Factor Levels In Patients Research Articles

Association Between Depressive Symptoms and Serum Brain-Derived Neurotrophic Factor Levels in Patients With First-Episode and Drug-Naïve Schizophrenia.

Previous studies have revealed that brain-derived neurotrophic factor (BDNF) levels are inversely associated with the severity of depressive symptoms. In addition, serum BDNF levels tend to increase with improvement in depressive symptoms. There is also evidence that BDNF has a possible role in the pathophysiology of schizophrenia. Therefore, the purpose of this study was to determine whether BDNF levels correlated with depressive symptoms in patients with first-episode and drug-naïve (FEDN) schizophrenia. In this study, 90 patients with FEDN schizophrenia and 60 healthy controls were recruited. The Positive and Negative Syndrome Scale (PANSS) and the 17-item Hamilton Depression Scale (HAMD-17) were used to gage psychopathological and depressive symptoms, respectively. All participants had their BDNF levels measured using a sandwich enzyme-linked immunosorbent test. Serum BDNF levels were lower in patients with FEDN schizophrenia compared with healthy controls. Moreover, patients with depressive symptoms exhibited a higher PANSS total score and a higher general psychopathology score than those without depressive symptoms (p < 0.05). For patients with depressive symptoms, serum BDNF levels were higher than in those without depressive symptoms (p < 0.05). An association between BDNF levels and the positive subscore was also observed (p < 0.01). However, there was no significant association between BDNF levels and HAMD scores (p > 0.05). In conclusion, BDNF levels were shown to be higher in the serum of patients with FEDN schizophrenia with depressive symptoms than in those without. Additionally, low levels of serum BDNF may contribute to the positive symptoms of FEDN schizophrenia but not to depressive symptoms.

Hippocampal Volume and Plasma Brain-Derived Neurotrophic Factor Levels in Patients With Depression and Healthy Controls.

The aim of the present study was to investigate associations between hippocampal subfield volumes and plasma levels of brain-derived neurotrophic factor (BDNF) in patients experiencing a first episode of major depression (MD) (n = 30) as compared to healthy controls (HC) (n = 49). Covariate-adjusted linear regression was performed to compare the MD and healthy groups, adjusting for age, sex, and total estimated intracranial volume. We demonstrated that there were no differences in total hippocampal volume between the MD and HC groups. However, the volumes of the hippocampus-amygdala-transition-area (HATA) on the left side of the brain as well as the parasubiculum, presubiculum, and fimbria on the right side were statistically significantly smaller in the MD group than in the HC group. Furthermore, the volume of the hippocampal fissure on the right side was statistically significantly smaller in the HC group than in the MD group. In the MD group, we found a positive linear correlation between hippocampal volume and plasma BDNF concentrations in the CA4 area on the left side (p = 0.043). In contrast, in the HC group, we found a negative linear correlation between parasubiculum volume on the right side and plasma BDNF concentrations (p = 0.04). These results suggest that some hippocampal subfields may already be atrophic at the start of MD. In addition, our findings suggest that the sensitivity of the right parasubiculum region to BDNF may differ between MD and HC groups. These findings guide future research directions and, if confirmed, may ultimately inform medical guidelines.

T239 Von Willebrand factor levels in patients with systemic lupus erythematosus and antiphospholipid syndrome

T239 Von Willebrand factor levels in patients with systemic lupus erythematosus and antiphospholipid syndrome

The Effects of Ticagrelor Combined with Tirofiban on Coagulation Function, Serum Myocardial Injury Markers, and Inflammatory Factor Levels in Patients with Acute Myocardial Infarction after Percutaneous Coronary Intervention.

Background Acute myocardial infarction (AMI) refers to the acute necrosis of part of the myocardium caused by persistent and severe myocardial ischemia. This study is aimed at investigating the efficacy of tirofiban combined with ticagrelor in AMI patients after percutaneous coronary intervention (PCI) and its effects on plasma activated partial thromboplastin time (APTT), fibrinogen (FIB), D-dimer (D-D) levels, myocardial injury markers, and inflammatory factors. Methods 68 AMI patients with AMI who received PCI were divided into control group and observation group (n =34) according to postoperative treatment methods. Both groups received ticagrelor tablets (90 mg). The observation group was additionally given tirofiban (10 μg/kg). APTT, FIB, D-D, serum myoglobin (MB), cardiac troponin I (cTnI), serum C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and IL-6, myeloperoxidase (MPO) levels and the peak time in both groups were detected. The incidence of cardiovascular events and drug safety were compared. Results After treatment, APTT was increased, and FIB and D-D levels were decreased in both groups. After treatment, the APTT in the observation group was longer, and FIB and D-D levels were lower than those in the control group. The peak time of serum MB and cTnI in the observation group was earlier than that in the control group. The levels of serum MB and cTnI in the observation group were lower than those in the control group. After treatment, serum CRP, TNF-α, IL-6, and MPO levels were decreased. And the incidence of cardiovascular events was reduced. Conclusion Tirofiban combined with ticagrelor can improve coagulation function, protect myocardium, relieve inflammation, and reduce the risk of cardiovascular events in patients with AMI after PCI.

Effects of Different Nonsteroidal Anti-Inflammatory Drugs Combined with Platelet-Rich Plasma on Inflammatory Factor Levels in Patients with Osteoarthritis.

Objective To investigate the effects of different nonsteroidal anti-inflammatory drugs combined with platelet-rich plasma on inflammatory factor levels in patients with osteoarthritis. Methods The clinic data of 120 patients with osteoarthritis who were treated in our hospital (June 2019-June 2021) were retrospectively reviewed. All the patients were given platelet-rich plasma. According to the different nonsteroidal anti-inflammatory drugs the patients received, they were equalized into diclofenac sodium group, celecoxib group, and iguratimod group, with 40 cases in each group. After treatment, the patients' clinical efficacy was compared and analyzed. Results After treatment, the pain degrees of the patients in the three groups were gradually reduced. After 4 weeks and 8 weeks of treatment, the statistical differences in the scores of Visual Analogue Scale (VAS) were found among the three groups. Specifically, compared with the other two groups, the iguratimod group had remarkably lower VAS scores (P < 0.05) and the celecoxib group had signally lower VAS scores compared with the diclofenac sodium group (P < 0.05). After treatment, the inflammatory factor levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and high-sensitivity C-reactive protein (hs-CRP) in the diclofenac sodium group were observably higher compared with the celecoxib group (P < 0.05), and the inflammatory factor levels in the celecoxib group were remarkably higher compared with the iguratimod group (P < 0.05). Before treatment, no notable difference in the Lysholm scores was found among the three groups, and the patients' knee joint function was gradually improved after treatment. To be specific, after 4 and 8 weeks of treatment, the iguratimod group had observably higher Lysholm scores compared with the other two groups (P < 0.05), and the celecoxib group had signally higher Lysholm scores compared with the diclofenac sodium group (P < 0.05). The iguratimod group got markedly lower Western Ontario and McMaster Universities (WOMAC) score compared with the celecoxib group (P < 0.05); Compared with the diclofenac sodium group, the celecoxib group got remarkably lower WOMAC score (P < 0.05). During treatment, few patients suffered from mild gastrointestinal discomfort and hepatic dysfunction in the three groups, and no other severe adverse reactions were found. No statistical difference in the total incidence of adverse reactions among the three groups was observed (P > 0.05). Conclusion The combination of nonsteroidal anti-inflammatory drugs with platelet-rich plasma can further reduce the inflammatory reactions of the patients with osteoarthritis and improve their knee joint function. Significantly, the iguratimod, with high safety, has observably better effects on inhibiting inflammatory factors and improving knee joint function compared with diclofenac sodium and celecoxib.

Effect of eplerenone on aldosterone and von Willebrand factor levelsin patients with myocardial infarction and chronic kidney disease

Aim: to study the levels of aldosterone and von Willebrand factor (VWF) in patients with Q-wave acute myocardial infarction (Q-AMI) and underling chronic kidney disease (CKD) using aldosterone antagonists. Materials and methods. The study group consisted of 106 patients with renal dysfunction who were hospitalized for acute Q-AMI. Serum levels of neurohumoral parameters (aldosterone and VWF) were determined in all the patients by enzyme-linked immunosorbent assay kits. Results. Reduction in the aldosterone levels was found in patients with Q-AMI and stage 2 CKD from 245.08 ± 17.38 pmol/l to 195.15 ± 13.82 pmol/l (P &lt; 0.05;) who received spironolactone and from 275.59 ± 23.43 to 169.37 ± 24.46 pmol/l (P &lt; 0.001) with eplerenone usage. Patients with stage 1 CKD showed a decreasing trend in aldosterone levels when using spironolactone (from 238.04 ± 20.37 pmol/l to 200.78 ± 9.15 pmol/l), and significantly decreased aldosterone levels when receiving eplerenone (from 229.77 ± 13.76 pmol/l to 156.76 ± 5.76 pmol/l; P &lt; 0.05). The serum concentration of VWF in stage 2 CKD patients was changed insignificantly on spironolactone therapy (from 0.99 ± 0.13 mg/l to 1.13 ± 0.06 mg/l) and it was significantly decreased in the eplerenone group – from 1.29 ± 0.19 mg/l to 0.71 ± 0.14 mg/l (P &lt; 0.05). In stage 1 CKD patients, the concentration of VWF was not decreased significantly with the use of spironolactone (from 1.22 ± 0.13 mg/l to 1.03 ± 0.06 mg/l), but it was decreased significantly when receiving eplerenone (from 1.14 ± 0.09 mg/l to 0.79 ± 0.08 mg/l; P &lt; 0.05). The data obtained indicate the significantly higher probability of declining both aldosterone (t = 2.91; P &lt; 0.01) and VWF (t = 2.59; P &lt; 0.01) with the use of eplerenone in the complex treatment as compared to the spironolactone administration. Conclusions. The effect of eplerenone to decrease the concentration of aldosterone and VWF is significantly greater than that of spironolactone, especially in AMI patients with stage 2 CKD.

Investigation of the effect of electroconvulsive treatment on serum glial cell line-derived neurotrophic factor levels in patients with schizophrenia and bipolar disorder

Investigation of the effect of electroconvulsive treatment on serum glial cell line-derived neurotrophic factor levels in patients with schizophrenia and bipolar disorder

Tanyu Tongzhi Formula Delays Atherosclerotic Plaque Progression by Promoting Alternative Macrophage Activation via PPARγ and AKT/ERK Signal Pathway in ApoE Knock-Out Mice.

We previously demonstrated that the Tanyu Tongzhi Formula (TTF) significantly alleviated the clinical symptoms of patients with coronary heart disease and lowered serum lipid and inflammatory factor levels in patients with coronary heart disease and atherosclerosis model rats. However, the mechanism underlying TTF remains unknown. In this study, we examined the effect of TTF on atherosclerotic plaques in ApoE-/- mice and underlying mechanisms involved in macrophage polarization. Sixty male ApoE-/- mice were randomly divided into four groups. Mice in the control group were fed a regular diet, whereas experimental mice were fed a high-fat diet and received either saline (HFD group) or TTF at concentrations of 0.60 (TTF-L group) or 2.25 g/ml (TTF-H group) by daily oral gavage for 16 weeks. In the TTF-L and TTF-H groups, the levels of serum cholesterol, triglyceride, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were decreased, lipid content was significantly decreased, and percentage area of collagen/lipid increased in atherosclerotic plaque compared to in the HFD group. Moreover, we found TTF promoted the expression of alternative macrophage markers (Fizz1, Arg1, and Mrc) and suppressed the expression of M1 macrophage markers (TNF-α, IL-1β, and IL-6) by regulating peroxisome proliferator-activated receptor γ (PPARγ) expression and AKT/extracellular signal-regulated kinase (ERK) activation. We further investigated whether alternative macrophage was reduced when PPARγ was inhibited or the AKT/ERK signaling pathway was activated. TTF delayed atherosclerotic plaque progression by promoting alternative macrophage activation through increasing PPARγ expression and inhibiting AKT/ERK phosphorylation, providing a theoretical basis for its clinical application.

Impact of obesity on factor VIII and von Willebrand factor levels in patients with Type 1 von Willebrand disease and low von Willebrand factor: An analysis of the ATHNdataset.

Obesity is associated with endothelial dysfunction, haemostatic and fibrinolytic disturbances, however the impact of obesity on von Willebrand factor (VWF) is unclear. The aim of this study was to test our hypothesis that the prevalence of obesity is higher among participants with low VWF (LVWF) compared to type 1 von Willebrand disease (T1VWD). A retrospective review of the ATHNdataset as of March 2018 was performed. Participants were categorized as T1VWD if their VWF ristocetin cofactor activity was 30IU/dL and LVWF if the values were 30-50IU/dL, and by the NIH definitions for body mass index (BMI) for adult participants (≥18 years of age) or BMI z-score for paediatric participants (<18 years). The prevalence of obesity was not significantly different between adults with T1VWD (n=186) and LVWF (n=362) (32%vs 36%; p=.345). The mean factor VIII (FVIII) increased with increasing BMIs in both groups. In the paediatric cohort (T1VWD, n=583; LVWF, n=1702), there was no difference in the prevalence of obesity, but BMI was positively correlated with mean FVIII (p<.001). Children<10 years were 27.6% more likely to be diagnosed with T1VWD compared to>10 years. Among participants in the ATHNdataset, the prevalence of obesity was similar among those with LVWF and T1VWD. However, higher BMI levels were associated with elevated FVIII. Further research is needed to evaluate the impact of obesity on bleeding phenotype and treatment practices.

Serum macrophage colony-stimulating factor levels in patients with essential hypertension after vaccination against SARS-CoV-2

The formation of immunity in the population to various variants of the COVID-19 pathogen is one of the most important problems for the world community. The aim of the study was to compare the dynamics of M-CSF and VEGF-A, IL-34 in the blood serum of patients with essential hypertension (EH) stage II, depending on the type of immunity formed (post-infectious, post-vaccination, “hybrid”) to analyze changes of M-CSF-mediated mechanisms of hypertension development. During the work, 2 groups of patients were formed: group 1-patients with stage II EH and SARS CoV-2 infection without pneumonia in the anamnesis, vaccination 6 months after laboratory recovery, group 2 – patients with stage II EH without COVID-19 in the anamnesis, vaccination during the follow-up period. Determination of M-CSF, IL-34, VEGF-A, IgG level to SARS-CoV-2 was determined using an enzyme-linked immunosorbent assay. The formation of post-infectious immunity in patients with stage II EH, despite the mild course of COVID-19, is accompanied by a long-term (up to 6 months) pathophysiologically significant increase in the serum level of M-CSF (p 0.001) with a decrease in IL-34 (p 0.001). Analysis of the dynamics of changes in M-CSF, IL-34, VEGF-A in the postvaccination period in the blood serum of patients with stage II EH with COVID-19 in the anamnesis (“hybrid” immunity), determined the absence (p 0.05) of changes in the levels of M-CSF, VEGF-A after the first component of “SPUTNIK V” against the background of an increase of the level of IgG to SARS-CoV-2. 21 days after the second component of the vaccine, an increase of M-CSF was detected when compared with both pre-vaccination indicators and data 21 days after the introduction of the first component of the vaccine (p 0.001). Comparing the dynamics of the of M-CSF, IL-34 and VEGF-A in patients with stage II EH without COVID-19 in the post-vaccination period with the data on the formation of “hybrid” immunity, an increase in M-CSF was recorded 21 days after the introduction of the first and second components against the background of a decrease in IL-34, but with the restoration of pre-vaccination concentrations in 100% of patients by day 180 with comparable immunogenicity after 180 days. In patients with EH II, the pathogenetic “summation” of the pre-infectious imbalance of cytokine regulation and postcovid changes is important, which in a number of patients may be the reason for the prolongation of the stabilization of the balance of the M-CSF-IL-34-VEGF-A system in the post-vaccination period during the formation of “hybrid” immunity.

The effect of methylethylpiridinol addition to the therapy on the level of pigment epithelium-derived factor and oxidative status in patients with diabetic nephropathy: randomized controlled open-label clinical study.

The diabetic nephropathy is associated with oxidative stress and increases in pigment epithelium-derived factor (PEDF) level in the patient's blood. For the first time, authors investigated the effect of methylethylpiridinol addition to the therapy on oxidative status and pigment epithelium-derived factor concentrations, and examined the relationship between these indicators and clinical markers of pathology development. Study design: open label randomized controlled trial study. Authors assessed the effect of methylethylpiridinol addition to the therapy vs basic treatment on antioxidant and NADPH-generating enzymes activity, glutathione's concentration and freeradical-induced oxidation's intensity using a spectrophotometric method and iron-induced biochemiluminescence. The pigment epithelium-derived factor concentration in the serum was measured by enzyme-linked immunosorbent assay. Patients receiving combination therapy with methylethylpiridinol showed a more substantial increase in activity of glutathione peroxidase (Δ = 0.04 ± 0.11, p = 0.002), glutathione transferase (Δ = 0.12 ± 0.08, p < 0.001) and the concentration of reduced glutathione (Δ = 0.30 ± 0.17, p = 0.039). In addition, there was a significant decrease in PEDF level (Δ = -6.4 ± 5.4, p = 0.004). Correlation analysis showed a negative link between Δ postprandial glucose and Δ NADP-isocitrate dehydrogenase (-0.39, p = 0.033), Δ reduced glutathione and Δ postprandial glucose (-0.372, p = 0.043), Δ glutathione transferase and Δ PEDF (-0.37, p = 0.044). The methylethylpiridinol addition to the therapy had a more potent stimulating effect on the patients' oxidative status in comparison with standard treatment, and reliably decreased pigment epithelium-derived factor level in patients' serum. The observed differences seem to be associated with the antioxidant activity of methylethylpiridinol which contributing to the mitigation of oxidative stress reducing at diabetes mellitus.

Residual cardiovascular risk reduction guided by lifetime benefit estimation in patients with symptomatic atherosclerotic disease: effectiveness and cost-effectiveness.

To determine the (cost)-effectiveness of blood pressure lowering, lipid-lowering, and antithrombotic therapy guided by predicted lifetime benefit compared to risk factor levels in patients with symptomatic atherosclerotic disease. For all patients with symptomatic atherosclerotic disease in the UCC-SMART cohort (1996-2018; n = 7697) two treatment strategies were compared. The lifetime benefit-guided strategy was based on individual estimation of gain in cardiovascular disease (CVD)-free life with the SMART-REACH model. In the risk factor-based strategy, all patients were treated the following: low-density lipoprotein cholesterol (LDL-c) < 1.8 mmol/L, systolic blood pressure <140 mmHg, and antithrombotic medication. Outcomes were evaluated for the total cohort using a microsimulation model. Effectiveness was evaluated as total gain in CVD-free life and events avoided, cost-effectiveness as incremental cost-effectivity ratio (ICER). In comparison to baseline treatment, treatment according to lifetime benefit would lead to an increase of 24 243 CVD-free life years [95% confidence interval (CI) 19 980-29 909] and would avoid 940 (95% CI 742-1140) events in the next 10 years. For risk-factor based treatment, this would be an increase of 18 564 CVD-free life years (95% CI 14 225-20 456) and decrease of 857 (95% CI 661-1057) events. The ICER of lifetime benefit-based treatment with a treatment threshold of ≥1 year additional CVD-free life per therapy was €15 092/QALY gained and of risk factor-based treatment €9933/QALY gained. In a direct comparison, lifetime benefit-based treatment compared to risk factor-based treatment results in 1871 additional QALYs for the price of €36 538/QALY gained. Residual risk reduction guided by lifetime benefit estimation results in more CVD-free life years and more CVD events avoided compared to the conventional risk factor-based strategy. Lifetime benefit-based treatment is an effective and potentially cost-effective strategy for reducing residual CVD risk in patients with clinical manifest vascular disease.

Determination of Pentraxin-3, Interleukin-8 and Vascular Endothelial Growth Factor Levels in Patients with Gastric Adenocarcinoma.

Introduction and Aim:The purpose of this study was to determine the value, in terms of diagnosis, resectability and prognosis of pentraxin-3 (PTX3), interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) in cases of gastric adenocarcinoma, an important condition both worldwide and in Turkey, and to determine their levels in order to contribute to elucidating the pathogenesis of the disease. Materials and Methods:Serum was separated from blood specimens collected from 45 patients diagnosed with gastric adenocarcinoma and from a 30-member healthy control group. Serum PTX3, IL-8 and VEGF levels were studied by ELISA method. Results:Serum PTX3 values differed significantly between the patient group and the control group (p<0.05). Serum IL-8 values also differed significantly between the patient group and the control group (p<0.05). A significant difference was also observed between serum VEGF values in the patient group and the control group (p<0.05). Significant correlation was determined between serum PTX3 and VEGF (p<0.01; r=0.833), between serum PTX3 and IL-8 (p<0.01; r=0.818), and between serum VEGF and IL-8 (p<0.01; r=0.803), measurements when the entire study population was evaluated irrespectively of groups. Conclusion:Serum PTX3, IL-8 and VEGF levels decreased in cases of gastric adenocarcinoma compared to the control group, and their levels affected one another.

Variable alterations in plasma erythropoietin and brain-derived neurotrophic factor levels in patients with major depressive disorder with and without a history of suicide attempt

It is hypothesized that major depression disorder (MDD) is associated with impaired neuronal plasticity, and that antidepressant treatments restore neuroplasticity. Brain-derived neurotrophic factor (BDNF) and erythropoietin (Epo) show neurotrophic and neuroprotective effects. We evaluated plasma Epo and BDNF levels in 50 MDD inpatients before treatment and in 50 healthy controls. The MDD inpatients consisted of 20 MDD patients without and 30 MDD patients with a recent suicide attempt. The plasma Epo level was significantly higher in nonsuicidal and suicidal MDD patients than in healthy controls (p ≤ 0.001), while the plasma BDNF level was significantly lower in suicidal MDD than in nonsuicidal MDD patients and healthy controls (p ≤ 0.001). When classifying study participants into low-Epo and high-Epo and low-BDNF and high-BDNF subgroups based on the cutoff of Epo or BDNF calculated using receiver operating characteristics (ROC) curve analysis, logistic regression analysis revealed that high-Epo and low-BDNF status correlated with a respective significant odds ratio of 7.367 (p = 0.015) and 33.123 (p ≤ 0.001) for suicidal MDD. In conclusion, plasma BDNF level was decreased in untreated MDD patients, which was presumed to be a dysfunctional effect of the onset of MDD. However, an increase in plasma Epo was observed in MDD in connection with a recent suicide attempt, indicating that this triggers hypoxic stress to induce a compensatory increase in Epo.

Serum brain-derived neurotrophic factor levels in patients with diabetic neuropathic pain

ObjectiveDiabetic neuropathic pain (DNP) is one of the most common and severe complications in patients with diabetes. This study aimed to investigate serum brain-derived neurotrophic factor (BDNF) levels in patients with DNP and to evaluate the association between BDNF and disease severity. MethodsA total of 143 T2DM patients were included, according to clinical characteristics and douleur neuropathique 4 (DN4) questionnaire are divided into the DNP group (n = 78) and without the DNP group (n = 65). BDNF levels were measured by an enzyme-linked immunosorbent assay. Additionally, other biochemical characteristics were measured using routine laboratory methods. ResultsSerum levels of BDNF was increased significantly in the DNP group compared to without DNP group. Meanwhile, a binary logistic regression model identified as revealed BDNF (OR = 1.178, 95 %CI = 1.064−1.305,p = 0.002) was a risk factor in T2DM patients. Furthermore, the serum BDNF levels positively correlated with VAS score in the DNP patients. ConclusionsSerum BDNF was elevated in DNP patients and increased gradually with the VAS score. BDNF was identified as risk factors for pain in all T2DM patients.

Motor recovery and brain-derived neurotrophic factor level in patients with poststroke depression

ObjectiveThe aim was to assess motor recovery and brain-derived neurotrophic factor level in patients with poststroke depression (PSD).BackgroundPSD is a common problem of stroke that negatively interferes with the outcome of patients with stroke.Patients and methodsThis is a case–control study conducted in Neurology Department, Faculty of Medicine, Menoufia University. The authors included all 200 patients, and then patients with acute ischemic stroke were randomized into two groups: control group (100 patients) and depression group (100 patients). Each patient was subjected to complete history taking, detailed neurological examination, brain-derived neurotrophic factor level assessment, and neurological and psychological evaluation using the following scales: Fugl-Meyer stroke scale-motor assessment, National Institute of Health Stroke Scale, Modified Rankin scale, and Beck depression inventory scale at baseline and 3-month follow-up timing.ResultsThere was a highly significant decrease in follow-up Fugl-Meyer assessment in the depressed group compared with the control group (P < 0.01). Moreover, the authors found a highly significant decrease in follow-up brain-derived neurotrophic factor level in the depressed group compared with the control group (P < 0.01). Spearman's correlation analysis shows that follow-up Beck depression inventory-II had a highly significant negative correlation with 90-day Fugl-Meyer assessment, with a highly significant statistical difference (P = 0.0012).ConclusionCorrelation between PSD and functional outcome has been shown, and it has a negative effect on upper limb function and performance of self-care, with decrease in the levels of brain-derived neurotrophic factor.

Levels of anti-oxidative molecules and inflammatory factors in patients with vascular dementia and their clinical significance

Objectives:To explore levels of anti-oxidative molecules and inflammatory factors in patients with vascular dementia (VD) and their clinical significance.Methods:Sixty VD patients admitted in our hospital from January 2016 to January 2019 were classified into an experimental group, while another 60 healthy patients seeking physical examinations in the corresponding period were selected as a control group. Various indexes related to serum inflammatory factors and anti-oxidative molecules were compared among patients in such two groups. For the purpose of comparing anti-oxidative molecular expression levels and inflammatory factor levels in patients with VD of different severities, 60 cases in the experimental group were divided, based on a Mini-mental State Examination (MMSE) scale, into patients with mild symptoms (n=20, score: 21~26), patients with moderate symptoms (n=22, score: 10~20) and patients with severe symptoms (n=18, score: 0~9).Results:By contrast to the control group, levels of inflammatory factors (e.g., TNF-a, CRP and IL-6) in VD patients are all significantly increased and their differences show statistical significance (p<0.05); and, expression levels of anti-oxidative factors, including superoxide dismutase (SOD), glutathion peroxidase (GSH-Px), total antioxidant capacity (TAC), catalase (CAT) and glutathione reductase (GR), in the experimental group are apparently below those of the control group (P<0.05). As dementia degree increases, expression levels of serum anti-oxidative molecules in such patients are inclined to drop in a significant way (P<0.05), while inflammatory factor levels tend to go up gradually (P<0.05).Conclusions:If compared with the normal population, inflammatory factor levels in serum of VD patients are higher; however, expression levels of anti-oxidative molecules become below those of the normal population. Additionally, levels of inflammatory factors and anti-oxidative molecules may change obviously as severity of illness increases. This suggests that inflammation and oxidation play a certain role of auxoaction in VD patients.

Serum Macrophage Migration Inhibitory Factor Levels in Patients with Ischemic Stroke in Iraqi Populations

Serum Macrophage Migration Inhibitory Factor Levels in Patients with Ischemic Stroke in Iraqi Populations

Serum Macrophage Migration Inhibitory Factor Levels in Patients with Ischemic Stroke in Iraqi Populations

Background: Stroke is one of the leading causes of permanent disability worldwide. The most commoncause of stroke is the occlusion of blood circulation by a thrombus (or embolism) although it can also beproduced by the rupture of a vessel and subsequent bleeding in a certain region of the brain. Strokes can,therefore, be classified as ischemic or hemorrhagic.Aim: The present study was conducted to investigate whether serum MIF levels are associated with severityin patients with ischemic stroke.Method: A total of 40 patients with ischemic stroke were included in the study who were admitted tohospital from the period between March to August 2019, and other groups consist of 40 apparently healthyindividuals. Two blood sample were taken from each patients one during attack (within 24 hours) and theother sample during follow up (within 1-3 months) for serum concentration of MIF by ELISA technique.Results: Mean serum concentration of MIF in Ischemic stroke during attack (within 24 hours) wassignificantly higher than that of Ischemic stroke during follow up (within 1-3 months) and healthy controlgroup; 17.094±2.25ng/ml versus 12.83± 4.16ng/ml and 6.407± 3.33ng/ml respectively.

Serum macrophage colony-stimulating factor levels in patients with essential hypertension after SARS-CoV-2 infection

Understanding changes in the cytokine-mediated mechanisms in immunopathogenesis of essential hypertension (EH) after COVID-19 poses a pressing scientific issue. SARS-CoV-2 exerts direct effects on macrophages with high probability altering regulatory M-CSF-VEGF-A-IL-34 axis, thereby accounting for change in cytokine-mediated patterns of hypertension progression. Immunopathogenesis of complications after SARS-CoV-2 infection and a role of M-CSF in EH pathogenesis justify study objective – to compare the serum M-CSF and VEGF-A, IL-34 levels in stage II EH patients prior to COVID-19 and one month after recovery to assess modality of altered M-CSF-mediated mechanisms behind hypertension progression. Four groups of patients were stratified depending on EH and clinical characteristics of COVID-19 (without/with pneumonia). Blood sampling was performed one month after COVID-19. The serum M-CSF and VEGF-A, IL-34 level was measured by using enzyme-linked immunosorbent assay. The data were statistically processed by using Stat Soft Statistica 13.5. Comparative analysis of serum M-CSF level in patients with stage II EH prior and after COVID-19 revealed that regardless of clinical course (with/without pneumonia) they were featured with higher levels of M-CSF one month after recovery (p 0.001) vs baseline level. The serum VEGF-A level in patients with stage II EH did not change in papallel with increased M-CSF (458 pg/ml or more) one month after SARS CoV 2 infection. However, M-CSF stimulated rise in serum VEGF-A level and accounted for formation of marked coronary collateral network prior to infection. A relationship between the increased serum M-CSF level (higher than 392 pg/ml) and elevated percentage of COVID-19 with pneumonia in patients with stage II EH prior to the infection might be related to the hypothesis about “a role of dysregulated activation of mononuclear phagocytes in development of lung tissue damage”. The data presented prove scientific and clinical value of assessing a role for M-CSF with respect to altered cytokine-mediated patterns of EH progression after COVID-19 recovery.