A Novel t(10;22) Translocation Harboring an IGL Gene Deletion in a CLL Patient Transforming to B-PLL with 1q Gain.

We report on a rare case of B-cell prolymphocytic leukemia (B-PLL) in a patient with a history of chronic lymphocytic leukemia (CLL) that showed a novel translocation t(10;22)(q21;q11.22) and an interstitial deletion of 11q14.1-q23.

Skin lesion in a patient after hematopoietic stem cell transplant.

We present a case of a 61-year-old Caucasian woman who was hospitalized with fever on day 176 after a matched unrelated stem cell transplant for acute myelogenous leukemia. She developed hemorrhagic bullae on the skin of her right thigh, and both blood cultures and skin biopsy confirmed Fusarium proliferatum. Despite antifungal therapy, her condition worsened and she died while on comfort-only measures.

Activation of extracellular regulated kinase and mechanistic target of rapamycin pathway in focal cortical dysplasia.

Neuropathology of resected brain tissue has revealed an association of focal cortical dysplasia (FCD) with drug-resistant epilepsy (DRE). Recent studies have shown that the mechanistic target of rapamycin (mTOR) pathway is hyperactivated in FCD as evidenced by increased phosphorylation of the ribosomal protein S6 (S6) at serine 240/244 (S(240/244) ), a downstream target of mTOR. Moreover, extracellular regulated kinase (ERK) has been shown to phosphorylate S6 at serine 235/236 (S(235/236) ) and tuberous sclerosis complex 2 (TSC2) at serine 664 (S(664) ) leading to hyperactive mTOR signaling.

mTOR inhibition suppresses established epilepsy in a mouse model of cortical dysplasia.

Objective: Hyperactivation of the mechanistic target of rapamycin (mTOR; also known as mammalian target of rapamycin) pathway has been demonstrated in human cortical dysplasia (CD) as well as in animal models of epilepsy. Although inhibition of mTOR signaling early in epileptogenesis suppressed epileptiform activity in the neuron subset-specific Pten knockout (NS-Pten KO) mouse model of CD, the effects of mTOR inhibition after epilepsy is fully established were not previously examined in this model. Here, we investigated whether mTOR inhibition suppresses epileptiform activity and other neuropathological correlates in adult NS-Pten KO mice with severe and well-established epilepsy.

Rapamycin reverses status epilepticus-induced memory deficits and dendritic damage.

Cognitive impairments are prominent sequelae of prolonged continuous seizures (status epilepticus; SE) in humans and animal models. While often associated with dendritic injury, the underlying mechanisms remain elusive. The mammalian target of rapamycin complex 1 (mTORC1) pathway is hyperactivated following SE.

Repression of calcitonin gene-related peptide expression in trigeminal neurons by a Theobroma cacao extract.

Ethnopharmacological Relevance: Cocoa bean preparations were first used by the ancient Maya and Aztec civilizations of South America to treat a variety of medical ailments involving the cardiovascular, gastrointestinal, and nervous systems. Diets rich in foods containing abundant polyphenols, as found in cocoa, underlie the protective effects reported in chronic inflammatory diseases. Release of calcitonin gene-related peptide (CGRP) from trigeminal nerves promotes inflammation in peripheral tissues and nociception.

Neuron-glia signaling in trigeminal ganglion: implications for migraine pathology.

Objective: The goal of this study was to investigate neuronal-glial cell signaling in trigeminal ganglia under basal and inflammatory conditions using an in vivo model of trigeminal nerve activation.

Background: Activation of trigeminal ganglion nerves and release of calcitonin gene-related peptide (CGRP) are implicated in the pathology of migraine. Cell bodies of trigeminal neurons reside in the ganglion in close association with glial cells.