Hepatic Arterial Buffer Response: Pathologic Evidence in Non-Cirrhotic Human Liver with Portal Vein Thrombosis

poster abstractHepatic arterial buffer response (HABR) is the ability of the hepatic artery (HA) to compensate for changes in portal flow. Experimentally, occlusion of the portal vein leads to compensatory increase in HA flow with minimal parenchymal effects. Wether portal vein thrombosis (PVT) causes similar effects in the human liver is unknown. This study aims to answer this question as well as elucidate any microscopic features that may reliably assist diagnosis of PVT in the non-cirrhotic liver. We studied patients with PVT and no concomitant liver pathology. Age and gender matched livers with normal morphology served as controls. Following parameters were graded as subtle or obvious and focal or diffuse in a blinded fashion: sinusoidal dilatation, central and portal vein (PV) dilatation, PV absence, hepatic plate thinning and thickening. Outer and luminal diameters and wall thickness of HA, and outer diameter of accompanying bile ducts (BD) were measured. There were 16 patients (8 men, 8 women; mean age, 46.5 years) who presented with varices (12), ascites (8) and splenomegaly (11). Subtle and or focal dilatations of CV, PV and sinusoids as well as thinning/thickening of hepatic plates were common findings in both groups but were diffuse and obvious predominantly in cases of PVT. Absence or attenuation of PV was seen only in cases of PVT. The large HA were dilated in resection specimens of patients with PVT, p<0.05. This difference was not seen in biopsy specimens. There was no difference in the small HA in either biopsy or resection specimens or other measurements of HA or BD. In conclusion, septal branches of the HA dilate as a compensatory response to long standing thrombosis. Microscopic features of PVT are subtle but when obvious and/or diffuse in a patient with non-cirrhotic portal hypertension should raise suspicion for this diagnosis

No One Left Behind: Real-World Federated Class-Incremental Learning

Federated learning (FL) is a hot collaborative training framework via aggregating model parameters of decentralized local clients. However, most FL methods unreasonably assume data categories of FL framework are known and fixed in advance. Moreover, some new local clients that collect novel categories unseen by other clients may be introduced to FL training irregularly. These issues render global model to undergo catastrophic forgetting on old categories, when local clients receive new categories consecutively under limited memory of storing old categories. To tackle the above issues, we propose a novel Local-Global Anti-forgetting (LGA) model. It ensures no local clients are left behind as they learn new classes continually, by addressing local and global catastrophic forgetting. Specifically, considering tackling class imbalance of local client to surmount local forgetting, we develop a category-balanced gradient-adaptive compensation loss and a category gradient-induced semantic distillation loss. They can balance heterogeneous forgetting speeds of hard-to-forget and easy-to-forget old categories, while ensure consistent class-relations within different tasks. Moreover, a proxy server is designed to tackle global forgetting caused by Non-IID class imbalance between different clients. It augments perturbed prototype images of new categories collected from local clients via self-supervised prototype augmentation, thus improving robustness to choose the best old global model for local-side semantic distillation loss. Experiments on representative datasets verify superior performance of our model against comparison methods. The code is available at https://github.com/JiahuaDong/LGA.Comment: 17 pages, 8 figure

Changes of procedural learning in Chinese patients with non-demented Parkinson disease

To study procedural learning changes in patients with non-demented Parkinson disease (PD) but without depression. The Nissen serial reaction time task (SRTT) software version II (as a task of procedural learning), the Wechsler Memory Scale-Chinese version (WMS-CR), and two tasks of implicit memory were applied to 20 PD patients with a Hoehn-Yahr score at I-II degrees and 20 matched healthy controls were enrolled for the Nissen Version test. In the explicit WMS-CR and the implicit (word stem completion and degraded picture naming) tasks, the patients\u27 scores fell within normal limits. In the SRTT, healthy controls displayed significantly reduced response times and error rates across the blocks of repeated sequence trials. In contrast, PD patients only showed a reduction in error rates but no change in response times. Impairment of nigrostriatal pathways selectively affects the performance in visuo-motor learning tasks such as the SRTT, but not in both the explicit tasks of WMS-CR and the implicit tasks

Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats

Stroke breaks the oxidative balance in the body and causes extra reactive oxygen species (ROS) generation, leading to oxidative stress damage. Long noncoding RNAs (lncRNAs) and microRNAs play pivotal roles in oxidative stress-mediated brain injury. Safflor yellow B (SYB) was able to effectively reduce ischemia-mediated brain damage by increasing antioxidant capacity and inhibiting cell apoptosis. In this study, we investigated the putative involvement of lncRNA AK046177 and microRNA-134 (miR-134) regulation in SYB against ischemia/reperfusion- (I/R-) induced neuronal injury. I/R and oxygen-glucose deprivation/reoxygenation (OGD/R) were established in vivo and in vitro. Cerebral infarct volume, neuronal apoptosis, and protein expression were detected. The effects of SYB on cell activity, cell respiration, nuclear factor erythroid 2-related factor 2 (Nrf2), antioxidant enzymes, and ROS were evaluated. I/R or OGD/R upregulated the expression of AK046177 and miR-134 and subsequently inhibited the activation and expression of CREB, which caused ROS generation and brain/cell injury. SYB attenuated the effects of AK046177, inhibited miR-134 expression, and promoted CREB activation, which in turn promoted Nrf2 expression, and then increased antioxidant capacities, improved cell respiration, and reduced apoptosis. We suggested that the antioxidant effects of SYB were driven by an AK046177/miR-134/CREB-dependent mechanism that inhibited this pathway, and that SYB has potential use in reducing or possibly preventing I/R-induced neuronal injury

No One Left Behind: Real-World Federated Class-Incremental Learning

ISSN:0162-8828ISSN:1939-353

Autophagy inhibition promotes 5-fluorouraci-induced apoptosis by stimulating ROS formation in human non-small cell lung cancer A549 cells.

Chemotherapy is an important option for the treatment of various cancers including lung cancer. However, tumor resistance towards cytotoxic chemotherapy has become more common. It has been reported that autophagy is one of the processes contributing to this resistance. In the present study, we found that the anti-cancer drug 5-fluorouraci(5-FU) could induce autophagy in A549 cells. 5-FU treatment could lead to the conversion of LC3 I/II, the up-regulation of Beclin-1, the down-regulation of p62 and the formation of acidic vesicular organelles (AVOs) in A549 cells. Pre-treatment of cancer cells with 3-MA or siAtg7 could enhance 5-FU-induced apoptosis through the activation of caspases, and the caspase inhibitor z-VAD-fmk rescued the cell viability reduction. Furthermore, the inhibition of autophagy also stimulated ROS formation and scavenging of ROS by antioxidant NAC inhibited caspase-3 activity, prevented the release of cyt-c from mitochondria and eventually rescued cancer cells from 5-FU-mediated apoptosis. These results suggest that 5-FU-elicited autophagic response plays a protective role against cell apoptosis and the inhibition of autophagy could sensitize them to 5-FU-induced caspase-dependent apoptosis through the stimulation of ROS formation

IGH/BCL2 status better predicts clinico-pathological behavior in primary splenic follicular lymphoma than histological grade and other molecular markers

Splenic lymphoma may be primary or secondary. Primary splenic lymphoma\u27s are rare and usually of follicular cell origin representing \u3c 1% of Non-Hodgkin\u27s Lymphoma\u27s. Most are secondary with 35% representing Marginal Cell sub-type with the rest being Diffuse Large B-Cell Lymphoma\u27s. Unlike the uniformly aggressive clinical course of Diffuse Large B-Cell Lymphoma\u27s, biological behavior of Primary Splenic CD10-Positive Small B-Cell Lymphoma/Follicular Lymphoma remains less well defined. We present here a solitary splenic mass confirmed as Primary Splenic CD10-Positive Small B-Cell Lymphoma/Follicular Lymphoma after a diagnostic splenectomy. Biopsy revealed monomorphic small lymphoid cells with low grade mitotic activity. Flow cytometry showed a lambda restricted population of B-Cells displaying dim CD19 and CD10. The cells were negative for CD5, CD11c, and CD103. FISH was negative for IGH/BCL2 fusion unlike nodal Follicular Lymphoma\u27s which are usually positive for this translocation. Evidence from this case and a review of literature support the finding that Primary Splenic CD10-Positive Small B-Cell Lymphoma/Follicular Lymphoma is less likely to have the classic IGH-BCL2 fusion and the associated chromosomal 14;18 translocation. This profile is associated with less aggressive clinical behavior even when histopathology represents a high-grade pattern. In such cases splenectomy alone is adequate for localized disease when negative for IGH/BCL2 fusion regardless of histological grade