An increased incidence of CAD events was noted in IBD patients despite having a lower burden of traditional risk factors. Additionally, these risk factors had a lower impact on CAD development in the IBD group. Further investigation into how nontraditional risk factors, including WBC count, and the effect of attenuating systemic inflammation in IBD patients change CAD risk is warranted.

Mitochondrial dysfunction, oxidative stress and reductions in thiamine-dependent enzymes have been implicated in multiple neurological disorders including Alzheimer's disease (AD). Experimental thiamine deficiency (TD) is an established model for reducing the activities of thiamine-dependent enzymes in brain. TD diminishes thiamine dependent enzymes throughout the brain, but produces a time-dependent selective neuronal loss, glial activation, inflammation, abnormalities in oxidative metabolism and clusters of degenerating neurites in only specific thalamic regions. The present studies tested how TD alters brain pathology in Tg19959 transgenic mice over expressing a double mutant form of the amyloid precursor protein (APP). TD exacerbated amyloid plaque pathology in transgenic mice and enlarged the area occupied by plaques in cortex, hippocampus and thalamus by 50%, 200% and 200%, respectively. TD increased Aβ 1-42 levels by about three-fold, β-CTF (C99) levels by 33% and β-secretase (BACE1) protein levels by 43%. TD induced inflammation in areas of plaque formation. Thus, the induction of mild impairment of oxidative metabolism, oxidative stress and inflammation induced by TD alters metabolism of APP and/or Aβ and promotes accumulation of plaques independent of neuron loss or neuritic clusters.

arterial therapies. This study sought to assess the major complication rates associated with arterial and venous lytic therapies with the hypothesis that the complication rates may be higher with venous as compared to arterial treatments.Methods: This study is a single-center, retrospective review of arterial and venous lytic treatments that were performed between the dates of December 2010 and April 2015. Treatment areas included all arterial and venous beds; however, dialysis access and pulmonary embolism treatments were excluded from the analysis. Treatment protocols for lytic therapy were standardized, with modifications made according to attending discretion. During the pharmacomechanical thrombectomy portion, the appropriate AngioJet rheolytic catheter was used based on the target vessel diameter. A maximum of 10 mg of tPA was used at the index treatment. Lytic therapy was continued postoperatively at a rate of 1 mg/h. This was titrated postoperatively based on serial laboratory examinations of fibrinogen, CBC, PTT, and CPK (arterial cases). The tPA was titrated based on the fibrinogen level: fibrinogen 200-250 (tPA at 0.5 mg/h); fibrinogen <200 (tPA held); fibrinogen <100 or any sign of bleeding (tPA reversal). Access site and systemic complications were evaluated.Results: A total of 93 patients were included in the cohort (A-52 vs V-41). The gender breakdown (% women) did not differ significantly between the two cohorts (A-63% vs V-78%; P ¼ .17). The age did differ significantly between the two cohorts (A-68 years vs V-50 years; P < .01). There were 6 complications (11.5%) in the arterial lytic group, with one associated mortality, and 6 complications (14.6%) in the venous lytic group (P ¼ NS). There were no significant differences in the total number of complications, although the complication types trended towards an increase in systemic complications in the venous patients (P ¼ .2; Table ).Conclusions: This study suggests that the overall complication rates as related to venous lytic therapy are equivalent to those for arterial lytic therapy; however, the nature of the complications may differ, with a trend toward increased systemic complications in venous patients. This study provides for further impetus to evaluate venous lytic treatments as a separate entity from arterial lytic treatments, specifically with regards to indications for treatment, procedural technique and tPA dosing.

Thiamine-dependent enzymes are diminished in multiple neurodegenerative diseases. Thiamine deficiency (TD) reduces the activity of thiamine dependent-enzymes [e.g., the α-ketoglutarate dehydrogenase complex (KGDHC)], induces regional selective neurodegeneration and serves as a model of a mild impairment of oxidative metabolism. The current experiments tested whether changes in KGDHC protein subunits (E1k, E2k and E3) or activity or message levels underlie the selective loss of neurons in particular brain regions. Thus, TD-induced changes in these variables in the brain region most vulnerable to TD [the sub-medial thalamic nucleus (SmTN)] were compared to those in a region that is relatively resistant to TD (cortex) at stages of TD when the neuron loss in SmTN is not present, minimal or severe. Impaired motor performance on rotarod was apparent by 8 days of TD (-32%) and was severe by 10 days of TD (-97%). At TD10, the overall KGDHC activity measured by an in situ histochemical staining method declined 52% in SmTN but only 20% in cortex. Reductions in the E2k and E3 mRNA in SmTN occurred as early as TD6 (-28% and -18%, respectively) and were more severe by TD10 (-61% and -66%, respectively). On the other hand, the level of E1k mRNA did not decline in SmTN until TD10 (-48%). In contrast, TD did not alter mRNA levels of the subunits in cortex at late stages. Western blots and immunocytochemistry revealed different aspects of the changes in protein levels. In SmTN, the immunoreactivity of E1k and E3 by Western blotting increased 34% and 40%, respectively, only at TD8. In cortex, the immunoreactivity of the three subunits was not altered. Immunocytochemical staining of brain sections from TD10 mice indicated a reduction in the immunoreactivity of all subunits in SmTN, but not in cortex. These findings demonstrate that the response of the KGDHC activity, mRNA and immunoreactivity of E1k, E2k and E3 to TD is region-and time-dependent. Loss of KGDHC activity in cortex is likely related to post-translational modification rather than a loss of protein, whereas in SmTN transcriptional and post-translational modifications may account for diminished KGDHC activity. Moreover, the earlier detection in TD induced-changes of the transcripts of KGDHC indicates that transcriptional modification of the two subunits (E2k and E3) of KGDHC may be one of the early events in the cascade leading to selective neuronal death.

No abstract

Myositis due to the etiologic agent of Lyme disease, Borrelia burgdorferi, has been reported nine times in the English-language literature; there has been but a single report of exacerbation of dermatomyositis due to B. burgdorferi in a patient with known dermatomyositis. Multiple infectious agents, but not B. burgdorferi, have been hypothesized to trigger dermatomyositis. We report the first case of dermatomyositis that appears to have been triggered by B. burgdorferi. This case involved an individual from Westchester County, NY, who presented with skin lesions suggestive of erythema migrans and who was seropositive for Lyme disease. He soon developed a clinical syndrome suggestive of dermatomyositis: periorbital edema, dysphagia, proximal muscle weakness, and a markedly elevated level of creatine phosphokinase. We also review the clinical presentation and response to treatment of patients with Lyme myositis.

BackgroundUnplanned postoperative reintubation (UPR) is a marker for severe adverse outcomes following general and vascular surgery.Study designA retrospective analysis of 8809 adult patients, aged 18 years and older, who underwent major general and vascular surgery at a large single-center urban hospital was conducted from January 2013 to September 2016. Patients were grouped into those who experienced UPR and those who did not. Univariate and multivariate regression analyses were used to identify predictors of UPR, and association of UPR with adverse postoperative outcomes. All regression models had Hosmer-Lemeshow P > 0.05, and C-statistic >0.75, indicating excellent goodness-of-fit and discrimination.ResultsOf the 8809 patients included, 138 (1.6%) experienced UPR. There was no statistical difference in incidence of UPR between general and vascular surgery patients (p = 0.53). Independent predictors of UPR advanced age (OR 5.1, 95%CI 3.5–7.5, p < 0.01), higher ASA status (OR 7.9, 95%CI 5.6–11.1, p < 0.01), CHF (OR 7.0, 95%CI 3.6–13.9, p = 0.02), acute renal failure or dialysis (OR 3.1, 95%CI 1.8–5.7, p = 0.01), weight loss (OR 5.2, 95%CI 2.8–9.6, p = 0.01), systemic sepsis (OR 4.8, 95%CI 3.4–6.9, p < 0.01), elevated preoperative creatinine (OR 4.2, 95%CI 3.0–5.9, p = 0.01), hypoalbuminemia (OR 5.3, 95% CI 3.8–7.5, p = 0.01), and anemia (OR 4.0, 95%CI 2.8–5.9, p < 0.01). Following surgery, UPR was associated with increased mortality (OR 3.8, 95%CI 2.7–5.2, p < 0.01), pulmonary complications (OR 1.8, 95%CI 1.7–2.0, p < 0.01), renal complications (OR 2.6, 95%CI 1.7–3.5, p < 0.01), cardiac complications (OR 4.6, 95%CI 2.0–6.7, p < 0.01), postoperative RBC transfusion (OR 5.7, 95%CI 3.8–8.6,p < 0.01), and prolonged hospitalization (OR 1.8, 95%CI 1.5–2.4, p < 0.01).ConclusionUPR is significantly associated with postoperative morbidity and mortality. Perioperative management aimed at decreasing incidences of UPR after noncardiac surgery should target preoperative anemia in addition to previously identified predictors.

Pseudoangiomatous stromal hyperplasia (PASH) is a rare benign proliferation of breast stromal cells with a complex pattern of interanastomosing spaces lined by myofibroblasts. The exact etiology is still unknown, but a proliferative response of myofibroblasts to hormonal stimuli has been postulated. PASH is a relatively common incidental finding in breast tissue removed for other reasons and rarely manifests as a localized mass. Fewer than 150 cases of tumoral PASH have been reported since it was first described in 1986. Although PASH tends to grow over time, most lesions are cured by surgical excision and the prognosis is excellent. We report an unusual case of bilateral axillary tumoral PASH in a 44-year-old man. Awareness of this disease is important when considering the differential diagnosis of axillary masses. To our knowledge, only one other case of unilateral axillary tumoral PASH in a male patient has been described in English and this is the first case of PASH occurring in male bilateral axillary gynecomastia.