Molecular profiling refines minimal residual disease‐based prognostic assessment in adults with Philadelphia chromosome‐negative B‐cell precursor acute lymphoblastic leukemia

Minimal residual disease (MRD) assessment is an essential tool in contemporary acute lymphoblastic leukemia (ALL) protocols, being used for therapeutic decisions such as hematopoietic stem cell transplantation in high‐risk patients. However, a significant proportion of adult ALL patients with negative MRD still relapse suggesting that other factors (ie, molecular alterations) must be considered in order to identify those patients with high risk of disease progression. We have identified partial IKZF1 gene deletions and CDKN2A/B deletions as markers of disease recurrence and poor survival in a series of uniformly treated adolescent and adult Philadelphia chromosome‐negative B‐cell progenitor ALL patients treated according to the Programa Español de Tratamientos en Hematología protocols. Importantly, CDKN2A/B deletions showed independent significance of MRD at the end of induction, which points out the need for treatment intensification in these patients despite being MRD‐negative after induction therapy.     

Bilateral bifid mandibular condyle: case report and literature review

Bifid mandibular condyle is an infrequent and normally asymptomatic morphological alteration of the mandibular condyle. Although the underlying cause is not clear, a number of theories have been proposed, including teratogenic effects in the embryo, vascular alterations during condyle development, and condylar remodeling following fracture. Since Schier first described this anomaly in 1948 in live individuals, further cases have been documented in the literature. We present a new case of bilateral bifid condyle. The disorder was asymptomatic and constituted a casual finding in a young male presenting for the surgical extraction of two impacted molars.     

Familiarity and face emotion recognition in patients with schizophrenia

Objective

To assess the emotion recognition in familiar and unknown faces in a sample of schizophrenic patients and healthy controls.

Methods

Face emotion recognition of 18 outpatients diagnosed with schizophrenia (DSM-IVTR) and 18 healthy volunteers was assessed with two Emotion Recognition Tasks using familiar faces and unknown faces. Each subject was accompanied by 4 familiar people (parents, siblings or friends), which were photographed by expressing the 6 Ekman’s basic emotions. Face emotion recognition in familiar faces was assessed with this ad hoc instrument. In each case, the patient scored (from 1 to 10) the subjective familiarity and affective valence corresponding to each person.

Results

Patients with schizophrenia not only showed a deficit in the recognition of emotions on unknown faces (p = .01), but they also showed an even more pronounced deficit on familiar faces (p = .001). Controls had a similar success rate in the unknown faces task (mean: 18 +/− 2.2) and the familiar face task (mean: 17.4 +/− 3). However, patients had a significantly lower score in the familiar faces task (mean: 13.2 +/− 3.8) than in the unknown faces task (mean: 16 +/− 2.4; p < .05). In both tests, the highest number of errors was with emotions of anger and fear. Subjectively, the patient group showed a lower level of familiarity and emotional valence to their respective relatives (p < .01).

Conclusions

The sense of familiarity may be a factor involved in the face emotion recognition and it may be disturbed in schizophrenia.     

A switch from inter‐ocular to inter‐hemispheric suppression following monocular deprivation in the rat visual cortex

Binocularity is a key property of primary visual cortex (V1) neurons that is widely used to study synaptic integration in the brain and plastic mechanisms following an altered visual experience. However, it is not clear how the inputs from the two eyes converge onto binocular neurons, and how their interaction is modified by an unbalanced visual drive. Here, using visual evoked potentials recorded in the juvenile rat V1, we report evidence for a suppressive mechanism by which contralateral eye activity inhibits responses from the ipsilateral eye. Accordingly, we found a lack of additivity of the responses evoked independently by the two eyes in the V1, and acute silencing of the contralateral eye resulted in the enhancement of ipsilateral eye responses in cortical neurons. We reverted the relative cortical strength of the two eyes by suturing the contralateral eye shut [monocular deprivation (MD)]. After 7 days of MD, there was a loss of interocular suppression mediated by the contralateral, deprived eye, and weak inputs from the closed eye were functionally inhibited by interhemispheric callosal pathways. We conclude that interocular suppressive mechanisms play a crucial role in shaping normal binocularity in visual cortical neurons, and a switch from interocular to interhemispheric suppression represents a key step in the ocular dominance changes induced by MD. These data have important implications for a deeper understanding of the key mechanisms that underlie activity‐dependent rearrangements of cortical circuits following alteration of sensory experience.