Gastroesophageal reflux disease was defined in 22 patients, of whom 19 patients had pathological distal esophageal acid exposure and 5 were defined as erosive esophagitis. The time to response showed a significant hazard ratio for patients with increased distal esophageal acid exposure time (ß: 0.93; HR: 2.55; 95% CI: 1.24-5.24; P = 0.011) and increased laryngopharyngeal bolus exposure time (BET; ß: 0.96; HR: 2.61; 95% CI: 1.36-5.00; P = 0.004). The latter had the best Youden Index (0.34) and accuracy (68.5%). CONCLUSIONS & INFERENCES: The success of acid suppression on chronic laryngitis could be predicted using reflux parameters detected by MII-pH, among which increased laryngopharyngeal BET is the best.

Combined transplantation of neural stem cells and olfactory ensheathing cells for the repair of spinal cord injuries.

Spinal cord repair is a problem that has long puzzled neuroscientists. The failure of the spinal cord to regenerate and undergo reconstruction after spinal cord injury (SCI) can be attributed to secondary axonal demyelination and neuronal death followed by cyst formation and infarction as well as to the nature of the injury environment, which promotes glial scar formation. Cellular replacement and axon guidance are both necessary for SCI repair. Multipotent neural stem cells (NSCs) have the potential to differentiate into both neuronal and glial cells and are, therefore, likely candidates for cell replacement therapy following SCI. However, NSC transplantation alone is not sufficient for spinal cord repair because the majority of the NSCs engrafted into the spinal cord have been shown to differentiate with a phenotype which is restricted to glial lineages, further promoting glial scaring. Olfactory ensheathing cells (OECs) are a unique type of glial cell that occur both peripherally and centrally along the olfactory nerve. The ability of olfactory neurons to grow axons in the mature central nervous system (CNS) milieu has been attributed to the presence of OECs. It has been shown that transplanted OECs are capable of migrating into and through astrocytic scars and thereby facilitating axonal regrowth through an injury barrier. Given the complementary properties of NSCs and OECs, we predict that the co-transplantation of NSCs and OECs into an injured spinal cord would have a synergistic effect, promoting neural regeneration and functional reconstruction. The lost neurocytes would be replaced by NSCs, while the OECs would build "bridges" crossing the glial scaring that conduct axon elongation and promote myelinization simultaneously. Furthermore, the two types of cells could first be seeded into a bioactive scaffold and then the cell seeded construct could be implanted into the defect site. We believe that this type of treatment would lead to improved neural regeneration and functional reconstruction after SCI.

Selective induction of necrotic cell death in cancer cells by beta-lapachone through activation of DNA damage response pathway.

Most efforts thus far have been devoted to develop apoptosis inducers for cancer treatment. However, apoptotic pathway deficiencies are a hallmark of cancer cells. We propose that one way to bypass defective apoptotic pathways in cancer cells is to induce necrotic cell death. Here we show that selective induction of necrotic cell death can be achieved by activation of the DNA damage response pathways. While beta-lapachone induces apoptosis through E2F1 checkpoint pathways, necrotic cell death can be selectively induced by beta-lapachone in a variety of cancer cells. We found that beta-lapachone, unlike DNA damaging chemotherapeutic agents, transiently activates PARP1, a main regulator of the DNA damage response pathway, both in vitro and in vivo. This occurs within minutes of exposure to beta-lapachone, resulting in selective necrotic cell death. Inhibition of PAR blocked beta-lapachone-induced necrosis. Furthermore, necrotic cell death induced by beta-lapachone was significantly reduced in PARP1 knockout cell lines. Our data suggest that selective necrotic cell death can be induced through activation of DNA damage response pathways, supporting the idea of selective necrotic cell death as a therapeutic strategy to eliminate cancer cells.

Protective effects of extract of Ginkgo biloba (EGb 761) on nerve cells after spinal cord injury in rats.

STUDY DESIGN: An experimental animal model was used to assess spinal cord injury following lateral hemitransection at thoracic spinal cord level. OBJECTIVE: To determine whether extract of Ginkgo biloba (EGb) could have a neuroprotective effect in spinal cord injury (SCI) in rats. SETTING: Department of Biological Sciences and Biotechnology, Tsinghua University, China. METHODS: A total of 72 adult rats were divided randomly into three groups: the EGb group, normal saline (NS) group, and sham operation group (sham group). After thoracic spinal cord hemitransection was performed at the level of the 9th thoracic vertebra (T9), rats in the EGb group were given 100 mg/kg EGb 761 daily, while rats in the NS group received NS. The rats in the sham group only underwent laminectomy without spinal cord hemitransection. At various time points after surgery, thoracic spinal cords were sampled and sliced for histochemistry, immunohistochemistry of inducible nitric oxide synthase (iNOS), and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) of apoptotic cells. RESULTS: Myelin staining showed that the area of cavities was small and the demyelinated zones were limited at and around the injury site of the spinal cord in the EGb group, while the area of cavities was large and the demyelinated zones were serious in the NS group. Nissl staining showed that the ratio of bilateral ventral horn neurons (transection side/uninjured side) in the EGb group was higher than that in the NS group (P<0.05). The apoptotic index and the percentage of iNOS-positive cells were lower in the EGb group than in the NS group. Furthermore, the percentage of iNOS-positive cells positively correlated with the apoptotic index (r( 2)=0.729, P<0.01) after SCI. CONCLUSION: This study demonstrated that EGb 761 could inhibit iNOS expression and have neuroprotective effect by preventing nerve cells from apoptosis after SCI in rats.

[Effect of LH-FSH releasing hormone on the sensitivity of cholinergic and adrenergic receptors in toad spinal ganglion neurons].

Intracellular recordings were performed on 81 neurons from 53 isolated toad spinal ganglia (SG). The effects of LH-FSH releasing hormone on the sensitivities of muscarinic receptors and alpha-adrenoceptors located on the soma of SG neurons were observed. Perfusing SG with atropine 10 mumol.L-1 in Ringer's solution depressed the amplitude of depolarization response induced by acetylcholine (ACh, 10-100 mumol.L-1). The depolarization and hyperpolarization induced by norepinephrine (NE, 10-100 mumol.L-1) were blocked by alpha 1-adrenoceptor antagonist prazosin and alpha 2-adrenoceptor antagonist yohimbine respectively. These results indicated that ACh-induced depolarization was mediated by muscarinic receptors while NE-induced depolarization and hyperpolarization were mediated by alpha 1- and alpha 2-adrenoceptors respectively. On the other hand, perfusing SG with LH-FSH releasing hormone 10 mumol.L-1 in Ringer's solution increased the depolarization response caused by ACh or NE, but attenuated NE-caused hyperpolarization response. The above results suggest that LH-FSH releasing hormone may modulate the sensitivities of muscarinic receptors and alpha-adrenoceptors on the soma membrane of toad SG neurons.