Chemosensory Function in Burning Mouth Syndrome a Comparative Cross-Sectional Study

Taste and smell are considered to be functions that contribute to the maintenance of good nutritional status. The present study evaluates taste and smell function in patients with burning mouth syndrome (BMS) versus a control group. A cross-sectional study was made of 36 consecutive patients with BMS and 56 healthy patients. Smell was assessed using the Sniffin’ Sticks test, while taste was evaluated with Taste Strips. Oral quality of life was assessed with the Oral Health Impact Profile-14 (OHIP-14), and the severity of dry mouth with the Thompson Xerostomia Inventory. The patients with BMS had a mean age of 60.4 ± 10.5 years, while the controls had a mean age of 61.3 ± 19 years. No significant differences in smell were recorded between the two groups. In contrast, significant differences in taste function were observed between the patients with BMS and the controls. In the patients with BMS, 44.4% suffered taste alterations compared with the 3.4% healthy controls. Further studies in such patients are needed to allow improved management of the chemosensory problems, mouth dryness, and oral health-related quality of life in BMS.     

Food quality,effects on health and sustainability today: a model case report

The Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico is a five-century institution that, besides the unique clinical role in the center of Milan, may rely on benefactor donations such as fields and farming houses not far from the city, for a total of 8500?ha, all managed by the “Sviluppo Ca’ Granda’ Foundation”. Presently, the main products of these fields are represented by rice and cow’s milk. During the latest years, farmers and managers have developed a model of sustainable food production, with great attention to the product quality based on compositional analysis and functional nutritional characteristics. This experience represents a new holistic model of food production and consumption, taking great care of both sustainability and health.     

First year growth among very low birth weight infants

Aim: The aim of this study was to describe first‐year growth among very low birth weight infants and the effect of growth restriction at hospital discharge on first year growth. Method: Anthropometric measures and background information for 118 very low birth weight infants were collected from medical records. Z‐scores were calculated based on recent Norwegian growth references. Results: Significant catch‐up growth for weight and length was observed during the first year with mean z‐score change (SD) of 0.40 (1.05) and 1.01 (1.25) respectively. However, the very low birth weight infants remained lighter and shorter than full‐term peers until 12 months corrected age with mean z‐score of ?0.93 (1.09) and ?0.48 (1.06) respectively. Head circumference followed a normal growth pattern after 2 months. Infants discharged from hospital as growth restricted had increased catch‐up in weight and length, but remained smaller than infants not subjected to early growth restriction and full‐term peers. Multiple regression showed that weight below the 10th percentile at discharge is important for weight and length during the first year of life. Conclusion: Very low birth weight infants showed catch‐up growth during the first year, but their weight and length remained less than full‐term peers. Growth deficiencies were more pronounced among infants subjected to early growth restriction, despite increased catch‐up growth.     

Polymerase chain reaction-based identification of <Emphasis Type="Italic">Plasmodium</Emphasis> (<Emphasis Type="Italic">Huffia</Emphasis>) <Emphasis Type="Italic">elongatum</Emphasis>, with remarks on species identity of haemosporidian lineages deposited in GenBank

Numerous lineages of avian malaria parasites of the genus Plasmodium have been deposited in GenBank. However, only 11 morphospecies of Plasmodium have been linked to these lineages. Such linking is important because it provides opportunities to combine the existing knowledge of traditional parasitology with novel genetic information of these parasites obtained by molecular techniques. This study linked one mitochondrial cytochrome b (cyt b) gene lineage with morphospecies Plasmodium (Huffia) elongatum, a cosmopolitan avian malaria parasite which causes lethal disease in some birds. One species of Plasmodium (mitochondrial cyt b gene lineage P-GRW6) was isolated from naturally infected adult great reed warblers (Acrocephalus arundinaceus) and inoculated to one naive juvenile individual of the same host species. Heavy parasitaemia developed in the subinoculated bird, which enabled identification of the morphospecies and deposition of its voucher specimens. The parasite of this lineage belongs to P. elongatum. Illustrations of blood stages of this parasite are given. Other lineages closely related to P. elongatum were identified. The validity of the subgenus Huffia is supported by phylogenetic analysis. Mitochondrial cyt b gene lineages, with GenBank accession nos. AF069611 and AY733088, belong to Plasmodium cathemerium and P. elongatum, respectively; these lineages have been formerly attributed to P. elongatum and P. relictum, respectively. Some other incorrect species identifications of avian haematozoa in GenBank have been identified. We propose a strategy to minimise the number of such mistakes in GenBank in the future.     

Activation of the unfolded protein response by deltaF508 CFTR

Environmental insults and misfolded proteins cause endoplasmic reticulum (ER) stress and activate the unfolded protein response (UPR). The UPR decreases endogenous cystic fibrosis transmembrane conductance regulator (CFTR) mRNA levels and protein maturation efficiency. Herein, we investigated the effects of the folding-deficient deltaF508 CFTR on ER stress induction and UPR activation. For these studies, we developed and characterized stable clones of Calu3deltaF cells that express different levels of endogenous wild-type (WT) and recombinant deltaF508 CFTR. We also present a novel RT-PCR-based assay for differential quantification of wild-type CFTR mRNA in the presence of deltaF508 CFTR message. The assay is based on a TaqMan minor groove binding (MGB) probe that recognizes a specific TTT sequence (encoding phenylalanine at position 508 in human CFTR). The MGB probe is extremely specific and sensitive to changes in WT CFTR message levels. In RNA samples that contain both WT and deltaF508 CFTR mRNAs, measurement of WT CFTR mRNA levels (using the MGB probe) and total CFTR mRNA (using commercial primers) allowed us to calculate deltaF508 CFTR mRNA levels. The results indicate that overexpression of deltaF508 CFTR causes ER stress and activates the UPR. UPR activation precedes a marked decrease in endogenous WT CFTR mRNA expression. Furthermore, polarized airway epithelial cell lines are important tools in cystic fibrosis research, and herein we provide an airway epithelial model to study the biogenesis and function of WT and deltaF508 CFTR expressed within the same cell.     

Surveying germline genomic landscape of breast cancer

The recent large genotyping studies have identified a new repertoire of breast cancer susceptibility genes and loci which are characterized by common risk alleles and low relative risks. Because of these properties, these loci explain a much larger proportion of the etiology of the particular cancers, described by the population attributable fraction (PAF), than of their familial risks. PAF is particularly suitable for ‘genomic landscaping’ because it defines the proportion of breast cancer explained by the variant under study. The joint PAF for the previously described high-penetrance alleles is about 1%, for moderate-penetrance alleles it is 1.5% and for low-penetrance susceptibility alleles it is 58%. The evidence appears compelling in pointing to the remarkably high population impacts of the recently described heritable loci compared to the ‘classical’ high-penetrance genes.     

Bortezomib‐induced peripheral neuropathy: A genome‐wide association study on multiple myeloma patients

The proteasome‐inhibitor bortezomib was introduced into the treatment of multiple myeloma more than a decade ago. It is clinically beneficial, but peripheral neuropathy (PNP) is a side effect that may limit its use in some patients. To examine the possible genetic predisposing factors to PNP, we performed a genome‐wide association study on 646 bortezomib‐treated German multiple myeloma patients. Our aim was to identify genetic risk variants associated with the development of PNP as a serious side effect of the treatment. We identified 4 new promising loci for bortezomib‐induced PNP at 4q34.3 (rs6552496), 5q14.1 (rs12521798), 16q23.3 (rs8060632), and 18q21.2 (rs17748074). Even though the results did not reach genome‐wide significance level, they support the idea of previous studies, suggesting a genetic basis for neurotoxicity. The identified single nucleotide polymorphisms map to genes or next to genes involved in the development and function of the nervous system (CDH13, DCC, and TENM3). As possible functional clues, 2 of the variants, rs12521798 and rs17748074, affect enhancer histone marks in the brain. The rs12521798 may also impact expression of THBS4, which affects specific signal trasduction pathways in the nervous system. Further research is needed to clarify the mechanism of action of the identified single nucleotide polymorphisms in the development of drug‐induced PNP and to functionally validate our in silico predictions.     

Survival in breast cancer is familial

Several earlier studies have assessed survival in breast cancer based on familial risk of this disease. The results have been conflicting and suggest that the risk and prognostic factors of cancer are largely distinct. As a novel concept, we searched for familial clustering of survival, i.e., concordance of survival among family members. We used the nation-wide Swedish Family-Cancer Database to estimate hazard ratios (HRs) for cause-specific and overall survival in invasive breast cancer. HR shows the probability of death in the study group compared the reference group. The study covered 1277 mother-daughter pairs with familial breast cancer. Their median follow-up times for survival ranged from 96 to 122 months. When the survival in daughters was analyzed according to the mothers' length of survival, there was a concordance of prognosis. The HR was 0.65 in daughters whose mothers had survived > or = 120 months compared to daughters whose mothers had survived less than 36 months (P-value for trend 0.02). When the analysis was reversed and HRs were derived for mothers, the results were essentially similar (P-value for trend 0.02). The survival did not differ between patients with familial or sporadic breast cancer. The results are consistent in showing that both good and poor survival in breast cancer aggregates in families, which is a novel population-level finding for any cancer. The consistency of the results suggests that the prognosis in breast cancer is in part heritable which is likely to be explained by yet unknown genetic mechanisms.