instruction:
Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
question:
Context: Genetic haploinsufficiency of SYNGAP1/Syngap1 commonly occurs in developmental brain disorders, such as intellectual disability, epilepsy, schizophrenia, and autism spectrum disorder. Thus, studying mouse models of Syngap1 haploinsufficiency may uncover pathologic developmental processes common among distinct brain disorders.', 'A Syngap1 haploinsufficiency model was used to explore the relationship between critical period dendritic spine abnormalities, cortical circuit assembly, and the window for genetic rescue to understand how damaging mutations disrupt key substrates of mouse brain development.', 'Syngap1 mutations broadly disrupted a developmentally sensitive period that corresponded to the period of heightened postnatal cortical synaptogenesis. Pathogenic Syngap1 mutations caused a coordinated acceleration of dendrite elongation and spine morphogenesis and pruning of these structures in neonatal cortical pyramidal neurons. These mutations also prevented a form of developmental structural plasticity associated with experience-dependent reorganization of brain circuits. Consistent with these findings, Syngap1 mutant mice displayed an altered pattern of long-distance synaptic inputs into a cortical area important for cognition. Interestingly, the ability to genetically improve the behavioral endophenotype of Syngap1 mice decreased slowly over postnatal development and mapped onto the developmental period of coordinated dendritic insults.
Answer: Pathogenic Syngap1 mutations have a profound impact on the dynamics and structural integrity of pyramidal cell postsynaptic structures known to guide the de novo wiring of nascent cortical circuits. These findings support the idea that disrupted critical periods of dendritic growth and spine plasticity may be a common pathologic process in developmental brain disorders.
answer:
Does syngap1 haploinsufficiency damage a postnatal critical period of pyramidal cell structural maturation linked to cortical circuit assembly?

question:
Context: Complications after immediate breast reconstruction pose a significant challenge to the reconstructive surgeon. Known risk factors include smoking, obesity, age, and adjuvant oncologic therapies. Less is known about the association between axillary lymph node dissection (ALND) and the development of postoperative complications.', 'We conducted a retrospective study of all patients who underwent immediate breast reconstruction after mastectomy at our institution over a 10-year period. Our outcome was an occurrence of a major complication within 90 days postoperatively. For each patient, we recorded data on demographics, smoking status, pertinent medical history, reconstruction type, adjuvant chemotherapy and radiation, tumor pathology, and whether an ALND was performed. Odds ratios (OR) were calculated to estimate the risk of a complication if an ALND was performed.', 'One hundred eighty-four women, with 270 surgically treated breasts, were identified as having mastectomy with immediate reconstruction between 2002 and 2012. Mean age was 49.4 years (range, 25-84 years). There were 71 mastectomies with ALND performed, with 22 complications, and 199 mastectomies without ALND, with 20 complications (31% complication rate vs 10%, respectively; OR, 3.84; P < 0.001). When adjusted for reconstruction type, smoking history, obesity, age, presence of invasive disease, chemotherapy, and radiation therapy, the OR for complications was 3.49 (P < 0.01). The most common complication was infection in both groups.
Answer: Mastectomy with ALND is associated with a 3-fold increase in risk of major complications in women undergoing immediate breast reconstruction, even after adjustment for known risk factors and confounders. Further studies are warranted to elucidate how ALND leads to these complications and what measures can reduce their occurrence.
answer:
Does axillary Lymph Node Dissection be a Risk Factor for Major Complications After Immediate Breast Reconstruction?

question:
Context: Developmental dyslexia (DD) is a complex heritable condition associated with impairments in multiple neurocognitive domains. Substantial heritability has been reported for DD and related phenotypes, and candidate genes have been identified. Recently, a candidate gene for human cognitive processes, that is, GRIN2B, has been found to be associated significantly with working memory in a German DD sample. In this study, we explored the contribution of six GRIN2B markers to DD and key DD-related phenotypes by association analyses in a sample of Italian nuclear families. Moreover, we assessed potential gene-by-environment interactions on DD-related phenotypes.', 'We carried out a family-based association study to determine whether the GRIN2B gene influences both DD as a categorical trait and its related cognitive traits in a large cohort of 466 Italian nuclear families ascertained through a proband affected by DD. Moreover, we tested the role of the selected GRIN2B markers and a set of commonly described environmental moderators using a test for GE interaction in sib pair-based association analysis of quantitative traits in 178 Italian nuclear families.', 'Evidence for a significant association was found with the categorical diagnosis of DD, performance intelligence quotient, phonemic elision, and auditory short-term memory. No significant gene-by-environment effects were found.
Answer: Our results add further evidence in support of GRIN2B contributing toward DD and deficits in DD. More specifically, our data support the view that GRIN2B influences DD as a categorical trait and its related quantitative phenotypes, thus shedding further light on the etiologic basis and the phenotypic complexity of this disorder.
answer:
Does gRIN2B mediate susceptibility to intelligence quotient and cognitive impairments in developmental dyslexia?