Publications by authors named "L Mittelman"

Objectives: Language is a critical aspect of human cognition and function, and its preservation is a priority for neurosurgical interventions in the left frontal operculum. However, identification of language areas can be inconsistent, even with electrical mapping. The use of multimodal structural and functional neuroimaging in conjunction with intraoperative neuromonitoring may augment cortical language area identification to guide the resection of left frontal opercular lesions.

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Supplementary motor area (SMA) syndrome is characterized by contralateral akinesia and mutism, and frequently occurs following resection of tumors involving the superior frontal gyrus. The frontal aslant tract (FAT), involved in functional connectivity of the supplementary area and other related large-scale brain networks, is implicated in the pathogenesis of, and recovery from, SMA syndrome. However, intraoperative neuromonitoring of the FAT is inconsistent and poorly reproducible, leading to a high rate of postoperative SMA syndrome.

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Article Synopsis
  • The text discusses a correction made to a previously published article, specifically the one identified by DOI: 10.18632/oncotarget.15343.
  • The correction likely addresses errors or clarifications needed in the original research findings.
  • This update plays a crucial role in ensuring the accuracy and credibility of scientific literature.
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We identified target proteins modified by phenanthrenes that cause exclusive eradication of human cancer cells. The cytotoxic activity of the phenanthrenes in a variety of human cancer cells is attributed by these findings to post translational modifications of NuMA and kinesins HSET/kifC1 and kif18A. Their activity prevented the binding of NuMA to α-tubulin and kinesins in human cancer cells, and caused aberrant spindles.

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The NAP motif of activity-dependent neuroprotective protein (ADNP) enhanced memory scores in patients suffering from mild cognitive impairment and protected activities of daily living in schizophrenia patients, while fortifying microtubule (MT)-dependent axonal transport, in mice and flies. The question is how does NAP fortify MTs? Our sequence analysis identified the MT end-binding protein (EB1)-interacting motif SxIP (SIP, Ser-Ile-Pro) in ADNP/NAP and showed specific SxIP binding sites in all members of the EB protein family (EB1-3). Others found that EB1 enhancement of neurite outgrowth is attenuated by EB2, while EB3 interacts with postsynaptic density protein 95 (PSD-95) to modulate dendritic plasticity.

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