Vessel Damage Research Articles

Open Surgical Retrieval of a Foreign Body in the Neck: A Case Report

Foreign body retention in the neck may be either traumatic or iatrogenic. Penetrating neck injuries with retained bodies are critical, as the neck serves as a passage for structures essential to life. Therefore, prompt detection and retrieval of the foreign body are paramount in preventing mortality. Here, authors present a case in which a successful surgical retrieval was performed without any postprocedural complications, despite the patient presenting relatively late after the injury. In this case report, a 23-year-old male labourer presented with a right-sided neck swelling two months after a workplace injury involving a shattered metal plate. Imaging confirmed a 15×5 mm hyperdense metallic object penetrating the sternocleidomastoid muscle. Successful open exploration extracted a 1.5 cm metallic shard at the C6 vertebral level, with no major vessel or airway damage. Postoperatively, the patient exhibited no movement restrictions, highlighting the atypical presentation of a retained metallic foreign body and the importance of timely intervention and comprehensive imaging for successful management.

Newer Modalities and Updates in the Management of Sickle Cell Disease: A Systematic Review.

Sickle cell disease (SCD), the most common autosomal recessive genetic disorder, affects the hemoglobin (Hb) chains in human red blood cells. It is caused by mutations in the β-globin genes, leading to the production of hemoglobin S, which results in the formation of sickle-shaped red blood cells (RBCs). These abnormal cells cause hemolysis, endothelial damage, and small vessel occlusion, leading to both acute and long-term complications. According to the World Health Organization's 2008 estimates, SCD affects approximately 2.28 per 1000 individuals globally. Despite this high prevalence, therapeutic advancements have been slow. For many years, the only FDA-approved medications for managing SCD complications were hydroxyurea and deferiprone. However, recent years have seen the approval of several new therapies, including L-glutamine (2017), voxelotor and crizanlizumab (2019), as well as exagamglogene autotemcel (Casgevy) and lovotibeglogene autotemcel (Lyfgenia) (2023). These treatments have proven effective in managing both the acute and chronic effects of SCD, including hemolytic anemia, chronic pain, stroke, vaso-occlusive crises, and multiple organ damage syndromes. This review explores the mechanisms of action, practical considerations, and side effects of these emerging therapies, drawing from a comprehensive search of databases such as PubMed, Medline, and Cochrane.

Dexmedetomidine protects against sepsis-induced lung injury through autophagy and Smad2/3 signaling pathway.

Dexmedetomidine (Dex) is a potent α2-adrenergic receptor(α2-AR) agonist that has been shown to protect against sepsis-induced lung injury, however, the underlying mechanisms of this protection are not fully understood. Autophagy and the Smad2/3 signaling pathway play important roles in sepsis-induced lung injury, but the relationship between Dex and Smad2/3 is not clear. This study aimed to investigate the role of autophagy and the Smad2/3 signaling pathway in Dex-mediated treatment of sepsis-induced lung injury. Sepsis was performed using cecal ligation and puncture (CLP) in C57BL/6J mice. Mice were randomly assigned to four groups (n=6 per group): sham, CLP, CLP-Dex, and CLP-Dex-YOH, Yohimbine hydrochloride (YOH) is an α2-AR blocker. The cecum was carefully separated to avoid blood vessel damage and was identified and punctured twice with an 18-gauge needle. The pathological changes, inflammatory factor levels, oxidative stress, autophagy, Smad2/3 signaling pathway-related protein levels in lung tissues, and the activity of superoxide dismutase (SOD) and malonaldehyde (MDA) in the serum were measured. CLP-induced lung injury was reflected by increased levels of inflammatory cytokines, apoptosis, and oxidative stress, along with an increase in the expression of autophagy and Smad2/3 signaling pathway-related proteins. Dex could reverse these changes and confer a protective effect on the lung during sepsis. However, the administration of YOH significantly reduced the positive effects of Dex in mice with sepsis. Dex exerts its beneficial effects against sepsis-induced lung injury through the regulation of autophagy and the Smad2/3 signaling pathway.

Коморбидный неврологический пациент: в фокусе метаболический синдром

INTRODUCTION. The article discusses the problem of managing patients suffering from metabolic syndrome and chronic cerebrovascular disorders. Metabolic syndrome is an important interdisciplinary problem. Metabolic syndrome significantly increases the incidence of strokes. Systemic metabolic disorders, insulin resistance and oxidative stress, as well as large vessel damage and microangiopathy play an important role. In addition, special attention is paid to low-grade chronic inflammation, which may be associated with the patient’s age. The most important risk factor for the development of acute cerebral ischemia is the combination of components of the metabolic syndrome, in particular, the combination of insulin resistance and arterial hypertension, which increase the likelihood of developing atrial fibrillation and increase the risk of an unfavorable outcome. CONCLUSION. Cognitive impairment is quite common in metabolic syndrome. When treating cognitive impairment as part of metabolic syndrome, it is advisable to use neuroprotectors. The use of citicoline (the drug “Ronocit”) has a clinically significant effect in restoring cognitive functions and reducing the risk of developing post-infarction and post-stroke dementia in patients with metabolic syndrome. The use of various approaches to the treatment of cognitive impairment in metabolic syndrome increases the likelihood of a favorable outcome. It is recommended to use the drugs “Ronocit” and “Cocarnit®” together in the treatment of patients with a predominance of cognitive and asthenic impairments and a clinical symptom complex of diabetic polyneuropathy. KEYWORDS: comorbidity, cognitive disorders, metabolic syndrome

Age characteristics of myocardial blood supply in comorbid pathology

Understanding the age-related changes in myocardial blood supply under conditions of diabetes mellitus and stress will help reveal the pathway of diabetic cardiomyopathy, considering the age aspect. Therefore, the aim of our work is to investigate the age-related morpho-functional changes in the hemomicrocirculatory bed (HMB) of the myocardium in rats with experimental streptozotocin-induced diabetes mellitus (SDM) under conditions of chronic immobilization stress (CIS). The study used heart fragments and blood from 56 2-month-old and 6-month-old male white rats, which were divided into 3 groups: 1 group with comorbid pathology, including modeled SDM and CIS, 2 group with SDM, and 3 – control group. The material was collected 14th and 56th days from the start of the experiment. According to our findings, hyperglycemia, and stress on the 14th day of the experiment lead to spasm of the arterioles of the HMB and a significant deterioration in their permeability, as evidenced by a likely increase in the Vongenwort index in the arterioles. On the 56th days, in the experimental groups of 6-month-old rats, vacuolar dystrophy and coagulation necrosis of endotheliocytes and myocytes, focal destruction of capillary walls, thickening, and proliferation of their basement membrane, pronounced micro- and macroclasmatic changes, and capillarosclerosis are observed. In contrast, 2-month-old rats alongside destructive changes in HMB vessels show phenomena of neovascularization. Thus, SCD leads to the development of diabetic microangiopathy in the vessels of the myocardium of rats of different age groups. In animals with comorbid pathology, damage of HMB vessels are more pronounced on the 56th day of observation and is manifested by: destruction of capillary walls, capillarosclerosis. In 2-month-old rats, alongside destructively changed capillaries, we found to former new vessels with a characteristic ultrastructure. Keywords: heart, heart failure, diabetic cardiomyopathy, diabetes mellitus, cardiovascular diseases, hemomicrocirculatory bed.

Kwas alfa-liponowy w prewencji powikłań cukrzycowych

Diabetes is a group of metabolic disorders characterized by a high blood sugar level (hyperglycemia) over a prolonged period of time. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced (insulin resistance). Chronic hyperglycemia is associated with damage of small and large blood vessels in many tissues and organs (micro- and macroangiopathy). Microvascular complications may contribute to the diabetic retinopathy and neuropathy. Diabetes is strongly associated with increased oxidative stress, which could be a consequence of either increased production of free radicals or reduced antioxidant defenses. Many of the biochemical pathways (e.g., protein glycation, polyol pathway, protein kinase C activation) associated with hyperglycemia can result in increased reactive oxygen species. An ideal therapeutic antioxidant should fulfill several criteria. These include absorption from the diet, conversion in cells and tissues into usable form, a variety of antioxidant actions (including interactions with other antioxidants) in both membrane and aqueous phases, and low toxicity. Alpha-lipoic acid is unique among natural antioxidants in its ability to fulfill all of these requirements. Alpha-lipoic acid has been shown to have diverse beneficial effects suggesting that it acts by multiple mechanisms on oxidative stress parameters. Alpha-lipoic acid’s antioxidant properties consist of the following: 1) its capacity to directly scavenge reactive oxygen species, 2) its ability to regenerate endogenous antioxidants, such as glutathione, vitamins E and C, and 3) its metal chelating activity, resulting in reduced reactive oxygen species production. Alpha-lipoic acid prevents micro-vascular damage through normalized pathways downstream of mitochondrial overproduction of reactive oxygen species. Alpha-lipoic acid inhibits diabetes-induced apoptosis of both endothelial cells and pericytes, signs and predictor of retinopathy, and prevents nerve ischemia and hypoxia whitch could cause neuropathy. Alpha-lipoic acid supplementation is an achievable adjunct therapy to help prevent vision loss and reduce neuropathic symptoms in diabetic patients. Honokiol is a natural polyphenolic compound extracted from the bark, cone and leaves of Magnolia. Honokiol is used in traditional Chinese and Japanese medicine for the treatment of various diseases. This promising bioactive compound presented an wide range of therapeutic and biological activities which include neuroprotective, anti-spasmodic, antidepressant, anti-tumorigenic, antithrombotic, antimicrobial, analgesic properties, and others. Some of its mechanism for exhibiting its pharmacological effects includes inhibition of oxidative stress and suppression of pro-inflammatory cytokines (TNF-α, IL-10 and IL-6). Honokiol might exert its protective effect on hyperglycemia-induced cell damage in human endothelial cells through the inhibition of NF-κB and COX-2 upregulation. Low-dose of honokiol may have the potential to protect endothelial cells from damage associated with elevated glucose.

ERYTHROPOIETIN SYNTESIS IN PATIENTS WITH CHRONIC HEART FAILURE DEPENDING ON COMORBID PATHOLOGY

Introduction. Decreased production of erythropoietin by the kidneys plays crucial role in the development of anemia in patients with chronic heart failure, especially on the background of comorbid diabetes mellitus type 2. In diabetic patients due to early damage of the kidney vessels and following erythropoietin deficiency anemia develops much earlier than clinically significant decrease of glomerular filtration rate.
 The aim of the study was to find out possible dependence of changes in the erythropoietinsynthesizing function of the kidneys on the degree of severity of anemic hypoxia in elderly and senile patients with chronic heart failure, including those with comorbid type 2 diabetes mellitus.
 Materials and methods. 120 patients with chronic heart failure of ischemic origin, type 2 diabetes mellitus and mild and moderate anemia were examined. Control group comprised 12 people with chronic heart failure without comorbid pathology. The examined groups were comparable in terms of gender and age, differing in the presence of comorbid diabetes mellitus and degree of severity of anemic syndrome. The level of erythropoietin in blood serum was determined by standard enzymelinked immunosorbent assay.
 Results. Type 2 diabetes mellitus in patients with chronic heart failure results in a significant decrease in erythropoietin production by 25 % compared to the control group (p<0,05). Comorbid to heart failure anemia leads to an increase in the level of erythropoietin by 74,4 % (р<0,05), and in the case of chronic heart failure and type 2 diabetes mellitus on the background of concomitant anemia – only by 39,5 % (р<0,05). As the severity of anemia in patients with chronic heart failure without diabetes progresses, the severity of the compensatory response of the kidneys to chronic anemic hypoxia is significantly higher than in patients with heart failure and comorbid type 2 diabetes.
 Conclusions. Diabetic nephropathy in patients with chronic heart failure and comorbid anemia leads to a significant deterioration of the erythropoietin-synthesizing function of the kidneys, complicating the course of both main and comorbid diseases.

Effectiveness and safety of a 26-week taper regimen of glucocorticoid in GCA patients: Results from a prospective cohort study

To assess the effectiveness and safety of the 26-week tapering regimen of glucocorticoids (GC) used in the GiACTA trial in a prospective cohort of treatment-naive, biopsy-proven GCA patients. Patients with a new diagnosis of biopsy-proven GCA enrolled in the GC arm of the START project (molecular stratification of patients with GCA to tailor GC and tocilizumab therapy) were included. All patients were treated with the 26-week taper regimen of GC used in the GiACTA trial. The primary endpoint was the rate of relapse-free remission at week 52. The secondary endpoints were the proportion of patients with incident aortic damage, cumulative GC doses and GC-related adverse events (AE). 22 patients were included between December 2018 and February 2022. At week 52, 10 patients (45%, 95% CI 24-68) were in relapse-free remission. After a median (IQR) follow-up of 35 (22-40) months, 7 patients (32%, 95% CI 14-55) were in relapse-free remission. 18 patients with baseline large-vessel imaging underwent CT angiography at the end of the follow-up. No patients had evidence of new aortic dilation, significant progression of aortic damage or large vessel stenosis. 15/22 patients (68%) had at least one relapse during follow-up. No patients developed visual or cerebrovascular manifestations during relapses. 15/22 (68%) patients had at least one GC-related AE. A 26 week taper regimen of GC was effective and safe in inducing and maintaining remission in a sizeable proportion of newly diagnosed GCA patients. However, the frequency of GC-related adverse events was high.

Beta-Amyloid Enhances Vessel Formation in Organotypic Brain Slices Connected to Microcontact Prints.

In Alzheimer's disease, the blood-brain barrier breakdown, blood vessel damage and re-organization are early events. Deposits of the small toxic peptide beta-amyloid (Aβ) cause the formation of extracellular plaques and accumulate in vessels disrupting the blood flow but may also play a role in blood clotting. In the present study, we aim to explore the impact of Aβ on the migration of endothelial cells and subsequent vessel formation. We use organotypic brain slices of postnatal day 10 wildtype mice (C57BL/6) and connect them to small microcontact prints (µCPs) of collagen. Our data show that laminin-positive endothelial cells migrate onto collagen µCPs, but without any vessel formation after 4 weeks. When the µCPs are loaded with human Aβ40, (aggregated) human Aβ42 and mouse Aβ42 peptides, the number and migration distance of endothelial cells are significantly reduced, but with a more pronounced subsequent vessel formation. The vessel formation is verified by zonula occludens (ZO)-1 and -2 stainings and confocal microscopy. In addition, the vessel formation is accompanied by a stronger GFAP-positive astroglial formation. Finally, we show that vessels can grow towards convergence when two opposed slices are connected via microcontact-printed lanes. In conclusion, our data show that Aβ promotes vessel formation, and organotypic brain slices connected to collagen µCPs provide a potent tool to study vessel formation.

Pulmonary hemorrhage in cystic fibrosis: a review of current data

Pulmonary hemorrhage is a serious complication of cystic fibrosis (CF) with a prevalence up to 9.1%. According to the Registry of Patients with Cystic Fibrosis of the Russian Federation for 2020, the prevalence of pulmonary hemorrhage was 1.5% in the general population, and 6.5% in patients over 18 years of age. Despite the importance of this problem, there is no systematic information on pulmonary hemorrhage in CF.Aim. The purpose of this study was to review current data on the pathogenesis, risk factors, and approaches to the treatment of pulmonary hemorrhage in patients with CF. Information was searched in еLibrary and PubMed databases.Results. During the literature review, we summarized and systematized the collected scientific data on pulmonary hemorrhage in CF. The pathogenesis of pulmonary hemorrhage is chronic inflammation in the bronchial wall accompanied by increased angiogenesis factors that promote neovascularization with development of many tortuous, thin-walled vessels. Exacerbation of bronchial inflammation and mechanical strain contribute to erosion and damage of fragile vessels and cause the bleeding. The main risk factors for pulmonary hemorrhage were colonization with Pseudomonas aeruginosa, Staphylococcus aureus, diabetes mellitus, and FEV1 < 70%. Complex therapy for pulmonary hemorrhage includes the use of antibiotics and antifibrinolytic agents. Some of the published regimens use β-blockers and blood coagulation factor VII. Data on the efficacy of vitamin K are unclear, but it is also used in the treatment of pulmonary hemorrhage. In cases of massive bleeding, temporarily discontinuation of inhalations of hypertonic solution and kinesiotherapy is recommended. In case of recurrent massive bleedings, bronchial artery embolization is performed and lung resection can be done in extreme cases.Conclusion. Hemoptysis in CF is a complex clinical problem that requires a multidisciplinary approach. Currently, important aspects of the pathogenesis of pulmonary hemorrhage remain unclear. Given the increasing life expectancy of CF patients and the age-related risk of pulmonary hemorrhage, it is important to investigate the pathogenetic aspects of this complication for the subsequent development of effective and justified treatment algorithms.

Effect of neutrophil extracellular traps (NET) on thrombosis: A literature review

Neutrophils are used by the innate immune system to form thrombi during many types of thrombosis. The inactivation of endogenous anticoagulants results in increased intravascular coagulation by increasing factor XII activation, decreasing plasmin production, or boosting the tissue factor-dependent extrinsic pathway. The creation of neutrophil extracellular traps (NET) by the externalization of decondensed nucleosomes and granule proteins supports neutrophil-dependent prothrombotic processes. Experimental thrombosis has been demonstrated to be caused by these traps, whether intact or fragmented, since they provide the means to enhance microvascular thrombosis. The von Willebrand factor increases platelet adhesion when neutrophils and activated platelets combine to form NET. Thus, neutrophils and externalized nucleosomes promote intravascular blood coagulation and thrombosis during infections and during conditions resulting from blood vessel damage.

Relationship between COVID-19 and Neurological Disorder

Abstract: The COVID-19 pandemic has resulted in a socially isolating way of life, and dementia patients are among those who are most affected. Lockdown procedures and the inability to monitor illnesses have led to a rapid decline in cognitive function in these individuals, with neuropsychiatric symptoms, such as agitation, delirium, and impaired motor performance being prevalent. However, the use of antipsychotics in treating these symptoms can increase the risk of death during COVID-19. Effective pain therapy can be used as an alternative to reduce or avoid the use of antipsychotics, given the consistent relationship between agitation and pain in dementia patients. The importance of properly assessing and managing pain in dementia patients is highlighted. Additionally, the article discusses how COVID-19 can affect brain health through inflammation, blood clotting, and blood vessel damage, leading to potential long-term effects on cognitive function. Healthcare professionals must be aware of the increased risk of neuropsychiatric symptoms in dementia patients during the pandemic and prioritize pain management as a viable alternative to antipsychotics. Proper care and attention are necessary to prevent cognitive decline and potential long-term effects on brain health in these vulnerable individuals.

Experimental investigation on the deformation and damage of steel ribbon wound vessel for hydrogen storage under external impact and blast loading

Steel ribbon wound vessel is a preferred type for stationary storage of high-pressure hydrogen in refueling stations. However, it is under the threat of fragment impact and blast loads caused by accidental explosions of hydrogen or other vessels. For the first time, the fragment-simulating projectile (FSP) impact tests with impact kinetic energy range from 1.8 × 103 J–4.9 × 103 J and external blast loading tests with TNT equivalent range from 157 g–4 kg of industrial-grade 50 MPa steel ribbon wound vessel were carried out. The damage of vessel under FSP impact loading was studied. The effect of concentrated and distributed blast loads on the deformation and damage of gas-filled vessel was analyzed, and the explosion resistance of vessel under near-field blast loading was explored. It is revealed that: 1) the steel ribbon wound vessels generally have good resistances to external blast and impact loads, 2) the primary damage characteristics of vessel under contact/near-field blast loading was localized depression deformation, accompanied by steel ribbons warping as the shock wave impulse increases, 3) the saddle fails earlier than the vessel under the near-field blast loading. Further, the failure modes of vessel under extreme blast loads were revealed. Results can provide reference for the safe design and validation of dynamic damage/failure analysis models of steel ribbon wound vessels.

TMIC-74. SPATIAL LANDSCAPE OF MELANOMA BRAIN METASTASES WITH AND WITHOUT PRE-SURGICAL IMMUNE CHECKPOINT BLOCKADE

Abstract We recently characterized the immune populations of brain metastases samples with or without immune checkpoint blockade (ICB) treatment. In that study, we utilized single cell RNAseq (scRNAseq) and multiplex immunofluorescence (mIF) to demonstrate that ICB induced T cell infiltration and the migration of a unique MRC1+ macrophage subset from the perivascular space into the tumor parenchyma. However, scRNAseq’s tissue dissociation step loses spatial information of cells while mIF has low dimensionality, covering only a few markers for each tissue section. Thus, we applied sequencing-based Visium spatial transcriptomics (ST) to study the spatial architecture of melanoma brain metastases with/without ICB treatment and developed a pipeline that leverages public scRNAseq data as a reference to resolve fine-grained cell types on each Visium spot. ICB was associated with an increased CXCL13+ terminally exhausted T cell subset in close spatial proximity to tumor cells, suggestive of tumor specificity. ICB also reduced multiple MRC1+ macrophage subtypes in the blood vessel regions, supporting our mIF observation. Furthermore, we discovered that MRC1+ macrophages in close proximity to blood vessels expressed elevated TIMP1. TIMP1 is a known inhibitor of MMP9 that prevents ECM degradation and blood vessel damage, thus limiting T cell extravasation. In contrast, MRC1+ macrophages that migrated into the tumor had higher interferon activation and expressed CXCL9 and CXCL12 chemokines, which could recruit T cells via CXCR3 and CXCR4. Such findings could explain the increased T cell infiltration with ICB even in metastatic brain tumors. However, these MRC1+ macrophages also had an M2 signature and expressed multiple immune checkpoint ligands. Such data suggest these cells might also increase immunosuppressive interactions with T cells. In summary, our study reveals how ICB affects the spatial architecture and crosstalk of different cell types within melanoma brain metastases and will provide insights into new therapeutic strategies for brain metastases patients.

South Asian adults with ASCVD exhibit a reduction in circulating vascular regenerative cell content compared to White European adults: a sub-analysis of the ORIGINS-RCE CardioLink-13 study

Abstract Background Compared to people of other races and ethnicities, South Asian (SA) adults are disproportionately affected by a higher burden of type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD). We previously found that compared to individuals of White European (WE) descent with T2D, SA individuals with T2D exhibited profoundly less vascular regenerative (VR) cell content. Given that VR cells critically regulate vessel homeostasis, we postulated that the "vascular regenerative cell exhaustion" phenomenon we had observed may also contribute to the prevalence of ASCVD in SA populations. Purpose The ORIGINS-RCE CardioLink-13 study compared the frequencies of VR cells and cell types in individuals of SA and WE ethnicities with either 1) T2D and cardiovascular-risk factors or 2) documented ASCVD. This sub-analysis was conducted to determine if there are differences in the frequency of circulating VR cells and cell types in SA and WE individuals with ASCVD. Methods Among the 120 self-identified SA and WE adult participants (≥40 years of age), 23 SA and 41 WE individuals had ASCVD. Peripheral blood samples were processed for pro-inflammatory vs. pro-vascular progenitor cell enumeration as well as measurement of reactive oxygen species (ROS) production using a unique high aldehyde dehydrogenase (ALDHhi) activity-based flow cytometry assay in combination with side scatter properties (SSC) and lineage specific cell surface markers to identify progenitor cell populations. Results Compared to samples from the WE participants, the SA adults had a lower frequency of ALDHhiSSClowCD133+ (59% vs. 48%, P<0.001) cells and ALDHhiSSClowCD34+CD133+ (56% vs. 45%, P<0.001) progenitor cells with previously established pro-angiogenic properties. We also observed that SA participants had a decreased frequency of ALDHhiSSClowCD34+CD133+CD45- (0.0019% vs. 0.0005%, P<0.05) cells which may represent a rare population of circulating endothelial progenitor cells with vasculogenic functions. SA participants also exhibited a shift in monocyte polarization from a reparative phenotype towards a pro-inflammatory state, as demonstrated by a decrease in ALDHhiSSCmidCD14+CD163+ (86% vs. 78%, P<0.01) monocytes and an increase in ALDHhiSSCmidCD86+CD163- (8.2% vs. 13%, P<0.01) cells. There were no significant differences in the frequency of circulating granulocytes (ALDHhiSSChi cells) suggesting comparable inflammatory granulocyte burden between SA and WE adults, with no meaningful difference in intracellular ROS production in ALDHhi progenitor cell subsets, as previously observed in participants with T2D. Conclusions South Asian adults with ASCVD demonstrate a loss of vascular regenerative cells suggesting a compromised ability to repair damaged vessels which may contribute to their elevated cardiovascular risk.

Diabetic Prediction Using Hybrid Smote-Tree Big Data Classification with Artificial Neural Network

Diabetes is one of the worst illnesses now plaguing humanity. The condition is caused by the body's abnormal reaction to insulin, a vital hormone that transforms sugar into the energy required for the normal functioning of daily living. In addition to increasing the chance of developing kidney disease, heart disease, and retinal eye disease, nerve damage, and blood vessel damage, diabetes causes serious consequences in the body. This research provides diabetes prognosis based on hybrid SMOTE-TREE large data categorization utilizing Artificial Neural networks (ANN). Artificial Neural Networks deliver promising results for nonlinear data. Hence ANN is picked for creating the model to predict diabetes among numerous ML (machine learning) techniques. The goal is to develop a decision support system to predict and diagnose diabetes with maximum accuracy, given the parameters. The parameters are set such that the best accuracy is obtained.

Moringa Oleifera Leaf Extract as an Antioxidant on Malondialdehyde (MDA) and Glutathione Peroxidase (GSH-Px) Levels in Rats with Hyperglycemia: A Systematic Literature Review

Hyperglycaemia is a clinical indicator of Diabetes Mellitus (DM), chronic hyperglycemia in diabetes is associated with damage to organ systems, such as kidney damage, eyes, nerves, and blood vessels, and even death through oxidative stress processes, resulting in an imbalance between antioxidants and free radicals. One of the plants that contain antioxidants is Moringa Oleifera (MO), MO has been utilized as a food source material. This plant has low toxicity, natural antioxidants, and important bioactive phytochemicals and is an excellent source of alternative natural therapies to synthetic drugs. Exogenous antioxidants in Moringa leaves may have potential as free radical scavengers. Studies published between 2017 and 2023 were systematically reviewed through identification in Research Gate, Science Direct, PubMed, and Google Scholar databases. Studies that met the inclusion criteria were included for review. The results of the literature review of the articles carried out can be concluded that the administration of moringa leaf extract is able to reduce blood sugar levels, reduce MDA levels and increase antioxidants in the body, such as Superoxide Dismutase (SOD), Catalase (CAT) and Glutathione Peroxidase (GSH-Px). Keywords: Hyperglycaemia, Diabetes, Leaf Extract Moringa Oleifera, Oxidative Stress, Antioxidant

Expression of Tie2 (angiopoietin receptor) on the monocyte subpopulations from ischemic stroke patients: Histological and flowcytometric studies.

Different subpopulations of monocytes play roles in phagocytosis, inflammation, and angiogenic processes e.g., Tie2-expressing monocytes (TEMs). The brain is flooded with macrophages that are derived from monocytes within 3-7 days after a stroke. This study aimed to determine the expression level of Tie2 (an angiopoietin receptor) on monocytes and their subpopulations in ischemic stroke patients using the histological and immunohistological study of bone marrow biopsies and blood flow cytometry examination. Ischemic stroke patients within two days were selected. Participants in the control group were healthy volunteers of matched age and gender. Sample collection was performed within 24 to 48 hours after medical consultants confirmed the stroke diagnosis. An iliac crest bone marrow biopsy was obtained and fixed for histological and immunohistological staining with antiCD14 and antiCD68. Flow cytometry was used to determine the total monocyte population, monocyte subpopulations, and TEMs after staining with monoclonal antibodies to CD45, CD14, CD16, and Tie2. Post-stroke patients' bone marrow cells were hypercellular. There was an apparent increase in CD68 and CD14-positive cells. Ischemic stroke patients exhibited low percentages of nonclassical monocytes CD14lowCD16++, with an increase in intermediate monocytes CD14highCD16+. Moreover, ischemic stroke patients had significantly higher levels of TEMs than control group. The results of this study demonstrate dysregulation of angiogenesis in monocyte subsets in ischemic stroke patients, which could be used as an early diagnostic marker of neurovascular damage and may need angiogenic therapy or improved medications to prevent further damage of blood vessels.

Adverse neurological effects after exposure to copper, manganese, and mercury mixtures in a Spraque-Dawley rat model: an ultrastructural investigation

ABSTRACT Exposure to environmental metal pollutants is linked to oxidative stress and the subsequent development of neurological disease. In this study, the effects of copper, manganese, and mercury, were evaluated at X100 the World Health Organization safety limits for drinking water. Using a Sprague-Dawley rat model, following exposure for 28 days, the effects of these metals on biochemical blood parameters and tissue and cellular structure of the brain were determined. Biochemical analysis revealed no hepatocellular injury with minor changes associated with the hepatobiliary system. Minimal changes were found for renal function and the Na+/K+ ratio was reduced in the copper and manganese (Cu + Mn) and copper, manganese, and mercury (Cu, Mn + Hg) groups that could affect neurological function. Light microscopy of the brain revealed abnormal histopathology of Purkinje cells in the cerebellum and pyramidal cells in the cerebrum as well as tissue damage and fibrosis of the surface blood vessels. Transmission electron microscopy of the cerebral neurons showed microscopic signs of axonal damage, chromatin condensation, the presence of indistinct nucleoli and mitochondrial damage. Together these cellular features suggest the presence and influence of oxidative stress. Exposure to these metals at X100 the safety limits, as part of mixtures, induces changes to neurological tissue that could adversely influence neurological functioning in the central nervous system.

Rheumatoid Vasculitis and Blepharitis Caused By Rheumatoid Arthritis In 6 Years Old Boy: A Case Report

Link of Video Abstract: https://youtu.be/4Guk_6foSxw Introduction: Rheumatoid Vasculitis (RV) is a rare complication affecting approximately 1% of patients with severe rheumatoid arthritis. This condition is an extra-articular manifestation of rheumatoid arthritis that affects the small and medium arteries in the body. Vasculitis is an inflammatory necrotizing vascular wall disease that can occur in autoimmune disease. This inflammation leads to damage in blood vessels due to stenosis or occlusion and thrombosis, resulting in pain, necrosis, and aneurysm. Inflammation can be primary or secondary. Skin, fingers, peripheral nerves, eyes and the heart are the most commonly affected areas. Case description: We report a case of a 6-year-old boy who presented RV and blepharitis. The patient subsequently experienced nail fold infarcts and gangrene of his left finger. He was found to fulfill Jones Criteria, and treatment with aspirin and corticosteroids significantly improved his symptoms. This rare case describes the early onset of rheumatoid vasculitis in a patient with rheumatoid arthritis. Rheumatoid vasculitis is a systemic disease that develops from rheumatoid arthritis with rheumatoid autoantibodies and extra-articular manifestations characterized by tissue damage or ischemia involving the skin and peripheral nerves. The incidence of rheumatoid vasculitis in children is less than 1%, with 12 to 53 cases per 100,000 children under 17 years old. Conclusion: Rheumatoid vasculitis is a rare complication of rheumatoid. This condition occurs in patients who have rheumatoid arthritis for a long period. The patient will prevent further complications with early diagnostic and proper treatment.