Serum MicroRNA-155 in Acute Graft-Versus-Host-Disease (aGVHD)
Published on: 16th August, 2019
OCLC Number/Unique Identifier: 9059393117
Allogeneic hematopoietic stem cell transplant (alloHSCT) is a curative treatment for many hematologic malignancies. Unfortunately, about 30-50% of all recipients undergoing alloHSCT develop acute graft-versus-host-disease (aGVHD), which is associated with high morbidity and mortality [1,2]. Treatment of aGVHD involves the use of immune suppressive drugs such as high dose of steroids that leads to further immunosuppression and risk for opportunistic infections. Often patients are refractory to steroids therapy making the prognosis dismal. Thus, it is critical to identify robust biomarkers to detect aGVHD before onset of clinical symptoms so that therapeutic strategies can be implemented that may result in better treatment responses and less toxicity.
Correlation of plasma protein from MDS, young and elderly patients by SDS-page
Published on: 11th November, 2019
OCLC Number/Unique Identifier: 8330254423
Summary: Myelodysplastic Syndrome (MDS) is a heterogeneous group of clonal hematopoietic malignancies characterized by progressive cytopenias, ineffective hematopoiesis, bone marrow hypercellularity and transformation to acute myeloid leukemia (AML).
Objectives: Identify plasma proteins from MDS patients and from two healthy controls groups (young and elderly) by SDS-Page.
Methods: Plasma from 08 healthy young, 08 healthy elderly and 08 MDS patients were used for this study. Proteins were fractionated, precipitated, used for SDS-PAGE gel analysis, stained with comassie brilliant blue, scanned and bands were analyzed.
Results: It was possible to identify in both, 20% fraction and supernatant, proteins that were differentially expressed in each group. The ones that have showed some clinical relevance. Fibronectin was highly expressed only in the young control group. α2-Macroglobulin was also expressed in both control groups, but it was not expressed in the MDS group. Haptoglobin was highly expressed only in the elderly control and SMD groups.
Conclusion: Protein expression in plasma can be a biomarker for MDS, and may play a key role in the process of aging and hematologic malignancies development.
The motivational factors and adverse events experienced by healthy volunteers donating bone marrow for research
Published on: 5th December, 2019
OCLC Number/Unique Identifier: 8479094098
Background: With the advancement of cell therapy research, there is an increasing need for healthy volunteers (HV) to donate small volumes (30 ml) of human bone marrow (BM). The BM procedure required to procure small volumes is invasive, although short-lived (25 seconds), is not without risk. To ensure a sustainable supply of BM for research and cell therapy, greater information of the risks and factors that motivate HV to donate small volumes of BM will help optimize the procedure and HV enrolment, ensuring donors are fully informed of the potential risks.
Objective: To identify the adverse events (AE) experienced by HV during and after small volume BM procedure and understand the motivating factors that influence HV to donate BM for research.
Method: HV (n = 55) who donated BM (30 ml) for scientific research and provided informed consent were administered a questionnaire to identify the type, duration and severity of AE experienced during and post-BM aspiration; and to determine the motivating factors that influenced their willingness to donate BM.
Results: Pain was experienced by 89% of participants during the BM procedure with moderate grade reported by 40%. One/more of the following AE were experienced by 73% of the volunteers post-BM procedure: pain, fatigue, site reaction, nausea and transient hypotension. AE resolved within an average of three days. The reported motivational factors ranked in the following order: first, to advance research for the benefit of future patients; compensation for participation; free medical check-up; lastly, the research question was interesting.
Conclusion: Young HV, motivated primarily by altruism and financial compensation, risk the occurrence of transient AE following donation of small-volume BM for research.
Novel European Asiatic Clinical, Laboratory, Molecular and Pathobiological (2015-2020 CLMP) criteria for JAK2V617F trilinear polycythemia vera (PV), JAK2exon12 PV and JAK2V617F, CALR and MPL515 thrombocythemias: From Dameshek to Constantinescu-Vainchenker, Kralovics and Michiels
Published on: 3rd April, 2020
OCLC Number/Unique Identifier: 8576367174
The Myeloproliferative Neoplasms (MPN) of trilinear polycythemia vera (PV) and megakaryocytic leukemia (ML = primary megakaryocytic granulocytic myeloproliferation: PMGM) and Essential Thrombocythemia (ET) in the studies of Dameshek and Michiels are caused by the MPN driver mutations JAK2V617F, JAK2exon12, CALR and MPL515 discovered by Constantinescu-Vainchenker, Green and Kralovics. The JAK2V617F mutated trilinear myeloproliferative neoplasms (MPN) include a broad spectrum of clinical laboratory and bone marrow features in essential thrombocythemia (ET), prodromal PV and erythrocythemic PV, classical PV and advanced stages of masked PV and PV complicated by splenomegaly and secondary myelofibrosis (MF). Heterozygous JAK2V617F mutated ET is associated with low JAK2 allele and MPN disease burden and normal life expectance. In combined heterozygous and homozygous or homozygous JAK2V617F mutated trilinear PV, the JAK2 mutation load increases from less than 50% in prodromal PV and classical PV to above 50% up to 100% in hypercellular PV, advanced PV and PV with MF. Bone marrow histology show diagnostic features of eryhrocytic, megakaryocytic and granulocytic (EMG) myeloproliferation in JAK2V617F mutated trilinear MPN, which clearly differs from monolinear megakaryocytic (M) myelproliferation in MPL and CALR thrombocythemia and dual megakaryocytic granulocytic (MG) myeloproliferation in CALR mutated thrombocythemia. The morphology of clustered large pleomorphic megakaryocytes with hyperlobulated nuclei are similar in JAK2V617F thrombocythemia, prodromal PV and classical PV patients. Monolinear megakaryocytic (M) myeloproliferation of large to giant megakaryocytes with hyperlobulated staghorn-like nuclei is the hallmark of MPL515 mutated normocellular thrombocythemia. CALR mutated thrombocythemia usually presents with high platelet count around 1000x109/l and normocellular megakaryocytic (M) proliferation of immature megakaryocytes with cloud-like hyperchromatic nuclei followed by dual megakaryocytic granulocytic (MG) myeloproliferation followed by various degrees of bone marrow fibrosis. Natural history and life expectancy of MPN patients are related to the response to treatment and the degree of anemia, splenomegaly, myelofibrosis and constitutional symptoms. The acquisition of epigenetic mutations at increasing age on top of MPN disease burden independently predict unfavorable outcome in JAK2V617F, MPL515 and CALR mutated myeloproliferative neoplasms (MPNs, which mutually exclude each other).
Role of plants, environmental toxins and physical neurotoxicological factors in Amyotrophic lateral sclerosis, Alzheimer Disease and other Neurodegenerative Diseases
Published on: 4th March, 2019
OCLC Number/Unique Identifier: 8056301487
Aim of this work is to verify the effect of some neurotoxins, physical factors and geography in presentation of some Relevant Neurological disorder like some form of ASL, PD, AD.
The geographic diffusion of the ASL/PD in west pacific (GUAM foci), and mutation of SOD 1 and other mutations are interesting facts to verify the recent literature about the neurotoxic process.
Related to the references presented a global conclusion about the pathogenetic progression of some neurological disease will be produced as instrument for new hypothesis and for the introduction of new innovative therapeutic strategies.
Mimicking multiple sclerosis - Ghost tumor that comes and goes in different parts of the brain without any treatment
Published on: 9th July, 2019
Lesions that spontaneously come and go in central nervous system without any treatment at different time points and at different locations (CNS) usually lead ones to think of the possibilities of multiple sclerosis. However, sometimes there are exceptions. Surgical biopsy remains an important tool for definitive diagnosis in difficult cases. We report a case of intracranial diffuse large B cell lymphoma that spontaneously disappeared without any treatment and then reappeared at different time points and different locations.
Comparative study of carboxylate and amide forms of HLDF-6 peptide: Neuroprotective and nootropic effects in animal models of ischemic stroke
Published on: 24th July, 2019
OCLC Number/Unique Identifier: 8195621281
Aim:The work was to perform a comparative study of the neuroprotective and nootropic activities of two pharmaceutical substances, the HLDF-6 peptide and its amide form (HLDF-6-NH2).
Materials and Methods: We used in the study healthy adult male Wistar rats aged 180–200 days weighing 280–300 g. We modelled ischemic stroke in rats by chronical occlusion of carotid arteries. Solutions of the HLDF-6-NH2 and HLDF-6 peptides were administered intranasally. Cognitive functions we assessed with Novel object recognition test and Morris maze.
Results: The amide form of HLDF-6 peptide is more efficient: the neuroprotective activity of HLDF-6-NH2, evaluated by improvement of cognitive functions in animals, surpassed that of the native HLDF-6 peptide. A dose of 250 µg/kg of HLDF-6-NH2 peptide resulted in practically complete restoration of the disturbed functions. In the model of ischemic stroke, the amide form of the peptide significantly excelled the reference substance mexidol both in the effective dose and biological activity.
Conclusion: The results of study of the agent allow hoping for its success in further clinical investigation. In view of high demand for the agent and in case of successful clinical trials, it will surely become widely used in clinical practice in treatment of IS.
Gastrointestinal stromal tumor resulting in recurrent colic in a arabian horse gelding a report of case
Published on: 2nd November, 2020
OCLC Number/Unique Identifier: 8697203989
Background: A Grey 12-year-old Arabian endurance horse gelding was referred to the SHS Veterinary Center for anorexia, mild colic of 5 days duration, and melena of 1 day duration. The owner reported recurring colic, 12 episodes of mild colic in the previous year.
Methods: On admission, vital signs were within normal limits and body condition score was estimated to be 3/9.
Results: Packed cell volume (PCV) was 28% [reference range (RR): 31% to 47%] and plasma total protein was 58 g/L (RR: 60 to 80 g/L). Hematochezia was observed. Abdominal ultrasound examination detected no abnormalities. Over the next 12 h, the horse experienced hematochezia and several mild episodes of colic and death. A necropsy was performed. A mass arising from the right dorsal ascending colon near the base of the cecum and extending transmurally from the colonic mucosa into the mesocolon was a 8 cm × 5 cm × 8 cm firm, homogenous, tan mass. The portion of the mass that extended into the colonic lumen was pedunculated, with an ulcerated surface. The adjacent segments of colon were markedly reddened and edematous. Histologically, the mass was comprised of large interweaving sheets of small, spindle cells with ill-defined cell borders embedded in abundant myxomatous matrix. Tumor cells contained scant eosinophilic cytoplasm and oval to elongate nuclei with finely stippled chromatin and inconspicuous nucleoli. Mitotic figures were rare (1/10) high power fields. Tumor infiltrated between the muscularis interna and the muscularis externa at the myenteric plexi.
Conclusion: Gross and histologic appearance, were consistent with a diagnosis of gastrointestinal stromal tumor.
Carbonic Anhydrase I modifies SOD1-induced motor neuron toxicity in Drosophila via ER stress pathway
Published on: 1st August, 2019
OCLC Number/Unique Identifier: 8195612915
Background: Drosophila models of amyotrophic lateral sclerosis (ALS) have been widely used in understanding molecular mechanisms of ALS pathogenesis as well as discovering potential targets for therapeutic drugs. Mutations in the copper/zinc superoxide dismutase (SOD1) cause ALS by gain of toxic functions and induce toxicity in fly motor neurons.
Results: In this study, we have determined that human carbonic anhydrase I (CA1) can alleviate mutant SOD1-induced motor neuron toxicity in the transgenic fly model of ALS. Interestingly, we found that motor neuron expression of CA1 could independently induce locomotion defect as well as decreasing the survival rate. In addition, CA1-induced toxicity in motor neurons is anhydrase activity-dependent. Mechanistically, we identified that both SOD1- and CA1-induced toxicity involve the activation of eIF2α in the ER stress response pathway. Downstream activation of the JNK pathway has also been implicated in the induced toxicity.
Conclusion: Our results have confirmed that SOD1-induced toxicity in fly motor neuron also involves endoplasmic reticulum (ER) stress pathway. More importantly, we have discovered a new cellular role that CA1 plays by antagonizing mutant SOD1-induced toxicity in motor neurons involving the ER stress pathway. Such information can be potentially useful for further understanding disease mechanisms and developing therapeutic targets for ALS.
Protection from the Pathogenesis of Neurodegenerative Disorders, including Alzheimer’s Disease, Amyotrophic Lateral Sclerosis, Huntington’s Disease, and Parkinson’s Diseases, through the Mitigation of Reactive Oxygen Species
Published on: 4th November, 2019
OCLC Number/Unique Identifier: 8302209826
The biological changes caused by oxidative stress (OS) are known to be involved in the etiology of neurodegenerative disorders, including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. The brain is particularly vulnerable to OS due to its high lipid content and extensive consumption of oxygen. OS processes, particularly the excessive production of reactive oxygen species (ROS), play a critical role in how neurodegenerative disorders develop. This is evidenced by in vivo studies investigating various biomolecules related to OS, such as products of lipid and DNA oxidation. Accordingly, ROS can also cause oxidative-related damage in neurodegenerative disorders, including dopamine auto-oxidation, mitochondrial dysfunction, glial cell activation, α-synuclein aggregation, excessive free iron, and changes in calcium signaling. Furthermore, excessive levels of cellular oxidants reduce antioxidant defenses, which in turn propagate the cycle of OS. As such, it is increasingly important to determine the linkage between a high intake of antioxidants through dietary interventions and a lower risk of developing neurodegenerative diseases. Indeed, in addition to modulating the immune system, optimal nutritional status is capable of changing various processes of neuroinflammation known to be involved in the pathogenesis of neurodegeneration. Accordingly, a better understanding of the role ROS plays in the etiology of neurodegeneration is needed, along with the identification of dietary interventions that may lead to improved therapeutic strategies for both the treatment and prevention of neurodegenerative disorders. Therefore, this review presents a comprehensive summary of the role of ROS in the pathogenesis of neurodegenerative disorders. In addition, nutrients believed to be useful for mitigating and counteracting ROS are discussed.
Immunohistochemical expression of Nestin as Cancer Stem Cell Marker in gliomas
Published on: 11th November, 2019
OCLC Number/Unique Identifier: 8457474432
Background: Gliomas represent the most frequent primary tumors of central nervous system (CNS), contributing to more than half of the incidence of brain tumors. Cancer stem cell markers (CSC) identify a group of patients at high risk for progression. Nestin is an intermediate filament (IF) protein was first described as a neural stem cell/progenitor cell marker. Nestin-positive neuroepithelial stem cells are detected in the subventricular zone of the human adult brain and they remain mitotically active throughout adulthood. The expression of Nestin in gliomas has been suggested to be related to dedifferentiation, improved cell motility, invasive potential and increased malignancy. This study aims to investigate Nestin immunohistochemical expression in different types of glioma and its correlation with different clinicopathological parameters.
Materials and Methods: Nestin immunostaining was studied in 60 specimens of glioma using avidin-biotin peroxidase method.
Results: Nestin was strongly expressed in 11/60 (18.33%), moderately expressed in 29/60 (48.33%) and weekly expressed in 15/60 (25%) of studied gliomas. A significant positive correlation was found between Nestin expression and histologic type (p < 0.001) and increasing grade of gliomas (p < 0.001).
Conclusion: Increased Nestin expression is correlated with tumor progression, increasing grade and poor prognostic parameter of glioma. Nestin is a useful marker for detection of CSC in high-grade glioma which is responsible for resistance to chemo-radiotherapy and may serve as a predictor for patient outcomes.
Central nervous system diseases associated with blood brain barrier breakdown - A Comprehensive update of existing literature
Published on: 25th August, 2020
OCLC Number/Unique Identifier: 8799409922
Blood vessels that supply and feed the central nervous system (CNS) possess unique and exclusive properties, named as blood–brain barrier (BBB). It is responsible for tight regulation of the movement of ions, molecules, and cells between the blood and the brain thereby maintaining controlled chemical composition of the neuronal milieu required for appropriate functioning. It also protects the neural tissue from toxic plasma components, blood cells and pathogens from entering the brain. In this review the importance of BBB and its disruption causing brain pathology and progression to different neurological diseases like Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD) etc. will be discussed.
Primary intracranial Hodgkin’s lymphoma after a blunt trauma: A case report
Published on: 15th December, 2020
We report a case of 30-year-old immunocompetent man, with a previous history of cranial-facial trauma, who presented with progressive left exophthalmos due to an intracranial left frontal-ethmoidal-orbital mass. Histology of the resected tumor revealed a classical Hodgkin’s Lymphoma (HL). Epstein-Barr virus encoded RNA/EBER was detected in typical Hodgkin and Reed-Sternberg cells. After postoperative radiotherapy and chemotherapy administration, the patient remains free of systemic disease or recurrence on 4 years of follow-up.
Intracranial involvement by HL has rarely been described, mostly as a late localization or as a recurrence of a disseminated disease, in a setting of immunosuppression. Primary HL of the central nervous system occurring as an isolated disease is even more uncommon, with only 16 reported cases documented to date. The prognosis of these rare cases appears comforting with appropriate treatment. Tumor resection and, in appropriate cases, treatment with radiation and/or chemotherapy seem to warrant a durable response. For this reason a systemic disease should be excluded in all cases intracranial HL by a comprehensive work-up.
To the best of our knowledge, this case represents the first report that documents the association of intracranial HL and local trauma with subsequent intracranial infection.
Impact of mandibular advancement device in quantitative electroencephalogram and sleep quality in mild to severe obstructive sleep apnea
Published on: 30th December, 2020
OCLC Number/Unique Identifier: 8899350400
Sleep related breathing disorders (SRBD) are among seven well-established major categories of sleep disorders defined in the third edition of The International Classification of Sleep Disorders (ICSD-3), and Obstructive Sleep Apnea (OSA) is the most common SRBD [1,2]. Several studies have demonstrated that obstructive sleep apnea treatment increases the quality of life in OSA patients [3-8]. Indeed, excessive daytime sleepiness (EDS), cognitive impairment (e.g., deficits in attention-concentration, memory, dexterity, and creativity), traffic accidents, and deterioration of social activities are frequently reported in untreated patients [9-11]. Furthermore, an increase in cardiovascular morbidities and mortality (systemic hypertension, stroke, cardiac arrhythmias, pulmonary arterial hypertension, heart failure) [12], metabolic dysfunction, cerebrovascular ischemic events and chemical/structural central nervous system cellular injuries (gray/white matter) has been reported in OSA patients [13-17].
Continuous positive airway pressure (CPAP) therapy is considered the gold standard for treatment of moderate-severe OSA, nevertheless there is an increasing body of evidence supporting the usefulness of mandibular advancement devices (MADs) for improving quality of life and respiratory parameters even among patients with a high severity of OSA burden [5,10,18,19]. According to the standard of care of the American Academy of Sleep Medicine (AASM), MADs are indicated for mild to moderate OSA particularly in the context of CPAP intolerance or refusal, surgical contraindication, or the need for a short-term substitute therapy [9,15,20-22]. In Cuba, CPAP machines are not readily available; they are expensive and the majority of OSA patients cannot obtain this mode of therapy. Taking into account this problem, our hypothesis was based in the scientific evidences of MAD effectiveness, considering that low cost MADs could offer a reasonable alternative treatment for patients with OSA where CPAP technology are not handy. In this way our purpose was to assess the efficacy of one of the most simple, low cost, manufactured monoblock MAD models (SAS de Zúrich) in terms of improvements in cerebral function, sleep quality and drowsiness reports in a group of Cuban OSA patients with mild to severe disease. Outcome measures included changes in the brain electrical activity, sleep quality, and respiratory parameters, measured by EEG recording with qEEG analysis and polysomnographic studies correspondingly, which were recorded before and during treatment with an MAD, as well as subjective/objective improvements in daytime alertness.
A pilot study on treatment of infantile cystinosis with mesenchymal stem cells
Published on: 9th December, 2019
OCLC Number/Unique Identifier: 9272394663
Infantile cystinosis is a lysosomal storage disease leading to end stage kidney disease at early ages. There is no effective treatment and patients require long term dialysis or kidney transplant for survival. We present our experience on three affected children who received HLA matched allogeneic stem cell transplant. The protocol used was novel and designed to promote engraftment. The primary endpoint was safety for treatment related mortality or morbidity; All three children survived without serious adverse effects during extended follow up for over 4 years. Although we could not prove engraftment, all three children met secondary end point of sustained target functions over a 6 month follow-up. Further studies are warranted to further evaluate safety and efficacy of MSC treatment for infantile cystinosis.
Glomerular hyperfiltration in Yemeni children with sickle cell disease
Published on: 12th January, 2021
OCLC Number/Unique Identifier: 8899350598
Background: Glomerular hyperfiltration (GH) is a common feature of sickle cell nephropathy (SCN) starting at infancy and represents an early marker of incipient glomerular injury and renal dysfunction.
Methods: This study aimed to determine the prevalence and correlates of GH among children (≤ 16 years) with sickle cell disease (SCD) at their steady state, recruited over 6 months at the Pediatric Outpatient Clinic in Al-Sadaqa General Teaching Hospital, Aden, Yemen. Glomerular filtration rate (eGFR) was estimated using the Schwartz formula. Data on clinical history, anthropometry, blood pressure (BP) and laboratory investigations were collected.
Results: Of 101 children (mean age 7.2 ± 3.9 years), 65 (64.4%) were males. The prevalence of GH was observed in 36 (35.6%) children, who were significantly older (10.7 ± 3.2 vs. 5.2 ± 2.7 years, p < 0.001) and had a lower fetal Hb level (5 ± 3.3 vs. 9 ± 7.1, p = 0.02). All children were normotensive, but hyperfiltrating children showed significantly higher systolic (97.2 ± 7.3 vs. 89.7 ± 5.2 mmHg) and diastolic pressure (55.1 ± 5.0 vs. 49 ± 4.3 mmHg) (all p < 0.001). Among evaluated children, 25.7% had hyperfiltration alone, whereas 9.9% had an associated microalbuminuria (MA), and no significant difference in eGFR between those with and without MA (158.4 ± 33.7 vs. 160.7 ± 29.8 ml/min/173m2, p = 0.84).
Conclusion: This study demonstrated a relatively high prevalence of GH in Yemeni children with SCD that increased with age. Recognition of hyperfiltration and other early markers of nephropathy in this population could help to develop renal protective strategies to prevent progressive loss of kidney function.
Acute urinary retention and hyponatremia from central hypothyroidism
Published on: 8th January, 2021
OCLC Number/Unique Identifier: 8899349889
A mass arising from the pituitary gland commonly damages cells of the anterior pituitary gland and affects the secretion of gonadotropins and growth hormone. However, central hypothyroidism and secondary adrenal insufficiency from such damage is a rare phenomenon. Acute urinary retention as the main symptom of central hypothyroidism is also an unusual initial presentation. We report a male patient who comes with frequent urinary retention and hyponatremia at our hospital.
Cortical spreading depolarizations in the context of subarachnoid hemorrhage and the role of ketamine
Published on: 23rd March, 2021
OCLC Number/Unique Identifier: 9026724760
Delayed cerebral ischemia (DCI) is one of the main complications of spontaneous subarachnoid haemorrhage and one of its causes is the cortical spreading depolarizations (CSDs). Cortical spreading depolarizations are waves of neuronal and glial depolarizations in which there is loss of neuronal ionic homeostasis with potassium efflux and sodium and calcium influx. In damaged brain areas and brain areas at risk, such as those adjacent to subarachnoid haemorrhage (SAH), CSDs induce microvascular vasoconstriction and, therefore, hypoperfusion and spread of ischemia. Several studies have been devoted to minimize secondary injuries that occur hours to days after an acute insult. Ketamine, a drug until recently contraindicated in the neurosurgical population for potentially causing intracranial hypertension, has re-emerged as a potential neuroprotective agent due to its pharmacodynamic effects at the cellular level. These effects include anti-inflammatory mechanisms, and those of microthrombosis and cell apoptosis controls, and of modulation of brain excitotoxicity and CSDs. A literature review was performed at PubMed covering the period from 2002 to 2019. Retrospective studies confirmed the effects of ketamine on the control of CSDs and, consequently, of DCI in patients with SAH, but did not show improvement in clinical outcome. The influence of ketamine on the occurrence/development of DCI needs to be further confirmed in prospective randomized studies
Characterization of the immune response in neuroimmune disorders in children
Published on: 20th April, 2021
OCLC Number/Unique Identifier: 9026721284
Background: A misguided auto-reactive injury is responsible for several types of central nervous system (CNS) conditions in pediatrics. We propose that, in some of these conditions, the adaptive immune system has a common cellular immune pathogenesis, driven predominantly by T cells, despite variability on the phenotypical clinical presentation.
Methods: We have characterized the CD4+/CD8+ adaptive immune response (AIR) on pediatric patients presenting with clinical symptoms compatible with Neuroimmune Disorders (NID). Flow cytometry with deep immunophenotyping of T cells was performed on peripheral blood obtained during the acute clinical phase and compared to an age-matched cohort group (Co).
Results: We found that pediatric patients with confirmed NID, exhibit a pattern of dysregulation of CD4+ lineages associated with autoimmune processes.
Discussion: The autoimmune associated CD4+ dysregulation was associated with patients with NID, as compared to healthy controls and patients with non-autoimmune diagnoses. If we can improve our capacity for early accurate diagnosis and meaningful disease monitoring of pathogenic T cell subsets, we can both expedite disease detection and may serve as a guide to the administration of effective immunotherapeutic agents.
Role of neuron specific enolase as a biomarker in Parkinson’s disease
Published on: 6th July, 2021
OCLC Number/Unique Identifier: 9137583301
Parkinson’s disease (PD) is thought to be the most common neurodegenerative disease with movement disorder. The key motor symptoms are rigidity, tremor, akinesis/hypokinesia/bradykinesia, and postural instability. However, in our day-to-day clinical practice we tend to see several other symptoms which may be motor or non-motor. Non-motor symptoms (NMS) are quite common and debilitating. The pathological hallmarks of PD are loss of dopaminergic neurons in the substantia nigra pars compacta (SNPc) and accumulation of unfolded or misfolded alpha-synuclein. Diagnosis of PD is difficult in the pre-motor stage. Late diagnosis renders a substantial loss of dopaminergic neurons in SNPc and spread of disease in other parts of the brain. This may manifest as either full blown symptoms requiring multiple medications or may even lead to life threatening condition due to lack of early diagnostic tools and techniques. Biomarkers are required to diagnose PD at a very early stage when prevention is possible. Hence, we see a lot of interest among researchers involved in finding a biomarker specific to the disease. Biomarkers may be clinical, image based, genetic, and biochemical. Cerebrospinal fluid (CSF) and serum markers which may correlate with disease pathophysiology are of great significance. One such molecule which recently gained a lot of attention is neuron-specific enolase (NSE). The main aim of this paper is to highlight the role of NSE in predicting neurodegeneration and neuroinflammation ultimately reflecting damage of brain cells in PD.
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