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Mechanism and significance of diffusion restriction followed by calcification in high-grade glioma treated with bevacizumab.
Sci Rep
November 2024
Division of Neurosurgery, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University, 36-1, Nishi-cho, Yonago, 683-8504, Tottori, Japan.
In this study, we focused on calcification and diffusion restriction, which sometimes appear around the resection cavity or periventricular white matter in patients with high-grade glioma (HGG) treated with bevacizumab (BVZ), as candidate imaging biomarkers for BVZ treatment efficacy. We investigated the timing of the appearance of diffusion restriction and calcification using magnetic resonance imaging and computed tomography in 35 patients with newly diagnosed or recurrent HGG treated with BVZ. In 17 (48.
View Article and Find Full Text PDFSymmetric, Bilateral Auricular Calcifications in Twins With Noonan Syndrome.
J Craniofac Surg
January 2025
Division of Plastic and Oral Surgery, Baylor Scott and White Medical Center and McLane Children's Hospital, Temple, TX.
Noonan syndrome (NS) is a rare, genetic multisystem disorder often presenting with associated craniofacial abnormalities. The authors report an identical twin pair with classical features of NS including short stature, mild ptosis, hypertelorism, down-slanting palpebral fissures, low-set angulated ears, and giant cell tumors in the craniofacial skeleton. Interestingly, these patients also presented with bilateral, symmetric, dystrophic auricular calcifications.
View Article and Find Full Text PDFUnraveling the Pathogenesis of Calcinosis in Systemic Sclerosis: A Molecular and Clinical Insight.
Int J Mol Sci
October 2024
Unit of Immunology, Rheumatology, Allergy and Rare Diseases, IRCCS San Raffaele Hospital, Vita-Salute San Raffaele University, 20132 Milan, Italy.
Article Synopsis
- Dystrophic calcinosis is a condition where calcified materials accumulate in tissues despite normal calcium and phosphorus levels, commonly seen in systemic sclerosis (SSc) and significantly impacting patient quality of life.
- The management of calcinosis in SSc is challenging due to risks like infection, pain, and the absence of standardized treatment options, with its precise causes still unclear.
- Factors contributing to calcinosis development include cell differentiation, mineralization imbalances, and local disturbances in mineral levels, alongside pathophysiological changes in SSc that may promote its formation, highlighting the need for further research into underlying mechanisms for potential treatment strategies.
[Calcifications and phosphocalcic metabolism].
Ann Pathol
November 2024
Anatomie et cytologie pathologiques, Institut de cancérologie de l'Ouest, Centre René-Gauducheau, boulevard Jacques-Monod, 44805 Saint-Herblain cedex, France. Electronic address:
Extraosseous calcifications correspond to ubiquitous deposits of intra-tissue calcium salts leading to dysfunction of the affected tissue or organ. There are two types: metastatic calcifications and dystrophic calcifications. Their formation mechanism is by mimicking the physiological mineralization process with an "osteoblast-like" cell.
View Article and Find Full Text PDFCalcification following tongue necrosis induced by vasopressor use in a nonintubated patient with septic shock: a case report.
J Med Case Rep
September 2024
Division of Pulmonology and Critical Care Medicine, Department of Internal Medicine, College of Medicine, Chungnam National University, 282 Munhwa-Ro, Jung-Gu, Daejeon, 35015, Republic of Korea.
Article Synopsis
- Tongue necrosis is a rare condition often linked to issues like vasculitis or septic shock, which can lead to serious damage and calcification.
- A case study details a 70-year-old man who experienced bilateral tongue necrosis after septic shock, with symptoms including discoloration and swelling, but without leg ischemia.
- Successful treatment involved cleaning the affected area, highlighting the importance of regular tongue inspection during ICU care to catch complications early and reduce long-term damage.
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