Acute colonic pseudo-obstruction (ACPO) is a condition characterized by acute dilation of the large bowel without evidence of mechanical obstruction that occurs in a variety of hospitalized patients with many predisposing factors. Management includes supportive care and limitation of offending medications with mainstays of treatment of neostigmine administration and colonic decompression. https://www.selleckchem.com/products/p22077.html We report the case of a critically ill patient with ACPO who experienced bradycardia and a brief episode of asystole when receiving concomitant dexmedetomidine and neostigmine infusions but who later remained hemodynamically stable when receiving propofol and neostigmine infusions. The bradycardia and associated hemodynamic instability experienced while on dexmedetomidine and neostigmine infusions were rapidly corrected with atropine and cessation of offending agents. Because ACPO is encountered frequently and the use of dexmedetomidine as a sedative agent in the ICU is increasing, practitioners should be aware of the additive risk of bradycardia and potential for asystole with the combination of neostigmine and dexmedetomidine. Electronic drug interaction databases should be updated and drug information sources should include a drug-drug interaction between dexmedetomidine and neostigmine to reduce the likelihood of concomitant administration.Objectives To identify the effective approach between neoadjuvant chemotherapy (NCT) and chemoradiotherapy (NCRT) by comparing patient survival and complications. Methods A systematic literature search of articles published between January 1980 and October 2020 was conducted. Data were extracted and analyzed with STATA 12.0. Results Five randomized trials and 15 retrospective studies, including 4529 patients (NCT 2035; NCRT 2494), were enrolled. Compared with NCT, NCRT provided a higher 3-year survival benefit, higher R0 resection and pathological complete response rates and lower local recurrence and distant metastasis rates, but no increase in 5-year survival. Perioperative mortality and cardiovascular complications were more common in patients with adenocarcinoma. Conclusions Further studies should concentrate on identifying the optimal neoadjuvant approach and suitable beneficiaries.The branching ratio method is usually used to evaluate the optical thinness conditions in laser-generated plasmas, which are important for the application of analytical methods such calibration free laser induced breakdown spectroscopy (CF-LIBS). In this communication, we warn on the possibility that in some circumstances, the branching-ratio method might give results close to the one characterizing optically thin plasma conditions, even in the presence of a substantial self-absorption for the transitions considered.Coronary computed tomographic angiography (CCTA) is a promising technique for ruling out coronary artery disease (CAD) in patients with chest pain. We aimed to investigate the prognostic impact of nonobstructive CAD on CCTA. We retrospectively reviewed patients who underwent CCTA between 2010 and 2016 at our institution. We divided them into 3 groups (1) patients with no CAD, (2) patients with nonobstructive CAD, and (3) patients with obstructive CAD. We investigated the incidence of the primary outcome (combination of death, nonfatal myocardial infarction, unstable angina, and late revascularization). A total of 989 patients were included 540 patients had CAD, which was obstructive (≥50% stenosis) in 256 cases. During the follow-up period, 99 events occurred (32 [7%] in patients without CAD, 26 [9%] in patients with nonobstructive CAD, and 41 [16%] in patients with obstructive CAD; P less then .001). The presence of nonobstructive and obstructive CAD was an independent predictor of events (HR 2.33 [1.15-4.69], P less then .001; and 4.02 [1.98-8.13], P = .019, respectively) compared with no CAD. Nonobstructive CAD on CCTA is associated with a 2-fold increase in risk of coronary events compared with patients with no CAD.Polypharmacy is common in older adults with cancer and deprescribing potentially inappropriate medications becomes very relevant when life expectancy decreases due to metastatic disease. Especially preventive medications may no longer be beneficial, because they may decrease quality of life and reduction in morbidity and mortality may be futile. Although deprescribing of preventive medication is common in the last period of life, it is still unusual during active cancer treatment for advanced disease, although life expectancy is often limited to less than 1 to 2 years in that stage. We performed a systematic search of the literature in Pubmed and Embase on the discontinuation of commonly utilized groups of preventive medication and evaluated the evidence of potential benefits and harms in patients aged 65 years or older with cancer and a limited life expectancy (LLE). From 21 included studies, it can be concluded that deprescribing lipid lowering drugs, antihypertensive drugs, osteoporosis drugs and antihyperglycemic drugs is feasible in a considerable part of patients with a LLE. Discontinuation may be performed safely, without the occurrence of serious adverse events or decrease of survival. The only study that addressed quality of life after deprescribing showed that discontinuation of statins improves quality of life in patients with a LLE. Recurrence of symptoms requiring reintroduction occurred in 0-13% of patients on antihyperglycemic treatment and 8-60% of patients using antihypertensive drugs. In order to reduce pill burden and futile treatment clinicians should discuss deprescribing of preventive medication with older patients with advanced cancer and a LLE.Long QT syndrome type 2 is a life-threatening disorder of cardiac electrophysiology. It can lead to sudden cardiac death as a result of QT prolongation and can remain undetected until it presents clinically in the form of life-threatening cardiac arrythmias. Current treatment relies on symptom management largely through the use of β-adrenergic blockade and presently no mechanism-based therapies exist to treat the dysfunction in the hERG channels responsible for the rapid delayed rectifier K+ current which is the pathological source of long QT syndrome type 2. We review the pathophysiology, diagnosis and current management of this life-threatening condition and also analyze some promising potential mechanism-based therapies.