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1.
Cureus ; 16(4): e58532, 2024 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-38957833

RESUMO

Introduction Cancer exerts a substantial influence on the body's metabolism through varied mechanisms, instigating a metabolic reprogramming that maintains the unchecked growth and survival of cancer cells, consequently perturbing diverse metabolic parameters. The introduction of positron emission tomography-computed tomography (PET/CT), delivering detailed insights into both metabolic and morphological aspects, has brought about a revolutionary shift in modern cancer detection. Exploring the potential connection between PET-CT metabolic features and the metabolic parameters of liver enzymes in an individual can unveil novel avenues for cancer diagnosis and prognosis. Materials and methods This study conducted a retrospective analysis of patient records from our institution, covering the period from January 2021 to September 2023, focusing on individuals with various malignancies. The data included information on gender, age, clinical history, and liver serum parameters, which were compiled into tables. Additionally, inflammatory indicators such as ALT (alanine transaminase), ALP (alkaline phosphatase), total protein (TP), ALT/AST ratio, and SUVmax were collected and plotted. The study used Pearson correlation analysis to assess the relationship between each inflammatory variable and SUV (max) as determined by PET-CT. Results In breast cancer, there was a statistically significant positive correlation (R2=0.0651) between serum ALP levels and SUVmax as determined by regression analysis. Hodgkin lymphoma, on the other hand, showed a statistically significant negative correlation between the ALT-to-AST ratio (ALT/AST) and SUVmax (r = -0.45, R2 = 0.204). In non-Hodgkin lymphoma patients, total protein (TP) was negatively correlated with SUVmax (R2=-0.081, r= -0.28), while in lung cancer patients, there was a significant positive correlation with regression correlation coefficients (R2 = 0.026, 0.024, 0.024, and 0.018 for ALT/AST, TP, ALP, albumin, and ALT, respectively). Conclusion Aligning with these results, it can be a recent addition to acknowledge that both the tumor metabolic parameter (SUVmax) and the levels of liver serum enzymes exhibit a potential for predicting patient prognosis in various cancers.

2.
Neurol India ; 68(5): 1144-1150, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33109865

RESUMO

BACKGROUND: Folic acid and multivitamin supplements ((FAMVS) and genetics involvement is one of the major roles in the development of neural tube defects (NTDs). OBJECTIVE: Our prior aim and objective is to establish an unique guideline and helps the policy decision making for our country India and the World. MATERIALS AND METHODS: We have collected the data through the literature from the World for their necessary action, rehabilitation part all objectively in PubMed/Medline, Scopous, Embase, Cochrane Review, Hinari, and Google scholar. STATISTICAL ANALYSIS: Statistical analysis was performed with very simple and logistic statistics, percentage, mean, total as collection through the available software SPSS with new version 17.0. RESULTS: The overall (70-95%) we find out those infants with neural tube defects (NTDs) associated with genes involvement and maternal vitamin intake (MVI). Before pregnancy relative risk (PRR) prior to non intake noted as 90% significantly reduced their risk of the NTDs. Now (40-60%) of the women of child-bearing age (CBA) don't use the folic acid intake and supplements (FAISs) in proper way in villages, urban, industrial and sewage areas. We find out that the genetic variants of the fourteen special reported genes, had the major risk factor (MRF) for the (NTDs) and associated abnormalities rate (AAR) within the developmental process in the human brain. CONCLUSIONS: The (45-55%) people still having at ignorant zone, due to lack of education, genetic counseling, and awareness till date.


Assuntos
Medicina Molecular , Defeitos do Tubo Neural , Suplementos Nutricionais , Feminino , Ácido Fólico , Humanos , Índia , Defeitos do Tubo Neural/genética , Gravidez
3.
J Pediatr Neurosci ; 13(1): 46-57, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29899771

RESUMO

AIM: Split cord malformation (SCM) is associated with extensive vertebral fusions (Klippel-Feil anomaly). In light of previous embryological theories and recent research findings, we attempt to document the origin of split cord, and vertebral fusions involvement of spectrum of genes is necessary to know better the etiopathogenesis of SCM and its associated diseases. MATERIALS AND METHODS: We used the various databases such as PubMed/MEDLINE, Cochrane Review, Hinari, and Google Scholar for the recently published medical literature. The women had been living and still born infants had SCM. The relative risk (RR) and possible molecular mechanism are described details of major genes and its variants in details. Although molecular genetics involvement including with recent advances of study add an evidence of both Mendelian and Non-Mendelian fashion is discussed with all genetic components. We mentioned our earlier experience and responsibility of SCM and its associated diseases. RESULTS: Although different mechanisms are suggested for the development of SCM observed in our experience, there is a midline lesion bisecting the neuroepithelium and the notochordal plate, which is responsible for complete splitting of the cervical cord with anterior bony defect. The localized disturbance of cervical neural tube closure accounts for SCM with partial dorsal splitting of the cord with posterior vertebral defect and associated diseases. CONCLUSIONS: According to the best of our knowledge, this report is the first one to be documented by wider spectrum of variants from (experimental studies to human subject). This add a complex interaction of mutant variants drive toward an additional second-hit alterations for the SCM. The up-to-date information, documented in proper order, derived the bench-to-bedside approach to overcome this burden of SCM, which is globally noticed with other additional diseases.

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