Cerebral infarction leading to hemiplegia: A rare complication of acute pancreatitis

Peripancreatic vascular thrombosis is a known complication of acute pancreatitis (AP) and chronic pancreatitis. However, hemiplegia resulting from cerebral infarction due to cerebral arterial thrombosis is a rare complication of AP. Here, we report a case of alcohol related severe AP with multi-organ dysfunction, which was complicated by large left sided middle cerebral artery territory infarct - leading to right sided hemiplegia in a 48-year-old male patient. The neurological and vascular thrombotic complications of pancreatitis, their pathogenesis and management are discussed in brief.     

The global effect for antisaccades

In the global effect, prosaccades are deviated to a position intermediate between two targets or between a distractor and a target, which may reflect spatial averaging in a map encoded by the superior colliculus. Antisaccades differ from prosaccades in that they dissociate the locations of the stimulus and goal and generate weaker collicular activity. We used these antisaccade properties to determine whether the global effect was generated in stimulus or goal computations, and whether the global effect would be larger for antisaccades, as predicted by collicular averaging. In the first two experiments, human subjects performed antisaccades while distractors were placed in the vicinity of either the stimulus or the saccadic goal. Global effects occurred only for goal-related and not for stimulus-related distractors, indicating that this effect emerges from interactions with motor representations. In the last experiment, subjects performed prosaccades and antisaccades with and without goal-related distractors. When the results were adjusted for differences in response latency, the global effect for rapid responses was three to four times larger for antisaccades than for prosaccades. Finally, we compared our findings with predictions from collicular models, to quantitatively test the spatial averaging hypothesis: we found that our results were consistent with the predictions of a collicular model. We conclude that the antisaccade global effect shows properties compatible with spatial averaging in collicular maps and likely originates in layers with neural activity related to goal rather than stimulus representations.     

Evaluation of the Hybrid III and Q-Series Pediatric ATD Upper Neck Loads as Compared to Pediatric Volunteers in Low-Speed Frontal Crashes

Debate exists in the automotive community regarding the validity of the pediatric ATD neck response and corresponding neck loads. Previous research has shown that the pediatric ATDs exhibit hyper-flexion and chin-to-chest contact resulting in overestimations of neck loads and neck injury criteria. Our previous work comparing the kinematics of the Hybrid III and Q-series 6 and 10-year-old ATDs to pediatric volunteers in low-speed frontal sled tests revealed decreased ATD cervical and thoracic spine excursions. These kinematic differences may contribute to the overestimation of upper neck loads by the ATD. The current study compared upper neck loads of the Hybrid III and Q-series 6 and 10-year-old ATDs against size-matched male pediatric volunteers in low-speed frontal sled tests. A 3-D near-infrared target tracking system quantified the position of markers on the ATD and pediatric volunteers (head top, nasion, bilateral external auditory meatus). Shear force (F _x ), axial force (F _z ), bending moment (M _y ), and head angular acceleration ( $ \ddot{\theta }_{\text{head}} $ ) were calculated about the upper neck using standard equations of motion. In general, the ATDs underestimated axial force and overestimated bending moment compared to the human volunteers. The Hybrid III 6, Q6, and Q10 exhibited reduced head angular acceleration and modest increases in upper neck shear compared to the pediatric volunteers. The reduction in axial force and bending moment has important implications for neck injury predictions as both are used when calculating N _ij . These analyses provide insight into the biofidelity of the pediatric ATD upper neck loads in low-speed crash environments.     

A case of arrhythmogenic right ventricular cardiomyopathy-Naxos disease

We present a case of arrhythmogenic right ventricular cardiomyopathy (ARVC)-Naxos disease. The patient is 21-year-old male with no history of previous heart disease admitted in a private hospital for rhythm disorder in heart. The condition was diagnosed as ventricular tachycardia (VT) and was treated with cardioversion. The patient was referred to our hospital for further evaluation. On examination patient had palmoplantar keratoderma, wooly hair, and dystrophic nails. The cardiovascular system examination was clinically normal. His electrocardiogram showed epsilon wave in lead V1; echocardiography showed hypo-echogenic tissues in the right ventricular (RV) apex and free wall; magnetic resonance imaging (MRI) investigation revealed fibrofatty replacement of RV free wall and dyskinetic RV wall with diastolic outbulging.     

Demystifying seronegative autoimmune pancreatitis

BackgroundAutoimmune pancreatitis (AIP) has been classified into type 1 and type 2 subtypes. Serum immunoglobulin G4 (IgG4) elevation characterizes type 1 AIP. Type 2 AIP and a subset of type 1 AIP are seronegative, i.e., have normal serum IgG4 levels.AimWe compared the profiles of the three subsets of AIP to identify the unique characteristics of seronegative type 1 AIP and type 2 AIP.MethodsWe compared the clinical profiles of 69 seropositive type 1 AIP patients, 21 seronegative type 1 AIP patients and 22 type 2 AIP patients.ResultsAmong type 1 AIP, seronegative group had similar clinical profiles when compared to seropositive group except that they were more likely to undergo surgical resection than seropositive patients (p = 0.001). Seronegative type I AIP patients were older (61.9 ± 13.7 vs 45.3 ± 17.4; p = 0.004), and differed in the occurrence of other organ involvement (OOI) (71.4% vs 0%; p < 0.001) and disease relapse (33.3% vs 0%; p = 0.005) when compared with type 2 AIP. All seronegative type 1 AIP patients had at least one of the following –OOI, disease relapse, and age >50 years while none of the type 2 AIP had OOI or disease relapse.ConclusionsSeronegative and seropositive type 1 AIP patients have similar clinical profiles, which are distinct from that of type 2 AIP. Among the seronegative AIP group, patients are more likely to have type 1 AIP rather than type 2 AIP if they are older than 50 years or have OOI or disease relapse.     

Pathogenic Mechanisms in Type 1 Diabetes: The Islet is Both Target and Driver of Disease

Recent advances in our understanding of the pathogenesis of type 1 diabetes have occurred in all steps of the disease. This review outlines the pathogenic mechanisms utilized by the immune system to mediate destruction of the pancreatic beta-cells. The autoimmune response against beta-cells appears to begin in the pancreatic lymph node where T cells, which have escaped negative selection in the thymus, first meet beta-cell antigens presented by dendritic cells. Proinsulin is an important antigen in early diabetes. T cells migrate to the islets via the circulation and establish insulitis initially around the islets. T cells within insulitis are specific for islet antigens rather than bystanders. Pathogenic CD4⁺ T cells may recognize peptides from proinsulin which are produced locally within the islet. CD8⁺ T cells differentiate into effector T cells in islets and then kill beta-cells, primarily via the perforin-granzyme pathway. Cytokines do not appear to be important cytotoxic molecules in vivo. Maturation of the immune response within the islet is now understood to contribute to diabetes, and highlights the islet as both driver and target of the disease. The majority of our knowledge of these pathogenic processes is derived from the NOD mouse model, although some processes are mirrored in the human disease. However, more work is required to translate the data from the NOD mouse to our understanding of human diabetes pathogenesis. New technology, especially MHC tetramers and modern imaging, will enhance our understanding of the pathogenic mechanisms.