From Chest Trauma to Coronary Artery Dissection.

Despite being rare, traumatic coronary artery dissection after blunt chest trauma can lead to life-threatening consequences that can be fatal. This case report focuses on a 51-year-old woman who suffered chest trauma at home and was later found to have right coronary artery dissection. This manuscript aims to elucidate the risk factors, diagnostic challenges, and management strategies associated with traumatic coronary artery dissection. This case report emphasizes the evaluation of risk factors, the significance of early detection with appropriate imaging modalities while maintaining high clinical suspicion, and the critical necessity of optimizing patient outcomes in such circumstances.

Unlocking the Hidden Pathway: A Rare Encounter With Right Coronary Artery Fistula to Coronary Sinus and Right Ventricle.

Coronary artery fistulas (CAFs) are rare vascular anomalies characterized by abnormal connections between coronary arteries and cardiac chambers or adjacent structures. Advances in cardiac interventions have led to an increasing recognition of acquired CAFs, which are typically congenital. We present a case of a 62-year-old male with a complex medical history, including hypertension, atrial fibrillation, and heart failure, who presented with exertional chest pain and palpitations. Diagnostic evaluation revealed a significant CAF originating from the right coronary artery (RCA) and terminating into the coronary sinus and right ventricle. Despite the absence of significant coronary artery occlusions, the fistula was deemed clinically significant due to its potential to cause myocardial ischemia. Management involved guideline-directed medical therapy and lifestyle modifications. This case underscores the importance of early recognition and appropriate management of CAFs to optimize patient outcomes. Further research is needed to better understand the natural history and optimal management strategies of CAFs.

Role and mechanism of autophagy-regulating factors in tumorigenesis and drug resistance.

A hallmark feature of tumorigenesis is uncontrolled cell division. Autophagy is regulated by more than 30 genes and it is one of several mechanisms by which cells maintain homeostasis. Autophagy promotes cancer progression and drug resistance. Several genes play important roles in autophagy-induced tumorigenesis and drug resistance including Beclin-1, MIF, HMGB1, p53, PTEN, p62, RAC3, SRC3, NF-2, MEG3, LAPTM4B, mTOR, BRAF and c-MYC. These genes alter cell growth, cellular microenvironment and cell division. Mechanisms involved in tumorigenesis and drug resistance include microdeletions, genetic mutations, loss of heterozygosity, hypermethylation, microsatellite instability and translational modifications at a molecular level. Disrupted or altered autophagy has been reported in hematological malignancies like lymphoma, leukemia and myeloma as well as multiple solid organ tumors like colorectal, hepatocellular, gall bladder, pancreatic, gastric and cholangiocarcinoma among many other malignancies. In addition, defects in autophagy also play a role in drug resistance in cancers like osteosarcoma, ovarian and lung carcinomas following treatment with drugs such as doxorubicin, paclitaxel, cisplatin, gemcitabine and etoposide. Therapeutic approaches that modulate autophagy are a novel future direction for cancer drug development that may help to prevent issues with disease progression and overcome drug resistance.

Novel Targeted Therapies for Chronic Lymphocytic Leukemia in Elderly Patients: A Systematic Review.

Chronic lymphocytic leukemia (CLL) typically affects older patients; administration of traditional cytotoxic therapies in old patients has very modest benefit with no survival improvement. With better understanding of CLL biology, trends are shifting towards the use of targeted therapies. The objective of this article is to review the safety and efficacy of various novel agents that specifically target the dysregulated pathways, with particular attention to elderly patients. Agents like B-cell receptor (BCR) inhibitors (Bruton's tyrosine kinase inhibitors [ibrutinib]), phosphatidylinositol 3-kinase inhibitors (idelalisib), spleen tyrosine kinase inhibitors (entospletinib), Bcl-2 inhibitors (venetoclax), immunomodulators (lenalidomide), and monoclonal antibodies (obinutuzumab, ofatumumab) have shown activity in CLL with a very favorable toxicity profile. Newer agents have improved clinical outcomes, and have tolerable toxicity profiles in elderly patients, resulting in the treatment with individualized therapy approach for CLL.

Revisiting Role of Vaccinations in Donors, Transplant Recipients, Immunocompromised Hosts, Travelers, and Household Contacts of Stem Cell Transplant Recipients.

Vaccination is an effective strategy to prevent infections in immunocompromised hematopoietic stem cell transplant recipients. Pretransplant vaccination of influenza, pneumococcus, Haemophilus influenza type b, diphtheria, tetanus, and hepatitis B, both in donors and transplant recipients, produces high antibody titers in patients compared with recipient vaccination only. Because transplant recipients are immunocompromised, live vaccines should be avoided with few exceptions. Transplant recipients should get inactive vaccinations when possible to prevent infection. This includes vaccination against influenza, pneumococcus, H. influenza type b, diphtheria, tetanus, pertussis, meningococcus, measles, mumps, rubella, polio, hepatitis A, human papillomavirus, and hepatitis B. Close contacts of transplant recipients can safely get vaccinations (inactive and few live vaccines) as per their need and schedule. Transplant recipients who wish to travel may need to get vaccinated against endemic diseases that are prevalent in such areas. There is paucity of data on the role of vaccinations for patients receiving novel immunotherapy such as bispecific antibodies and chimeric antigen receptor T cells despite data on prolonged B cell depletion and higher risk of opportunistic infections.