Differentiating between Lymphoma and Metastasis Presenting as Solid Cerebellar Mass Lacking Necrosis.

Objectives: This study aimed to identify radiologic features that differentiate lymphoma from metastasis manifesting as a solid enhancing mass lacking necrosis in the cerebellum. Methods: Pathologically confirmed 24 primary central nervous system lymphoma (PCNSL) and 32 metastasis patients with solid enhancing cerebellar masses without necrotic or hemorrhagic components were retrospectively analyzed. We evaluated the imaging characteristics using contrast-enhanced magnetic resonance imaging (MRI). The serrate sign was defined as a tumor spreading along white matter with branch-like enhancement or outward spikes. Results: The serrate sign was exclusively identified in the PCNSL group, showing a significant difference compared to the metastasis group (75.0% vs. 0%, p < 0.001). Homogeneous enhancement occurred more frequently in PCNSL than in metastasis (91.7% vs. 21.9%, p < 0.001). Conversely, bulging contour (62.5% vs. 4.2%, p < 0.001) and surface involvement (71.9% vs. 29.2%, p = 0.003) were more prevalent in metastasis than PCNSL. For predicting PCNSL, the serrate sign demonstrated 75.0% sensitivity, 100% specificity, 100% positive predictive value, 84.2% negative predictive value, and 89.3% accuracy. Conclusions: This study found that the serrate sign and homogeneous enhancement are reliable MRI features for differentiating cerebellar PCNSL from metastasis, whereas a bulging contour and surface involvement suggest metastasis. The serrate sign demonstrated diagnostic significance in differentiating PCNSL from metastasis.

Neutrophil extracellular traps promote ΔNp63+ basal cell hyperplasia in chronic rhinosinusitis.

BACKGROUND: Neutrophil extracellular traps (NETs) are observed in chronic rhinosinusitis (CRS), although their role remains unclear. OBJECTIVES: This study aimed to investigate the influence of NETs on the CRS epithelium. METHODS: Forty-five sinonasal biopsy specimens were immunofluorescence-stained to identify NETs and p63+ basal stem cells. Investigators treated human nasal epithelial cells with NETs and studied them with immunofluorescence staining, Western blotting, and quantitative real-time PCR. NET inhibitors were administered to a murine neutrophilic nasal polyp model. RESULTS: NETs existed in tissues in patients with CRS with nasal polyps, especially in noneosinophilic nasal polyp tissues. p63+ basal cell expression had a positive correlation with the release of NETs. NETs induced the expansion of Ki-67+p63+ cells. We found that ΔNp63, an isoform of p63, was mainly expressed in the nasal epithelium and controlled by NETs. Treatment with deoxyribonuclease (DNase) I or Sivelestat (NET inhibitors) prevented the overexpression of ΔNp63+ epithelial stem cells and reduced polyp formation. CONCLUSIONS: These results reveal that NETs are implicated in CRS pathogenesis via basal cell hyperplasia. This study suggests a novel possibility of treating CRS by targeting NETs.

Superior cerebellar artery occlusion remaining after thrombectomy for acute basilar artery occlusion.

To investigate the incidence and impact of superior cerebellar artery (SCA) occlusion remaining after thrombectomy for acute basilar artery occlusion (BAO). We retrospectively analyzed data from 116 patients who underwent thrombectomy for BAO. The patency of SCA was assessed on final angiograms. Clinical and radiologic data of the patients were retrieved from a prospectively collected database and analyzed. All patients underwent pretreatment and follow-up DWI to detect new infarctions in SCA territory. Ten patients (8.6%) had SCA occlusions on final angiograms. Of these, two patients had bilateral occlusions. A new infarction with a diameter ranged from 4 to 11 mm in corresponding SCA territory occurred in 5 of 10 patients. No patients with SCA occlusions experienced symptomatic cerebellar hemorrhage or malignant cerebellar infarction. Nine of 12 SCA occlusions showed spontaneous recanalization on follow-up CT angiography. Four of 10 patients showed 90-day favorable outcome (mRS 0-3) and 90-day mortality occurred in one patient. SCA occlusions remaining after thrombectomy for acute BAO had a benign clinical course. Most of these lesions recanalized spontaneously. Our study suggests that attempts to recanalize remnant SCA occlusion may be unnecessary after basilar artery thrombectomy.

Four-dimensional flow MR imaging for evaluating treatment response after transcatheter arterial chemoembolization in cirrhotic patients with hepatocellular carcinoma.

PURPOSE: To prospectively evaluate the potential of four-dimensional (4D) flow magnetic resonance imaging (MRI) in predicting treatment responses after transcatheter arterial chemoembolization (TACE) in cirrhotic patients with hepatocellular carcinoma (HCC). METHODS: A total of 195 patients were classified into four groups (A-D): A, cirrhotic patients without HCC (n = 30); B, cirrhotic patients with HCC before TACE (n = 75); C, cirrhotic patients with HCC showing an incomplete response following TACE (n = 56); and D, cirrhotic patients with HCC achieving a complete response (CR) following TACE (n = 34). The patients were subjected to routine laboratory tests and 4D flow MRI using a 3-T MRI system to measure the quantitative parameters of blood flow in the portal vein (PV), splenic vein (SV), and superior mesenteric vein. The data collected by 4D flow MRI were compared among the groups using one-way analysis of variance. A multivariate analysis was performed to verify the association of clinical characteristics and 4D flow parameters with CR after TACE treatment. RESULTS: The average through-plane velocity, peak velocity magnitude, average net flow, peak flow, and net forward volume in the PV and SV were significantly lower in groups B and C (P < 0.05) compared to those in group A. Moreover, average through-plane velocity and peak velocity magnitude in the PV in groups B and C were significantly lower than those in group D (P < 0.05). The multivariate analysis demonstrated that the average through-plane velocity and peak velocity magnitude in the PV were independently associated with CR in HCC patients after TACE (P < 0.05). CONCLUSION: The quantitative flow data obtained by 4D flow MRI may be useful for predicting CR after TACE in cirrhotic patients with HCC.

Preoperative prediction of Ki-67 and p53 status in meningioma using a multiparametric MRI-based clinical-radiomic model.

Purpose: To investigate the utility of preoperative multiparametric magnetic resonance imaging (mpMRI)-based clinical-radiomic analysis combined with machine learning (ML) algorithms in predicting the expression of the Ki-67 proliferative index and p53 tumor suppressor protein in patients with meningioma. Methods: This multicenter retrospective study included 483 and 93 patients from two centers. The Ki-67 index was classified into high (Ki-67≥5%) and low (Ki-67<5%)-expressed groups, and the p53 index was classified into positive (p53≥5%) and negative (p53<5%)-expressed groups. Clinical and radiological features were analyzed using univariate and multivariate statistical analyses. Six ML models were performed with different types of classifiers to predict Ki-67 and p53 status. Results: In the multivariate analysis, larger tumor volumes (p<0.001), irregular tumor margin (p<0.001), and unclear tumor-brain interface (p<0.001) were independently associated with a high Ki-67 status, whereas the presence of both necrosis (p=0.003) and the dural tail sign (p=0.026) were independently associated with a positive p53 status. A relatively better performance was yielded from the model constructed by combined clinical and radiological features. The area under the curve (AUC) and accuracy of high Ki-67 were 0.820 and 0.867 in the internal test, and 0.666 and 0.773 in the external test, respectively. Regarding p53 positivity, the AUC and accuracy were 0.858 and 0.857 in the internal test, and 0.684 and 0.718 in the external test. Conclusion: The present study developed clinical-radiomic ML models to non-invasively predict Ki-67 and p53 expression in meningioma using mpMRI features, and provides a novel non-invasive strategy for assessing cell proliferation.

Image-guided in situ cancer vaccination with combination of multi-functional nano-adjuvant and an irreversible electroporation technique.

Cancer immunotherapy is a next-generation treatment strategy; however, its side effects limit its clinical translation. Here, a novel combination of a multi-functional nano-adjuvant (M-NA) prepared with an iron oxide/gold core and a cationic polymer shell via multilayer synthesis with CpG oligodeoxynucleotide (CpG-ODN) electrostatically complexed on its surface, and irreversible electroporation (IRE) technique was developed for effective image-guided in situ cancer vaccination. The M-NA can be retained long-term in the dense tumoral extracellular matrix after intratumoral injection and internalized by antigen-presenting cells (APCs). The IRE can induce immunogenic cell death. Indeed, in a mouse tumor model, the M-NA showed longer tumor retention time than free CpG-ODN. Compared with other treatments, the combined treatment significantly inhibited tumor growth with 100% survival rate for ∼60 days. The therapy induced the activation of cytotoxic lymphocytes and the maturation of APCs in vivo. This treatment could be effective in image-guided local cancer immunotherapy.

House dust mite-induced Akt-ERK1/2-C/EBP beta pathway triggers CCL20-mediated inflammation and epithelial-mesenchymal transition for airway remodeling.

House dust mite (HDM) allergens cause inflammatory responses and chronic allergic diseases such as bronchial asthma and atopic dermatitis. Here, we investigate the mechanism by which HDM induces C-C chemokine ligand 20 (CCL20) expression to promote chronic inflammation and airway remodeling in an HDM-induced bronchial asthma mouse model. We showed that HDM increased CCL20 levels via the Akt-ERK1/2-C/EBPß pathway. To investigate the role of CCL20 in chronic airway inflammation and remodeling, we made a mouse model of CCL20-induced bronchial asthma. Treatment of anti-CCL20Ab in this mouse model showed the reduced airway hyper-responsiveness and inflammatory cell infiltration into peribronchial region by neutralizing CCL20. In addition, CCL20 induced the Nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation through NLRP3 deubiquitination and transcriptional upregulation in BEAS-2B cells. As expected, anti-CCL20Ab markedly suppressed NLRP3 activation induced by CCL20. Moreover, HDM-induced CCL20 leads to epithelial-mesenchymal transition in the lung epithelium which appears to be an important regulator of airway remodeling in allergic asthma. We also found that anti-CCL20Ab attenuates airway inflammation and remodeling in an HDM-induced mouse model of bronchial asthma. Taken together, our results suggest that HDM-induced CCL20 is required for chronic inflammation that contributes airway remodeling in a mouse model of asthma.

Successful Management of Massive Congenital Hepatic Hemangioma and Systemic Hypertension With Sirolimus.

Congenital hepatic hemangioma (CHH) is a common benign vascular tumor of the liver, seen in infancy. The clinical manifestations vary from incidental findings to life-threatening complications. The authors present here a case of an infant with massive CHH who developed systemic hypertension because of compression of the right renal artery by the CHH and did not respond to other lines of treatment. After sirolimus therapy, the CHH size decreased and antihypertensive drugs were no longer necessary. In a critical situation, if the embolization and/or steroids do not seem to control the situation, then adding sirolimus may be considered as secondary therapy with good additive effects.

Identification of potential metabolic biomarkers in predicting esophageal varices needing treatment in patients with liver cirrhosis.

The goal of this study was to determine the diagnostic performance of in vivo quantitative proton magnetic resonance spectroscopy (1H-MRS) to identify the presence of esophageal varices needing treatment (VNT), as well as investigate its correlation with clinical characteristics in patients with liver cirrhosis. Forty cirrhotic patients without VNT showing the negative red color sign, and 40 cirrhotic patients with VNT showing positive red color sign underwent laboratory tests, esophago-gastro-duodenoscopy, and 1H-MRS with single-voxel localization in the cirrhotic liver parenchyma. The levels of lactate + triglyceride (TG) and choline in cirrhotic patients with VNT were significantly higher than those in cirrhotic patients without VNT. In multivariate analysis, spleen diameter, platelet count, and platelet count/spleen diameter ratio, as well as lactate + TG, and choline were associated with the presence of VNT. Moreover, lactate + TG and choline levels were positively correlated with spleen diameter and negatively correlated with platelet count in the combined group of cirrhotic patients with and without VNT. Our study demonstrated that higher hepatic lactate + TG and choline levels in cirrhotic patients in conjunction with longer spleen diameter, lower platelet counts, and lower ratios of platelet count to spleen diameter were associated with the presence of esophageal VNT and the risk of developing variceal bleeding. Therefore, in vivo 1H-MRS might be an effective tool for diagnosing and predicting esophageal VNT in patients with liver cirrhosis.

T-Cell-Derived Nanovesicles for Cancer Immunotherapy.

Although T-cell therapy is a remarkable breakthrough in cancer immunotherapy, the therapeutic efficacy is limited for solid tumors. A major cause of the low efficacy is T-cell exhaustion by immunosuppressive mechanisms of solid tumors, which are mainly mediated by programmed death-ligand 1 (PD-L1) and transforming growth factor-beta (TGF-ß). Herein, T-cell-derived nanovesicles (TCNVs) produced by the serial extrusion of cytotoxic T cells through membranes with micro-/nanosized pores that inhibit T-cell exhaustion and exhibit antitumoral activity maintained in the immunosuppressive tumor microenvironment (TME) are presented. TCNVs, which have programmed cell death protein 1 and TGF-ß receptor on their surface, block PD-L1 on cancer cells and scavenge TGF-ß in the immunosuppressive TME, thereby preventing cytotoxic-T-cell exhaustion. In addition, TCNVs directly kill cancer cells via granzyme B delivery. TCNVs successfully suppress tumor growth in syngeneic-solid-tumor-bearing mice. Taken together, TCNV offers an effective cancer immunotherapy strategy to overcome the tumor's immunosuppressive mechanisms.

Association of pretreatment pontine infarction with extremely poor outcome after endovascular thrombectomy in acute basilar artery occlusion.

BACKGROUND: The association between pretreatment brain stem infarction and thrombectomy outcomes remains to be elucidated in patients with acute basilar artery occlusion (BAO). We aimed to assess the association between pretreatment pontine infarction and extremely poor outcome in patients who underwent endovascular thrombectomy due to acute BAO. METHODS: We retrospectively reviewed data from a stroke database to identify patients with acute BAO who underwent thrombectomy between January 2011 and August 2019. Patient characteristics, pretreatment diffusion-weighted imaging (DWI) data, and outcomes were evaluated. The largest infarct core was expressed as the percentage of infarct core area in each brain stem region on the DWI slice displaying the largest lesion. Extremely poor outcome was defined as a 90-day modified Rankin Scale score of 5 or 6. RESULTS: A total of 113 patients were included, 37 of whom had extremely poor outcome. Among the 15 patients with extensive pontine infarction (largest pontine infarct core of ≥70%), 93.3% had extremely poor outcome. Multivariate logistic regression analysis revealed that the following variables were independent predictors of extremely poor outcome: extensive pontine infarction (adjusted OR 22.494; 95% CI 2.335 to 216.689; p=0.007), posterior circulation ASPECTS on DWI (adjusted OR per 1-point decrease 1.744; 95% CI 1.197 to 2.541; p=0.004), age (adjusted OR per 1-year increase 1.067; 95% CI 1.009 to 1.128; p=0.023), and baseline NIHSS (adjusted OR per 1-point increase 1.105; 95% CI 1.004 to 1.216; p=0.040). CONCLUSION: Our results showed that a large pontine infarct core of ≥70% on pretreatment DWI was strongly associated with extremely poor outcome among patients treated with endovascular thrombectomy for acute BAO.

Nitration of protein phosphatase 2A increases via Epac1/PLCε/CaMKII/HDAC5/iNOS cascade in human endometrial stromal cell decidualization.

Decidualization of the endometrial stroma is an essential differentiation process for embryo implantation and maintenance of pregnancy. We previously reported that protein phosphatase 2A (PP2A) acts as a key mediator during cAMP-induced decidualization of human endometrial stromal cells (hESCs). However, the mechanism underlying its activation has remained obscure in hESCs. In the present study, we aimed to reveal the mechanism that induces the nitration of PP2A catalytic subunit (PP2Ac) during cAMP-induced decidualization of hESCs. First, cAMP-induced PP2Ac nitration was significantly repressed using L-NAME, an inhibitor of nitric oxide synthase (NOS). Among several NOS isoforms, only inducible NOS (iNOS) was highly expressed in hESCs, indicating that iNOS directly induces the nitration of PP2Ac. Second, cAMP-induced iNOS expression and PP2Ac nitration were decreased by treatment with TSA, an inhibitor of histone deacetylase 5 (HDAC5). cAMP-induced phosphorylation of CaMKII and HDAC5 was suppressed by treatment with U73122 (an inhibitor of phospholipase C) or transfection of PLCε siRNA. Finally, small G protein Rap1 and its guanine nucleotide exchange factor Epac1 were found to be involved in cAMP-induced PP2A activation. Taken together, our results suggest that PP2Ac nitration during cAMP-induced decidualization of hESCs is induced through the Epac1-Rap1-PLCε-CaMKII-HDAC5-iNOS signaling pathway.

Incidentally detected sellar spine in a patient with Cushing's syndrome: a case report.

Sellar spine, a bony spur extending anteriorly from the dorsum sellae, is a very rare anatomical variant. Several hypotheses regarding its etiology have been proposed, including the strongly supported theory of a cephalic ossified notochordal remnant. Sellar spine is usually detected incidentally in patients who have no definite symptoms, but several cases have reportedly accompanied endocrinopathies such as precocious puberty, hypopituitarism, or galactorrhea/oligomenorrhea. However, no published reports have described sellar spine in a patient with Cushing's syndrome. We herein report a case of sellar spine detected during the evaluation of Cushing's disease in a 29-year-old woman who underwent inferior petrosal sinus sampling, computed tomography, magnetic resonance imaging, and exploratory surgery. There was no evidence of a pituitary microadenoma, but a sellar spine was present in the operative field. Thus, the sellar spine might have caused Cushing's syndrome in this case, although the exact mechanism is unknown.

Bcl-2 Overexpression Induces Neurite Outgrowth via the Bmp4/Tbx3/NeuroD1 Cascade in H19-7 Cells.

Bcl-2 is overexpressed in the nervous system during neural development and plays an important role in modulating cell survival. In addition to its anti-apoptotic function, it has been suggested previously that Bcl-2 might act as a mediator of neuronal differentiation. However, the mechanism by which Bcl-2 might influence neurogenesis is not sufficiently understood. In this study, we aimed to determine the non-apoptotic functions of Bcl-2 during neuronal differentiation. First, we used microarrays to analyze the whole-genome expression patterns of rat neural stem cells overexpressing Bcl-2 and found that Bcl-2 overexpression induced the expression of various neurogenic genes. Moreover, Bcl-2 overexpression increased the neurite length as well as expression of Bmp4, Tbx3, and proneural basic helix-loop-helix genes, such as NeuroD1, NeuroD2, and Mash1, in H19-7 rat hippocampal precursor cells. To determine the hierarchy of these molecules, we selectively depleted Bmp4, Tbx3, and NeuroD1 in Bcl-2-overexpressing cells. Bmp4 depletion suppressed the upregulation of Tbx3 and NeuroD1 as well as neurite outgrowth, which was induced by Bcl-2 overexpression. Although Tbx3 knockdown repressed Bcl-2-mediated neurite elaboration and downregulated NeuroD1 expression, it did not affect Bcl-2-induced Bmp4 expression. While the depletion of NeuroD1 had no effect on the expression of Bcl-2, Bmp4, or Tbx3, Bcl-2-mediated neurite outgrowth was suppressed. Taken together, these results demonstrate that Bcl-2 regulates neurite outgrowth through the Bmp4/Tbx3/NeuroD1 cascade in H19-7 cells, indicating that Bcl-2 may have a direct role in neuronal development in addition to its well-known anti-apoptotic function in response to environmental insults.

Predictors and impact of hemorrhagic transformations after endovascular thrombectomy in patients with acute large vessel occlusions.

BACKGROUND: Predictors and impact of hemorrhagic transformation (HT) after thrombectomy remain to be elucidated. OBJECTIVE: To investigate the independent predictors and impact of each hemorrhagic infarction (HI) and parenchymal hematoma (PH) after thrombectomy in patients with acute stroke due to intracranial large vessel occlusion (LVO). MATERIALS AND METHODS: We retrospectively reviewed data from 400 patients with acute LVO who underwent thrombectomy. Logistic regression analyses were performed to determine independent predictors of HI and PH on post-treatment CT scans. Associations between HT and poor outcome (modified Rankin Scalescore ≥3) at 90 days were analyzed. RESULTS: HT was observed in 98 patients (62 HIs (15.5%) and 36 PHs (9%)). Independent predictors of HI were male sex, atrial fibrillation, and time from symptom onset to groin puncture. Hyperlipidemia (OR=0.221, 95% CI 0.064 to 0.767, P=0.017) and successful reperfusion (OR=0.246, 95% CI 0.093 to 0.651, P=0.005) were independently associated with a lower chance of PH, while hypertension (OR=2.260, 95% CI 1.014 to 5.035, P=0.046) and longer procedure duration (OR=1.046, 95% CI 1.016 to 1.077, P=0.003) were independently associated with a higher chance of PH. Only PH (OR=10.154, 95% CI 3.260 to 31.632, P<0.001) was an independent predictor of poor outcome. CONCLUSIONS: PH is independently associated with poor outcome, whereas HI does not predict outcome after thrombectomy in patients with acute LVO. Our findings suggest that rapid and successful reperfusion is essential to prevent PH in patients undergoing thrombectomy for acute LVO. In addition, our study suggests that hyperlipidemia is associated with a lower risk of PH in such patients.

CCAAT/enhancer-binding protein beta (C/EBPß) is an important mediator of 1,25 dihydroxyvitamin D3 (1,25D3)-induced receptor activator of nuclear factor kappa-B ligand (RANKL) expression in osteoblasts.

Receptor activator of nuclear factor kappa B ligand (RANKL) expression in osteoblasts is regulated by 1,25-dihydroxyvitamin D3 (1,25D3). CCAAT/enhancer-binding protein beta (C/EBPß) has been proposed to function as a transcription factor and upregulate RANKL expression, but it is still uncertain how C/EBPß is involved in 1,25D3-induced RANKL expression of osteoblasts. 1,25D3 stimulation increased the expression of RANKL and C/EPBß genes in osteoblasts and enhanced phosphorylation and stability of these proteins. Moreover, induction of RANKL expression by 1,25D3 in osteoblasts was downregulated upon knockdown of C/EBPß. In contrast, C/EBPß overexpression directly upregulated RANKL promoter activity and exhibited a synergistic effect on 1,25D3-induced RANKL expression. In particular, 1,25D3 treatment of osteoblasts increased C/EBPß protein binding to the RANKL promoter. In conclusion, C/EBPß is required for induction of RANKL by 1,25D3. [BMB Reports 2019; 52(6): 391-396].

Inflammatory mediator expression within retrieved clots in acute ischemic stroke.

Objective: In this study we investigate the association between the expression of inflammatory mediators measured in clots retrieved by mechanical thrombectomy, stroke etiology, and the susceptibility vessel sign (SVS) on gradient-echo (GRE) MR imaging in acute ischemic stroke patients. Methods: We performed molecular analysis of intracranial clots retrieved by mechanical thrombectomy from 82 patients with acute stroke. Seventy-two of these patients underwent GRE imaging before endovascular therapy. We measured the relative expression of inflammatory mediators by performing the quantitative real-time polymerase chain reaction on the retrieved clots and assessed associations between the expression of inflammatory mediators and stroke subtypes as well as with GRE SVS. Results: Classifications of stroke etiology for the cohort were as follows: cardioembolism (51, 62.2%), large artery atherosclerosis (9, 11%), and undetermined etiology (22, 26.8%). Clots associated with large artery atherosclerosis showed significantly higher interleukin (IL)-1ß expression than clots from both cardioembolism and undetermined etiology (P = 0.008). A positive SVS was identified in 48 of 72 patients (66.7%) who had GRE imaging. IL-1ß, tumor necrosis factor-α, and matrix metalloproteinase-9 expressions were significantly higher in clots with a negative SVS than in those with a positive SVS (P = 0.010, 0.049, and 0.004, respectively). Interpretation: Expression of inflammatory mediators in intracranial clots differs significantly based on stroke etiology or presence or the absence of SVS on GRE imaging. This study suggests that molecular analysis of inflammatory mediators in retrieved clots is a promising tool for determining stroke mechanism in acute ischemic stroke patients.

Phosphatidic acid induces decidualization by stimulating Akt-PP2A binding in human endometrial stromal cells.

Decidualization of human endometrial stromal cells (hESCs) is crucial for successful uterine implantation and maintaining pregnancy. We previously reported that phospholipase D1 (PLD1) is required for cAMP-induced decidualization of hESCs. However, the mechanism by which phosphatidic acid (PA), the product of PLD1 action, might regulate decidualization is not known. We confirmed that PA induced decidualization of hESCs by observing morphological changes and measuring increased levels of decidualization markers such as IGFBP1 and prolactin transcripts (P < 0.05). Treatment with PA reduced phosphorylation of Akt and consequently that of FoxO1, which led to the increased IGFBP1 and prolactin mRNA levels (P < 0.05). Conversely, PLD1 knockdown rescued Akt phosphorylation. Binding of PP2A and Akt increased in response to cAMP or PA, suggesting that their binding is directly responsible for the inactivation of Akt during decidualization. Consistent with this observation, treatment with okadaic acid, a PP2A inhibitor, also inhibited cAMP-induced decidualization by blocking Akt dephosphorylation.

A case of cecal volvulus presenting with chronic constipation in lissencephaly.

Cecal volvulus is uncommon in pediatric patients and there are few reports of cecal volvulus with cerebral palsy. Here, we report the case of a 19-year-old male patient who presented with abdominal distension, a history of cerebral palsy, refractory epilepsy due to lissencephaly, and chronic constipation. An abdominal x-ray and computed tomography without contrast enhancement showed fixed dilated bowel intensity in the right lower abdomen. Despite decompression with gastric and rectal tube insertion, symptoms did not improve. The patient underwent an exploratory laparotomy that revealed cecal volvulus. Cecal volvulus usually occurs following intestinal malrotation or previous surgery. In this patient, however, intestinal distension accompanying mental disability and chronic constipation resulted in the development of cecal volvulus. We suggest that cecal and proximal large bowel volvulus should be considered in patients presenting with progressive abdominal distension combined with a history of neuro-developmental delay and constipation.

Predictors of the feasibility of primary endoscopic management of biliary strictures after adult living donor liver transplantation.

Biliary strictures are a major cause of morbidity and mortality for liver transplant recipients. The endoscopic management of biliary strictures is not well established after living donor liver transplantation (LDLT) in comparison with deceased donor liver transplantation. The aims of this study were to assess the initial success rate of primary endoscopic treatment of biliary strictures after LDLT and to identify predictors of the feasibility of endoscopic management. One hundred thirty-seven adult patients who underwent LDLT and were confirmed to have biliary strictures by endoscopic retrograde cholangiopancreatography (ERCP) were enrolled. The biliary strictures were primarily managed endoscopically with internal drainage or nasobiliary catheterization. The initial success rate for the primary endoscopic management of biliary strictures after LDLT was 46.7% (64 of 137 patients), and the feasibility of endoscopic management was associated with the stricture-to-ERCP interval (the interval between the development of the total bilirubin, aspartate aminotransferase, or alanine aminotransferase level to >2 times the upper limit of normal and the performance of ERCP) as well as cholangiographic findings (eg, the stricture morphology and the tip shape of the distal duct). In conclusion, when biliary strictures are noticed after LDLT, prompt endoscopic interventions may improve the initial success rate of primary endoscopic management. In addition, the feasibility of primary endoscopic management can be predicted by the cholangiographic findings, which may help with the choice of the therapeutic modality.