Comparison of Biocompatibility of Calcium Silicate-Based Sealers and Epoxy Resin-Based Sealer on Human Periodontal Ligament Stem Cells

The aim of this study was to evaluate the biocompatibility of calcium silicate-based sealers (CeraSeal and EndoSeal TCS) and epoxy resin-based sealer (AH-Plus) in terms of cell viability, inflammatory response, expression of mesenchymal phenotype, osteogenic potential, cell attachment, and morphology, of human periodontal ligament stem cells (hPDLSCs). hPDLSCs were acquired from the premolars (n = 4) of four subjects, whose ages extended from 16 to 24 years of age. Flow cytometry analysis showed stemness of hPDLSCs was maintained in all materials. In cell viability test, AH-Plus showed the lowest cell viability, and CeraSeal showed significantly higher cell viability than others. In ELISA test, AH-Plus showed higher expression of IL-6 and IL-8 than calcium silicate-based sealers. In an osteogenic potential test, AH-Plus showed a lower expression level than other material; however, EndoSeal TCS showed a better expression level than others. All experiments were repeated at least three times per cell line. Scanning electronic microscopy studies showed low degree of cell proliferation on AH-Plus, and high degree of cell proliferation on calcium silicate-based sealers. In this study, calcium silicate-based sealers appear to be more biocompatible and less cytotoxic than epoxy-resin based sealers.     

Low literacy is associated with uncontrolled blood pressure in primary care patients with hypertension and heart disease

Objectives

To evaluate the association between low literacy and uncontrolled blood pressure (BP) and their associations with medication adherence.

Methods

Cross-sectional study of 423 urban, primary care patients with hypertension and coronary disease. The relationship between low literacy (Rapid Estimate of Adult Literacy in Medicine ≤ 44) and uncontrolled BP (≥140/90 mmHg, ≥130/80 mmHg for patients with diabetes) was evaluated by crude and adjusted logistic regression. Relationships with self-reported adherence and refill adherence were explored using adjusted linear and logistic regression.

Results

Overall, 192 (45%) subjects had low literacy and 227 (52.9%) had uncontrolled BP. Adjusting for age, gender, race, employment, education, mental status, and self-reported adherence, low literacy was associated with uncontrolled BP (OR 1.75, 95% CI 1.06–2.87). Lower self-reported adherence was associated with uncontrolled BP; the relationship between refill adherence and uncontrolled BP was not statistically significant.

Conclusion

Low literacy is independently associated with uncontrolled BP.

Practice implications

Awareness of the relationships among patient literacy, BP control, and medication adherence may guide healthcare providers as they communicate with patients.     

Permissive hypercapnia: Is there any upper limit?

A 19-year-old male presented with history of massive hemoptysis. The patient was kept on mechanical ventilation because of severe hypoxia. Lung protective ventilation with low tidal volume was given in view of very poor pulmonary compliance. During the course of treatment, the patient developed a very high CO₂ level of 373 mmHg. The patient was successfully weaned off on the 9^th day without any obvious adverse consequences.     

Toll‐like receptor 6 mediated inflammatory and functional responses of zinc oxide nanoparticles primed macrophages

Macrophages are among the most sensitive immune cells because of their phagocytic activity and are prone to become dysfunctional or not able to perform properly if nanoparticle load increases. We have previously reported that zinc oxide nanoparticles (ZNPs) induce inflammatory responses in macrophages that contribute to their death. Recognition of ZNPs by pattern recognition receptors such as toll‐like receptors (TLRs) might be a factor in the initiation of these responses in macrophages. Therefore, in this study we explored the role played by TLR6 and mitogen‐activated protein kinase (MAPKs) pathways in the inflammatory responses of macrophages during ZNPs exposure. ZNPs‐activated macrophages showed enhanced expression of activation and maturation markers (CD1d, MHC‐II, CD86 and CD71). Among various TLRs screened, TLR6 emerged as the most potent activator for ZNPs‐induced inflammatory responses. Downstream signalling proteins myeloid differentiation 88, interleukin‐1 receptor associated kinase and tumour necrosis factor receptor‐associated factor were also enhanced. On inhibiting MAPKs pathways individually, the inflammatory responses such as interleukin‐1β, interleukin‐6, tumour necrosis factor‐α, cyclooxygenase‐2 and inducible nitric oxide synthase were suppressed. TLR6 silencing significantly inhibited the pro‐inflammatory cytokine levels, reactive nitrogen species generation and inducible nitric oxide synthase expression. Also, inhibition of MAPKs in the absence of TLR6 signalling validated the link between TLR6 and MAPKs in ZNPs‐induced inflammatory responses. TLR6 was found to be co‐localized with autophagosomes. Macrophages lacking TLR6 inhibited the autophagosome marker protein‐microtubule‐associated protein1 light chain 3‐isoform II formation and phagocytosis. These results demonstrate that inflammatory responses caused by ZNPs‐activated macrophages strongly depend on TLR6‐mediated MAPK signalling.     

Neonatal Diabetes Mellitus Due to a Novel ABCC8 Gene Mutation Mimicking an Organic Acidemia

Neonatal diabetes mellitus and organic acidemias, may present with similar features like hyperglycemia, ketoacidosis and failure to thrive. A four-mo-old girl presented with diabetic ketoacidosis following a febrile respiratory illness during which high anion gap metabolic acidosis and hyperglycemia were detected. She also had hyperammonemia, which led to diagnostic uncertainty. Euglycemia was achieved with insulin injections. Genotyping revealed a homozygous novel mutation of the ABCC8 gene coding for the SUR1 subunit of the pancreatic beta cell potassium channel. Subsequently, the child was successfully transitioned to oral glibenclamide therapy. Developmental delay was noted on follow-up which raised the possibility of intermediate DEND syndrome. A possible cause for hyperammonemia in neonatal diabetes mellitus has been postulated in the discussion.