scholarly journals The role of Helicobacter pylori in the process of 43 carcinogenesis by means of dysregulation of miRNA expression

2014 ◽  
Vol 19 (6) ◽  
pp. 43-47
Author(s):  
O. F Belaia ◽  
E. V Volchkova ◽  
O. A Paevskaya ◽  
S. N Zuevskaya ◽  
Yu. V Yudina ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Intracellular Signaling ◽  
Severe Disease ◽  
Biological Significance ◽  
Cancer Of The Stomach ◽  
Increased Risk ◽  
New Directions ◽  
Stomach Adenocarcinoma ◽  
Few Data

Duodenal ulcer is associated with Helicobacter pylori almost in 90-100% of cases. Severe disease of the stomach - adenocarcinoma - is caused by infection with Helicobacter pylori in 70-90% of cases. Persons infected with this bacterium were proven statistically to be in group of the increased risk of the development of gastric cancer. Helicobacter pylori expresses a spectrum of virulence factors which cause dysregulation of intracellular signaling pathways in a host cell, that reduces the resistance to neoplastic transformation. In the review there are presented data about identified to the present time deregulated miRNAs associated with H.pylori diseases, including cancer of the stomach, and a few data on their biological significance. The growing number of studies confirming the involvement of miRNAs in various stages of carcinogenesis - from gastritis to the formation of metastases - demonstrates the importance of the new directions of the research.

scholarly journals Role of Helicobacter pylori in Upper Gastrointestinal Bleeding Among Ischemic Stroke Hospitalizations: A Nationwide Study of Outcomes

2019 ◽  
Vol 1 (3) ◽  
pp. 358-371
Author(s):  
Urvish K. Patel ◽  
Mihir Dave ◽  
Anusha Lekshminarayanan ◽  
Nidhi Patel ◽  
Abhishek Lunagariya ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Ischemic Stroke ◽  
Risk Stratification ◽  
Gastrointestinal Bleeding ◽  
Health Care Cost ◽  
Upper Gastrointestinal Bleeding ◽  
Increased Risk ◽  
H Pylori ◽  
Upper Gastrointestinal

Introduction: Helicobacter pylori (H. pylori) is a well-recognized risk factor for upper gastrointestinal bleeding (UGIB). The exposure to tissue plasminogen activator (tPA), anti-platelets, and anticoagulants increases the risk of UGIB in acute ischemic stroke (AIS) patients, the risk stratification of H. pylori infection is not known. In this retrospective cross-sectional study, we aimed to evaluate the relationship between H. pylori and GIB in patients hospitalized with AIS. Methods: In the nationwide data, hospitalization for AIS was identified by primary diagnosis using International Classification of Diseases, clinical modification (ICD-9-CM) codes. Subgroup of patients with GIB and H. pylori were identified in AIS cohort. A stepwise multivariable logistic regression model was fitted to evaluate the outcome of upper GIB and role of H. Pylori in UGIB. Results: Overall 4,224,924 AIS hospitalizations were identified, out of which 18,629 (0.44%) had UGIB and 3122 (0.07%) had H. pylori. The prevalence of H. pylori-induced UGIB among UGIB in AIS was 3.05%. The prevalence of UGIB was markedly elevated among the H. pylori infection group (18.23% vs. 0.43%; p < 0.0001) compared to the non-H. pylori group. In multivariable regression analysis, H. pylori was associated with markedly elevated odds of UGIB (aOR:27.75; 95%CI: 21.07–36.55; p < 0.0001). Conclusion: H. pylori infection had increased risk-adjusted occurrence of UGIB amongst the AIS hospitalized patients. H. pylori testing may improve risk stratification for UGIB and lower the health care cost burden in stroke hospitalization.

Preverbal skills in 8-month-old children with sex chromosome trisomies

2020 ◽  
pp. 014272372096294
Author(s):  
Laura Zampini ◽  
Tiziana Burla ◽  
Gaia Silibello ◽  
Elena Capelli ◽  
Francesca Dall’Ara ◽  
...  
Keyword(s):  
Sex Chromosome ◽  
Word Comprehension ◽  
Lexical Development ◽  
Observation Session ◽  
Number Of Children ◽  
Increased Risk ◽  
Predictive Role ◽  
Few Data ◽  
Vocal Productions

Individuals with sex chromosome trisomies (SCTs) have an increased risk of language delays and impairments. However, there are only a few data relative to their language development in early childhood. The present study aimed to investigate the preverbal skills shown by a group of 8-month-old children with SCTs to assess the presence of a possible early communicative delay. Moreover, the predictive role of early preverbal productions on later lexical development at 24 months was analysed. Twenty-six children with SCTs and 24 typically developing (TD) children participated in the study. Their use of vocal productions and gazes addressed to the communicative partner was assessed during a parent–child observation session held when the children were 8 months old. In addition, the children’s word comprehension at 8 months and their word production at 24 months were indirectly assessed by a parental report. Children’s word comprehension was similar in the two groups of children, whereas a significantly lower frequency per minute of gazes was found in children with SCTs than in TD children. A significantly lower proportion of children with SCTs showed the ability to produce babbling during the observation session, and significant differences were also found in the frequency of babbling utterances. No significant differences emerged among the subgroups of children with different types of SCTs. The predictive role of babbling on later lexical size was found in TD children but not in children with SCTs. This result could be probably explained by the small number of children in this group who could produce babbling utterances. The study leads to identify early signals of delay in the preverbal skills of children with SCTs. Early monitoring of their communicative development could help the clinicians in intervening with well-timed and targeted programmes.

scholarly journals Association of Occupational Distress and Low Sleep Quality with Syncope, Presyncope, and Falls in Workers

2021 ◽  
Vol 18 (23) ◽  
pp. 12283
Author(s):  
Nicola Magnavita ◽  
Reparata Rosa Di Prinzio ◽  
Gabriele Arnesano ◽  
Anna Cerrina ◽  
Maddalena Gabriele ◽  
...  
Keyword(s):  
Mental Health ◽  
Sleep Quality ◽  
Ad Hoc ◽  
Unknown Origin ◽  
Poor Mental Health ◽  
Occupational Performance ◽  
Increased Risk ◽  
Few Data ◽  
Health Promotion Interventions

Syncope and presyncope episodes that occur during work could affect one’s safety and impair occupational performance. Few data are available regarding the prevalence of these events among workers. The possible role of sleep quality, mental stress, and metabolic disorders in promoting syncope, presyncope, and falls in workers is unknown. In the present study, 741 workers (male 35.4%; mean age 47 ± 11 years), employed at different companies, underwent clinical evaluation and blood tests, and completed questionnaires to assess sleep quality, occupational distress, and mental disorders. The occurrence of syncope, presyncope, and unexplained falls during working life was assessed via an ad hoc interview. The prevalence of syncope, presyncope, and falls of unknown origin was 13.9%, 27.0%, and 10.3%, respectively. The occurrence of syncope was associated with an increased risk of occupational distress (adjusted odds ratio aOR: 1.62, confidence intervals at 95%: 1.05–2.52), low sleep quality (aOR: 1.79 CI 95%: 1.16–2.77), and poor mental health (aOR: 2.43 CI 95%: 1.52–3.87). Presyncope was strongly associated with occupational distress (aOR: 1.77 CI 95%: 1.25–2.49), low sleep quality (aOR: 2.95 CI 95%: 2.08–4.18), and poor mental health (aOR: 2.61 CI 95%: 1.78–3.84), while no significant relationship was found between syncope or presyncope and metabolic syndrome. These results suggest that occupational health promotion interventions aimed at improving sleep quality, reducing stressors, and increasing worker resilience might reduce syncope and presyncope events in the working population.

PTEN and Autism With Macrocepaly

2013 ◽  
Author(s):  
Craig M. Powell
Keyword(s):  
Tumor Cell ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Clinical Phenotype ◽  
Model Systems ◽  
Tumor Cell Lines ◽  
Gene Encoding ◽  
Increased Risk ◽  
The Brain

Phosphatase and Tensin homolog deleted on chromosome 10 (PTEN) is a gene encoding an intracellular signaling molecule. PTEN was originally discovered as the gene responsible for a subset of familial hamartoma (tumor) syndromes associated with increased risk for certain cancers (Nelen et al., 1997) and as a gene often mutated in human cancers and tumor cell lines (Li et al., 1997; Steck et al., 1997). More recently, mutations in PTEN have been linked genetically to the clinical phenotype of autism or developmental delay with macrocephaly (Boccone et al., 2006; Butler et al., 2005; Buxbaum et al., 2007; Goffin, Hoefsloot, Bosgoed, Swillen, & Fryns, 2001; Herman, Butter, et al., 2007; McBride et al., 2010; Orrico et al., 2009; Stein, Elias, Saenz, Pickler, & Reynolds, 2010; Varga, Pastore, Prior, Herman, & McBride, 2009; Zori, Marsh, Graham, Marliss, & Eng, 1998). This chapter examines the role of PTEN in intracellular signaling, the link between PTEN signaling pathways and other autism-related genes and signaling pathways, the genetic relationship between PTEN and autism, model systems in which effects of Pten deletion on the brain have been studied, and promising preclinical data identifying therapeutic targets for patients with autism/macrocephaly associated with PTEN mutations.

Helicobacter Pylori Infection and the Risk of Myocardial Infarction: Role of Fibrinogen and Its Genetic Control

1999 ◽  
Vol 82 (07) ◽  
pp. 14-18 ◽  
Author(s):  
Francesco Zito ◽  
Augusto Di Castelnuovo ◽  
Andria D’Orazio ◽  
Riccardo Negrini ◽  
Domenico De Lucia ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Genetic Control ◽  
Case Control Study ◽  
Case Control ◽  
Increased Risk ◽  
Confounding Variables ◽  
Control Study

SummaryThe contribution of Helicobacter pylori (HP) infection to the risk of myocardial infarction was evaluated. The role of fibrinogen and its genetic control as a possibile mechanism by which HP may influence myocardial infarction risk was explored in this context. A case-control study was performed in 101 patients with myocardial infarction and in 101 controls.HP infection was associated with an increased risk of myocardial infarction independently for confounding variables (OR 4.1, CI95: 1.8-9.4). HP infection was significantly associated with higher levels of fibrinogen, both in cases and in controls. Furthermore, there was an additive effect of HP infection and B2 allele of BclI fibrinogen poly-morphism in increasing fibrinogen levels. HP infection showed a stronger effect on the risk of myocardial infarction in B2 allele carriers (OR 7.6, CI95: 1.8-31.6) as compared to subjects carrying the B1B1 genotype (OR 3.3, CI95: 1.2-9.2).We showed that a previous HP infection is a risk factor for myocardial infarction. An increase in fibrinogen levels is a possible mechanism by which HP may act. Concomitant conditions, like a genetic predisposition in increasing fibrinogen levels, seem to further increase the effect of HP on myocardial infarction risk.

scholarly journals NSAIDs and Cardiovascular Diseases: Role of Reactive Oxygen Species

2015 ◽  
Vol 2015 ◽  
pp. 1-25 ◽  
Author(s):  
Rajeshwary Ghosh ◽  
Azra Alajbegovic ◽  
Aldrin V. Gomes
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Side Effects ◽  
Intracellular Signaling ◽  
Reactive Oxygen ◽  
Cell Types ◽  
Oxygen Species ◽  
Beneficial Effects ◽  
Increased Risk

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most commonly used drugs worldwide. NSAIDs are used for a variety of conditions including pain, rheumatoid arthritis, and musculoskeletal disorders. The beneficial effects of NSAIDs in reducing or relieving pain are well established, and other benefits such as reducing inflammation and anticancer effects are also documented. The undesirable side effects of NSAIDs include ulcers, internal bleeding, kidney failure, and increased risk of heart attack and stroke. Some of these side effects may be due to the oxidative stress induced by NSAIDs in different tissues. NSAIDs have been shown to induce reactive oxygen species (ROS) in different cell types including cardiac and cardiovascular related cells. Increases in ROS result in increased levels of oxidized proteins which alters key intracellular signaling pathways. One of these key pathways is apoptosis which causes cell death when significantly activated. This review discusses the relationship between NSAIDs and cardiovascular diseases (CVD) and the role of NSAID-induced ROS in CVD.

scholarly journals Possible Influence of Resistance to Malaria in Clinical Presentation of Rheumatoid Arthritis: Biological Significance of Natural Selection

Arthritis ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Fabio Bonilla-Abadía ◽  
Gabriel J. Tobón ◽  
Carlos A. Cañas
Keyword(s):  
Rheumatoid Arthritis ◽  
Natural Selection ◽  
Chemokine Receptors ◽  
Biological Significance ◽  
Immunological Response ◽  
Immune Reactivity ◽  
Loss Of Function ◽  
Special Group ◽  
Increased Risk

Rheumatoid arthritis (RA) is a common autoimmune disease that affects all ethnic groups. Genetic factors, mainly HLA alleles, are highly associated with increased risk to develop RA. However, there are few available data about the role of these genetic polymorphisms in the prevalence or severity of RA in the Afrodescendant population, who have evolutionarily and by natural selection developed mutations that allowed them to acquire resistance to infectious diseases like malaria. Some of the mechanisms, by which this resistance was developed as a product of natural selection, are involved in different forms of immunological response, many of them of a well-known importance in the pathophysiology of RA. This paper focuses on presenting the known mechanisms of resistance to malaria and their possible contribution to the pathophysiology of RA, including “loss-of-function” mutations, lack of expression of chemokine receptors, decrease of immune complexes clearance by asplenia, or increase of immune reactivity mediated by B cells, among other mechanisms in this special group of patients.

scholarly journals NLRP3-Inflammasome Inhibition during Respiratory Virus Infection Abrogates Lung Immunopathology and Long-Term Airway Disease Development

Viruses ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 692
Author(s):  
Carrie-Anne Malinczak ◽  
Charles F. Schuler ◽  
Angela J. Duran ◽  
Andrew J. Rasky ◽  
Mohamed M. Mire ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Severe Disease ◽  
Critical Role ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Increased Risk ◽  
Rsv Infection ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) infects most infants by two years of age. It can cause severe disease leading to an increased risk of developing asthma later in life. Previously, our group has shown that RSV infection in mice and infants promotes IL-1β production. Here, we characterized the role of NLRP3-Inflammasome activation during RSV infection in adult mice and neonates. We observed that the inhibition of NLRP3 activation using the small molecule inhibitor, MCC950, or in genetically modified NLRP3 knockout (Nlrp3−/−) mice during in vivo RSV infection led to decreased lung immunopathology along with a reduced expression of the mucus-associated genes and reduced production of innate cytokines (IL-1β, IL-33 and CCL2) linked to severe RSV disease while leading to significant increases in IFN-β. NLRP3-inflammasome inhibition or deletion diminished Th2 cytokines and inflammatory cell infiltration into the lungs. Furthermore, NLRP3 inhibition or deletion during early-life RSV infection led to reducing viral-exacerbated allergic response in a mouse model of RSV-induced allergy exacerbation. Here, we demonstrated the critical role of NLRP3-inflammasome activation in RSV immunopathology and the related long-term airway alteration. Moreover, these findings suggest the NLRP3-inflammasome as a potential therapeutic target to attenuate severe RSV disease and limit childhood asthma development.

scholarly journals Elevated D-Dimer Levels are Associated with Increased Risk of Mortality in COVID-19: A Systematic Review and Meta-Analysis

2020 ◽  
Author(s):  
Siddharth Shah ◽  
Kuldeep Shah ◽  
Siddharth B Patel ◽  
Forum S Patel ◽  
Mohammed Osman ◽  
...  
Keyword(s):  
Systematic Review ◽  
Meta Analysis ◽  
Severe Disease ◽  
Case Fatality ◽  
Inclusion Criteria ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Novel Coronavirus ◽  
D Dimer

AbstractIntroductionThe 2019 novel Coronavirus (2019-nCoV), now declared a pandemic has an overall case fatality of 2–3% but it is as high as 50% in critically ill patients. D-dimer is an important prognostic tool, often elevated in patients with severe COVID-19 infection and in those who suffered death. In this systematic review, we aimed to investigate the prognostic role of D-dimer in COVID-19 infected patients.MethodsWe searched PubMed, Medline, Embase, Ovid, and Cochrane for studies reporting admission D-dimer levels in COVID-19 patients and its effect on mortality.Results18 studies (16 retrospective and 2 prospective) with a total of 3,682 patients met the inclusion criteria. The pooled mean difference (MD) suggested significantly elevated D-dimer levels in patients who died versus those survived (MD 6.13 mg/L, 95% CI 4.16 − 8.11, p <0.001). Similarly, the pooled mean D-dimer levels were significantly elevated in patients with severe COVID-19 infection (MD 0.54 mg/L, 95% CI 0.28 − 0.8, p< 0.001). In addition, the risk of mortality was four-fold higher in patients with positive D-dimer vs negative D-dimer (RR 4.11, 95% CI 2.48 − 6.84, p< 0.001) and the risk of developing the severe disease was two-fold higher in patients with positive D-dimer levels vs negative D-dimer (RR 2.04, 95% CI 1.34 − 3.11, p < 0.001).ConclusionOur meta-analysis demonstrates that patients with COVID-19 presenting with elevated D-dimer levels have an increased risk of severe disease and mortality.

Association of interleukin-1 gene polymorphisms with gastric cancer: A meta-analysis

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 21142-21142
Author(s):  
B. Vincenzi ◽  
D. Santini ◽  
G. Patti ◽  
F. Pantano ◽  
O. Venditti ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Meta Analysis ◽  
Interleukin 1 ◽  
Strong Association ◽  
Pooled Analysis ◽  
Epidemiologic Studies ◽  
Caucasian Population ◽  
Increased Risk ◽  
Stomach Adenocarcinoma

21142 Introduction: Previous studies on the association between interleukin-1 (IL-1) genetic polymorphisms and the risk of gastric cancer have produced conflicting results. The purpose of this study was to examine the association between IL-1 genotype and gastric cancer by systematically reviewing the original studies. Materials and Methods: We searched the MEDLINE, CENTRAL, and PubMed databases (last research performed on July 2005) and reviewed cited references to identify relevant studies. Search key words were: gastric cancer (OR stomach cancer OR gastric adenocarcinoma OR stomach adenocarcinoma) and IL-1 (OR IL1). The literature review identified 23 titles that met the search criteria. Data from 15 articles that investigated the association between any of IL-1B-511 and IL-1B-31 polymorphisms and gastric cancer met the inclusion criteria, and they were included in the meta-analysis. Eight studies evaluated the role of IL-1B-511, four the role of IL- 1B-31 and three investigated both IL-1B-511 and IL-1B-31. Results: By pooling all the studies identified, our study shows that individuals IL-1B-31T carrier have got an increased risk developing gastric cancer (OR of 1.25; 95% CI 1.06–1.47) in particular in Caucasian sub-group (OR of 1.41; 95% CI 0.97–2.05). IL-1B-31CC genotype confers a decreased risk (OR of 0.80; 95% CI 0.68–0.95) especially in Caucasian population (OR of 0.71; 95% CI 0.49–1.03) compared to Asians (OR of 0.83; 95% CI 0.69–0.99). This association might be explained with the well-known near complete linkage disequilibrium between IL1B-511T and IL1B-31C polymorphism. Furthermore our results suggest a strong association between IL1B-511T polymorphism and gastric cancer risk only in Caucasians and not in Asians. Conclusions: In conclusion, although affected by the common bias of each epidemiologic studies, this pooled analysis suggests that IL1B-511T polymorphism is associated with an increased risk of developing gastric cancer in Caucasian population. No significant financial relationships to disclose.

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