The diagnostic value of neurogranin in patients with carbon monoxide poisoning: Can it show early neurological damage?

BACKGROUND AND AIM: Carbon monoxide poisoning is a toxicological emergency that causes neurological complications. High serum neurogranin can be detected in acute or chronic conditions where brain tissue is damaged. This study aimed to investigate the diagnostic value of serum neurogranin level and its role in demonstrating neurological damage in patients admitted to the emergency department with carbon monoxide poisoning. MATERIALS AND METHODS: The study was conducted prospectively on patients with carbon monoxide poisoning (patient group) and healthy volunteers (control group). Demographic characteristics and serum neurogranin level of all participants and symptoms at admission, neurological examination findings, laboratory results, and Diffusion-Weighted Magnetic Resonance Imaging results of the patient group were recorded. We used an independent sample t-test to compare neurogranin levels and bivariate correlation analysis to compare the relationship between serum neurogranin levels and data belonging to the patient group. RESULTS: Sixty eight participants (patient group, n = 36; control group, n = 32) were included in the study. Serum neurogranin level was significantly higher in patients with carbon monoxide poisoning (0.31 ± 0.16 ng/ml) compared to control group (0.22 ± 0.10 ng/ml) (p = 0.015). The mean Glasgow Coma Scale of the patients with carbon monoxide poisoning was 14.59 ± 0.23, and of Diffusion Weighted Magnetic Resonance Imaging results were completely normal in 94.4% (n = 34). There was no correlation between serum neurogranin level and Diffusion Weighted Magnetic Resonance Imaging results (r = -0.011; p = 0.953). CONCLUSION: Serum neurogranin level may be a new diagnostic biomarker in patients admitted to the emergency department with carbon monoxide poisoning. The high serum neurogranin levels detected in patients with normal diffusion-weighted imaging after carbon monoxide poisoning suggest that there is neurological damage in these patients, even if imaging methods cannot detect it.

Investigation of the relationship between betatrophin and certain key enzymes involved in carbohydrate and lipid metabolism in insulin-resistant mice.

OBJECTIVES: The present study sought to examine the relationship of betatrophin with certain key enzymes, namely lactate dehydrogenase-5 (LDH5), citrate synthase (CS), and acetyl-CoA carboxylase-1 (ACC1), in insulin-resistant mice. METHODS: Eight-week-old male C57BL6/J mice were used in this study (experimental group n=10 and control group n=10). S961 was administered using an osmotic pump to induce insulin resistance in the mice. The betatrophin, LDH5, CS, and ACC1 expression levels were determined from the livers of the mice using the real-time polymerase chain reaction (RT-PCR) method. Moreover, biochemical parameters such as the serum betatrophin, fasting glucose, insulin, triglyceride, total cholesterol, and high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol levels were analyzed. RESULTS: The betatrophin expression and serum betatrophin (p=0.000), fasting glucose, insulin, triglyceride (p≤0.001), and total cholesterol (p=0.013) levels were increased in the experimental group. In addition, the CS gene expression level was statistically significantly decreased in the experimental group (p=0.01). Although strong correlation was found between the expression and serum betatrophin and triglyceride levels, no correlation was found between the betatrophin gene expression and the LDH5, ACC1, and CS gene expression levels. CONCLUSIONS: The betatrophin level appears to play an important role in the regulation of triglyceride metabolism, while insulin resistance increases both the betatrophin gene expression and serum levels and decreases the CS expression level. The findings suggest that betatrophin may not regulate carbohydrate metabolism through CS and LDH5 or lipid metabolism directly through the ACC1 enzyme.

Why do multiple sclerosis and migraine coexist?

BACKGROUND: Migraine coexistence, which is high in multiple sclerosis (MS), is reported. To better understand the etiology of the coexistence of MS and migraine and the outcomes of this relationship, the vitamin D, vitamin D-binding protein (VITDBP), vitamin D receptor (VITDR), high-sensitivity C-reactive protein (hs-CRP), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), total antioxidant status (TAS), total oxidant status (TOS), and Oxidative Stress Index (OSI) values were examined in patients with the coexistence of relapsing-remitting multiple sclerosis (RRMS) and migraine. METHODS: This study was conducted between January 1, 2019, and July 25, 2019, at the neurology and biochemistry clinics of two different tertiary hospitals simultaneously. Overall, 50 RRMS patients with migraine, 50 RRMS patients without migraine, and 50 healthy volunteers were included in the study. The participants' vitamin D, VITDBP, VITDR, hs-CRP, SOD, CAT, GSH-Px, TAS, TOS, and OSI values were measured. RESULTS: The vitamin D and VITDR values of the RRMS patients with migraine were lower than those of the RRMS patients without migraine (respectively, p = 0.014, p < 0.001). There was no significant difference between the RRMS patients with and without migraine in terms of their VITDBP values (p = 0.570). The SOD, CAT, GSH-Px, and TAS values of the RRMS patients with migraine were lower than those without migraine (all p < 0.001). The hs-CRP and TOS values of the RRMS patients with migraine were higher than those without migraine (all p < 0.001). CONCLUSION: To the best of our knowledge, this is the first study on this topic to date. Based on the results, our study may shed light on the etiopathogenesis of the coexistence of MS and migraine and new treatments. However, more studies are needed to better understand the etiology of this relationship and its negative effects.