Reduced Iron Levels Research Articles

Penambahan Media Kapas Dan Kerikil Pada Multi Tray Aerator Untuk Pengolahan Air Daerah Rususnawa Untan Dalam Mengurangi Kandungan Logam Sebagai Pre-treatment Pada Sistem Membran RO

Rivers are surface water used for public purposes. Rivers are used for water storage, transportation, irrigation, livestock, industry, housing, water availability, fish rearing and recreation. Various activities carried out in the river cause pollution and have an impact on the decline in water quality, such as in Sepakat 2 river water which is used by the surrounding community for daily needs. The purpose of this study was to determine the Fe contained in Sepakat 2 river water and the effectiveness of using multi tray aerators with the addition of cotton and gravel media in reducing iron levels. Processing of Sepakat 2 river water through a pretreatment process using a 5-level multi tray aerator method and 6 perforated trays to drop water to the bottom of the container, then the water that has been aerated is collected in a box and deposited for 1 and 2 hours after which the water is taken and stored using a bottle container to be analyzed by the Pontianak Industrial Standardization and Services Center Laboratory. The results of this study are the quality of river water Sepakat 2 iron levels 6.37 mg / L before processing, after aeration 4.99 mg / L, after settling 1 and 2 hours with the same value of 5.09 mg / L. The efficiency of the multi tray aerator tool to reduce iron parameters from iron by 20.09%, TDS 52.1%, mercury (Hg) 43.08% and salinity is 63.3%.

Components of Iron Deficiency Anemia: Understanding Pathophysiology, Diagnosis, and Management

Iron deficiency anemia (IDA) is a prevalent global health concern, marked by a significant reduction in iron levels, leading to diminished hemoglobin production and compromised oxygen transport. This condition disproportionately affects vulnerable populations, including women of reproductive age, infants, and individuals in low-resource settings, resulting in a multitude of health complications. The pathophysiology of IDA involves complex interactions between dietary iron intake, increased physiological demands, chronic blood loss, and malabsorption syndromes. Clinically, IDA manifests through symptoms such as fatigue, pallor, and cognitive impairments, necessitating a thorough diagnostic approach that includes complete blood counts, iron studies, and reticulocyte counts. Effective management strategies encompass dietary modifications, iron supplementation, and treatment of underlying causes. Furthermore, preventive measures—such as public health initiatives and food fortification—are crucial in addressing the root causes of IDA. Emerging research suggests innovative approaches, including bioavailable iron sources and genetic studies, to enhance prevention and treatment efforts. This review comprehensively examines the components of IDA, providing insights into its pathophysiology, diagnosis, management, and future directions for research and intervention. Keywords Iron deficiency anemia (IDA), Pathophysiology, Diagnosis, Management, Dietary iron.

Butylphthalide mitigates traumatic brain injury by activating anti-ferroptotic AHR-CYP1B1 pathway

Ethnopharmacological relevanceIncreasing evidence suggests that ferroptosis, an iron-dependent form of cell death characterized by lipid peroxidation, may play a substantial role in the traumatic brain injury (TBI) pathophysiology. 3-n-butylphthalide (NBP), a compound extracted from the seeds of Apium graveolens Linn (Chinese celery) and used in China to treat ischemic stroke, has demonstrated encouraging anti-reactive oxygen species (ROS) effects. Ascertaining whether NBP can inhibit ferroptosis and its mechanism could potentially expand its use in models of neurological injury and neurodegenerative diseases. Methods and resultsIn this study, we used erastin-induced in vitro ferroptosis models (HT22 cells, hippocampal slices, and primary neurons) and an in vivo controlled cortical impact mouse model. Our study revealed that NBP administration mitigated erastin-induced death in HT-22 cells and decreased ROS levels, lipid peroxidation, and mitochondrial superoxide indicators, resulting in mitochondrial protection. Moreover, the ability of NBP to inhibit ferroptosis was confirmed in organotypic hippocampal slice cultures and a TBI mouse model. NBP rescued neurons, inhibited microglial activation, and reduced iron levels in the brain tissue. The protective effect of NBP can be partly attributed to the inhibition of the AHR-CYP1B1 axis, as evidenced by RNA-seq and CYP1B1 overexpression/inhibition experiments in HT22 cells and primary neurons. ConclusionsOur study underscores that NBP inhibition of the AHR-CYP1B1 axis reduces ferroptosis in neuronal damage and ameliorates brain injury.

Silibinin promotes healing in spinal cord injury through anti-ferroptotic mechanisms.

Pre-clinical animal experiment. In this study, we investigated therapeutic effects of silibinin in a spinal cord injury (SCI) model. In SCI, loss of cells due to secondary damage mechanisms exceeds that caused by primary damage. Ferroptosis, which is iron-dependent non-apoptotic cell death, is shown to be influential in the pathogenesis of SCI. The study was conducted as an in vivo experiment using a total of 78 adult male/female Sprague Dawley rats. Groups were as follows: Sham, SCI, deferoxamine (DFO) treatment, and silibinin treatment. There were subgroups with follow-up periods of 24 h, 72 h, and 6 weeks in all groups. Malondialdehyde (MDA), glutathione (GSH), and Fe2+ levels were measured by spectrophotometry. Glutathione peroxidase-4 (GPX4), ferroportin (FPN), transferrin receptor (TfR1), and 4-hydroxynonenal (4-HNE)-modified protein levels were assessed by Western blotting. Functional recovery was assessed using Basso-Beattie-Bresnahan test. Silibinin achieved significant suppression in MDA and 4-HNE levels compared to the SCI both in 72-h and 6 weeks group (p < 0.05). GSH, GPX4, and FNP levels were found to be significantly higher in the silibinin 24 h, 72 h, and 6 weeks group compared to corresponding SCI groups (p < 0.05). Significant reduction in iron levels was observed in silibinin treated rats in 72 h and 6 weeks group (p < 0.05). Silibinin substantially suppressed TfR1 levels in 24 h and 72 h groups (p < 0.05). Significant difference among recovery capacities was observed as follows: Silibinin > DFO > SCI (p < 0.05). Impact of silibinin on iron metabolism and lipid peroxidation, both of which are features of ferroptosis, may contribute to therapeutic activity. Within this context, our findings posit silibinin as a potential therapeutic candidate possessing antiferroptotic properties in SCI model. Therapeutic agents capable of effectively and safely mitigating ferroptotic cell death hold the potential to be critical points of future clinical investigations.

SYNTHESIS OF POROUS CARBON MATERIAL PROPYLENE MEDICAL MASK AS ADSORBENT HEAVY METAL IRON (Fe) IN WATER EX-TIN MINING BANGKA BELITUNG

Bangka Belitung Islands Province faces severe environmental challenges, exacerbated byillegal tin mining activities leading to heightened pollution levels, particularly in stagnantwater within former tin mining holes, reaching depths of up to 40 meters. The presence ofiron metal (Fe) in this water poses a health risk, potentially damaging intestinal walls andcompromising lung function upon ingestion. This study presents a novel approach to addressthis issue by synthesizing porous carbon material from propylene waste sourced frommedical masks. The process involves initial sulfonation for sterilization and pore sizeenhancement, followed by activation using KOH and carbonization at 750 °C.Characterization methods validate the successful synthesis, including FTIR highlightingpolypropylene groups at 822 cm-1, XRD indicating graphite carbon with high crystallinity,and SEM exhibiting rod shapes and cavities at 5,000í— magnification. The adsorption testdemonstrates outstanding performance, with porous carbon exhibiting a 100% adsorptionefficiency in purifying water, eliminating odors, and reducing iron (Fe) levels. Thisinnovative method effectively reduces iron levels in stagnant water environments, providinga sustainable solution to environmental pollution, particularly in Bangka Belitung.

Rosmarinic acid liposomes suppress ferroptosis in ischemic brain via inhibition of TfR1 in BMECs

BackgroundIron deposition and ferroptosis are involved in ischemic stroke injury, but the choice of drugs for treatment is limited. PurposeTo investigate the potential neuroprotective effects of Rosmarinic acid (RosA) encapsulated within nanoliposomes (RosA-LIP) on ischemic stroke. MethodsWild-type (WT) and TfR1EC cKO (specific knockout of the TfR1 gene in BMECs) mice used to establish a dMCAO model, with simultaneous administration of RosA-LIP (20 mg/kg/d, i.p.) or RosA (20 mg/kg/d, i.p.). ResultsThe successful synthesis of RosA-LIP resulted in enhanced stability and precise delivery in both the serum and brain. The administration of RosA-LIP effectively mitigated ischemia-induced behavioral abnormalities and pathological damage. RosA-LIP inhibited ferroptosis by ameliorating mitochondrial abnormalities, increasing GPX4 levels, and decreasing ACSL4/LPCAT3/Lox-dependent lipid peroxidation. RosA-LIP effectively improved blood‒brain barrier (BBB) permeability, increased tight junctions (TJs) protein expression and reduced iron levels in ischemic tissue and brain microvascular endothelial cells (BMECs) by modulating FPN1 and TfR1 levels. Furthermore, RosA-LIP suppressed TfR1 to attenuate ACSL4/LPCAT3/Lox-mediated ferroptosis in TfR1EC cKO mice subjected to dMCAO. ConclusionRosA-LIP effectively increased the brain level of RosA and protected against ferroptosis through the regulation of TfR1 in BMECs.

Electroacupuncture Downregulating Neuronal Ferroptosis in MCAO/R Rats by Activating Nrf2/SLC7A11/GPX4 Axis

Ischemic stroke involves various pathological processes, among which ferroptosis is crucial. Previous studies by our group have indicated that electroacupuncture (EA) mitigates ferroptosis after ischemic stroke; however, the precise mechanism underlying this effect remains unclear. In the present study, we developed a rat model of middle cerebral artery occlusion/reperfusion. We chose the main acupoint of the treatment methods of the “Awakening and Opening of the Brain”. Rats’ neurological function and motor coordination were evaluated by neurological function score and the rotarod test, respectively, and the volume of cerebral infarction was analyzed by 2,3,5-triphenyltetrazolium chloride Staining. The cerebrovascular conditions were visualized by time-of-flight magentic resonance angiography. In addition, we detected changes in lipid peroxidation and endogenous antioxidant activity by measuring the malondialdehyde, glutathione, superoxide dismutase activities, glutathione/oxidized glutathione and reduced nicotinamide adenine dinucleotide phosphate/oxidized nicotinamide adenine dinucleotide phosphate ratios. Inductively coupled plasma-mass spectrometry, western blot, reverse transcription-polymerase chain reaction, fluoro-jade B staining, immunofluorescence analysis, and transmission electron microscopy were utilized to examine the influence of EA. The results indicate that EA treatment was effective in reversing neurological impairment, neuronal damage, and protecting mitochondrial morphology and decreasing the cerebral infarct volume in the middle cerebral artery occlusion/reperfusion rat model. EA reduced iron levels, inhibited lipid peroxidation, increased endogenous antioxidant activity, modulated the expression of several ferroptosis-related proteins, and promoted nuclear factor-E2-related factor 2 (Nrf2) nuclear translocation. However, the protective effect of EA was hindered by the Nrf2 inhibitor ML385. These findings suggest that EA can suppress ferroptosis and decrease damage caused by cerebral ischemia/reperfusion by activating Nrf2 and increasing the protein expression of solute carrier family 7 member 11 and glutathione peroxidase 4.

Chronic Aroclor 1260 exposure alters the mouse liver proteome, selenoproteins, and metals in steatotic liver disease

The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) continues to increase due in part to the obesity epidemic and to environmental exposures to metabolism disrupting chemicals. A single gavage exposure of male mice to Aroclor 1260 (Ar1260), an environmentally relevant mixture of non-dioxin-like polychlorinated biphenyls (PCBs), resulted in steatohepatitis and altered RNA modifications in selenocysteine tRNA 34 weeks post-exposure. Unbiased approaches identified the liver proteome, selenoproteins, and levels of 25 metals. Ar1260 altered the abundance of 128 proteins. Enrichment analysis of the liver Ar1260 proteome included glutathione metabolism and translation of selenoproteins. Hepatic glutathione peroxidase 4 (GPX4) and Selenoprotein O (SELENOO) were increased and Selenoprotein F (SELENOF), Selenoprotein S (SELENOS), Selenium binding protein 2 (SELENBP2) were decreased with Ar1260 exposure. Increased copper, selenium (Se), and zinc and reduced iron levels were detected. These data demonstrate that Ar1260 exposure alters the (seleno)proteome, Se, and metals in MASLD-associated pathways.

Adsorption isotherm and kinetic study of Bengkulu Kaolinite in removing ferrous cation by continuous operation

Iron is a chemical element that is found in groundwater that can be suspended in the form of ferrous cations. Iron presence that exceeds the threshold can cause detrimental effects such as piping corrosion, bad smells, and health problems. According to observations, groundwater in Sukarame, Bandar Lampung, has smells and colors that indicate iron metal contamination. Hence, it is necessary to research reducing the iron content. The method used in this research is the adsorption method using kaolin adsorbent that has been activated by physical activation at 700°C. The adsorption was conducted continuously with various reactor heights of 20 cm, 15 cm, and 10 cm. The results showed that the most significant reduction in efficiency was found in the adsorption using reactors with a height of 20 cm by 92%. The adsorption phenomenon using a reactor height of 20 cm followed the Langmuir isotherm model (R2 = 0.9255) with an adsorption capacity of 17.03 mg/g. The kinetic data correlated well with the pseudo-second-order equation (R2 = 0.9313). It can be concluded that kaolin adsorbent can reduce iron levels, in which the adsorption using reactors with a height of 20 cm is the most effective.

Paroxysmal atrial fibrillation and hemochromatosis: a narrative review

Paroxysmal atrial fibrillation (PAF) and hemochromatosis have a complex relationship. This review explores its mechanisms, prevalence, correlations, and clinical manifestations. Hereditary hemochromatosis (HH) involves iron overload due to HFE protein mutations, while atrial fibrillation (AF) is characterized by irregular heart rhythms. Iron overload in hemochromatosis can promote cardiac arrhythmias. AF is prevalent in developed countries and may be linked to cryptogenic strokes. Genetic variations and demographic factors influence the occurrence of both conditions. HH affects multiple organ systems, including the heart, while AF causes palpitations and reduced exercise tolerance. Diagnosis involves iron markers, genotypic testing, and electrocardiogram (ECG) findings. Treatment strategies focus on reducing iron levels in hemochromatosis and managing AF through antithrombotic therapy and rhythm control. Untreated hemochromatosis carries a higher risk of complications, and PAF is associated with increased cardiovascular-related mortality. For better understanding of the mechanisms and to improve management, additional studies are required. Tailored approaches and combined treatments may enhance patient outcomes.

Deferasirox Targeting Ferroptosis Synergistically Ameliorates Myocardial Ischemia Reperfusion Injury in Conjunction With Cyclosporine A.

Ferroptosis, an iron-dependent form of regulated cell death, is a major cell death mode in myocardial ischemia reperfusion (I/R) injury, along with mitochondrial permeability transition-driven necrosis, which is inhibited by cyclosporine A (CsA). However, therapeutics targeting ferroptosis during myocardial I/R injury have not yet been developed. Hence, we aimed to investigate the therapeutic efficacy of deferasirox, an iron chelator, against hypoxia/reoxygenation-induced ferroptosis in cultured cardiomyocytes and myocardial I/R injury. The effects of deferasirox on hypoxia/reoxygenation-induced iron overload in the endoplasmic reticulum, lipid peroxidation, and ferroptosis were examined in cultured cardiomyocytes. In a mouse model of I/R injury, the infarct size and adverse cardiac remodeling were examined after treatment with deferasirox, CsA, or both in combination. Deferasirox suppressed hypoxia- or hypoxia/reoxygenation-induced iron overload in the endoplasmic reticulum, lipid peroxidation, and ferroptosis in cultured cardiomyocytes. Deferasirox treatment reduced iron levels in the endoplasmic reticulum and prevented increases in lipid peroxidation and ferroptosis in the I/R-injured myocardium 24 hours after I/R. Deferasirox and CsA independently reduced the infarct size after I/R injury to a similar degree, and combination therapy with deferasirox and CsA synergistically reduced the infarct size (infarct area/area at risk; control treatment: 64±2%; deferasirox treatment: 48±3%; CsA treatment: 48±4%; deferasirox+CsA treatment: 37±3%), thereby ameliorating adverse cardiac remodeling on day 14 after I/R. Combination therapy with deferasirox and CsA may be a clinically feasible and effective therapeutic approach for limiting I/R injury and ameliorating adverse cardiac remodeling after myocardial infarction.

Hydrogen Attenuates Chronic Intermittent Hypoxia-Induced Cardiac Hypertrophy by Regulating Iron Metabolism.

The present study aimed to investigate the impact of hydrogen (H2) on chronic intermittent hypoxia (CIH)-induced cardiac hypertrophy in mice by modulating iron metabolism. C57BL/6N mice were randomly allocated into four groups: control (Con), CIH, CIH + H2, and H2. The mice were exposed to CIH (21-5% FiO2, 3 min/cycle, 8 h/d), and received inhalation of a hydrogen-oxygen mixture (2 h/d) for 5 weeks. Cardiac and mitochondrial function, levels of reactive oxygen species (ROS), and iron levels were evaluated. The H9C2 cell line was subjected to intermittent hypoxia (IH) and treated with H2. Firstly, we found H2 had a notable impact on cardiac hypertrophy, ameliorated pathological alterations and mitochondrial morphology induced by CIH (p < 0.05). Secondly, H2 exhibited a suppressive effect on oxidative injury by decreasing levels of inducible nitric oxide synthase (i-NOS) (p < 0.05) and 4-hydroxynonenal (4-HNE) (p < 0.01). Thirdly, H2 demonstrated a significant reduction in iron levels within myocardial cells through the upregulation of ferroportin 1 (FPN1) proteins (p < 0.01) and the downregulation of transferrin receptor 1 (TfR1), divalent metal transporter 1 with iron-responsive element (DMT1(+ire)), and ferritin light chain (FTL) mRNA or proteins (p < 0.05). Simultaneously, H2 exhibited the ability to decrease the levels of Fe2+ and ROS in H9C2 cells exposed to IH (p < 0.05). Moreover, H2 mediated the expression of hepcidin, hypoxia-inducible factor-1α (HIF-1α) (p < 0.01), and iron regulatory proteins (IRPs), which might be involved in the regulation of iron-related transporter proteins. These results suggested that H2 may be beneficial in preventing cardiac hypertrophy, a condition associated with reduced iron toxicity.

Bioactive strawberry fruit (Arbutus unedo L.) extract remedies paraquat-induced neurotoxicity in the offspring prenatally exposed rats.

Paraquat (1,1'-dimethyl-4-4'-bipyridinium dichloride) exposure is well-established as a neurotoxic agent capable of causing neurological deficits in offspring. This study aimed to investigate therapeutic effects of Arbutus unedo L. aqueous extract (AU) against paraquat (PQ) exposure. For that the phytoconstituents of AU was determined by LC/MS, and then its antioxidant potential was assessed by DPPH and ABTS assays. The assessment included its impact on cell viability and mitochondrial metabolism using N27 dopaminergic cells. Additionally, we evaluated the effects of prenatal PQ exposure on motor coordination, dopamine levels, trace element levels, and total antioxidant capacity (TAC) in rat progeny. The phytochemical profile of AU extract revealed the presence of 35 compounds, primarily phenolic and organic acids, and flavonoids. This accounted for its strong in vitro antioxidant activities against DPPH and ABTS radicals, surpassing the activities of vitamin C. Our findings demonstrated that AU effectively inhibited PQ-induced loss of N27 rat dopaminergic neural cells and significantly enhanced their mitochondrial respiration. Furthermore, daily post-treatment with AU during the 21 days of the rat's pregnancy alleviated PQ-induced motor deficits and akinesia in rat progeny. These effects inhibited dopamine depletion and reduced iron levels in the striatal tissues. The observed outcomes appeared to be mediated by the robust antioxidant activity of AU, effectively counteracting the PQ-induced decrease in TAC in the blood plasma of rat progeny. These effects could be attributed to the bioactive compounds present in AU, including phenolic acids such as gallic acid and flavonoids such as quercetin, rutin, apigenin, glucuronide, and kaempferol, all known for their potent antioxidant capacity. In conclusion, this preclinical study provided the first evidence of the therapeutic potential of AU extract against PQ-induced neurotoxicity. These findings emphasize the need for further exploration of the clinical applicability of AU in mitigating neurotoxin-induced brain damage.

Iron chelation prevents nigrostriatal neurodegeneration in a chronic methamphetamine mice model

Methamphetamine (METH) has been established to selectively target and impair dopaminergic neurons through multiple pathways. Ferroptosis is a unique form of non-apoptotic cell death driven by cellular iron accumulation-induced lipid peroxidation. Nonetheless, it remains unclear whether METH can induce ferroptosis. In the present study, we sought to assess alterations in iron levels after chronic METH exposure and reveal the modulatory role of iron on METH-induced pathologies. Importantly, we demonstrated that METH increased iron deposition in the nigrostriatal system, including the substantia nigra (SN) and caudate putamen (CPu). Moreover, decreases in GPx4 levels, increases in lipid peroxidation products, and pathological alterations were observed in the nigrostriatal system as a consequence of chronic METH exposure. The iron chelator deferiprone not only alleviated nigrostriatal iron deposition, dopaminergic cell death, and lipid peroxidation, but alsoattenuated the decreases in GPx4 induced by METH. These findings suggest an alleviation of ferroptosis in dopaminergic neurons. In addition, we found that the ferroptosis inhibitor liproxstatin-1 attenuated METH-induced dopaminergic degeneration in the nigrostriatal system. Our findings corroborated that METH might induce dopaminergic neurodegeneration through iron-dependent ferroptosis. Interestingly, reducing iron levels or inhibiting ferroptosis may alleviate METH-induced dopaminergic neurodegeneration.

Pengolahan Air Gambut Menjadi Air Bersih Menggunakan Metode Elektrokoagulasi dan Filtrasi

Treating peat water with simple technology to meet clean water standards is a viable solution for addressing community water needs. This study combines electrocoagulation and filtration methods to achieve desired results. Electrocoagulation combines electrochemical processes with flocculation-coagulation, while filtration removes suspended solids through a porous medium. The research demonstrates the method's effectiveness in enhancing peat water quality. It reduces iron levels from 0.27 mg/l to 0.04 mg/l, changes water color from brown to clear white, increases pH from 5.0 to 8.2 (within clean water standards of 6.5-8.5), and lowers TDS from 33.1 mg/l to 10.1 mg/l. The design of this peat water treatment device utilizing electrocoagulation and filtration is remarkably simple, allowing for easy implementation by individuals in their regions. The process is uncomplicated, and required filter media are readily available in the market. These findings provide a practical solution to meet clean water needs by effectively treating abundant peat water sources.

Neuroprotective effects of morroniside from Cornus officinalis sieb. Et zucc against Parkinson’s disease via inhibiting oxidative stress and ferroptosis

Parkinson’s disease (PD) is the second most common neurodegenera­tive disorder after Alzheimer disease accompanied by the death of dopaminergic neurons and brain nigrostriatal mitochondrial damage in the elderly population. The features of the disease include tremor, rigidity, postural instability, and motor retardation. The pathogenesis of Parkinson’s disease is complex, and abnormal lipid metabolism resulting in ferroptosis due to the excessive accumulation of free radicals from oxidative stress in the substantia nigra of the brain was thought to be one of the factors causing the disease. Morroniside has been reported to have significant neuroprotective effects, although it has not been studied in PD. Therefore, this study focused on determining the neuroprotective effects of morroniside (25, 50, and 100 mg/kg) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg)-induced mice models of PD and explored 1-methyl-4-phenylpyridinium MPP+-induced ferroptosis in PC12 cells. Morroniside restored impaired motor function in the PD mice models while reducing neuronal injury. The activation of nuclear factor erythroid 2-related factor 2/antioxidant response elements (Nrf2/ARE) by morroniside promoted antioxidation, the content of reducing agent glutathione (GSH) increased, and the level of the lipid metabolite malondialdehyde (MDA) decreased. Notably, morroniside inhibited ferroptosis in substantia nigra of the brain and PC12 cells, reduced iron levels, and upregulated the expression of the iron-regulated proteins glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), ferritin heavy chain 1 (FTH-1), and ferroportin (FPN). More importantly, morroniside repaired the mitochondrial damage, restored the mitochondrial respiratory chain, and inhibited the production of reactive oxygen species (ROS). These data indicated that morroniside could activate the Nrf2/ARE signaling pathway to increase the antioxidant capacity, thereby inhibiting abnormal lipid metabolism and protecting dopaminergic neurons from ferroptosis in PD.

A Survey of Thalassemia and Iron Deficiency Anaemia Classification using a Voting Classifier

Thalassemia is viewed as a prevalent inherited blood disease that has gotten exorbitant consideration in the field of medical research around the world. Inherited diseases have a high risk that children will get these diseases from their parents. If both the parents are β-Thalassemia carriers then there are 25% chances that each child will have β-Thalassemia intermediate or β-Thalassemia major, which in most of its cases leads to death. Prenatal screening after counseling of couples is an effective way to control β-Thalassemia. Iron deficiency anemia (IDA) is considered one of the most common nutritional deficiencies globally, making it a prevalent health issue. Its prevalence varies among different populations and geographic regions. To diagnose iron deficiency anemia (IDA), healthcare professionals typically perform a series of tests to evaluate the patient's iron status and identify the underlying cause of the deficiency. Thalassemia and iron deficiency anemia are thus two common hematological disorders characterized by abnormal hemoglobin synthesis and reduced iron levels, respectively. Distinguishing between these conditions is crucial for accurate diagnosis and appropriate treatment. Hereby, we propose a classification approach based on an SGR-voting classifier to differentiate between thalassemia and iron deficiency anemia. SGR-VC is an ensemble of three machine learning algorithms: Support Vector Machine, Gradient Boosting Machine, and Random Forest.

Transcriptomic analysis identified SLC40A1 as a key iron metabolism-related gene in airway macrophages in childhood allergic asthma.

Introduction: Asthma is the most common chronic condition in children, with allergic asthma being the most common phenotype, accounting for approximately 80% of cases. Growing evidence suggests that disruption of iron homeostasis and iron regulatory molecules may be associated with childhood allergic asthma. However, the underlying molecular mechanism remains unclear. Methods: Three childhood asthma gene expression datasets were analyzed to detect aberrant expression profiles of iron metabolism-related genes in the airways of children with allergic asthma. Common iron metabolism-related differentially expressed genes (DEGs) across the three datasets were identified and were subjected to functional enrichment analysis. Possible correlations between key iron metabolism-related DEGs and type 2 airway inflammatory genes were investigated. Single-cell transcriptome analysis further identified major airway cell subpopulations driving key gene expression. Key iron metabolism-related gene SLC40A1 was validated in bronchoalveolar lavage (BAL) cells from childhood asthmatics with control individuals by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunofluorescence. The intracellular iron content in BAL cells was assessed by Perls iron staining and the iron levels in BAL supernatant was measured by iron assay to assess airway iron metabolism status in childhood asthmatics. Results: Five common iron metabolism-related DEGs were identified, which were functionally related to iron homeostasis. Among these genes, downregulated SLC40A1 was strongly correlated with type 2 airway inflammatory markers and the gene signature of SLC40A1 could potentially be used to determine type 2-high and type 2-low subsets in childhood allergic asthmatics. Further single-cell transcriptomic analysis identified airway macrophages driving SLC40A1 expression. Immunofluorescence staining revealed colocalization of FPN (encoded by SLC40A1) and macrophage marker CD68. Down-regulation of SLC40A1 (FPN) was validated by qRT-PCR and immunofluorescence analysis. Results further indicated reduced iron levels in the BAL fluid, but increased iron accumulation in BAL cells in childhood allergic asthma patients. Furthermore, decreased expression of SLC40A1 was closely correlated with reduced iron levels in the airways of children with allergic asthma. Discussion: Overall, these findings reveal the potential role of the iron metabolism-related gene SLC40A1 in the pathogenesis of childhood allergic asthma.

Effects of Carbonization Temperature from Activated Carbon of Water Hyacinth on the Flux and Its Ability on Iron Removal

The synthesis of activated carbon derived from water hyacinth has been successfully carried out as an iron adsorbent in a laboratory-scale water filter design system. In this article, activated carbon derived from water hyacinth is made through a carbonization process at 400°C and 500°C with NaOH as an activating agent. This activated carbon derived from water hyacinth acts as a filter media for purifying well water by assessing the flux, pH and iron removal efficiency before and after filtration. The results showed that the use of activated carbon derived from water hyacinth with a carbonization temperature of 500°C resulted in a water flux value greater than the carbonization temperature of 400°C. The pH value showed no difference between the use of activated carbon derived from water hyacinth (at a carbonization temperature 400°C and 500°C) before and after the filtration process, which was 7.5. Meanwhile, the effectiveness of activated carbon derived from water hyacinth at a carbonization temperature of 500°C as a filtration medium is more optimal in reducing iron levels compared to the use of activated carbon at a carbonization temperature of 400°C with percentage efficiency up to 98.09%.

Interferência do ferro na produção de hemoglobina de leitões do nascimento a desmama

ABSTRACT: Iron deficiency anemia (IDA) in humans is defined as the decrease of total hemoglobin concentration and the non-production of the adult hemoglobin subtype 2 - HbA2 (α2δ2 chains), which is considered a marker of IDA severity in humans, dosed together with the iron serum. This study aimed to determine the standard of hemoglobin types in piglets induced to experimentally IDA in the first 21 days of life (delivery to weaning). In the present study, 40 piglets born from four naïve gilts, were randomly and equally assigned among the gilts. On the third day after delivery, the groups were randomly distributed in different environments (cement and clay floors) and according to the iron supplementation (iron dextran and placebo). Erythrocyte parameters, serum iron, and hemoglobin trait were analyzed at four moments between birth and weaning days. The group of piglets that did not receive iron dextran supplementation on the third-day post-birth and were placed in the pen without soil did not present HbA2 from the seventh day onwards on the agarose electrophoretogram (pH 8.6) and this observation was correlated to decrease of serum iron (ρ: 0.156, p=0.003) when compared to the other groups’ piglets that did not present iron deficiency. In the present study was possible to determine the swine hemoglobin pattern in IDA, since HbA2 was absent in piglets with IDA in comparison to the non-ferropenic groups and the correlation between the reduction of iron levels and the absence of HbA2.