Coordinates: 32°30′6″N 35°59′39″E / 32.50167°N 35.99417°E / 32.50167; 35.99417King Abdullah University Hospital (Arabic: مُستشفى الملك المؤسس عبد الله الجامعي), often abbreviated KAUH, is a hospital in Ar Ramtha, Jordan. It is the largest medical structure in the north of the country, serving approximately one million inhabitants from Ramtha, Irbid, Ajloun, Jerash, and Mafraq governorates. It is also the teaching hospital affiliated with Jordan University of Science and Technology (JUST), located within the campus adjacent to the university's Medical Faculties Complex.The hospital is staffed with full-time physicians and surgeons who are faculty members of the JUST Faculty of Medicine, in addition to many others from the Ministry of Health, and the Royal Medical Services (RMS).The overall area of various hospital buildings is 95,583 m2, in addition to a double story car park of 9,000 m2 area. The hospital has a bed capacity of 750 which can be increased to 900 beds in an emergency situation. Structurally, the hospital is composed of a 15-story high-rise building, in which all hospital beds are located, and a 3-story low-rise buildings in which patient clinics, diagnostic and other services are located. The hospital is connected to various health science faculties via the ground floor of the low-rise building.During the COVID-19 pandemic, KAUH was designated by the Jordanian Ministry of Health as the main center for COVID-19 testing and isolation in the north of Jordan and one of 7 such centers in the country.
Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract and represent a paradigm of precision oncology in which histopathology and molecular profiling directly inform diagnosis, prognosis, and therapeutic strategy. Arising from the interstitial cells of Cajal or their precursors, GISTs display a wide morphological spectrum, including spindle cell, epithelioid, mixed, and rare histologic variants, often requiring immunohistochemical confirmation with KIT (CD117), DOG1, and CD34. Molecular characterization reveals a limited but clinically decisive range of driver mutations, most commonly in KIT and PDGFRA, with additional subsets involving SDH deficiency, NF1 alterations, and rare mutations such as BRAF, KRAS, or NTRK fusions. These molecular signatures underpin distinct biological behaviors, prognostic categories, and therapeutic sensitivities. Risk stratification incorporates tumor size, mitotic rate, anatomical location, and tumor rupture to predict recurrence and guide adjuvant therapy decisions. Targeted tyrosine kinase inhibitors (TKIs) have transformed GIST management, with imatinib as the foundational first-line therapy and subsequent agents, sunitinib, regorafenib, avapritinib, and ripretinib, addressing primary or secondary resistance driven by diverse mutational patterns. Nevertheless, challenges persist, including imatinib-resistant PDGFRA D842V mutations, SDH-deficient tumors lacking actionable kinase alterations, and the emergence of polyclonal secondary resistance due to heterogeneous KIT adenosine triphosphate (ATP)-binding pocket or activation loop mutations. Emerging therapeutic directions include next-generation kinase inhibitors, heat shock protein inhibitors, immunotherapy, metabolic and epigenetic targeting, and biomarker-driven individualized treatment strategies. This review synthesizes contemporary advances in the histopathological, molecular, and therapeutic landscape of GISTs, emphasizing an integrated diagnostic approach and highlighting ongoing efforts to overcome therapeutic resistance and optimize personalized care.
Cribriform morular thyroid carcinoma (CMTC) is a rare neoplasm more common in young euthyroid females, usually associated with familial adenomatous polyposis (FAP) syndrome, but also presenting as sporadic cases. These tumors result from the activation of the WNT/β-catenin signaling pathway, usually through germline APC gene mutations in FAP-associated disease, while sporadic cases may exhibit somatic mutations in APC, CTNNB1, and AXIN1. Additional possible molecular events include somatic mutations in KRAS, PIK3CA, KMT2C, KMT2D, TERT promoter or RET rearrangements. BRAF mutations do not occur. We describe a sporadic case of high-grade CMTC presented in a 44-year-old female with a large multilobulated, unifocal mass in the right thyroid lobe. The tumor showed the typical cribriform and morular patterns, high grade features (Ki-67 proliferative index of 20
Purpose/Objective(s) Glioblastoma (GBM) exhibits near-universal recurrence, with 80–90% of failures arising within the high-dose irradiated margin. This pattern suggests that resistance is not purely intrinsic but may involve radiation-induced adaptive survival programs. Sirtuin-3 (SIRT3), a mitochondrial NAD⁺-dependent deacetylase, regulates oxidative stress and metabolic fitness. We investigated whether ionizing radiation (IR) promotes a SIRT3-mediated mitochondrial defence axis that enhances glioma stem cell (GSC) survival and therapeutic escape. Materials/Methods A structured mechanistic synthesis of preclinical GBM models (2000–2025) was conducted, integrating laboratory data with clinical bioinformatic validation. Study quality was appraised using established risk-of-bias tools. Clinical correlation was performed using the TCGA-GBM dataset (n=157), evaluating SIRT3 transcript levels against overall survival (OS) using Cox proportional hazards modelling and Kaplan–Meier analysis. Results Evidence supports a cooperative two-step SIRT3 activation program following IR. First, radiation induces transcriptional upregulation of SIRT3 via NF-κB signalling. Second, Cyclin B1/CDK1 phosphorylates SIRT3 at Thr150/Ser159, enhancing its deacetylase activity. Activated SIRT3 deacetylates and stimulates MnSOD (SOD2), augmenting mitochondrial ROS detoxification and preserving mitochondrial integrity under radiation stress.In GSCs, SIRT3 functionally interacts with TRAP1 to sustain oxidative phosphorylation capacity while limiting ROS accumulation, supporting stemness and metabolic plasticity. Additionally, SIRT3 modulates ferroptosis susceptibility through the ATF4–SLC7A11 axis, maintaining glutathione synthesis and suppressing lipid peroxidation.Inhibition of SIRT3 (3-TYP or shRNA) or disruption of CDK1-mediated phosphorylation sensitized GBM models to radiation and increased ferroptotic vulnerability in vivo. TCGA analysis demonstrated that elevated SIRT3 expression was significantly associated with poorer OS (p=0.0322). Conclusion These findings support a model in which radiation actively engages a SIRT3-dependent mitochondrial stress adaptation program rather than merely selecting for pre-existing resistant clones. Targeting the CDK1–SIRT3–MnSOD axis may represent a rational radiosensitization strategy by collapsing mitochondrial redox buffering and lowering the ferroptotic threshold. Disrupting this adaptive “mitochondrial shield” offers a translational opportunity to enhance radiation response in GBM.
Aneurysmal subarachnoid hemorrhage (aSAH) in infants is exceptionally rare, posing unique diagnostic and therapeutic challenges due to nonspecific clinical features and lack of standardized management protocols. We report a 6-month-old male presenting with vomiting, decreased consciousness, and seizures. Neuroimaging revealed diffuse subarachnoid hemorrhage from a ruptured left middle cerebral artery (MCA) aneurysm. Despite aggressive stabilization, the patient suffered rebleeding and succumbed to catastrophic complications. A systematic review following PRISMA guidelines was conducted (CRD420251145008). PubMed, Embase, and Cochrane CENTRAL were searched (2005–2025) for aSAH cases in infants ≤ 12 months. Extracted individual patient data were combined into a pooled individual–level analysis comparing survival and functional outcomes between intervention (endovascular/microsurgical) and conservative management using Fisher’s exact test. Sixty cases were identified (median age 6 months; 56
