Squamous cell carcinoma arising in a below-knee stump of a patient with chronic lymphocytic leukemia.

We report a case of localized squamous cell carcinoma arising in the ulceration at the site of a below-knee amputation in a patient with chronic lymphocytic leukemia on treatment with ibrutinib. The patient underwent local excision of the skin and soft tissue with histopathology showing a small focus of well-differentiated squamous cell carcinoma in the specimen. This case highlights the importance of clinical evaluation and histopathological review for underlying malignancy in the setting of amputation stump ulceration.

How High Can You Get: A Case Report of an Unusual Cause of Ascending Paralysis.

Secondary hyperkalemic paralysis is a life-threatening manifestation of hyperkalemia seen with a potassium level of 7 or above 7 milliequivalents per liter (Meq/L) in an acute or chronic state. Standard hyperkalemic treatment should be initiated upon diagnosis with emergency dialysis in refractory cases. Here we present the case of a patient with end-stage renal disease (ESRD) compliant with dialysis three times a week. The patient presented with generalized ascending flaccid paralysis and was found to have serum potassium of 9.6 Meq/L. Spontaneous resolution of the paralysis was observed shortly after the completion of one hemodialysis session. The goal of this case report is to raise awareness of a life-threatening complication of electrolyte imbalances in ESRD even in patients that are compliant with dialysis.

A Rare Cause of Acute Abdomen in a 59-Year-Old Male.

Celiac artery dissection is often an inconspicuous cause of acute abdomen. Spontaneous celiac artery dissection is most often associated with aortic dissection, and thus isolated spontaneous celiac artery dissection is rare. Herein, we present a case of celiac artery dissection with no aortic involvement. This case emphasizes the importance of including such a condition in the differential diagnosis of patients presenting with acute abdomen.

Correction: Perinatal Choline Supplementation Reduces Amyloidosis and Increases Choline Acetyltransferase Expression in the Hippocampus of the APPswePS1dE9 Alzheimer's Disease Model Mice.

[This corrects the article DOI: 10.1371/journal.pone.0170450.].

Perinatal Choline Supplementation Reduces Amyloidosis and Increases Choline Acetyltransferase Expression in the Hippocampus of the APPswePS1dE9 Alzheimer's Disease Model Mice.

Prevention of Alzheimer's disease (AD) is a major goal of biomedical sciences. In previous studies we showed that high intake of the essential nutrient, choline, during gestation prevented age-related memory decline in a rat model. In this study we investigated the effects of a similar treatment on AD-related phenotypes in a mouse model of AD. We crossed wild type (WT) female mice with hemizygous APPswe/PS1dE9 (APP.PS1) AD model male mice and maintained the pregnant and lactating dams on a control AIN76A diet containing 1.1 g/kg of choline or a choline-supplemented (5 g/kg) diet. After weaning all offspring consumed the control diet. As compared to APP.PS1 mice reared on the control diet, the hippocampus of the perinatally choline-supplemented APP.PS1 mice exhibited: 1) altered levels of amyloid precursor protein (APP) metabolites-specifically elevated amounts of ß-C-terminal fragment (ß-CTF) and reduced levels of solubilized amyloid Aß40 and Aß42 peptides; 2) reduced number and total area of amyloid plaques; 3) preserved levels of choline acetyltransferase protein (CHAT) and insulin-like growth factor II (IGF2) and 4) absence of astrogliosis. The data suggest that dietary supplementation of choline during fetal development and early postnatal life may constitute a preventive strategy for AD.

Bicuspid aortic valve disease: systematic review and meta-analysis of surgical aortic valve repair.

Aortic valve repair is still emerging, and its role in the treatment of bicuspid aortic valve disease (BAVD) is not yet fully understood. Our objective is to synthesise available evidence on outcomes after surgical aortic valve repair in patients with BAVD. We conducted a systematic review of clinical studies using prespecified methods for searching, identifying and selecting eligible studies in 4 databases, and synthesising results (PROSPERO 2014:CRD42014014415). 2 researchers independently reviewed full-text articles and extracted data. The results of included studies were quantitatively synthesised in frequentist meta-analyses. We included 11 aortic valve repair studies or study arms with a total of 2010 participants. Pooled estimates for the proportion of patients surviving at 30 days, 1 year, 5 years and 10 years were 0.995 (95% CI 0.991 to 0.995), 0.994 (0.989 to 0.999), 0.945 (0.898 to 0.993) and 0.912 (0.845 to 0.979), respectively. The pooled proportion of late deaths from valve-related causes was 0.008 (0.000 to 0.019) at a mean follow-up of 3.5 years. Proportion of patients with valve-related reinterventions was 0.075 (0.037 to 0.113) at a mean follow-up of 3.9 years, and the linearised reintervention rate was 1.3 (0.7 to 1.9) per 100 patient-years. Outcome reporting was insufficient to pool the results for a number of predefined outcomes. In conclusion, existing evidence on aortic valve repair in BAVD is limited to mostly small case series, case-control and small retrospective cohort studies. Despite the low quality, available evidence suggests favourable survival outcomes after aortic valve repair in selected patients with BAVD. Valve-related reinterventions at follow-up are common in all patients undergoing repair surgery.

The neuropsychology of starvation: set-shifting and central coherence in a fasted nonclinical sample.

OBJECTIVES: Recent research suggests certain neuropsychological deficits occur in anorexia nervosa (AN). The role of starvation in these deficits remains unclear. Studies of individuals without AN can elucidate our understanding of the effect of short-term starvation on neuropsychological performance. METHODS: Using a within-subjects repeated measures design, 60 healthy female participants were tested once after fasting for 18 hours, and once when satiated. Measures included two tasks to measure central coherence and a set-shifting task. RESULTS: Fasting exacerbated set-shifting difficulties on a rule-change task. Fasting was associated with stronger local and impaired global processing, indicating weaker central coherence. CONCLUSIONS: Models of AN that propose a central role for set-shifting difficulties or weak central coherence should also consider the impact of short-term fasting on these processes.

IGF2 ameliorates amyloidosis, increases cholinergic marker expression and raises BMP9 and neurotrophin levels in the hippocampus of the APPswePS1dE9 Alzheimer's disease model mice.

The development of an effective therapy for Alzheimer's disease (AD) is a major challenge to biomedical sciences. Because much of early AD pathophysiology includes hippocampal abnormalities, a viable treatment strategy might be to use trophic factors that support hippocampal integrity and function. IGF2 is an attractive candidate as it acts in the hippocampus to enhance memory consolidation, stimulate adult neurogenesis and upregulate cholinergic marker expression and acetylcholine (ACh) release. We performed a seven-day intracerebroventricular infusion of IGF2 in transgenic APPswe.PS1dE9 AD model mice that express green fluorescent protein in cholinergic neurons (APP.PS1/CHGFP) and in wild type WT/CHGFP littermates at 6 months of age representing early AD-like disease. IGF2 reduced the number of hippocampal Aß40- and Aß42-positive amyloid plaques in APP.PS1/CHGFP mice. Moreover, IGF2 increased hippocampal protein levels of the ACh-synthesizing enzyme, choline acetyltransferase in both WT/CHGFP and APP.PS1/CHGFP mice. The latter effect was likely mediated by increased protein expression of the cholinergic differentiating factor, BMP9, observed in IGF2-treated mice as compared to controls. IGF2 also increased the protein levels of hippocampal NGF, BDNF, NT3 and IGF1 and of doublecortin, a marker of neurogenesis. These data show that IGF2 administration is effective in reversing and preventing several pathophysiologic processes associated with AD and suggest that IGF2 may constitute a therapeutic target for AD.