Latarcin 4a

According to the Interactive Specialization Theory, cognitive skill development is facilitated by a process of neural specialization. In line with this theory, the current study investigated whether neural specialization for phonological and semantic processing at 5-to-6 years old was predictive of growth in word reading skills 2 years later. Specifically, four regression models were estimated in which reading growth was predicted from: (1) an intercept-only model; (2) measures of semantic and phonological neural specialization; (3) performance on semantic and phonological behavioral tasks; or (4) a combination of neural specialization and behavioral performance. Results from the preregistered analyses revealed little evidence in favor of the hypothesis that early semantic and phonological skills are predictive of growth in reading. However, results from the exploratory analyses, which included a larger sample, added age at Time 1 as a covariate, and investigated relative growth in reading, demonstrated decisive evidence that variability in phonological processing is predictive of reading growth. The best fitting model included both measures of specialization within the posterior superior temporal gyrus (pSTG) and behavioral performance. This work provides important evidence in favor of the Interactive Specialization Theory and, more specifically, for the role of phonological neural specialization in the development of early word reading skills.

Maturity-onset diabetes of the young (MODY) is a group of monogenic disorders characterized by autosomal dominantly inherited non-insulin dependent form of diabetes classically presenting in adolescence or young adults before the age of 25 years. MODY is a rare cause of diabetes (1% of all cases) and is frequently misdiagnosed as Type 1 diabetes (T1DM) or Type 2 diabetes (T2DM). A precise molecular diagnosis is essential because it leads to optimal treatment of the patients and allows early diagnosis for their asymptomatic family members. Mutations in the glucokinase (GCK) (MODY 2) and hepatocyte nuclear factor (HNF)1A/4A (MODY 3 and MODY 1) genes are the most common causes of MODY. GCK mutations cause a mild, asymptomatic, and stable fasting hyperglycemia usually requiring no specific treatment. However, mutations in the HNF1A and HNF4A cause a progressive pancreatic β-cell dysfunction and hyperglycemia that can result in microvascular complications. Sulfonylureas are effective in these patients by acting on adenosine triphosphate (ATP)-sensitive potassium channels, although insulin therapy may be required later in life. Mutations in the HNF1B (MODY 5) is associated with pancreatic agenesis, renal abnormalities, genital tract malformations, and liver dysfunction. Compared to MODY 1, 2, 3, and 5, the remaining subtypes of MODY have a much lower prevalence. In this review, we summarize the main clinical and laboratory characteristics of the common and rarer causes of MODY.