Local response to the COVID-19 pandemic: The case of Nepal.

Outbreak of the coronavirus pandemic is testing governments' capacity. Generally, considerable attention is paid to the capacity and response of the central or national governments; however, COVID-19 pandemic is local in nature. Although central authorities have important roles to play in COVID-19 response, local governments, being closer to people, are best-positioned to form the first line of defense.

Molecular mechanisms of esophageal epithelial regeneration following repair of surgical defects with acellular silk fibroin grafts.

Constructive remodeling of focal esophageal defects with biodegradable acellular grafts relies on the ability of host progenitor cell populations to repopulate implant regions and facilitate growth of de novo functional tissue. Intrinsic molecular mechanisms governing esophageal repair processes following biomaterial-based, surgical reconstruction is largely unknown. In the present study, we utilized mass spectrometry-based quantitative proteomics and in silico pathway evaluations to identify signaling cascades which were significantly activated during neoepithelial formation in a Sprague Dawley rat model of onlay esophagoplasty with acellular silk fibroin scaffolds. Pharmacologic inhibitor and rescue experiments revealed that epithelialization of neotissues is significantly dependent in part on pro-survival stimuli capable of suppressing caspase activity in epithelial progenitors via activation of hepatocyte growth factor receptor (c-MET), tropomyosin receptor kinase A (TrkA), phosphoinositide 3-kinase (PI3K), and protein kinase B (Akt) signaling mechanisms. These data highlight the molecular machinery involved in esophageal epithelial regeneration following surgical repair with acellular implants.

BASP1 labels neural stem cells in the neurogenic niches of mammalian brain.

The mechanisms responsible for determining neural stem cell fate are numerous and complex. To begin to identify the specific components involved in these processes, we generated several mouse neural stem cell (NSC) antibodies against cultured mouse embryonic neurospheres. Our immunohistochemical data showed that the NSC-6 antibody recognized NSCs in the developing and postnatal murine brains as well as in human brain organoids. Mass spectrometry revealed the identity of the NSC-6 epitope as brain abundant, membrane-attached signal protein 1 (BASP1), a signaling protein that plays a key role in neurite outgrowth and plasticity. Western blot analysis using the NSC-6 antibody demonstrated multiple BASP1 isoforms with varying degrees of expression and correlating with distinct developmental stages. Herein, we describe the expression of BASP1 in NSCs in the developing and postnatal mammalian brains and human brain organoids, and demonstrate that the NSC-6 antibody may be a useful marker of these cells.

Evaluation of the Effect of Topical Hypericum perforatum Oil on Excisional Palatal Wound Healing in Rabbits.

Aim: The aim of this study was to evaluate the effect of Hypericum perforatum (HP) oil on wound-healing process in rabbit palatal mucosa. Materials and Methods: Thirty-six New Zealand albino rabbits were randomly allocated to following groups; (1) HP oil (test, n = 18) and (2) olive oil (control, n = 18). Palatinal excisional wounds were created and the oils were topically applied (0.1 ml, 30 s, twice a day). Gingival biopsies were excised, and analyzed for re-epithelialization (RE) and granulation tissue maturation (GTM) on days 3, 7, and 14 after surgery. Levels of vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF-2) were assessed using the immunohistochemical method. Apoptotic cells (ACs) were evaluated using TUNEL staining. Enzyme-linked immunosorbent assay was used to assess tissue catalase (CAT) and malondialdehyde (MDA) levels. Results: RE and GTM were completed earlier in the HP oil group than in the control group. The number of positively stained cells/vessels was higher in olive oil than in the test group on day 3 for FGF-2 and on days 3 and 7 for VEGF (p < 0.05). In contrast, on day 14, a higher number of vessels was observed in the HP oil group than in the control group. HP oil treatment reduced the number of ACs compared to olive oil (p < 0.05), but the difference during the healing period did not reach significance. Tissue CAT and MDA levels between groups were not different, and also the results were the same when the levels were analyzed by the evaluated time periods (p > 0.05). Conclusions: The results of this study demonstrated that topical HP oil treatment did not provide an additional benefit to its base, olive oil, in the early phase of secondary wound healing.

Heterogeneity of Stem Cells in the Hippocampus.

The discovery of neural stem cells in the adult mammalian hippocampus has attracted attention and controversy, which both continue to this day. Hippocampal neural stem cells and their immediate progeny, amplifying neuroprogenitor cells, give rise to neurons and astrocytes in the region. Envisioned as possible key for tissue regeneration, whether mobilized endogenously or transplanted exogenously, neural stem cells have been in the eye of both public and science over the course of the past 20 years. These cells are a heterogeneous population, and here, we review different aspects of their heterogeneity from morphology to metabolism and response to different stimuli.

Imaging Mass Spectrometry: A New Tool to Assess Molecular Underpinnings of Neurodegeneration.

Neurodegenerative diseases are prevalent and devastating. While extensive research has been done over the past decades, we are still far from comprehensively understanding what causes neurodegeneration and how we can prevent it or reverse it. Recently, systems biology approaches have led to a holistic examination of the interactions between genome, metabolome, and the environment, in order to shed new light on neurodegenerative pathogenesis. One of the new technologies that has emerged to facilitate such studies is imaging mass spectrometry (IMS). With its ability to map a wide range of small molecules with high spatial resolution, coupled with the ability to quantify them at once, without the need for a priori labeling, IMS has taken center stage in current research efforts in elucidating the role of the metabolome in driving neurodegeneration. IMS has already proven to be effective in investigating the lipidome and the proteome of various neurodegenerative diseases, such as Alzheimer's, Parkinson's, Huntington's, multiple sclerosis, and amyotrophic lateral sclerosis. Here, we review the IMS platform for capturing biological snapshots of the metabolic state to shed more light on the molecular mechanisms of the diseased brain.

Metabolomics of mammalian brain reveals regional differences.

BACKGROUND: The mammalian brain is organized into regions with specific biological functions and properties. These regions have distinct transcriptomes, but little is known whether they may also differ in their metabolome. The metabolome, a collection of small molecules or metabolites, is at the intersection of the genetic background of a given cell or tissue and the environmental influences that affect it. Thus, the metabolome directly reflects information about the physiologic state of a biological system under a particular condition. The objective of this study was to investigate whether various brain regions have diverse metabolome profiles, similarly to their genetic diversity. The answer to this question would suggest that not only the genome but also the metabolome may contribute to the functional diversity of brain regions. METHODS: We investigated the metabolome of four regions of the mouse brain that have very distinct functions: frontal cortex, hippocampus, cerebellum, and olfactory bulb. We utilized gas- and liquid- chromatography mass spectrometry platforms and identified 215 metabolites. RESULTS: Principal component analysis, an unsupervised multivariate analysis, clustered each brain region based on its metabolome content, thus providing the unique metabolic profile of each region. A pathway-centric analysis indicated that olfactory bulb and cerebellum had most distinct metabolic profiles, while the cortical parenchyma and hippocampus were more similar in their metabolome content. Among the notable differences were distinct oxidative-anti-oxidative status and region-specific lipid profiles. Finally, a global metabolic connectivity analysis using the weighted correlation network analysis identified five hub metabolites that organized a unique metabolic network architecture within each examined brain region. These data indicate the diversity of global metabolome corresponding to specialized regional brain function and provide a new perspective on the underlying properties of brain regions. CONCLUSION: In summary, we observed many differences in the metabolome among the various brain regions investigated. All four brain regions in our study had a unique metabolic signature, but the metabolites came from all categories and were not pathway-centric.

Evaluation of Pregnancy-Associated Plasma Protein-A Levels in Patients with Chronic Obstructive Pulmonary Disease and Associations with Disease Severity.

Chronic obstructive pulmonary disease (COPD) represents a systemic disorder characterized by chronic airflow limitation and an increased inflammatory response of the airways. Comorbidities are frequent in COPD and it is crucial to predict these in early stage for adequate management of COPD. Recent studies have reported that elevated levels of pregnancy-associated plasma protein-A (PAPP-A), a zinc-binding metalloproteinase, detected in patients with asthma, lung cancer, and pulmonary embolism and independently associated with cardiovascular events. We aimed to assess serum PAPP-A levels in COPD and the associations between disease severity. The study population consisted of 75 COPD patients and 35 healthy subjects as a control group. PAPP-A levels were measured by using ultrasensitive enzyme-linked immunosorbent assay. Elevated levels of PAPP-A were observed in patients with COPD on comparison with the controls (p = 0.000). The levels in stage 1 (34.73 ± 22.97) and stage 2 (48.29 ± 53.35) were significantly higher than stage 3 (20.58 ± 22.98) and stage 4 (27.36 ± 21.46) (p = 0.049). Increased PAPP-A levels may be a useful marker in management of COPD that seeks to prevent the development of comorbidities such as adverse cardiovascular diseases.

Serum Levels of Omentin in Pseudoexfoliation Syndrome.

PURPOSE: Omentin, a member of the adipocytokines family, is derived from adipose tissue and a lower level of serum omentin is considered as a metabolic risk factor. The aim of the present study is to evaluate the serum levels of omentin in patients with pseudoexfoliation syndrome (PES). MATERIALS AND METHODS: Patients without any systemic or ocular disease other than PES were included in the study. Age-matched and sex-matched healthy volunteers without PES were accepted as a control group. After detailed ophthalmologic examination, blood samples were obtained from a forearm vein. Serum levels of omentin were determined by the method of enzyme-linked immunosorbent assay. RESULTS: The mean age of the PES group (12 females, 12 males, n=24) was 75.2 ± 8.4 years, and the control group (10 females, 10 males, n=20) was 75 ± 6.7 years. There was no difference between the groups in terms of age (P=0.93) and sex (P=0.9). The mean serum levels of omentin in the PES group were 801.5 ± 317.1 ng/mL and in the control group were 1150.1 ± 584.1 ng/mL. The mean serum omentin levels were significantly lower in patients with PES (P=0.016). CONCLUSION: Lower levels of serum omentin in patients with PES compared with healthy subjects may support the theory of systemic nature of the disease.

Serum levels of visfatin, resistin and adiponectin in patients with psoriatic arthritis and associations with disease severity.

AIM: Psoriatic arthritis (PsA) is an inflammatory form of arthritis typically associated with psoriasis and/or psoriatic nail disease. Adipocytokines were once thought to influence development of (only) insulin resistance and diabetes mellitus. However, it is now clear that adipocytokines play important roles in development of the inflammation associated with either autoimmune or auto-inflammatory disorders. In the present study, we measured changes in the serum levels of adiponectin, resistin and visfatin, and the associations of such changes with the extent of disease activity and insulin resistance in PsA patients. MATERIAL AND METHODS: A total of 67 subjects (28 with PsA and 39 healthy controls) without hypertension or diabetes mellitus were enrolled. Adiponectin, resistin and visfatin levels, and the extent of insulin resistance (assayed using the homeostasis model [HOMA-IR]), were measured in all subjects. Assessment of PsA disease activity was done with the Disease Activity Index for Psoriatic Arthritis (DAPSA). RESULTS: Psoriatic arthritis patients had considerably higher serum levels of adiponectin, resistin and visfatin than did healthy controls (all P < 0.05). In the logistic regression analysis, the following variables may contribute to complex pathogenesis of PsA: adiponectin (P = 0.001, OR = 3.1, 95% CI = 1.6-6.0), resistin (P = 006, OR = 1.8, 95% CI = 1.2-2.9) and visfatin (P = 0.031, OR = 3.9, 95% CI = 1.1-13.9). In contrast, we have not detected any correlation between DAPSA and adipocytokine serum levels (P > 0.05). CONCLUSION: There is no correlation between adipocytokines and disease activity. Although serum adiponectin, resistin and visfatin levels are higher in patients with PsA, pathophysiological significance of the result has to be evaluated with more extensive studies.

Serum Uric Acid, Alanine Aminotransferase, Hemoglobin and Red Blood Cell Count Levels in Pseudoexfoliation Syndrome.

Purpose. The pathogenesis of pseudoexfoliation (PEX), the most common cause of secondary glaucoma, has not been clearly identified, but there is increasing evidence that points out the role of oxidative stress. The aim of this study is to evaluate some of the most commonly used blood parameters, hemoglobin (Hb), red blood cell count (RBC), alanine aminotransferase (ALT), and uric acid (UA) levels, in subjects with PEX. Materials and Methods. This study is performed in a state hospital between November 2011 and December 2012. Retrospective chart review of subjects who underwent cataract surgery was performed. Thirty-one healthy subjects with PEX and 34 healthy subjects without PEX were evaluated. Hb, RBC, ALT, and UA levels were recorded. Student's t-test was used to compare the two groups. Results. The mean age was 73.6 ± 14.1 years in PEX group and 70.1 ± 12.7 in control group (p = 0.293). Hb, RBC, ALT, and UA levels did not show a statistically significant difference among PEX and control groups (p > 0.05 for all). Conclusion. Serum levels of Hb, RBC, ALT, and UA levels were similar in subjects with and without PEX. Further studies are needed to clarify the precise role of Hb, RBC, ALT, and UA in the pathogenesis of PEX.

Serum and aqueous xanthine oxidase levels, and mRNA expression in anterior lens epithelial cells in pseudoexfoliation.

PURPOSE: The aim of this study was to determine serum and aqueous xanthine oxidase (XO) levels, and mRNA expression in anterior lens epithelial cells in pseudoexfoliation (PEX). METHODS: In this prospective study, serum, aqueous and anterior lens capsules were taken from 21 patients with PEX and 23 normal subjects who had undergone routine cataract surgery. Serum and aqueous XO levels were analyzed using the colorimetric method. mRNA expression of XO in anterior lens epithelial cells was evaluated using reverse transcription polymerase chain reaction analysis. RESULTS: Serum XO levels (means ± standard deviations) were 207.0 ± 86.1 IU/mL and 240.6 ± 114.1 IU/mL in the normal and PEX groups, respectively (p = 0.310). Aqueous XO levels (means ± standard deviations) were 65.5 ± 54.3 IU/mL in the normal group and 130.5 ± 117.4 IU/mL in the PEX group (p = 0.028). There was a 2.9 fold decrease in mRNA expression in anterior lens epithelial cells of PEX, which is significantly lower than the normal group (p = 0.01). CONCLUSIONS: Higher aqueous XO levels lacking associated different serum XO suggests higher oxidative stress in the aqueous. Higher aqueous XO levels in PEX with decreased mRNA expression in anterior lens epithelial cells indicate possible overexpression of XO in other structures related to the aqueous.

Tear and serum vitamin D levels in children with allergic rhinoconjunctivitis.

BACKGROUND: Although solid cohort studies confirmed a preventative role for the anti-oxidant vitamin D in allergic asthma, a limited number of studies focused on allergic rhinoconjunctivitis (ARC). Here, we aimed to determine 25-hydroxycholecalciferol levels in tear and serum in young allergic rhinoconjunctivitis patients as compared to their apparently healthy matched controls. METHODS: In total, 22 children with allergic rhinoconjunctivitis and 31 healthy control subjects underwent serum total IgE and 25-hydroxycholecalciferol measurements. Tear levels of 25-hydroxycholecalciferol were also determined in both groups. RESULTS: The mean serum total IgE level in the ARC group (143.6±132.8IU/ml) was significantly higher than that in the control group (54.8±44.1IU/ml; p=0.03). Serum 25(OH)D levels were significantly higher in the ARC group (34.1±12.7ng/ml) than in the healthy controls (21.8±11.3ng/ml; p=0.001). CONCLUSIONS: To our knowledge, this is the first reported study to show an association between serum 25-hydroxycholecalciferol and ARC in a childhood group. Higher levels of serum 25-hydroxycholecalciferol in children with allergic rhinoconjunctivitis may indicate a possible aetiopathogenic mechanism in the development of allergic rhinoconjunctivitis. This is also the first report to examine tear fluid vitamin D levels in paediatric ARC patients.

Effects of ivabradine therapy on heart failure biomarkers.

BACKGROUND: Heart rate (HR) reduction is associated with improved outcomes in patients with heart failure (HF) and biomarkers can be a valuable diagnostic tool in HF management. The primary aim of our study was to evaluate the short-term (6 months) effect of ivabradine on N-terminal pro B-type natriuretic peptide (NT-proBNP), CA-125, and cystatin-C values in systolic HF outpatients, and secondary aim was to determine the relationship between baseline HR and the NT-proBNP, CA-125, cystatin-C, and clinical status variation with ivabradine therapy. METHODS: Ninety-eight patients (mean age: 65.81 ± 10.20 years; 33 men), left ventricular ejection fraction < 35% with Simpson method, New York Heart Association (NYHA) class II-III, sinus rhythm and resting HR > 70/min, optimally treated before the study were included. Among them, two matched groups were formed: the ivabradine group and the control group. Patients received ivabradine with an average (range of 10-15) mg/day during 6 months of follow-up. Blood samples for NT-proBNP, CA-125, and cystatin-C were taken at baseline and at the end of a 6-month follow-up in both groups. RESULTS: There was a significant decrease in NYHA class in the ivabradine group (2.67 ± ± 0.47 vs. 1.85 ± 0.61, p < 0.001). When ivabradine and control groups were compared, a significant difference was also found in NHYA class 6 months later (p = 0.013). A significant decrease was found in HR in the ivabradine and control groups (84.10 ± 8.76 vs. 68.36 ± ± 8.32 bpm, p = 0.001; 84.51 ± 10 vs. 80.40 ± 8.3 bpm, p = 0.001). When both groups were compared, a significant difference was also found in HR after 6 months (p = 0.001). A significant decrease was found in cystatin-C (2.10 ± 0.73 vs. 1.50 ± 0.44 mg/L, p < 0.001), CA-125 (30.09 ± 21.08 vs. 13.22 ± 8.51 U/mL, p < 0.001), and NT-proBNP (1,353.02 ± 1,453.77 vs. 717.81 ± 834.76 pg/mL, p < 0.001) in the ivabradine group. When ivabradine and control groups were compared after 6 months, a significant decrease was found in all HF parameters (respectively; cystatin-C: p = 0.001, CA-125: p = 0.001, NT-proBNP: p = 0.001). Creatinine level was significantly decreased and glomerular filtration rate (GFR) was significantly increased in the ivabradine group (1.02 ± 0.26 vs. 0.86 ± 0.17, creatinine: p = 0.001; 79.26 ± 18.58 vs. 92.48 ± 19.88, GFR: p = 0.001). There was no significant correlation between NYHA classes (before and after ivabradine therapy) and biochemical markers, or HR. CONCLUSIONS: In the outpatients with systolic HF, persistent resting HF > 70/min with optimal medical therapy, the NT-proBNP, CA-125, and cystatin-C reductions were obtained with ivabradine treatment. Measurement of NT-proBNP, CA-125, and cystatin-C may prove to be useful in biomarker panels evaluating ivabradine therapy response in HF patients.

Pentraxin 3 as a novel biomarker of inflammation in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease of the lungs in which inflammatory markers are involved with significant extrapulmonary effects that may contribute to its severity and complications. Moreover, some of the inflammatory markers such as C-reactive protein (CRP) are associated with COPD. Pentraxin 3 (PTX3) is the member of long pentraxins. The aim of the present study was to investigate the level of PTX3 in patients with COPD. Fifty-four COPD patients and 31 controls were enrolled in this study. Demographical data such as age, sex, cigarette smoking status, comorbidities, drugs, habits, and modified Medical Research Council (MMRC) dyspnea scores were recorded. All patients were asked for COPD Assessment Test™ (CAT). The mean age was 65.7 ± 9.8 years, 92 % male. Plasma levels of PTX3 were found to be markedly higher in COPD patients [1.65 (0.32-12.72) ng/ml] than in controls [1.05 (0.43-3.26) ng/ml; p = 0.005]. On the other hand, PTX3 values did not differ between COPD stages [A, 1.73 (0.69-11.03); B, 1.49 (0.84-12.52); C, 0.79 (0.52-1.06); and D, 2.09 (0.32-12.72); p = 0.27]. The plasma PTX3 levels were positively correlated with MMRC scores. We conclude that circulating PTX3 levels are elevated in COPD patients. Plasma levels of PTX3 were correlated with dyspnea (MMRC scores). But PTX3 levels were not correlated with the severity of COPD.

Treatment of ankylosing spondylitis with TNF inhibitors does not have adverse effect on results of liver function tests: a longitudinal study.

AIM: To retrospectively investigate and compare the effects of tumor necrosis factor alpha inhibitors (TNFi) on hepatic enzymes in ankylosing spondylitis (AS) patients. METHODS: A retrospective analysis of the records of 94 AS (66 male, 28 female) patients using TNFi was performed. Patients' clinical data, Bath Ankylosing Spondylitis Disease Activity (BASDAI) scores, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were all examined. Liver function test (LFTs) results of patients before the treatment and 3, 6 and 12 months after treatment with TNFi were investigated. Aspartate transaminase (AST) and alanine transaminase (ALT) levels were investigated as indicators of LFTs. RESULTS: The TNFi drugs used were infliximab (n = 28), adalimumab (n = 32) and etanercept (n = 34). Pre-treatment values of ESR, CRP and BASDAI scores were 28.3 ± 20.1 mm/h, 1.5 ± 1.2 ng/dL and 5.2 ± 0.8, respectively. Following TNFi use there was a statistically significant decrease in disease activity score (P = 0.001). There was a significant increase in LFT at the third month evaluation compared to the initial values, while the average value was within normal range (baseline AST 19.6 ± 10.8 U/L, ALT 19.1 ± 6.4 U/L, third month AST 31.3 ± 21.6 U/L, ALT 28.1 ± 18.1 U/L, P = 0.001). Drug group comparison analysis revealed a significant difference in the adalimumab group value at the end of the first year, but no other significant difference in the data for the other months (P > 0.05). No significant correlation was determined between initial disease activity scores and LFT. CONCLUSION: TNFi use-associated rises in hepatic enzymes were determined compared to pre-treatment but the mean values remained within normal limits. Considering the cases in the literature, in daily practice patients must be carefully monitored for liver function before treatment and at follow-up.

Cardiac autonomic function in healthy young smokers.

The present study examined the heart rate turbulence (HRT) and heart rate variability (HRV) parameters in healthy young smokers (<40 years) to assess the effects of smoking on cardiac autonomic function. The study included 75 smokers with a history of habitual smoking for at least 1 year (41 males and 34 females; mean age, 29.3 ± 7.3 years) and 30 nonsmokers (hospital staff; 16 males and 14 females; mean age, 29.0 ± 6.1 years). Addiction to smoking was evaluated using the modified Fagerström test for nicotine-dependence index (NDI). HRT, HRV, basic clinical and echocardiographic, and Holter test parameters were compared between groups. No significant differences between the two groups were found in the basic clinical and echocardiographic variables. Turbulence onset (TO) was significantly higher in the smoking group than in the controls, and turbulence slope was significantly lower in the smokers, than in the controls (p < 0.05). Standard deviation of all normal-to-normal (NN) interval index (SDNNI) was the only HRV parameter that was significantly different between the smoking and control groups (p < 0.05). The NDI was positively correlated with the TO (p < 0.05). Smoking impairs the baroregulatory function in healthy young smokers, particularly the HRT parameters and SDNNI. Our findings highlight the importance of complete smoking cessation.

Elevated neutrophil/lymphocyte ratio in patients with schizophrenia.

BACKGROUND: Inflammatory mechanisms are reported to play important roles in the pathophysiology of schizophrenia. The neutrophil-lymphocyte ratio (NLR) is a simple and easily accessible indicator of the systemic inflammatory response. Our goal was to investigate whether NLR was higher in patients with schizophrenia than in healthy comparison subjects similar in age, sex, and body mass index. SUBJECTS AND METHODS: In this multicenter cross-sectional study, we analyzed 156 non-obese patients with schizophrenia and 89 healthy control subjects for complete blood count. The Brief Psychiatric Rating Scale was used to determine the severity of clinical pathology. RESULTS: The mean ± SD NLR of patients with schizophrenia was significantly higher than that of healthy controls (2.6 ± 1.1 vs. 1.9 ± 0.6, respectively, p < 0.001). NLR did not significantly correlate with severity and duration of schizophrenia (r = 0.065. p > 0.05). CONCLUSIONS: Our findings suggest that NLR levels are increased in physically healthy, non-obese, patients with schizophrenia when compared with physically and mentally healthy individuals. To our knowledge, this is the first study that demonstrated the association between NLR and schizophrenia.

Plasma omentin levels in drug-free patients with schizophrenia.

AIMS: We aimed to investigate plasma omentin concentrations in non-obese, drug-free patients with schizophrenia in comparison with healthy volunteers. METHOD: Thirty-two patients with schizophrenia and 33 control subjects were recruited. Plasma omentin levels were determined by enzyme-linked immunosorbent assay. RESULTS: Plasma levels of omentin (ng/ml) were found to be markedly lower in patients with schizophrenia (median = 7.7, 25th percentile = 6.3, 75th percentile = 604.9) than in controls (median = 486, 25th percentile = 326, 75th percentile = 794.2, p < 0.01). No significant difference was found between drug-free (n = 23) and drug-naive (n = 9) patients with respect to plasma omentin levels. Omentin concentrations correlated negatively with severity of illness, suggesting that patients with more severe pathology had lower fasting levels of omentin (n = 32; r = -0.387; p = 0.029). CONCLUSION: The present results suggest that plasma omentin levels are decreased in physically healthy, non-obese, antipsychotic-free patients with schizophrenia when compared with physically and mentally healthy individuals. To our knowledge, this is the first study that demonstrated the association between omentin and schizophrenia.