Inhibition of nuclear factor-kappaB DNA binding by organoselenocyanates through covalent modification of the p50 subunit

Most known chemopreventive agents including certain selenium compounds suppress the activation of the nuclear factor kappaB (NF-kappaB), but the mechanisms remain largely elusive. Toward this end, we initially showed that the inhibition of NF-kappaB DNA binding by benzyl selenocyanate (BSC) and 1,4-phenylenebis(methylene)selenocyanate (p-XSC) was reversed by the addition of DTT; this suggests the formation of DTT-reducible selenium-sulfur bonds between selenocyanate moieties and cysteine residues in NF-kappaB (p50) protein. Furthermore, the inhibitory effect of selenocyanates on NF-kappaB was not altered in the presence of physiologic level of reduced glutathione (1 mmol/L), suggesting that selenocyanates can also inhibit NF-kappaB in vivo. Using both matrix-assisted laser desorption/ionization-time of flight and tandem mass spectrometry fragmentation, we showed for the first time that the Cys(62) residue in the active site of NF-kappaB (p50) protein was modified by BSC through the formation of a selenium-sulfur bond. In addition, p-XSC-bound NF-kappaB (p50) protein was also detected by a radiotracer method. To provide further support, molecular models of both BSC and p-XSC positioned in the DNA binding pocket of the p50 were constructed through the covalent modification of Cys(62); the models reveal that DNA substrate could be hindered to enter its DNA binding region. This study shows for the first time that BSC and p-XSC may exert their chemopreventive activity, at least in part, by inhibiting NF-kappaB through covalent modification of Cys(62) of the p50 subunit of NF-kappaB.     

Streptococcus mutans and Streptococcus sobrinus detection by Polymerase Chain Reaction and their relation to dental caries in 12 and 15 year-old schoolchildren in Valencia (Spain)

A cross-sectional study was carried out to determine the prevalence of Streptococcus mutans and Streptococcus sobrinus and the association of the two in a random sample (n=614) of the child population of the region of Valencia (Spain). Saliva samples were analyzed by the quantitative polymerase chain reaction (PCR) method to study the relation of these bacteria to caries prevalence and the DMFT index.The prevalence of S. mutans was 35.4% at age 12 and 22.9% at age 15, that of S. sobrinus 18.9% and 8.4% and that of the S. mutans-S. sobrinus association 18.2% and 6.8% respectively. At both 12 and 15 years of age, the caries prevalence rates were lower in the Streptococcus-free group of children (37.6% and 48.5% respectively) and higher in the S.mutans-only group (67.3% and 74.0%). At the age of 12, the DMFT index was significantly higher in the mutans-only carriers (2.1) than in the Streptococcus-free and S. mutans-S. sobrinus association groups (both 0.9). At the age of 15, the DMFT index was significantly higher in the S. mutans-S. sobrinus association (3.71) and mutans-only (3.1) carrier groups than in the Streptococcus-free group (1.4). Determination of S. mutans and S. sobrinus by real-time quantitative PCR can provide valuable information for caries risk assessment in epidemiological studies. Key words:Streptococcus mutans, Streptococcus sobrinus, polymerase chain reaction, dental caries, cross-sectional studies.     

Do the filarial lymphoedema patients’‘3 months recall’ on acute dermato‐lymphangio‐adenitis (ADLA) correlate with streptococcal serology?

Aim The aim of this study was to know the correlation of patients’ 3 months recall on acute dermato‐lymphangio‐adenitis (ADLA) with anti‐streptolysin O (ASO) serology and its application as a tool to know the burden of ADLA in the community. Methods Fifty‐nine lymphoedema (LE) patients and 27 age matched controls were clinically assessed for LE and the occurrence of ADLA during the previous 3 months was obtained by recall. After obtaining the informed consent, 2 mL of venous blood sample was collected and ASO was quantified in Olympus AU400 auto‐analyzer. Results When the results were computed as two groups, controls and LE patients with no reported ADLA and LE patients with reported ADLA (by 3 months recall), the ASO positivity and ASO titre was significantly higher in the later group (P < 0.05). When the results were computed as three groups, controls with no reported ADLA, LE patients with no reported ADLA and LE patients with reported ADLA, the ASO titre was significantly higher in LE patients reported ADLA (P < 0.05). Conclusion As ASO was measured in post‐infection phase, we relied on the ASO titre for making conclusion. Patients’ 3 months recall on ADLA correlates with the ASO titre and therefore, it could be considered as a tool to measure the burden of ADLA in the community. Multicentre community‐based studies are needed to ascertain the findings.     

Diffusion imaging in neurological disease

Diffusion-weighted imaging can be used to assess the microscopic properties of measured tissues, providing insights into the architecture of neural tissues and how they change in physiological and pathological states. Such imaging data can be readily quantified to provide numerical values of parameters that have clinical relevance, particularly in regard to cellular constituents of tumours, chemical contents of cysts, the integrity of neuronal cell bodies and myelin sheaths. Diffusion based techniques have proven to be particularly useful in investigating cerebral infarction, cerebral infections, epidermoid and other cysts, cerebral tumours, and white matter disorders. The purpose of this review is to introduce key concepts in diffusion imaging and illustrate how it may be applied to clinical practice, with particular reference to head injury.     

The impact of blue light and digital screens on the skin

Introduction

The skin is frequently subjected to a variety of environmental trauma and stress. It is unavoidably subjected to blue light due to the increased use of electronic equipment, including indoor lighting and digital gadgets like smartphones and laptops, which have a range of detrimental effects. The method of action and numerous harmful consequences of blue light on the skin are the main subjects of this review.

Materials and Methods

A literature search has been performed using PubMed, GoogleScholar and EmBase databases and an updated review on the topic has been presented.

Results

Numerous studies have shown that being exposed to blue light accelerates the aging process and produces cutaneous hyperpigmentation. It also modifies the circadian rhythm. The two main molecules that mediate cellular responses to blue light are nitric oxide (NO) and reactive oxygen species. However, the precise process is still not fully known.

Conclusion

These negative consequences may eventually cause more general skin damage, which may hasten the aging process. At times, skin protection may be crucial for protection against blue light.