PCI vs. CABG in left main with multi-vessel coronary artery disease and diabetes: Case report.

This case challenges the conventional preference for coronary artery bypass grafting (CABG) over percutaneous coronary intervention (PCI) in patients with diabetes, left main coronary artery disease (LMCAD) and multivessel disease. Current guidelines generally recommend CABG, especially in the context of LMCAD. However, our case involves a male patient with diabetes with LMCAD and extensive multivessel disease who was successfully treated with PCI, demonstrating a favorable outcome. Despite the high-risk profile, including a SYNTAX score of 28, the PCI approach was selected. This decision was supported by evidence suggesting comparable outcomes between PCI and CABG in similar patients. Our case highlights the potential of PCI as not just a viable, but potentially superior alternative in specific high-risk patients with diabetes, contrary to the prevailing belief in favor of CABG for all patients with left main involvement.

Diagnostic and Therapeutic Ambiguities in Diabetic Ketoacidosis With Overlapping Acute Pancreatitis and Hypertriglyceridemia.

This case report discusses the diagnostic challenges and management complexities in a patient presenting with symptoms of diabetic ketoacidosis (DKA) and severe pancreatitis, complicated by concurrent hypertriglyceridemia (HTG) and superior mesenteric vein (SMV) thrombosis. The presence of DKA in acute pancreatitis suggests very severe impact on the pancreas. Hence, it calls for screening with CT imaging for complications like hemorrhagic pancreatitis, necrotizing pancreatitis, or even thrombus. Despite typical reliance on clinical presentation and serum lipase for diagnosing pancreatitis, this case emphasizes the necessity of contrast-enhanced CT imaging in ambiguous cases to identify critical complications like thrombosis and necrotizing pancreatitis. Furthermore, the patient's management involved insulin therapy for DKA and HTG-induced acute pancreatitis, deferring plasmapheresis and anticoagulation due to the risk of hemorrhagic transformation in pancreatitis. This approach highlights the need for individualized treatment strategies, especially in complex presentations with overlapping pathologies. The case also explores the potential for insulin as a first-line treatment in HTG-induced pancreatitis over plasmapheresis, contributing to evolving guidelines.

Crystal Structure of the YcjX Stress Protein Reveals a Ras-Like GTP-Binding Protein.

Stress proteins promote cell survival by monitoring protein homeostasis in cells and organelles. YcjX is a conserved protein of unknown function, which is highly upregulated in response to acute and chronic stress. Notably, heat shock induction of ycjX exceeded even levels observed for major stress-induced chaperones, including GroEL, ClpB, and HtpG, which use ATP as energy source. YcjX features a Walker-type nucleotide-binding domain indicating that YcjX might function as a molecular chaperone. Here, we present the first crystal structure of YcjX from Shewanella oneidensis solved at 1.9-Å resolution by SAD phasing. We show that YcjX is a GTP-binding protein that shares at its core the canonical alpha-beta domain of p21ras (Ras). However, unlike Ras, YcjX features several unique insertions, including an entirely α-helical domain not previously observed in Ras-like GTPases. We note that this helical domain is reminiscent of a similar domain in the Gα subunit of heterotrimeric G proteins, supporting a potential role for YcjX as a signal transducer of stress responses. To elucidate the mechanism of GTP hydrolysis, we determined crystal structures of YcjX bound to GDP and GDPCP, respectively, which crystallized in three different nucleotide switch conformations. Supported by targeted mutagenesis experiments, we show that YcjX utilizes a non-canonical switch 2' motif not previously observed in Ras-like GTPases. Together, our structures provide atomic snapshots of YcjX in different functional states, illustrating the structural determinants for stress signaling.