Molar-Incisor Hypomineralisation: Severity, caries and hypersensitivity.

Objectives: To investigate distribution of affected teeth and severity of molar-incisor hypomineralisation (MIH) in 8-9-year-old children. A second aim was to study association between severity of MIH and hypersensitivity, caries, and affection of incisors and second primary molars (SPM).

Methods: A total of 3013 children in one age cohort participated in a cross-sectional study, of which 851 children were diagnosed with MIH.

Molar-incisor hypomineralisation in Norwegian children: Prevalence and associated factors.

This study investigated the prevalence and associations of molar-incisor hypomineralisation (MIH) in 8-9 year-old children in Oslo. A total of 3013 children in one age cohort participated in the study during their regular dental examination at the Public Dental Service. Hypomineralised enamel defects were recorded according to the European Academy of Paediatric Dentistry criteria for MIH.

Molar incisor malformation in six cases: description and diagnostic protocol.

Objective: The term molar-incisor malformation (MIM) has recently been presented in the scientific literature, where it is described as a condition with localized impaired root development. Here we present 6 recently discovered cases referred to our departments.

Study Design: The patients were enrolled in the study after referral and were examined clinically and radiologically.

The TGFβ-SMAD3 pathway inhibits IL-1α induced interactions between human pancreatic stellate cells and pancreatic carcinoma cells and restricts cancer cell migration.

Background: The most abundant cells in the extensive desmoplastic stroma of pancreatic adenocarcinomas are the pancreatic stellate cells, which interact with the carcinoma cells and strongly influence the progression of the cancer. Tumor stroma interactions induced by IL-1α/IL-1R1 signaling have been shown to be involved in pancreatic cancer cell migration. TGFβ and its receptors are overexpressed in pancreatic adenocarcinomas.

Lysophosphatidic acid induces both EGFR-dependent and EGFR-independent effects on DNA synthesis and migration in pancreatic and colorectal carcinoma cells.

Lysophosphatidic acid (LPA) is a small glycerophospholipid ubiquitously present in tissues and plasma. It acts through receptors belonging to the G-protein-coupled receptor (GPCR) family, is involved in several biological processes, and is strongly implicated in different cancers. In this paper, we have investigated the effects of LPA on DNA synthesis and migration in a panel of pancreatic and colon cancer cells, with particular focus on the involvement of the epidermal growth factor (EGF) receptor (EGFR) in LPA-induced signaling.