Background: Several  studies  have  shown  a  genetic  role  in  the  pathogenesis  of   many  childhood  psychiatric  disorders.  The  most  common  childhood  psychiatric   disorder  is  the  attention  deficit  hyperactivity  disorder  (ADHD)  and  some  reports   showed  the  co-­occurance  in  ADHD  children  and  Autism  Spectrum  Disorders  (ASD).   Many  investigators  focused  their  attention  on  polymorphisms  affecting  gene  regions   coding  for  dopamine  receptors.  In  this  study  we  evaluate  the  association  of  three   single-­nucleotide  polymorphisms  (SNPs)  with  clinically  significant  level  of  autistic   symptoms  among  children  with  ADHD. Methods: We  enrolled  150  children  who   were  divided  into  four  groups:  children  with  ADHD,  children  with  ASD,  children  with   co-­occurance  of  ADHD/ASD,  and  control  subjects.  We  investigated  rs265975  C/T   (174862195C>T)  for  dopamine  receptor  D1  gene,  rs1076560  C/A  (113283688C>A)   and  rs1079597  G/A  (113296286C>T)  for  dopamine  receptor  D2  gene  utilizing   previous  DNA  extraction  and  amplification,  restriction  enzymes  that  recognized  one   of  two  allelic  variants. Results: Our  results  demonstrated  that  homozygosis  T/T  for   rs265975  had  a  lower  frequency  in  ADHD  patients  compared  to  other  groups,whereas  small  differences  were  seen  in  heterozygosis  C/T.  Both  heterozygosis  C/A   for  rs1076560  and  heterozygosis  G/A  for  rs1079597  showed  higher  frequency  in   ASD  group  with  respect  to  control  children  and  ADHD  patients,  whereas  in   ADHD/ASD  group  a  ratio  3:1  vs  unaffected  people  was  seen.  The  same  trend,  but   with  slight  differences,  was  observed  in  homozygosis  A/A  for  rs1076560  and   rs1079597. Conclusions: These  preliminary  data  pointing  to  differences  between   ADHD/ASD  and  other  groups  must  be  confirmed  and  encourage  us  to  enlarge  our   study  populations.

Current evidence indicates that periodontal disease is frequently due to inappropriate levels of gingival granulocyte functions. Reason of this failure may be the toxic effects of a number of local or systemic exogenous factors, capable of spreading through the gingival crevice environment, and strongly conditioning the granulocyte activities. The wide list includes bacteria and granulotoxic products, hedonistic drugs (mainly tobacco), and chemotherapeutic agents (especially antimicrobials used for preventing or reducing the accumulation of dental plaque). Almost always, their presence induces a time- and/or dose-dependent toxicity.

BACKGROUND: It is not known whether antibiotic therapy for lung disease in cystic fibrosis (CF) has an influence on circulating polymorphonuclear neutrophil (PMN) function and apoptosis. PATIENTS AND METHODS: Blood PMNs were obtained from 14 CF patients before and after antibiotic treatment for an acute exacerbation, and from 10 healthy controls. PMNs were evaluated for production of reactive oxygen species (ROS) by spectrophotometry, of cytokines in the conditioned medium by ELISA, and apoptotic response by cytofluorimetry. RESULTS: ROS and interleukin (IL)-8 were produced at higher levels by CF PMNs pre-therapy than control PMNs under basal conditions. IL-8 levels further increased after therapy. Early apoptotic response was higher in CF PMNs pre-therapy than in control PMNs, and this pattern did not change after antibiotic treatment. CONCLUSIONS: Circulating PMNs are primed in CF acute patients. Further studies are needed to consider PMN-produced IL-8 as a biomarker to evaluate response to antibiotic therapy in CF patients.

Accumulating evidence shows that chronic inflammation is associated to increased risk of cancer. An inflammatory component is present also in the microenvironment of tumours epidemiologically unrelated to inflammation. Extensive investigations over the past decade have uncovered many of the important mechanistic pathways underlying cancer-related inflammation. Pathways linking inflammation and cancer have been identified: an intrinsic one (driven by genetic events that cause neoplasia) and an extrinsic one (driven by inflammatory conditions which predispose to cancer). Smouldering inflammation is a component of the tumour microenvironment and is a recognized hallmark of cancer. Key orchestrators at the intersection of the intrinsic and extrinsic pathways include transcription factors (e.g. Nuclear Factor kappa-B, NFkB) that modulate the inflammatory response through soluble mediators (cytokines, chemokines) and cellular components (e.g. tumor-associated macrophages), promoting tumorige-nesis. NFkB aids in the proliferation and survival of malignant cells, promotes angiogenesis and metastasis, subverts adaptive immunity, and alters responses to hormones and chemotherapeutic agents. Emerging evidence also suggests that persistent inflammation promotes genetic instability. Thus, cancer-related inflammation represents a target for innovative diagnostic and therapeutic strategies.

The gram-positive pathogen Streptococcus pneumoniae is the most common cause of community-acquired pneumonia and is responsible for high morbidity and mortality worldwide. A major feature of pneumococcal pneumonia is an abundant neutrophil infiltration. In this work we observed that the R6 nonencapsulated S. pneumoniae strain induced a higher oxidative burst in neutrophils compared with its capsulated progenitor D39, by triggering neutrophil NADPH oxidase to produce more reactive oxygen intermediates (ROI) and by interfering with the neutrophil kinase signalling pathway. In addition, we evaluated the possibility that the capsule, lacking in R6 but present in D39, could modulate the S. pneumoniaeinduced neutrophil respiratory burst. In this respect, three knock-out isogenic mutants (D39DCPS2E, D39DCPS-R6 and R6DCPS-R6) that were unable to synthesize the capsule, were tested for their capability of inducing the release of neutrophil-ROIs. The results indicate that the mutants behaved similarly to their wild-type parental strains in enhancing respiratory burst activity, suggesting that the capsule itself is not directly involved in modulating the neutrophil oxidative burst induced by S. pneumoniae, but that other genetic differences between D39 and R6 present elsewhere in the genome could be responsible for these mechanisms.

Survivin (SVV) is a protein that belongs to the inhibitor of apoptosis proteins (IAP) family and is involved in the G2/M phase progression of the cell cycle as a spindle-associated molecule. The biological features of this protein are well documented and its activity appears to be involved in mitochondria-dependent and -independent antiapoptotic pathways. Overexpression of SVV at the transcriptional and translational level has been associated with cancer, a multifactorial disorder in which the occurrence of a -31G to C polymorphism in the promoter region may significantly contribute to the development of this pathology. To verify this hypothesis, the occurrence of a single nucleotide polymorphism (SNP) in cis-acting cell cycle-dependent elements (CDEs) and in cell cycle homology regions (CHRs) of the survivin TATA-less promoter was investigated. A total of 23 oral squamous cell carcinoma (OSCC) cell lines and normal epithelium-derived normal human epidermal keratinocyte (NHEK) cell lines were analyzed by RFLP and direct DNA sequencing of their promoter region. Furthermore, survivin expression at the transcriptional and translational levels was evaluated in these cells by RT-PCR and Western blotting, respectively. The findings indicate that the presence of a G or C allele is not directly correlated to survivin expression, at the mRNA or at the protein level, at least in the OSCC lines analyzed in this study.