Results 81 to 90 of about 23,942 (228)

No increased risk of spinal cerebrospinal fluid leak after spinal manipulative therapy: A retrospective cohort study

PM&R, EarlyView.
Abstract Background Spinal cerebrospinal fluid (CSF) leaks, a rare but debilitating condition, have been described following spinal manipulative therapy (SMT) in case reports. However, the nature of the potential association between SMT and CSF leak is uncertain, and symptoms such as neck pain or headache may reflect preexisting leaks rather than ...
Robert J. Trager, Collin M. Labak, Anthony N. Baumann, Tyler H. Snodgrass, Zachary A. Cupler   +4 more
wiley   +1 more source

Schwannomatosis of the Spinal Accessory Nerve: A Case Report. [PDF]

, 2019
Schwannomatosis is a distinct syndrome characterized by multiple peripheral nerve schwannomas that can be sporadic or familial in nature. Cases affecting the lower cranial nerves are infrequent.
Chin, Cynthia T, Jacques, Line, Lee, Anthony T, Lee, Young M, Morshed, Ramin A   +4 more
core  

Non-coding RNA ANRIL and the number of plexiform neurofibromas in patients with NF1microdeletions [PDF]

, 2012
BACKGROUND: Neurofibromatosis type-1 (NF1) is caused by mutations of the NF1 gene at 17q11.2. In 95% of non-founder NF1 patients, NF1 mutations are identifiable by means of a comprehensive mutation analysis. 5-10% of these patients harbour microdeletions
David N Cooper, Hildegard Kehrer-Sawatzki, Josef Högel, Lan Kluwe, Rosa Nguyen, Tanja Mußotter, Victor-Felix Mautner   +6 more
core   +2 more sources

Optic nerve sheath meningioma exhibits neural niche‐associated transcriptomic features and rare copy number variation‐linked evolution

Brain Pathology, EarlyView.
Optic nerve sheath meningiomas are typically NF2‐intact with few copy number alterations and are generally clinically indolent. Rare aggressive recurrences are associated with progressive accumulation of copy number variations, including CDKN2A/B homozygous deletion, 1q gain, and 14q loss.
Daisuke Sato, Satoru Miyawaki, Yu Sakai, Kenta Ohara, Yu Teranishi, Yudai Hirano, Motoyuki Umekawa, Takahiro Tsuchiya, Shotaro Ogawa, So Hirata, Hiroki Hongo, Hideaki Ono, Daisuke Komura, Tetsuo Ushiku, Shumpei Ishikawa, Nobuhito Saito   +15 more
wiley   +1 more source

Neurofibromin knockdown in glioma cell lines is associated with changes in cytokine and chemokine secretion in vitro. [PDF]

, 2018
The neurofibromin-1 tumor suppressor gene (NF1) is altered in approximately 20% of sporadic glioblastoma (GBM) cases. NF1 deficient GBM frequently shows a mesenchymal gene expression signature, suggesting a relationship between NF1 status and the tumor ...
Mukherjee, Joydeep, Pieper, Russell O, Wood, Matthew D   +2 more
core   +3 more sources

Novel drugs approved by the EMA, the FDA and the MHRA in 2025: A year in review

British Journal of Pharmacology, EarlyView.
Abstract In the 2025 novel drug mini‐review, one can take a full measure of the ingenuity that underlies current drug design and development, despite the year's smaller harvest (46 novel drugs) compared to 2024 (53) and 2023 (70). 54% of the novel drugs are first‐in‐class (FIC).
Andreas Papapetropoulos, Stavros Topouzis, Steve P. H. Alexander, Miriam M. Cortese‐Krott, Zsuzsanna Helyes, Kirill Martemyanov, Claudio Mauro, Nithyanandan Nagercoil, Reynold A. Panettieri Jr, Hemal H. Patel, Rainer Schulz, Barbara Stefanska, Gary J. Stephens, Nathalie Vergnolle, Xin Wang, Stephen Ward, Péter Ferdinandy   +16 more
wiley   +1 more source

Clinically aggressive central giant cell granulomas in two patients with neurofibromatosis 1 [PDF]

, 2006
Background Neurofibromatosis 1 (NF1) is an autosomal dominantly inherited disorder caused by a spectrum of mutations affecting the Nf1 gene. Affected patients develop benign and malignant tumors at an increased frequency.
Edwards, Paul C., Fantasia, John E, Rosenberg, Tracey J, Ruggiero, Salvatore, Sachs, Stephen A, Saini, Tamjit   +5 more
core   +1 more source

Deep‐Intronic Variant in RUNX2 Causing Pseudo‐Exon Inclusion in a Family With Cleidocranial Dysplasia

Clinical Genetics, EarlyView.
A deep‐intronic single nucleotide variant in RUNX2 causes the characteristic clinical features of cleidocranial dysplasia (CCD) in a family via pseudo‐exon inclusion into the mRNA. The pseudo‐exon contains a premature stop codon and triggers mRNA decay, which results in RUNX2 haploinsufficiency, the known disease mechanism.
Dorothea Stojanovic, Dorota Garczarczyk‐Asim, Julia Vodopiutz, Andreas R. Janecke   +3 more
wiley   +1 more source

Parental age and risk of genetic syndromes predisposing to nervous system tumors: nested case–control study

Clinical Epidemiology, 2018
Maral Adel Fahmideh,1 Giorgio Tettamanti,1 Catharina Lavebratt,2 Mats Talbäck,1 Tiit Mathiesen,3,4 Birgitta Lannering,5 Kimberly J Johnson,6,7 Maria Feychting1 1Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet ...
Adel Fahmideh M, Tettamanti G, Lavebratt C, Talbäck M, Mathiesen T, Lannering B, Johnson KJ, Feychting M   +7 more
doaj  

Molecular Features of a Primary Transmural Tracheal Schwannoma: Clinical Experience and Review of the Literature

Cancer Management and Research, 2022
Chunqiu Xia,1,* Minghui Liu,1,* Xiaoyu Niu,1 Xin Li,1 Jun Chen1– 3 1Department of Lung Cancer Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, People’s Republic of China; 2Tianjin Key Laboratory of Lung Cancer Metastasis and
Xia C, Liu M, Niu X, Li X, Chen J
doaj