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Does damage to hypothalamic paraventricular nucleus underlie symptoms of ultradian rhythm disorder and an increased anxiety in coronavirus disease 2019?
Get PDFPovezanost grelina i grelinskoga receptora sa stupnjem displazije u adenomima debeloga crijeva [Correlation of ghrelin and ghrelin receptor with the grade of dysplasia in colonic adenomas]
Get PDFAim of this study was to investigate the correlation of serum ghrelin and immunohistochemical expression of ghrelin and ghrelin receptor with the grade of dysplasia in colonic adenomas, and compare them with the presence of insulin resistance and metabolic syndrome. The study included 92 participants with colonic adenomas, of whom 43 had high grade dysplasia. In high grade adenomas high expression of ghrelin was 7 times more common than in low grade adenomas (13,95% to 2,04%) and it was absent in normal mucosa. High expression of ghrelin receptor was present in 12,24% low grade, 25,58% high grade adenomas and 2,17% of normal mucosa. Expression of ghrelin positively correlated with expression of ghrelin receptor in high grade dysplasia. Serum deacylated ghrelin negatively correlated with body mass, BMI, waist circumference, insulin, fasting plasma glucose levels and HOMA-IR. High expression of grelin in high grade adenomas is probably due to increased local production of ghrelin, and could in that way have a role in proliferation and tumorigenesis. Serum deacylated ghrelin is negatively correlated with insulin resistance and metabolic syndrome criteria, and could have a protective role in these two conditions
Meta-analysis is not always the best way to round out a systematic review: a few thoughts prompted by the COVID-19 pandemic and “spiced-up” with an earthquake
Get PDFRelationships of cerebrospinal fluid Alzheimer’s disease biomarkers and COMT, DBH, and MAOB single nucleotide polymorphisms
Get PDFThe noradrenergic and dopaminergic systems are affected in Alzheimer's disease (AD). Polymorphisms in genes encoding enzymes and proteins that are components of these systems can affect products of transcription and translation and lead to altered enzymatic activity and alterations in overall dopamine and noradrenaline levels. Catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAOB) are the enzymes that regulate degradation of dopamine, while dopamine β-hydroxylase (DBH) is involved in synthesis of noradrenaline. COMT Val158Met (rs4680), DBH rs1611115 (also called -1021C/T or -970C/T), and MAOB rs1799836 (also called A644G) polymorphisms have been previously associated with AD. We assessed whether these polymorphisms are associated with cerebrospinal fluid (CSF) AD biomarkers including total tau (t-tau), phosphorylated tau proteins (p-tau181, p-tau199, and p-tau231), amyloid-β42 (Aβ42), and visinin-like protein 1 (VILIP-1) to test possible relationships of specific genotypes and pathological levels of CSF AD biomarkers. The study included 233 subjects: 115 AD, 53 mild cognitive impairment, 54 subjects with other primary causes of dementia, and 11 healthy controls. Significant decrease in Aβ42 levels was found in patients with GG compared to AG COMT Val158Met genotype, while t-tau and p-tau181 levels were increased in patients with AA compared to AG COMT Val158Met genotype. Aβ42 levels were also decreased in carriers of A allele in MAO-B rs1799836 polymorphism, while p-tau181 levels were increased in carriers of T allele in DBH rs1611115 polymorphism. These results indicate that COMT Val158Met, DBH rs1611115, and MAOB rs1799836 polymorphisms deserve further investigation as genetic markers of AD
Current knowledge on the genetic background of developmental dysplasia of the hip and the histomorphological status of the cartilage
Get PDFDevelopmental dysplasia of the hip (DDH) represents a morphological abnormality characterized by the incongruity of femoral head and acetabulum. It ranges from mild dysplastic changes to complete dislocation. DDH has been associated with several hereditary and environmental risk factors, which could explain the incidence variability among different countries. Numerous genes may be involved in the disease etiology and progression. However, there are controversies in the literature regarding some of these genes. DDH-induced secondary osteoarthritis (OA) is characterized by changes in the macromolecule content of the cartilage and the expression of cartilage degradation markers. In addition, it exhibits a pattern of specific histological changes, with several reported differences between primary and DDH-induced secondary OA. The articular cartilage of patients with DDH shows specific radiological characteristics, including changes visible already in infancy, but also at pre-arthritic stages, early stages of OA, and in fully developed DDH-induced secondary OA. Although DDH has been extensively researched in different disease stages, the etiology of the disorder still remains uncertain. This review focuses on the current knowledge on the histomorphological status of the cartilage and the genetic background of DDH
Učinak pentadekapeptida BPC 157 na ishemijsko/reperfuzijske ozljede u mozgu štakora [The effect of pentadecapeptide BPC 157 on ischemic/reperfusion injuries in rat brain]
Get PDFIntroduction. Ischemic/reperfusion injuries are the basis of cardiovascular insult
(CVI) while pentadecapeptide BPC 157, is already been proven to affect vessel integrity,
it is a mediator of Robert's cytoprotection, it has beneficial effects on various injuries
and interacts with the NO system, making it a promising agent for cerebral
ischemic/reperfusion injuries. -----
Materials and methods. The effect of BPC 157 was examined using an animal
model of bilateral carotid artery occlusion (BCAO), in Wistar rats. After an occlusion of
20 min, the rats were randomly divided into groups, treated group was administered
BPC 157 (10μg/kg) while the control group was given saline (1ml, 0.9%NaCl), and
depending on the group the animals received an agonist and/or antagonist of NO
system (L-arginine and/or L-NAME). After 24 hours, the neurological assessment was
performed using the Morris water maze test, inlined beam walk test and lateral push test
and tissue samples were taken for pathohistological and RT-qPCR gene expression
analysis. -----
Results. The neurological assessment showed that BPC 157 has beneficial
effects on the neurological outcome, while the pathohistological analysis and gene
expression analysis further confirmed the beneficial effects of BPC 157. ----- Conclusion. This experiment has revealed the beneficial effect of BPC 157 and
thereby opened the possibility of using BPC 157 as a therapeutical agent in
ischemic/reperfusion injuries
Autologous blood coagulum is a physiological carrier for BMP6 to induce new bone formation and promote posterolateral lumbar spine fusion in rabbits
Get PDFIn the present study, we describe autologous blood coagulum (ABC) as a physiological carrier for BMP6 to induce new bone formation. Recombinant human BMP6 (rhBMP6), dispersed within ABC and formed as an autologous bone graft substitute (ABGS), was evaluated either with or without allograft bone particles (ALLO) in rat subcutaneous implants and in a posterolateral lumbar fusion (PLF) model in rabbits. ABGS induced endochondral bone differentiation in rat subcutaneous implants. Coating ALLO by ABC significantly decreased the formation of multinucleated foreign body giant cells (FBGCs) in implants, as compared with ALLO alone. However, addition of rhBMP6 to ABC/ALLO induced a robust endochondral bone formation with little or no FBGCs in the implant. In rabbit PLF model, ABGS induced new bone formation uniformly within the implant resulting in a complete fusion when placed between two lumbar transverse processes in the posterolateral gutter with an optimum dose of 100-μg rhBMP6 per ml of ABC. ABGS containing ALLO also resulted in a fusion where the ALLO was replaced by the newly formed bone via creeping substitution. Our findings demonstrate for the first time that rhBMP6, with ABC as a carrier, induced a robust bone formation with a complete spinal fusion in a rabbit PLF model. RhBMP6 was effective at low doses with ABC serving as a physiological substratum providing a permissive environment by protecting against foreign body reaction elicited by ALLO
Axon morphology of rapid Golgi-stained pyramidal neurons in the prefrontal cortex in schizophrenia
Get PDFAim To analyze axon morphology on rapid Golgi impregnated pyramidal neurons in the dorsolateral prefrontal cortex in schizophrenia. -----
Methods Postmortem brain tissue from five subjects diagnosed with schizophrenia and five control subjects without neuropathological findings was processed with the rapid Golgi method. Layer III and layer V pyramidal neurons from Brodmann area 9 were chosen in each brain for reconstruction with Neurolucida software. The axons and cell bodies of 136 neurons from subjects with schizophrenia and of 165 neurons from control subjects were traced. The data obtained by quantitative analysis were compared between the schizophrenia and control group with the t test. -----
Results Axon impregnation length was consistently greater in the schizophrenia group. The axon main trunk length was significantly greater in the schizophrenia than in the control group (93.7 ± 36.6 μm vs 49.8 ± 9.9 μm, P = 0.032). Furthermore, in the schizophrenia group more axons had visibly stained collaterals (14.7% vs 5.5%). -----
Conclusion Axon rapid Golgi impregnation stops at the beginning of the myelin sheath. The increased axonal staining in the schizophrenia group could, therefore, be explained by reduced axon myelination. Such a decrease in axon myelination is in line with both the disconnection hypothesis and the two-hit model of schizophrenia as a neurodevelopmental disease. Our results support that the cortical circuitry disorganization in schizophrenia might be caused by functional alterations of two major classes of principal neurons due to altered oligodendrocyte development
