scholarly journals Predicting of fentanyl-associated neurotoxicity in pancreatic cancer with clical, genetic model

Author(s):  
O. P. Bobrova ◽  
N. A. Shnayder ◽  
M. M. Petrova ◽  
S. N. Zobova ◽  
Yu. A. Dykhno ◽  
...  

Aim. To develop a model for the implementation of opioid - associated neurotoxicity in patients with pancreatic cancer based on an analysis of the relationship of clinical and genetic factors. Materials and methods. In 45 patients with pancreatic cancer, 54 clinical and genetic factors were studied for predicting the implementation of opioid-associated neurotoxicity, receiving a transdermal form of fentanyl. Results. A clinical genetic model of the implementation of opioid - associated neurotoxicity in patients with pancreatic cancer was developed using the example of a transdermal form of fentanyl Conclusion. The clinical genetic model for predicting the risk of opioid-associated neurotoxicity in patients with pancreatic cancer is important from the perspective of personalized medicine.

2001 ◽  
Vol 91 (6) ◽  
pp. 2776-2784 ◽  
Author(s):  
David M. Herrington ◽  
Karen Potvin Klein

There are a number of genetic factors that likely modulate both the beneficial and adverse effects of estrogen. An important domain of consideration is the relationship of estrogen and thrombosis risk. Gene polymorphisms among the key elements of the coagulation and fibrinolytic cascade appear to influence the effects of estrogen on risk for venous thromboembolic events and possibly arterial thrombosis as well. Emerging data also suggest that allelic variants in the estrogen receptor-α may modulate estrogen's effects, especially with respect to bone and lipid metabolism.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Pengfei Du ◽  
Xiaojie Ma ◽  
Changjiang Wang

Many studies have established that T-lymphocyte antigen-4 (CTLA4) is a susceptible gene for Graves’ disease (GD). Also many studies showed the association between the CTLA4 exon-1 49A/G polymorphism and the risk of developing Graves’ ophthalmopathy (GO) in GD patients. But those results were inconsistent. In recent years many new studies were published which helped to shed light on the relationship of CTLA4 SNP49 with GO. So we performed the meta-analysis to explore the association between the SNP49 and GO susceptibility in GD patients. Studies up to February 29, 2012, were searched by using PubMed. The odds ratio was used to evaluate the strength of the association. Altogether 12 case-control studies involving 2,505 participants were included in the meta-analysis. Results showed that the G allele was related to the increased risk of GO compared with the A allele under allelic genetic model (OR = 1.14, 95% CI: 1.14–1.72,P=0.001) in European subgroup. No publication bias was detected. Our results showed that the SNP49 polymorphism of CTLA4 gene was related to increased risk of GO.


2015 ◽  
Author(s):  
Elena Peretokina ◽  
Natalia Mokrysheva ◽  
Lyudmila Rozhinskaya ◽  
Ekaterina Zakharova

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1593-P
Author(s):  
BAQIYYAH CONWAY ◽  
WILLIAM J. BLOT

Twin Research ◽  
2000 ◽  
Vol 3 (1) ◽  
pp. 28-32 ◽  
Author(s):  
Michael J Lyons ◽  
Jonathan Huppert ◽  
Rosemary Toomey ◽  
Rebecca Harley ◽  
Jack Goldberg ◽  
...  

AbstractThere have been long questions about the relationship of schizophrenia to other mental disorders. Lifetime DSM-III-R diagnoses of mood and anxiety disorders in twins with clinically diagnosed schizophrenia (n = 24) and their non-affected co-twins (n = 24) were compared with twins from pairs without schizophrenia (n = 3327) using a sample from the Vietnam Era Twin Registry. Schizophrenic probands had significantly elevated rates of all included disorders (bipolar disorder, major depression, dysthymia, generalized anxiety disorder, panic disorder, and PTSD) compared with controls (P < 0.01). The odd ratios comparing co-twins of schizophrenic probands with controls was greater than three for every disorder, but did not attain statistical significance. A similar pattern was observed when analyses were restricted to only monozygotic twins (n = 12). Consistent with other studies, schizophrenics appeared to have higher rates of a range of mental disorders. Our results suggest that schizophrenia per se represents a risk factor for other psychiatric disorders, but the absence of significantly elevated risk among non-schizophrenic co-twins suggested that family environmental and/or genetic factors that contribute to risk of schizophrenia do not increase the risk of mood and anxiety disorders to the same extent that the risk of these other disorders is increased by the presence of schizophrenia. Twin Research (2000) 3, 28–32.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Enkhmaa Byambaa ◽  
Kyoungmi Kim ◽  
Wei Zhang ◽  
Kevin Truax ◽  
Anuurad Erdembileg ◽  
...  

Abstract Introduction: An elevated level of lipoprotein(a) [Lp(a)] is an independent causal risk factor for cardiovascular disease. Non-genetic factors do not appreciably influence Lp(a) levels due to a strong genetic control. However, inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) has been shown to reduce Lp(a) levels. The association of PCSK9 with Lp(a) level and its major genetic determinant—apolipoprotein(a) [apo(a)] size—is not fully understood. In this study, we assessed the relationship between PCSK9, Lp(a) level, apo(a) size, age, and race/ethnicity. Methods: Healthy Caucasian and African-American families were recruited from the general population (age range: 6–74 years, N=267). PCSK9 and Lp(a) levels were assayed enzymatically; apo(a) isoform and LPA allele sizes and isoform-specific Lp(a) levels were determined. Results: In all participants, PCSK9 levels differed significantly by race/ethnicity, age, and sex. Thus, the mean PCSK9 levels were significantly higher in African-Americans vs. Caucasians (104 ± 29 vs. 95 ± 30 ng/mL, respectively, p=0.020), in adults vs. children (102 ± 29 vs. 92 ± 31 ng/mL, respectively, p=0.001) and in females vs. males (103 ± 30 vs. 94 ± 29 ng/mL, respectively, p=0.007). PCSK9 levels were not associated with total plasma Lp(a) levels neither in all participants nor in ethnicity-specific analyses. However, PCSK9 levels were significantly and positively associated with isoform-specific Lp(a) levels carried by the larger apo(a) size in all subjects (r=0.139, p=0.0361). In race/ethnicity analyses, a significant association was seen for African-Americans (r=0.268, p=0.0199), but not for Caucasians. In contrast, there were no significant associations of PCSK9 with isoform-specific Lp(a) levels for the smaller apo(a) sizes in all participants nor in ethnic-specific analyses. Of note, PCSK9 levels were significantly negatively associated with the larger apo(a) isoform sizes in all participants (r=-0.139, p=0.0366). Although significant in both groups, heritability of PCSK9 level was higher in Caucasians than in African-Americans (47% vs. 22%, respectively). Conclusions: Among African-Americans, but not Caucasians, PCSK9 levels were associated with isoform-specific Lp(a) levels carried on larger, but not smaller, apo(a) sizes. The findings illustrate a diverging relationship of PCSK9 with isoform-specific Lp(a) levels.


2021 ◽  
Vol 03 (03) ◽  
pp. 93-103
Author(s):  
A.G. Ganiev ◽  

The importance of assessment in the educational process and international assessment systems were discussed. There is also information on the dependence of a child's educational opportunities on genetic factors and upbringing. In this regard, it is recommended to use Gardner's "theory of multiplicity of intelligence" to make the most of the child's potential. The article presents a map of the “multi-intelligence theory” of intellect and comments on the relationship of types of intellect to the cerebral hemispheres. A "Child Intelligence Diagram" is also recommended for practice.


2020 ◽  
Author(s):  
Xiaoli Liu ◽  
Dandan Li ◽  
Chunjuan He ◽  
Linna Peng ◽  
Shishi Xing ◽  
...  

Abstract Background: LOC105371267 (also known as PR-lncRNA1) was reported to be a p53-regulated lncRNA, which played essential roles in the pathogenesis of breast cancer (BC). We aimed to investigate the potential associations between LOC105371267 polymorphisms and BC risk. Method: Totally, 555 healthy individuals and 561 BC patients were recruited. Five candidate SNPs of LOC105371267 were genotyped with Agena MassARRAY system. Odds ratio (OR) and 95% confidence intervals (CIs) were applied to evaluate the relationship of LOC105371267 with BC susceptibility. Additionally, stratification analyses based on clinical features and haplotype analysis were also conducted. Results: A decreased BC risk was observed rs3931698 GG genotype (OR = 0.30, P = 0.018) and recessive genetic model (OR = 0.30, P = 0.021). Stratified analysis with age also revealed that this SNP was associated with a lower risk at age < 52 years. Meanwhile, multiple clinical characteristics, including ER and PR status and stage were all correlated with SNPs rs6499221, rs3931698, rs3852740 and rs8044565.Conclusion: Four LOC105371267 SNPs (rs6499221, rs3931698, rs8044565 and rs3852740) were found to be correlated with development of BC. Additionally, ER, PR, and stage were also linked to LOC105371267 polymorphisms, providing novel diagnostic and therapeutic targets for of BC management.


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