Eotaxin-1 Levels in Patients with Myocardial Infarction.

BACKGROUND: Acute myocardial infarction is one of the leading causes of morbidity and mortality worldwide. Eotaxin-1, an eosinophil-specific chemoattractant, has been shown to be overexpressed in human atherosclerotic lesions. Eotaxin-1 levels are higher in coronary artery disease patients than in healthy individuals. In this study, we aimed to determine the eotaxin-1 concentrations of patients with myocardial infarction and to investigate the role of eotaxin-1 in myocardial infarction. METHODS: The study included 42 patients diagnosed with AMI (patients with suspected AMI based on history, physical examination, ECG, and biochemical markers and confirmed by angiography) and 40 healthy controls. Plasma eotaxin-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Eotaxin-1, troponin-I, CK, and CKMB levels were statistically higher in the patient group than in the control group. ROC analysis demonstrated that eotaxin-1 gave a sensitivity of 93% and a specificity of 48% once the cutoff value was 341.6 pg/mL. Additionally, the ROC analysis showed that troponin I yielded a specificity of 100% and a sensitivity of 91% when the cutoff value was 0.025 µg/L. CONCLUSIONS: Eotaxin-1/eosinophils appear to have a role in coronary artery disease independent of known risk factors. Accordingly, this study and recent studies suggest that eotaxin-1 may be useful in the diagnosis of AMI in addition to other cardiac markers.

The Effectiveness of Ischemia Modified Albumin in Determining Acute Cholecystitis and its Severity.

BACKGROUND: Acute cholecystitis (AC) is caused by chemical and bacterial inflammation of the gallbladder. The use of Tokyo guidelines is recommended in determining the diagnosis of AC and its clinical severity. In the early stages of AC, many cytokines are secreted due to the local inflammatory cell activation, leading to exacerbation of inflammation and organ failure. Ischemia modified albumin (IMA) is a type of albumin that occurs in ischemia and oxidation and is used as a marker of hypoperfusion and oxidative stress. This study aims to investigate the effectiveness of ischemia modified albumin, C-reactive protein (CRP), and some other inflammation parameters in predicting the severity of the AC on admittance. METHODS: Forty-two patients diagnosed with AC and 30 healthy individuals in the control group were included in the study. The severity assessment of the patients was performed based on the revised Tokyo guidelines (TG 13). The patients were divided into 3 groups according to severity of the disease. Blood samples were taken from the subjects on admittance. Serum IMA levels were studied using an ELISA kit. SPSS 22.00 package program was used for statistical analysis. RESULTS: Thirty (71.4%) of the participants were in the mild group, while 12 (28.6%) were in the moderate group. There were no patients in the severe group. Leukocyte, CRP, and IMA values in the patient group were higher than those of the control group (p > 0.05). According to the Tokyo classification, a significant difference was found between the groups with mild and moderate grades in terms of CRP and IMA values (p < 0.001 and p < 0.05, respectively). When the cutoff value of IMA was 84 ng/mL, the sensitivity was found to be 76% and specificity was determined to be 40% (AUC: 0.665, p = 0.017, 95% Confidence Interval). CONCLUSIONS: It is considered that IMA could be useful in predicting the clinical severity of TG13-based acute cholecystitis and, therefore, could be used in the management of treatment by the clinician such as medical treatment, early surgery, and interval surgery.

The relationship between visfatin and cardiac markers on induced myocardial infarction in rats.

Myocardial infarction (MI) is one of the most important reason of mortality into worldwide. Visfatin is a novel adipokine which was reported increased in metabolic syndrome and obesity. Moreover, it is known that visfatin increases in aterosclerotic endotelial dysfunction. In our study we want to demonstrate how visfatin changes in isoproterenol (ISO) induced MI. Rats were allocated into 4 groups in which each group included 6 rats in this study. 200 mg/kg ISO was administered into rats except control group to induce MI. I. and II. Group rats in 6th hour, III. Group rats in 24th hour and IV. Group rats in 7th day were decapitated. Visfatin was searched in cardiac tissues of all groups by immunohistochemistry stainning. Visfatin and cardiac markers' levels were measured in serum samples. Serum visfatin levels gradually increased in 6th and 24th hour in MI rats compared to controls. In 7th day visfatin levels decreased to control levels. These changes correlated with serum troponin T levels. These findings were supported by immunohistochemistry stainning of visfatin in cardiac tissues. It has been shown that visfatin could be useful in diagnosing MI and may be a biomarker for cardiac ischemia because of increasing in systemic circulation and cardiac tissues in MI like troponins.

Plasma dermcidin levels in acne patients, and the effect of isotretinoin treatment on dermcidin levels.

Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit. Dermcidin (DCD) is an antimicrobial peptide released from eccrine sweat glands and sebaceous glands. Studies investigating the role of DCD expression in acne development are scarce. The aim of this study was to determine the relationship between DCD expression and acne vulgaris and the effect of oral isotretinoin treatment on DCD levels. Two groups (one patient group and one control group) were included in the study. The patient group consisted of 30 patients with acne vulgaris who were given oral isotretinoin treatment for 6 months until the cumulative dose was attained. Plasma DCD levels were investigated before and 6 months after treatment. The control group comprised 30 volunteer individuals without acne vulgaris or any inflammatory dermatosis. Of the patients, 24 (80%) had Grade 3, 3 (10%) had Grade 1, and 3 (10%) had Grade 4 acne vulgaris, as determined according to the Pillsbury scoring method. The DCD levels in the control group were significantly higher than those in pretreatment patients (39.53 ± 20.2 vs. 28.60 ± 20.12, p = .004). Additionally, pretreatment DCD levels were significantly increased after 6 months of isotretinoin treatment in the patient group (28.60 ± 20.12 vs. 35.07 ± 24.02, p = .012). The mean pretreatment global acne grading system score of 20.86 ± 4.43 was decreased to 5.17 ± 1.91 in patients after treatment (p < .001). This study indicated that DCD plays an important role in the pathogenesis of acne. It demonstrates anti-inflammatory properties in acne vulgaris. Moreover, it was shown that isotretinoin treatment may improve acne vulgaris by increasing DCD levels.

Expression of adropin in rat brain, cerebellum, kidneys, heart, liver, and pancreas in streptozotocin-induced diabetes.

We have investigated how diabetes affects the expression of adropin (ADR) in rat brain, cerebellum, kidneys, heart, liver, and pancreas tissues. The rats in the diabetic group were administered an intraperitoneal (i.p.) injection of a single dose of 60 mg/kg streptozotocin (STZ) dissolved in a 0.1 M phosphate-citrate buffer (pH 4.5). The rats were maintained in standard laboratory conditions in a temperature between 21 and 23 °C and a relative humidity of 70 %, under a 12-h light/dark cycle. The animals were fed a standard commercial pellet diet. After 10 weeks, the animals were sacrified. ADR concentrations in the serum and tissue supernatants were measured by ELISA, and immunohistochemical staining was used to follow the expression of the hormones in the brain, cerebellum, kidneys, heart, liver, and pancreas tissues. The quantities were then compared. Increased ADR immunoreaction was seen in the brain, cerebellum, kidneys, heart, liver, and pancreas in the diabetes-induced rats compared to control subjects. ADR was detected in the brain (vascular area, pia mater, neuroglial cell, and neurons), cerebellum (neuroglial cells, Purkinje cells, vascular areas, and granular layer), kidneys (glomerulus, peritubular interstitial cells, and peritubular capillary endothelial cells), heart (endocardium, myocardium, and epicardium), liver (sinusoidal cells), and pancreas (serous acini). Its concentrations (based on mg/wet weight tissues) in these tissues were measured by using ELISA showed that the levels of ADR were higher in the diabetic rats compared to the control rats. Tissue ADR levels based on mg/wet weight tissues were as follows: Pancreas > liver > kidney > heart > brain > cerebellar tissues. Evidence is presented that shows ADR is expressed in various tissues in the rats and its levels increased in STZ-induced diabetes; however, this effect on the pathophysiology of the disorder remains to be understood.

Increased ghrelin and decreased leptin levels in patients with antisocial personality disorder.

OBJECTIVE: The study aimed to compare acyl ghrelin (AG), des-acyl ghrelin (DAG), and leptin levels considered to be used as biological markers in the etiopathogenesis of antisocial personality disorder (ASPD) with healthy controls, and to investigate the relationship between these hormones and aggression and impulsivity. METHOD: The study included 45 patients with ASPD and 61 healthy people in the control group. Sociodemographic data form, Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI), Barratt Impulsiveness Scale (BIS-11), and Buss-Durkee Aggression Scale (BDAS) were applied to all participants. Fasting venous blood samples were taken from all participants at the same time of the day and the height and weight of the participants were measured. RESULTS: It was found that the mean serum AG and DAG levels were significantly higher than that of healthy controls whereas leptin hormone levels were significantly lower in patients compared to healthy controls. BDI, BAI, BIS-11, and BDAS scores of the patients were significantly higher compared to healthy controls. There was a positive correlation between AG and DAG hormone levels and impulsivity and aggression. DISCUSSION: The present study is the first in the literature to examine AG, DAG, and leptin hormone levels of patients diagnosed with ASPD. According to the results of the study, it is believed that changes in serum leptin and ghrelin levels will bring a new perspective in terms of understanding the pathophysiological mechanism of ASPD. Further studies are required to explain the definitive roles of these hormones in ASPD.

Can laboratory parameters be an alternative to CT and RT-PCR in the diagnosis of COVID-19? A machine learning approach.

In this study, a machine learning-based decision support system that uses routine laboratory parameters has been proposed in order to increase the diagnostic success in COVID-19. The main goal of the proposed method was to reduce the number of misdiagnoses in the RT-PCR and CT scans and to reduce the cost of testing. In this study, we retrospectively reviewed the files of patients who presented to the coronavirus outpatient. The demographic, thoracic CT, and laboratory data of the individuals without any symptoms of the disease, who had negative RT-PCR test and who had positive RT-PCR test were analyzed. CT images were classified using hybrid CNN methods to show the superiority of the decision support system using laboratory parameters. Detection of COVID-19 from CT images achieved an accuracy of 97.56% with the AlexNet-SVM hybrid method, while COVID-19 was classified with an accuracy of 97.86% with the proposed method using laboratory parameters.

Scat-NET: COVID-19 diagnosis with a CNN model using scattergram images.

The acute respiratory syndrome COVID-19 disease, which is caused by SARS-CoV-2, has infected many people over a short time and caused the death of more than 2 million people. The gold standard in detecting COVID-19 is to apply the reverse transcription polymerase chain reaction (RT-PCR) test. This test has low sensitivity and produces false results of approximately 15%-20%. Computer tomography (CT) images were checked as a result of suspicious RT-PCR tests. If the virus is not infected in the lung, the virus is not observed on CT lung images. To overcome this problem, we propose a 25-depth convolutional neural network (CNN) model that uses scattergram images, which we call Scat-NET. Scattergram images are frequently used to reveal the numbers of neutrophils, eosinophils, basophils, lymphocytes and monocytes, which are measurements used in evaluating disease symptoms, and the relationships between them. To the best of our knowledge, using the CNN together with scattergram images in the detection of COVID-19 is the first study on this subject. Scattergram images obtained from 335 patients in total were classified using the Scat-NET architecture. The overall accuracy was 92.4%. The most striking finding in the results obtained was that COVID-19 patients with negative RT-PCR tests but positive CT test results were positive. As a result, we emphasize that the Scat-NET model will be an alternative to CT scans and could be applied as a secondary test for patients with negative RT-PCR tests.

Nesfatin-1 Hormone Levels in Patients with Antisocial Personality Disorder and Their Relationship with Clinical Variables.

OBJECTIVE: This study aims to investigate the levels of nesfatin-1-hormone in patients with Antisocial Personality Disorder (ASPD) and their relationship with clinical variables. METHODS: A total of 90 people (45 ASPD, 45 controls) were included in our study. Sociodemographic Data Form, Beck-Depression-Inventory (BDI), Beck-Anxiety-Inventory (BAI), Barratt Impulsivity Scale (BIS-11), Buss-Durkee-Hostility-Inventory (BDHI) were applied to all participants. Venous blood samples were taken from participants at the same time of the day when they were hungry. RESULTS: It was found that the BDI and BAI scores of the ASPD were higher than those of the controls (p<0.001, for both scales). The scores in BIS-11; motor and nonplanning-impulsivity subscales were higher than those of the controls (p<0.001, 0.036, respectively). The scores obtained by the ASPD were higher in all subscales of BDHI (p<0.001). For the nesfatin-1-hormone, the values of the ASPD were lower than those of the controls (p=0.044). No relationship was found between the nesfatin-1-hormone and any other laboratory parameters and applied scales (p>0.05). CONCLUSION: This is the first study to examine the nesfatin-1-hormone levels in patients with any personality disorder. Further studies with more participants are needed in different types of personality disorders to understand the relationship between personality disorder and nesfatin-1-hormone levels.

Chemerin and Dermcidin in Human Milk and Their Alteration in Gestational Diabetes.

BACKGROUND: Chemerin and dermcidin, which have antimicrobial properties, are molecules that are also related to insulin resistance and inflammation. RESEARCH AIMS: The aims were to determine the amounts of chemerin and dermcidin in the milk and blood of mothers with gestational diabetes, and to compare the amounts of chemerin and dermcidin in the milk and blood of mothers with and without diabetes. METHODS: This was a two-group nonrandomized longitudinal study with a convenience sampling of mothers without gestational diabetes (n = 27) and mothers with gestational diabetes (n = 26). Human milk and blood samples were obtained from these mothers during colostrum, transitional, and mature milk periods. The amount of chemerin and dermcidin in these samples was measured by enzyme-linked immunosorbent assay. RESULTS: The presence of chemerin and dermcidin was first detected in human milk. The amounts of chemerin and dermcidin in the blood of all the mothers were greater in the colostrum period and lowest in the mature period. The amount of chemerin and dermcidin in the milk of all the mothers was greater than that in the blood. The amounts of chemerin and dermcidin were significantly increased in both blood and human milk within the gestational age samples. CONCLUSIONS: Chemerin and dermcidin may contribute to the protection of infants from infections during infancy. Increased amounts of these molecules found within the gestational diabetes group may also prevent adverse maternal and fetal outcomes.

ENHO gene expression and serum adropin level in rheumatoid arthritis and systemic lupus erythematosus.

BACKGROUND: Adropin, a secreted protein, is encoded by the energy homeostasis-associated gene (ENHO). It is expressed by a variety of tissues and cells. It has been implicated in several physiological and pathological processes, such as angiogenesis and apoptosis. OBJECTIVES: The aim of the present study was to investigate the ENHO gene expression and serum adropin levels in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). MATERIAL AND METHODS: The study included 36 patients with RA, 22 patients with SLE and 20 healthy controls (HC). Patients with a disease activity score-28-erythrocyte sedimentation rate (DAS28-ESR) >2.6 in the RA group and an SLE disease activity index (SLEDAI) >6 in the SLE group were accepted as active. Serum adropin levels were analyzed by the enzyme-linked immunosorbent assay (ELISA) method. The ENHO gene and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) gene expressions in peripheral blood mononuclear cells were analyzed by real-time polymerase chain reaction (PCR). RESULTS: The ENHO gene mRNA expression was significantly higher in the RA group than in the HC group (p = 0.024), although it was similar between the SLE and HC groups (p = 0.920). On the other hand, there were no significant differences among the study groups in terms of serum adropin levels (p > 0.05 for all). Moreover, there was no significant difference in terms of the ENHO expression and serum adropin levels between active and inactive RA and SLE patients. CONCLUSIONS: Although the ENHO gene expression is increased, serum adropin level is not altered in RA. Similarly, adropin seems not to be associated with SLE. However, the potential link between adropin and inflammatory diseases need to be tested by further studies.

Adropin as a potential marker of enzyme-positive acute coronary syndrome.

AIM: Enzyme-positive acute coronary syndrome (EPACS) can cause injury to or death of the heart muscle owing to prolonged ischaemia. Recent research has indicated that in addition to liver and brain cells, cardiomyocytes also produce adropin. We hypothesised that adropin is released into the bloodstream during myocardial injury caused by acute coronary syndrome (ACS), so serum and saliva levels rise as the myocytes die. Therefore, it could be useful to investigate how ACS affects the timing and significance of adropin release in human subjects. METHODS: Samples were taken over three days after admission, from 22 EPACS patients and 24 age- and gendermatched controls. The three major salivary glands (submandibular, sublingual and parotid) were immunohistochemically screened for adropin production, and serum and saliva adropin levels were measured by an enzyme-linked immunosorbent assay (ELISA). Salivary gland cells produce and secrete adropin locally. RESULTS: Serum adropin, troponin I, CK and CK-MB concentrations in the EPACS group became gradually higher than those in the control group up to six hours (p < 0.05), and troponin I continued to rise up to 12 hours after EPACS. The same relative increase in adropin level was observed in the saliva. Troponin I, CK and CK-MB levels started to decrease after 12 hours, while saliva and serum adropin levels started to decrease at six hours after EPACS. In samples taken four hours after EPACS, when the serum adropin value averaged 4.43 ng/ml, the receiver operating characteristic curve showed that the serum adropin concentration indicated EPACS with 91.7% sensitivity and 50% specificity, while when the cut-off adropin value in saliva was 4.12 ng/ml, the saliva adropin concentration indicated EPACS with 91.7% sensitivity and 57% specificity. CONCLUSION: In addition to cardiac troponin and CK-MB assays, measurement of adropin level in saliva and serum samples is a potential marker for diagnosing EPACS.

Comparison of the therapeutic effects of sildenafil citrate, heparin and neuropeptides in a rat model of acetic acid-induced gastric ulcer.

AIMS: The purpose of our investigative work has been to determine whether there can be therapeutic roles in the administration of sildenafil citrate, heparin and several neuropeptides on an animal model where gastric ulcers were induced with acetic acid, and to compare their efficacy. MATERIALS AND METHODS: The animals were divided into 13 groups, with 4 animals in each. Gastric ulcers was induced in the animals of 12 groups with one untreated group being left as the control (Group I - control; given normal saline (NS)). The other groups were: Group II (ulcer+NS); Group III (5mg/kg sildenafil citrate, low dose); Group IV (10mg/kg sildenafil citrate, high dose); Group V (0.6mg/kg heparin, low dose); Group VI (6mg/kg heparin, high dose); Group VII (20nmol/kg des-acyl ghrelin); Group VIII (40nmol/kg des-acyl ghrelin); Group IX (4nmol/kg acyl ghrelin); Group X (8nmol/kg acly ghrelin); Group XI (20pmol/kg Nesfatin-1); Group XII (15nmol/kg Obestatin) and Group XIII (5nmol/kg Neuropeptide Y). Gastric neuropeptide expression was measured using an immunohistochemical method, and the amount in circulation was detected using ELISA. To compare with no treatment, the controls and other treatment groups, we recorded loss of the surface epithelium of the stomach, erosion, bleeding and inflammatory cell infiltration in the upper halves of the gastric glands. KEY FINDINGS: The muscularis and the layers beneath it were, however, apparently normal. The gastric mucosa healed with little or no inflammation when sildenafil citrate, low dose heparin, ghrelin, NUCB2/Nesfatin-1, obestatin, Neuropeptide Y were administered. SIGNIFICANCE: Overall the data indicate that low dose heparin, and especially sildenafil citrate and neuropeptides, can be used clinically as an alternative approach in the treatment of the gastric ulcer.

Serum, Saliva, and Urine Irisin with and Without Acute Appendicitis and Abdominal Pain.

A 112-amino-acid protein irisin (IRI) is widely expressed in many organs, but we currently do not know whether appendix tissue and blood cells express it. If appendix tissue and neutrophil cells express IRI, measuring its concentration in biological fluids might be helpful in the diagnosis of acute appendicitis (AA), since neutrophil cells are the currently gold-standard laboratory parameters for the diagnosis of AA. Therefore, the purpose of this study was to investigate the suitability of enzyme-linked immunosorbent assay-based measurements of the proposed myokine IRI for the discrimination of patients with AA from those with acute abdominal pain (AP) and healthy controls. Moreover, immunoreactivity to IRI was investigated in appendix tissues and blood cells. Samples were collected on admission (T1), 24 hours (T2), and 72 hours (T3) postoperatively from patients with suspected AA and from patients with AP corresponding to T1-T3, whereas control subject blood was once corresponding to T1. IRI was measured in serum, saliva, and urine by using enzyme-linked immunosorbent assay, whereas in appendix tissue and blood cells, IRI was detected by immunohistohcemistry. Appendix tissue and blood cells (except for erythrocytes) are new sources of IRI. Basal saliva, urine, and serum levels were higher in children with AA compared with postoperative levels (T2) that start to decline after surgery. This is in line with the finding that IRI levels are higher in children with AA when compared with those with AP or control subject levels, most likely due to a large infiltration of neutrophil cells in AA that release its IRI into body fluids. Measurement of IRI in children with AA parallels the increase or decrease in the neutrophil count. This new finding shows that the measurement of IRI and neutrophil count can together improve the diagnosis of AA, and it can distinguish it from AP. IRI can be a candidate marker for the diagnosis of AA and offers an additional parameter to neutrophil count. The promising receiving operating curve results indicate the following sensitivities and specificities, respectively, for IRI: serum 90% and 55%, saliva 90% and 60%, and urine 90% and 50%. Serum neutrophil count gave a sensitivity of 90% and a specificity of 90%. This promising result now needs to be confirmed in a larger group of patients.

Maternal and umbilical cord copeptin levels in pregnancies complicated by fetal growth restriction.

OBJECTIVE: The aim of this study was to compare maternal and fetal serum copeptin concentrations in pregnancies complicated by isolated fetal growth restriction (FGR), and uncomplicated pregnancies, and to investigate relationships between copeptin levels and clinical parameters. METHODS: Maternal and fetal serum copeptin levels were measured in 21 women with pregnancies complicated by isolated FGR and 20 women with normal pregnancies (control group). Doppler assessment of the uterine and umbilical arteries was performed in each patient. RESULTS: Maternal serum copeptin levels were significantly higher in women with isolated FGR compared to controls (p = 0.042). In addition, maternal copeptin levels were inversely correlated with the uterine artery pulsatility and resistance indices and positively correlated with neonatal birth weight. Umbilical vein copeptin levels were significantly increased in neonates with adverse outcomes (p = 0.001). CONCLUSIONS: Increased maternal copeptin concentration may reflect a response to stress, thus serving as a compensatory mechanism in pregnancies complicated by FGR.

Neuron-Specific Enolase, S100 Calcium-Binding Protein B, and Heat Shock Protein 70 Levels in Patients With Intracranial Hemorrhage.

The authors evaluated neuron-specific enolase (NSE), S100 calcium-binding protein B (S100B), and heat shock protein 70 (HSP 70) levels and their relationships with in-hospital mortality, Glasgow Coma Scale (GCS) scores, and National Institute of Health Stroke Scale (NIHSS) scores. In total, 35 patients older than 18 years were presented to our emergency department and were diagnosed with non-traumatic intracranial hemorrhage (ICH) and 32 healthy controls were included. Blood samples were drawn on days 0 and 5. S100 calcium-binding protein B and HSP levels were significantly higher in patients than in controls on days 0 and 5. Neuron-specific enolase levels were higher in patients than in controls on day 0, but there was no significant difference on day 5. S100 calcium-binding protein B was negatively correlated with GCS, whereas it was positively correlated with NIHSS and bleeding volume. There was also a negative correlation between NSE and GCS, but it was not statistically significant. In addition, no significant correlation was found in terms of bleeding volume or NIHSS. Heat shock protein 70 was negatively correlated with GCS and positively correlated with bleeding volume and NIHSS, but these results were not statistically significant. S100 calcium-binding protein B and HSP 70 levels were significantly higher in those who died compared with survivors. The areas under the curve of S100 B, NSE, and HSP 70 for mortality were 0.635, 0.477, and 0.770, respectively. Neuron-specific enolase, S100B, and HSP 70 levels are simple, inexpensive, and objective measures in cases of ICH. These tests can be used to support an assessment for screening ICH patients with clinical scoring systems, such as GCS and NIHSS.

Ghrelin in the pilosebaceous unit: alteration of ghrelin in patients with acne vulgaris.

BACKGROUND: Ghrelin in the pilosebaceous tissues of human skin and ghrelin levels in patients with acne vulgaris have not yet been investigated. OBJECTIVE: The purpose of this study was to screen ghrelin immunoreactivity by immunohistochemistry in human pilosebaceous tissues of human skin and also to determine the quantities of ghrelin in the serum of the patients with acne vulgaris. METHODS: 30 patients presenting with acne vulgaris and 30 control subjects participated in this study. Ghrelin levels were determined by enzyme linked immunosorbent assay (ELISA). Human hair follicles and sebaceous glands were immunohistochemically examined. RESULTS: Immunohistochemistry results showed that there is a strong ghrelin immunoreactivity in the hair follicles and sebaceous glands in sections of human skin. The mean serum ghrelin levels (27.58 ・} 15.44 pg/mL) in patients with acne vulgaris was significantly lower than those of controls (35.62・}20.46 pg/mL). CONCLUSIONS: Ghrelin produced in hair follicles and sebaceous glands of the skin might participate in the pathogenesis of acne vulgaris and also acne vulgaris in humans might be associated with decreased serum ghrelin.

Effect of carnosine, methylprednisolone and their combined application on irisin levels in the plasma and brain of rats with acute spinal cord injury.

Spinal cord injury (SCI) might occur to anybody at any time and any age. In its treatment, methylprednisolone (MP) is a first choice worldwide, but there is still no significant breakthrough in truly beneficial treatment due to SCI's complex pathophysiology. We investigated the effect of carnosine, methylprednisolone (MP) and its combination on irisin levels in the plasma, brain and medulla spinalis tissues in SCI using a rat model. The rats were divided into 6 groups: I (Control, saline); II (sham animals with laminectomy without cross-clamping); III (SCI); IV (SCI treated with 150mg/kg carnosine); V (SCI treated with 30mg/kg methylprednisolone); and VI (SCI treated with a combination of carnosine and MP). The animals were given traumatic SCI after laminectomy, using 70-g closing force aneurysm clips (Yasargil FE 721). Irisin concentration was measured by ELISA. The distribution of irisin in brain and spinal cord tissues was examined by immunochemistry. Irisin was mainly expressed in the astrocytes and microglia of brain tissues, and multipolar neurones of the anterior horn of spinal cord tissue in rats of all groups, indicating that irisin is physiologically indispensable. MP and carnosine and the combination of the two, significantly increased irisin in plasma and were accompanied by a significant rise in irisin immunoreactivity of brain and spinal cord tissues of the injured rats compared with control and sham. This finding raises the possibility that methylprednisolone and carnosine regulate the brain and spinal cord tissues in SCI by inducing irisin expression, and may therefore offer a better neurological prognosis.

Today's and yesterday's of pathophysiology: biochemistry of metabolic syndrome and animal models.

During the past 20 y, there has been much interest in sugars and especially fructose in relation to human health. Over the past decade, considerable scientific debate and controversy have arisen about the potential health effects of sucrose, high-fructose corn syrup (HFCS), and fructose itself. HFCS increasingly has been used as a sweetener in thousands of food products and soft drinks, leading to the development of obesity, diabetes, dyslipidemia, and metabolic syndrome (MetS) in both rodents and humans, which is associated with an increase in body weight. There is a need for detailed research on the mechanism underlying MetS that could lead to a remedy. This review will first systematically present a definition of MetS, its history, prevalence, and comparative diagnostic criteria. We will then consider fructose and its effects on human health, the diet-induced obesity model (various fat contents), the hypercholesterolemic model, the diabetes model, the hypertensive model, the MetS or insulin resistance model, and biomarkers related to MetS, in light of contemporary data using multiple databases (PubMed, MEDLINE, and OVID).