Hormone Molecular Biology and Clinical Investigation最新文献

Objectives: Human chorionic gonadotropin (hCG) assays are commonly used as a pregnancy test. False-positive human chorionic gonadotropin (hCG) values in urine were reported in 15 patients (nine males and six females) presenting with urinary tract infection.

Methods: Extopic hCG production and presence of heterophilic antibodies were excluded as potential causes of interference.

Results: Orbitrap mass spectrometry revealed the presence of uromodulin, an abundant urinary glycoprotein, as the likely cause of the interference. Falsely elevated hCG values correlated well with urinary alpha 1 microglobulin (a tubular protein) concentrations and with the urinary leukocyte count. The false positive hCG signal disappeared after antibiotic administration.

Conclusions: These data suggest that false-positive hCG test results in urine may occur in patients presenting with upper urinary tract infections due to uromodulin interference.

Objectives: Non-alcoholic fatty liver disease (NAFLD), recently reclassified as metabolic dysfunction-associated fatty liver disease (MAFLD), can also manifest in patients classified as non-MAFLD who do not meet MAFLD criteria. The involvement of cortisol and thyroid hormones may play a role in the pathogenesis of FLD by modifying the metabolism of specific lipoproteins, particularly apolipoprotein M (Apo M). This study investigated cortisol and thyroid hormones levels and Apo M gene expression in white blood cells (WBCs) of individuals with MAFLD, non-MAFLD, and healthy controls.

Methods: The serum and WBCs of the study subjects were collected from patients with FLD (n=99) including 58 MAFLD and 41 non-MAFLD and healthy individuals (n=23). To investigate the gene expression of Apo M and thyroid and cortisol hormones, qRT-PCR and ELISA methods were used, respectively.

Results: The Apo M gene expression was significantly lower in FLD patients, both non-MAFLD, and MAFLD patients compared to the control group (p<0.05). Total T4 and TSH hormone levels in the MAFLD patients were significantly decreased and increased compared to the control group, respectively (p<0.05). The cortisol level was significantly elevated in the FLD and MAFLD patients compared to the control group (p<0.01).

Conclusions: Alterations in Apo M gene expression also cortisol and thyroid hormones levels in non-MAFLD patients were milder than MAFLD patients when compared to the control. Also, likely Apo M may be involved in FLD pathogenesis.

Objectives: The present study evaluated the relationships of the serum levels of the cyclic dinucleotide 2'3'-cyclic GMP-AMP (cGAMP) marker of activation of pattern-recognition receptors with immunoglobulin G antibodies against severe acute respiratory syndrome-linked coronavirus (IgG-SARS)-positive status and endothelial dysfunction.

Methods: Selected groups from two cohorts (cohort 1 of 307 healthy volunteers and cohort 2 of 218 coronary heart disease [CHD] patients). COVID-19 infection was confirmed by detection of IgG-SARS against SARS-CoV-2 S1 protein receptor-binding domain. Cohort 1 was examined for systematic coronary risk evaluation by European Society of Cardiology (SCORE) starting from 2019 before the onset of the COVID-19 pandemic. Cohort 2 was processed starting from 2017 (three years prior to the COVID-19 pandemic) in a hospital setting to undergo coronary angiography to assess coronary lesions as Gensini score. The levels of cGAMP and endothelial markers (nitrate and nitrite combined as NOx and endothelin-1) were assessed in the serum to evaluate the associations with IgG-SARS status, SCORE, and extent of coronary lesions by correlation and receiver operating characteristic analyses.

Results: Serum cGAMP did not discriminate between SARS-positive and SARS-negative healthy subject of cohort 1. Moreover, the level of cGAMP was not associated with endothelial biomarkers in healthy subjects. However, Serum cGAMP was associated with atherosclerosis, with area under the curve 0.69 (95 % CI 0.587-0.806; p=0.001), and with endothelial markers in cohort 2.

Conclusions: Low cGAMP was associated with atherosclerosis in CHD patients, suggesting that cGAMP is a new biomarker in the context of sterile inflammation.

Autism spectrum disorder (ASD) is a pervasive neurobehavioral condition characterized by disruption of behavioral and emotional patterns in individuals with this condition. Given that various environmental and genetic factors play a fundamental role in the pathophysiology of ASD, it can be said that ASD is a multifaceted disease. This study used scientific databases including Google Scholar, PubMed, Scopus, and Semantic Scholar. In this review, we aimed to select manuscripts based on our field and relevant to the topic of our article. Emerging studies have shown that many neural, anatomical, and chemical factors play a role in the development of ASD. In this regard, an increasing body of studies has pointed out the relationship between chemical factors, including hormones, which play an important role in ASD. These hormones include melatonin, serotonin, thyroid, oxytocin, vasopressin, insulin-like growth hormone (IGF-1), etc. For instance, IGF-1 levels are low in ASD individuals, or melatonin levels are reduced in ASD individuals. Therefore, with take into account these findings, in this review, we decided to check over the association of these hormones to ASD and have a concise overview of their potential as therapeutic solutions to reduce the effects of ASD.

One of the biggest challenges of today's society is cancer, which imposes a significant financial, emotional and spiritual burden on human life. Breast cancer (BC) is one of the most common cancers that affects people in society, especially women, and due to advanced treatment strategies and primary prevention, it is still the second cause of cancer-related deaths in society. Various genetic and environmental factors are involved in the development of BC. MicroRNAs (miRNA)s are non-coding RNAs, that the degradation or inhibition of them plays an important role in the prevention or development of cancer by modulating many cellular pathways including apoptosis, drug resistance, and tumorigenesis. Drug resistance is one of the important defense mechanisms of cancer cells against anticancer drugs and is considered one of the main causes of cancer treatment failure. Different miRNAs, including mir-7, mir-21, mir-31, and mir-124 control different cell activities, including drug resistance, through different pathways, including PI3K/AKT/mTOR, TGF-β, STAT3, and NF-kB. Therefore, cell signaling pathways are one of the important factors that miRNAs control cellular activities. Hence, in this study, we decided to highlight an overview of the relationship between miRNAs and signaling pathways in the development of drug resistance in BC.

Objectives: The patient's family history of type 2 diabetes (FH-DM2) has been negatively associated with the functionality of endothelial cells (ECs). Our objectives in this work were to use human umbilical vein endothelial cells (HUVECs) as a model, to substantiate whether FH-DM2 influences endothelial phenotype and impairs NO and ROS synthesis, cell metabolism, and mitochondrial activity of ECs from individuals with FH-DM2.

Methods: In this study were evaluated the synthesis of reactive oxygen species (ROS) and nitric oxide (NO), mitochondrial membrane potential (MMP), mRNA of eNOS, glucose consumption, and lactate synthesis in HUVECs from newborns with FH-DM2. Furthermore, we also evaluated EC complexity and cell size through flow cytometry.

Results: Our results showed significant differences in HUVECs with FH-DM2, regarding their complexity and cell size, in the synthesis of ROS (p<0.01), and NO (p<0.05); they also reflected diminished glucose consumption and slight changes in the lactate levels.

Conclusion: In conclusion, our results showed that HUVECs from children with FH-DM2 have a reduced capability of synthesizing ROS and NO, which might be linked to the metabolism of endothelial cells. These results are relevant since early endothelial dysfunction has been reported in individuals with FH-DM2, and could be used to establish preventive measures to reduce the risk of developing atherosclerosis or cardiovascular diseases in healthy individuals, but with this family background.

Objectives: The objective of the study was to use anthropometric measurements (age, BMI, and subcutaneous fat) in conjunction with biochemical parameters (sex hormone-binding globulin (SHBG), homeostasis model assessment-insulin resistance (HOMA-IR), fasting glucose, serum insulin, and total cholesterol) to predict the probability of gestational diabetes mellitus (GDM) in the first trimester.

Methods: The study enrolled 48 pregnant women with GDM and 64 high-risk pregnant women without GDM. During the first-trimester examination, maternal blood samples were collected to measure SHBG, fasting blood glucose, serum insulin, and total cholesterol levels. Regression model analysis was used to examine the variables that showed statistically significant differences between the groups and were independent predictors of GDM. Receiver operating characteristic (ROC) curve analysis was employed to determine the risk of developing GDM based on cut-off values.

Results: The levels of SHBG, HOMA-IR, serum insulin, fasting glucose, and total cholesterol were identified as significant independent markers for predicting GDM. Meanwhile, age, body mass index, and subcutaneous fat values were found to be non-independent predictors of GDM. The areas under the ROC curve were calculated to determine the predictive accuracy of total cholesterol, HOMA-IR, SHBG, and subcutaneous fat for developing into GDM, and were 0.869, 0.977, 0.868, and 0.822 respectively. The sensitivities for a false positive rate of 5 % for predicting GDM were 68.7 , 91.67, 91.7, and 97.9 % for total cholesterol, HOMA-IR, SHBG, and subcutaneous fat, respectively.

Conclusions: The independent predictors for the subsequent development of GDM in high-risk pregnancies are HOMA-IR, SHBG, Total cholesterol, and subcutaneous fat (SC) levels. These parameters can be used to create a regression model to predict the occurrence of GDM.

Objectives: Neurodegenerative diseases are defined by specific protein accumulation and anatomic vulnerability leading to neuronal loss. Some studies have shown that lutein may have an effect on neurodegenerative diseases. As most of the neurodegenerative diseases don't have certain cure and therapies focus on symptom control, Lutein may be a complementary treatment. Due to controversies in studies investigating lutein effect on neurodegenerative diseases, we decided to perform a systematic review on these studies.

Methods: A systematic search was carried out in the available databases. We used all MeSH terms and relevant keywords. Studies that reported relationship between lutein and any neurodegenerative disease were included.

Results: We found 278 studies. After removing duplicates, screening by titles and abstracts and excluding irrelevant papers, 17 articles were included in this study. Fourteen studies investigated Alzheimer's disease, 2 studies Parkinson's disease and 1 study Amyotrophic lateral sclerosis. 1/17 study found that high serum levels of lutein at baseline were associated with a lower risk of AD mortality and lutein effect on lipid profile have been investigated in 2/17 studies. Also, 1/17 study has been shown that high intake of lutein may reduce the risk of ALS progression.

Conclusions: 4/17 studies confirm that lutein can improve cognitive function. 8/17 studies demonstrate a reduction in the progression of AD, and 2/17 studies indicate an improvement in lipid profiles. However, some studies did not find any significant associations. Additionally, there is a limited number of studies investigating the effects of lutein on other neurodegenerative diseases.

Objectives: Infertility affects approximately 15 % of couples globally, with 50 % cases of male factor infertility. Precise assessment of spermatogenesis is essential for evaluating male infertility. Recent studies suggest serum inhibin B as a promising biomarker for testicular function. This study aims to evaluate the diagnostic utility of serum inhibin B in predicting male infertility, particularly focusing on its relationship with sperm count.

Methods: A cross-sectional study was conducted on 80 adult men (mean age 31.4 ± 6.89 years) presenting with infertility at gynecology and urology outpatient departments. Semen analysis was performed following WHO (2010) guidelines, and serum inhibin B levels were quantified. The correlation between serum inhibin B levels and sperm parameters was assessed using Pearson's correlation test. Receiver operating characteristic (ROC) curve analysis was employed to evaluate the diagnostic accuracy of serum inhibin B and the inhibin B/FSH ratio for non-obstructive azoospermia (NOA) and oligozoospermia.

Results: A significant positive correlation was observed between serum inhibin B and sperm count (r=0.94, p<0.001). ROC analysis demonstrated that the inhibin B/FSH ratio had the highest diagnostic accuracy for NOA and oligozoospermia (AUC=0.986), with sensitivity of 100 % and specificity of 91.67 %. Serum inhibin B alone also showed high diagnostic value (AUC=0.965 for NOA and 0.969 for oligozoospermia).

Conclusions: Serum inhibin B is a reliable biomarker for assessing male infertility, particularly in evaluating spermatogenic function. The inhibin B/FSH ratio provides superior diagnostic accuracy for NOA and oligozoospermia, offering valuable clinical utility in male infertility diagnosis.