Iron Deposition Research Articles

Effect of Bovine Lactoferrin Treatment on Iron Homeostasis and Gene Expression Changes in Multiple Organ Dysfunctions During Wound Healing Process in Rats.

Injury systemically disrupts the homeostatic balance and can cause organ failure. LF mediates both iron-dependent and iron-independent mechanisms, and the role of LF in regulating iron homeostasis is vital in terms of metabolism. In this study, we evaluated the organ-level effect and gene expression change of bLf in the cutaneous repair process. An excisional full-thickness skin defect (FTSD) wound model was created in male Sprague Dawley rats (180-250 g) (n = 48) fed a high-fat diet (HFD) and the PHGPx, SLC7A11 and SLC40A1 genes and iron metabolism were evaluated. The animals were randomly divided into 6 groups: 1- Control, 2- bLf (200 mg/kg/day, oral), 3- FTSD (12 mm in diameter, dorsal), 4- HFD + bLf, 5- HFD + FTSD, 6- HFD + FTSD + bLf. Histologically, iron accumulation was demonstrated by Prussian blue staining in the liver, kidney, and intestinal tissues. Gene expression analysis was performed with qPCR. Histologically, iron accumulation was demonstrated by Prussian blue staining in the liver, kidney, and intestinal tissues. Prussian blue reactions were detected in the kidney. PHPGx and SLC7A11 genes in kidney and liver tissue were statistically significant (P < 0.05) except for the SLC40A1 gene (P > 0.05). Expression changes of the three genes were not statistically significant in analyses of rat intestinal tissue (P = 0.057). In the organ-level ferroptotic damage mechanism triggered by wound formation. BLf controls the expression of three genes and manages iron deposition in these three tissues. In addition, it suppressed the increase in iron that would drive the cell to ferroptosis and anemia caused by inflammation, thereby eliminating iron deposition in the tissues.

Assessment of transfusion-induced iron overload with T2*MRI in survivors of childhood acute lymphoblastic leukemia: A case control study

IntroductionChildhood acute lymphoblastic leukemia survivors receiving multiple packed red blood transfusions may be at risk of vital organ iron deposition causing long-term complications. This study was undertaken to assess the prevalence and severity of iron overload in the liver and heart by magnetic resonance imaging. MethodsA case-control study was conducted on 60 acute lymphoblastic leukemia survivors aged from 6 to 18 years and 60 healthy, age- and sex-matched children as a control group. The hematological profile, and serum ferritin was assessed and the iron content of the liver and heart was measured by T2* magnetic resonance imaging. ResultsTwenty-six (43.3 %) and two (3.3 %) patients had elevated liver and myocardial iron concentrations, respectively. The statistics show a significantly positive correlation between liver T2* magnetic resonance and serum ferritin. The total volume of blood transfused and duration of follow up were associated with elevated liver iron concentrations (p-values = 0.036 and 0.028 respectively). Myocardial T2* magnetic resonance lacked correlation with serum ferritin and transfusion therapy ConclusionLiver iron overload was detected in children and adolescents after acute lymphoblastic leukemia therapy. The risk of iron overload was related mainly to the transfusion burden during therapy. These patients need monitoring after therapy to assess their need for future chelation therapy.

Hippocampal iron overload and spatial reference memory impairment: Insights from a rat model

BackgroundBrain iron overload may induce neuronal death and lead to cognitive impairment. The hippocampus is a critical limbic structure involved in memory. This study aimed to investigate iron overload and its role in hippocampal damage and memory impairment using a rat model. MethodsYoung rats (2 weeks old) received intraperitoneal injections of high-dose iron solution (Group H, n = 10), low-dose iron solution (Group L, n = 10) and normal saline as control (Group D, n = 5). The Morris water maze (MWM) test was performed on all rats to evaluate their spatial reference memory by assessing their escape latency time and number of platform crossing. The iron content and neuronal damage in hippocampal tissue sections of the rats were assessed semi-quantitatively using diaminobenzidine (DAB)-enhanced Perl’s Prussian blue (PPB) staining, and their correlation with spatial reference memory performance was evaluated. ResultsThe escape latency in Group H was significantly longer compared to Groups L and D (P < 0.05). The number of platform crossings was significantly lower in Group H than in Group L or D (P < 0.001). The neuronal cells in Group H had more brown iron deposits than those of Groups L and D. There were significant correlations between the severity of structural damage in the hippocampal tissue and the number of platform crossings (P1 = 0.001 for Group H; P2 = 0.043 for Group L). ConclusionThis study showed an association between hippocampal iron-induced structural damage and spatial reference memory impairment in a rat model. This work should advance our understanding of hippocampal iron overload on cognitive functioning.

Iron accumulation/overload and Alzheimer's disease risk factors in the precuneus region: A comprehensive narrative review.

Alzheimer's disease (AD) is a neurodegenerative disease that is characterized by amyloid plaques, neurofibrillary tangles, and neuronal loss. Early cerebral and body iron dysregulation and accumulation interact with AD pathology, particularly in the precuneus, a crucial functional hub in cognitive functions. Quantitative susceptibility mapping (QSM), a novel post-processing approach, provides insights into tissue iron levels and cerebral oxygen metabolism and reveals abnormal iron accumulation early in AD. Increased iron deposition in the precuneus can lead to oxidative stress, neuroinflammation, and accelerated neurodegeneration. Metabolic disorders (diabetes, non-alcoholic fatty liver disease (NAFLD), and obesity), genetic factors, and small vessel pathology contribute to abnormal iron accumulation in the precuneus. Therefore, in line with the growing body of literature in the precuneus region of patients with AD, QSM as a neuroimaging method could serve as a non-invasive biomarker to track disease progression, complement other imaging modalities, and aid in early AD diagnosis and monitoring.

TREM1 induces microglial ferroptosis through the PERK pathway in diabetic-associated cognitive impairment

Ferroptosis is involved in neurodegenerative disorders including diabetes-associated cognitive impairment (DACI). As central immune cells, microglia have strong siderophilic properties. However, the role of iron deposition in microglia and the underlying regulatory mechanism remains unclear in DACI. Here, we established high glucose (HG) model in BV2/HMC3 cells and diabetes model in C57BL/6 J mice with HFD and STZ. Transmission Electron Microscopy, Western blot, assay kits of Fe2+, GSH/GSSG, MDA and ROS were carried out in vitro. Prussian blue staining, Western blot and immunofluorescence were implemented in vivo. Y-maze and novel object recognition were performed to assess cognitive performance. LP17 was used to inhibit TREM1 (triggering receptor expressed on myeloid cells 1) specifically in vivo and vitro. We found excessively deposited iron and significant reduction in antioxidants in hippocampal microglia of mice with DACI, concomitant with increased TREM1 (a microglia-specific inflammatory amplifier). Furthermore, LP17 (TREM1 specific inhibitor) ameliorated cognitive impairment caused by HFD/STZ through relieving iron accumulation and antioxidant inactivation. In vitro, ferroptosis was induced by HG in mice microglia-BV2 and human microglia-HMC3 cells, which could be blocked by a ferroptosis inhibitor-Fer-1 and LP17. Moreover, PERK pathway of endoplasmic reticulum stress was activated by HG, and then reversed by PERK inhibitor GSK2606414 and LP17 followed by improved ferroptosis in HG-cultured BV2. In summary, our results indicated that TREM1 effectively aggravates T2DM-associated microglial iron accumulation through the PERK pathway of ERS, which contributes to antioxidant inactivation and lipid peroxidation, eventually, massively boosted ROS result in microglial ferroptosis. The mechanism elucidation in our study may shed light on targeted therapy of DACI.

Les surcharges hépatiques en fer

Iron is essential for functioning of cells and of the body as a whole. Perls staining allows the histopathological identification of iron deposits. By classifying hepatic siderosis as parenchymal, mesenchymal or mixed, it may guide the search for its etiology. HFE1 hemochromatosis is the most common siderosis. Its diagnosis is currently based on genetic analysis. Its expressivity being variable and its penetrance incomplete, the demonstration of hepatic siderosis may represent a mode of discovery.

Vitamin D Deficiency among Blood Transfusion-Dependent Beta Thalassemia Children Admitted to Tertiary Level Pediatric Hospital in Nepal: A Descriptive Cross-Sectional Study

Introduction: Children with beta thalassemia are on regular blood transfusions, which could result in iron deposition in the liver causing decreased synthesis of Vitamin D-25OH. There are limited publications on the association of Vitamin D deficiency with blood transfusion-dependent thalassemia in the Nepalese population. This study aims to determine the prevalence of Vitamin D deficiency among blood transfusion-dependent beta-thalassemia patients.Methods: This was a descriptive cross-sectional study conducted among beta-thalassemia major patients under 15 years of age, receiving regular blood transfusion, from July 17, 2022, to July 16, 2023, after ethical approval obtained from Ethical Review Committee, Kanti Children’s Hospital (reference number 155). Data were collected using convenience sampling, and descriptive analyses were performed using Microsoft Excel and Statistical Package for Social Sciences (SPSS) 2024.Results: A total of 127 blood transfusion-dependent beta-thalassemia major patients were included in the study, of whom 82 (64.56%) were male. Among these patients, 104 (81.88%) were aged between 5 and 14 year. Almost one-third 41 (32.28%) had Vitamin D insufficiency, and a quarter, 34 (26.77%), had Vitamin D deficiency. Ten percent of the children were underweight, and a quarter were stunted.Conclusions: Children with blood transfusion dependent beta thalassemia major are at a greater risk for Vitamin D deficiency and iron overload

Foodborne iron overload induces oxidative stress and causes mitochondrial damage in the liver of grass carp (Ctenopharyngodon idellus)

Iron is essential to biological processes such as energy metabolism and oxygen transport. However, excessive iron can cause iron overload and ultimately result in tissue damage. To date, the damage mechanism of foodborne iron overload in aquatic animals is still unclear. This study used grass carp (Ctenopharyngodon idellas) as the research subject to establish a chronic iron overload model by feeding diets with different iron levels, and combined in vitro experiments to investigate the mechanisms of iron overload-induced damage. The growth performance and liver HE staining indicated that a high‑iron diet led to decreased growth in grass carp, accompanied by hepatic iron deposition. ELISA and qRT-PCR analysis data revealed that a high‑iron diet disrupted the antioxidant balance and modulated the expression of genes associated with iron metabolism. CCK-8 determination results revealed that treatment of L8824 cells with ferri ammonii citras (FAC) resulted in iron overload, led to disruption of iron metabolism and enhanced the intracellular production of reactive oxygen species (ROS), and caused lipid peroxidation. Furthermore, qRT-PCR analysis results showed that the treatment of L8824 cells with FAC resulted in a significant up-regulation of genes associated with antioxidant, apoptosis, and necrosis pathways, and increased the rate of apoptosis. In addition, fluorescence microscopy observation and mitochondrial DNA detection data showed that excess iron could increase the iron accumulation in mitochondria and the production of mtROS, reduce the mitochondrial membrane potential, and finally cause mitochondria damage. In conclusion, our research offers invaluable insights that iron overload leads to disrupted intracellular iron pool stability, causing mitochondrial damage and oxidative stress, eventually causing cell death.

Study on the mechanism of activating SIRT1/Nrf2/p62 pathway to mediate autophagy-dependent ferroptosis to promote healing of diabetic foot ulcers.

Diabetic foot (DF), a prevalent and grave diabetes sequela, is considered as a notable clinical concern, with SIRT1 downregulation observed in DF patients' blood specimens. Nonetheless, the regulatory mechanisms of SIRT1 in diabetic foot ulcer (DFU) remain unclear. Thus, in the current study, we investigated the role and mechanisms of SIRT1 in alleviating DFU. Western blotting was used to detect the expression of autophagy and ferroptosis-related proteins, CCK8 assay was used to measure cell proliferation. Plate colony method was used to measure bacterial growth, and the inhibitory effect on intracellular and extracellular Staphylococcus aureus was observed after drug intervention. ELISA was used to detect inflammatory cytokines and oxidative stress markers levels. ROS, total iron, and Fe2+ levels were detected using corresponding assays. Additionally, HE staining detected the thickness of the epidermis and dermis of the rat wound tissue while the collagen deposition in the wound tissue was detected using Masson staining. In addition, Prussian blue staining was used to detect iron deposition, and C11 BODIPY 581/591 lipid peroxidation probe was used to detect lipid ROS. Our results suggested that the activation of SIRT1/Nrf2/p62 signaling affects cell proliferation, colony formation, ferroptosis, and the production of lipid ROS in DFU-infected cell model through autophagy. In vivo experiments indicated that activating SIRT1/Nrf2/p62 signaling affects oxidative stress, inflammation, and autophagy in wound tissue and promotes wound healing in DFU rats through mediating autophagy-dependent ferroptosis. Taken together, the activation of SIRT1/Nrf2/p62 pathway can promote DFU healing, which might be mediated by autophagy-dependent ferroptosis.

Microglial CR3 promotes neuron ferroptosis via NOX2-mediated iron deposition in rotenone-induced experimental models of Parkinson's disease

The activation of complement receptor 3 (CR3) in microglia contributes to neurodegeneration in neurological disorders, including Parkinson's disease (PD). However, it remains unclear for mechanistic knowledge on how CR3 mediates neuronal damage. In this study, the expression of CR3 and its ligands iC3b and ICAM-1 was found to be up-regulated in the midbrain of rotenone PD mice, which was associated with elevation of iron content and disruption of balance of iron metabolism proteins. Interestingly, genetic deletion of CR3 blunted iron accumulation and recovered the expression of iron metabolism markers in response to rotenone. Furthermore, reduced lipid peroxidation, ferroptosis of dopaminergic neurons and neuroinflammation were detected in rotenone-lesioned CR3−/− mice compared with WT mice. The regulatory effect of CR3 on ferroptotic death of dopaminergic neurons was also mirrored in vitro. Mechanistic study revealed that iron accumulation in neuron but not the physiological contact between microglia and neurons was essential for microglial CR3-regulated neuronal ferroptosis. In a cell-culture system, microglial CR3 silence significantly dampened iron deposition in neuron in response to rotenone, which was accompanied by mitigated lipid peroxidation and neurodegeneration. Furthermore, ROS released from activated microglia via NOX2 was identified to couple microglial CR3-mediated iron accumulation and subsequent neuronal ferroptosis. Finally, supplementation with exogenous iron was found to recover the sensitivity of CR3−/− mice to rotenone-induced neuronal ferroptosis. Altogether, our findings suggested that microglial CR3 regulates neuron ferroptosis through NOX2 -mediated iron accumulation in experimental Parkinsonism, providing novel points of the immunopathogenesis of neurological disorders.

Chinese guidelines for the diagnosis and treatment of hereditary hemochromatosis

Hereditary hemochromatosis is an iron overload disease caused by mutations in iron-regulating genes, resulting in excessive iron deposition in organs such as the liver, heart, skin, pancreas, and gonads, leading to corresponding multi-system damage. This condition is relatively common in European and American populations, primarily caused by mutations in the HFE gene; however, it is rare in China and other Asian countries, almost exclusively due to mutations in non-HFE genes. Clinical features include unexplained chronic hepatitis or cirrhosis, accompanied by elevated serum ferritin and/or increased transferrin saturation. MRI shows iron deposition in the liver, liver biopsy reveals iron accumulation in hepatocytes, and genetic testing facilitate the diagnosis of this disease. Repeated phlebotomy is the first-line therapy for this condition. For those who cannot tolerate phlebotomy, iron chelation therapy may be used, and patients who progress to end-stage liver disease will require liver transplantation. To assist clinicians in making informed decisions on the diagnosis and treatment of hereditary hemochromatosis, the Chinese Society of Hepatology, Chinese Medical Association has invited experts from clinical medicine, molecular genetics, pathology, imaging, and methodology to systematically summarize the advancement in this field and collaboratively develop the current guidelines.

Variations in Temperature and Pressure in the “Reservoir–Well” System Triggered by Blasting Recovery of Iron Ore at the Kursk Magnetic Anomaly

This paper presents the results of precise measurements of temperature and pore pressure in the “reservoir–well” system during the development of iron ore deposits of the Kursk Magnetic Anomaly (KMA) via blasting. For the observation period from October 2021 to June 2024, variations in compressibility, permeability and temperature in the upper Albian-Cenomanian confined aquifer, which is used for district water supply, were determined. The general trend in a decrease in water temperature was traced (from 12 °C to 11.4 °C). It was accompanied by an increase in the hydrostatic head (from 3.7 m to 7.4 m). Water temperature in the upper aquifer was measured for 9 industrial explosions in the mine and for 30 explosions in the quarry. For one explosion in the mine and five explosions in the quarry the coseismic changes in water temperature with amplitudes of 0.06–0.09 °C were established, while changes in pore pressure in the “reservoir–well” system were 0.4–2.2 kPa. Local changes in the permeability of the reservoir in the vicinity of the well (the skin effect) are considered to be the main factor that controls the coseismic response of temperature during industrial explosions. As the reservoir permeability increases, the water temperature in the “reservoir–well” system can decrease and vice versa. The same pattern was observed according to regime measurements performed in 2022–2023. The recorded coseismic responses of water temperature in the upper aquifer in the high-frequency range are similar to the effects observed during propagation of seismic waves originated from earthquakes in the low-frequency range at different sites all over the world for the seismic energy density of 0.05–0.45 J/m3. The observed variations in aquifer temperature in the “reservoir–well” system under episodic dynamic impacts are of particular interest from the point of view of activating hydrogeochemical processes that accompany the development of iron ore deposits.

Fetal hemochromatosis: rare case of hepatic and extrahepatic siderosis involving thyroid on fetal MRI

BackgroundNeonatal hemochromatosis (NH) is a rare condition that is characterized by severe neonatal liver disease in association with hepatic and extrahepatic excess iron deposition (siderosis), while sparing the reticuloendothelial system. The most common cause of fetal liver injury leading to the NH phenotype (accounting for over 95% of cases) is gestational alloimmune liver disease. This condition is caused by the transfer of maternal IgG antibodies through the placenta, targeting a fetal hepatocyte antigen. Prenatal diagnosis, particularly the identification of iron overload involving both liver and thyroid, is of significant importance and can have a profound impact on patient care. To our knowledge, no case has been reported on prenatal diagnosis of iron overload involving both liver and thyroid.Case presentationWe present an exceptionally rare case of fetal hemochromatosis in a primigravida, a case that significantly contributes to our understanding of this condition. The diagnosis was made with the presence of hepatic and extrahepatic siderosis involving the thyroid using Ultrasonography (USG) and fetal Magnetic Resonance Imaging (MRI) findings. A 23-year-old primigravida was referred to our center in view of oligohydramnios, Intrauterine Growth Restriction (IUGR) and echogenic bowel at 29 weeks of gestation. USG and fetal MRI showed features of coarse liver echotexture and iron overload involving the liver and thyroid; this is the first case describing iron accumulation in the fetal thyroid gland diagnosed in utero.ConclusionThis case underscores the critical importance of performing MRI in suspected cases of fetal hemochromatosis for early diagnosis and intervention, emphasizing the potential to significantly improve patient outcomes.

Inhibition of ubiquitin-specific protease 7 ameliorates ferroptosis-mediated myocardial infarction by contrasting oxidative stress: An in vitro and in vivo analysis

BackgroundOur prior research determined that USP7 exacerbates myocardial injury. Additionally, existing studies indicate a strong connection between USP7 and ferroptosis. However, the influence of USP7 on ferroptosis-mediated myocardial infarction (MI) remains unclear. Given these findings, we are particularly interested in USP7's regulatory role in ferroptosis-mediated MI and its underlying mechanisms. MethodsIn this study, we established MI models and lentivirus-transfected groups to inhibit USP7 expression both in vivo and in vitro. Cardiac function was detected with Echocardiography. TTC and HE staining were employed to assess myocardial alterations. The expression of ferroptosis markers (PTGS2, ACSL4, GPX4) were analyzed by RT-qPCR and Western blotting. Flow cytometry and ELISA were used for measuring Fe2+, lipid ROS, GSH, and GSSG levels. TEM and Prussian blue staining were used to observe mitochondrial alterations and iron deposition. RT-qPCR, Western blotting, and immunofluorescence were conducted to analyze Keap1, Nrf2, and nuclear Nrf2 expression in vitro and in vivo. ResultsIn the MI model group, USP7 expression significantly increased, worsening ferroptosis-mediated MI. Conversely, in the USP7-inhibited group, activation of the Keap1-Nrf2 signaling pathway improved ferroptosis-mediated MI outcomes. In vitro, the MI model exhibited a marked decline in cardiomyocyte viability and notable mitochondrial damage. However, these issues improved in the USP7-inhibited groups. In vivo, USP7 intensified MI and iron deposition within the MI model group, with decreased values of LVEF, LVFS, SV, LVAWd, and LVPWs, all of which showed improvement in the USP7-inhibited group, except for LVPWd and LVPWs, which showed no significant variation. Importantly, both the in vitro and in vivo experiments revealed analogous results: a reduction in Keap1 expression and an increase in both Nrf2 and nuclear Nrf2 post USP7 inhibition. Additionally, GPX4 expression decreased while PTGS2 and ACSL4 expressions increased. Notably, concentrations of Fe2+, lipid ROS, GSH, and GSSG significantly decreased. ConclusionIn vitro and in vivo studies have found that inhibition of USP7 attenuates iron deposition and suppresses oxidative stress, resulting in amelioration of ferroptosis-induced MI.

Associations between quantitative susceptibility mapping with male obstructive sleep apnea clinical and imaging markers

PurposeTo quantitatively measure and compare whole-brain iron deposition between OSA patients and a healthy control group, we initially utilized QSM and evaluated its correlation with PSG results and cognitive function. Materials and methodsA total of 28 OSA patients and 22 healthy control subjects matched in age, education level, and BMI were enrolled in our study. Each participant underwent scanning with 3D T1 and multi-echo GRE sequences. Additionally, PSG results were collected from OSA patients, and they underwent simple cognitive assessments. Finally, we analyzed the relationship between iron content in different brain regions, PSG results, and cognitive ability. ResultsIn OSA patients, iron content increased in the left temporal-pole-sup and right putamen, while it decreased in the left fusiform gyrus, left middle temporal gyrus, right inferior occipital gyrus, and right superior temporal gyrus. The correlation analysis between brain iron content and PSG results/cognitive scales is as follows: left fusiform gyrus and MMSE (r = −0.416, p = 0.028); right superior temporal gyrus and MMSE (r = 0.422, p = 0.025); left middle temporal gyrus and average oxygen saturation (r = −0.418, p = 0.027); left temporal-pole-sup and REM stage (rs = 0.466, p = 0.012); the right putamen and N1 stage (rs = 0.393. p = 0.039). Moreover, both MoCA (r = 0.598, p = 0.001) and MMSE (r = 0.456, p = 0.015) show a positive correlation with average oxygen saturation. ConclusionThis study is the first to use QSM technology to show abnormal brain iron levels in OSA. Correlations between brain iron content, PSG, and cognition in OSA may reveal neuropathological mechanisms, aiding OSA diagnosis.

Postencephalitic Parkinsonism: Unique Pathological and Clinical Features-Preliminary Data.

Postencephalitic parkinsonism (PEP) is suggested to show a virus-induced pathology, which is different from classical idiopathic Parkinson's disease (PD) as there is no α-synuclein/Lewy body pathology. However, PEP shows a typical clinical representation of motor disturbances. In addition, compared to PD, there is no iron-induced pathology. The aim of this preliminary study was to compare PEP with PD regarding iron-induced pathology, using histochemistry methods on paraffin-embedded post-mortem brain tissue. In the PEP group, iron was not seen, except for one case with sparse perivascular depositions. Rather, PEP offers a pathology related to tau-protein/neurofibrillary tangles, with mild to moderate memory deficits only. It is assumed that this virus-induced pathology is due to immunological dysfunctions causing (neuro)inflammation-induced neuronal network disturbances as events that trigger clinical parkinsonism. The absence of iron deposits implies that PEP cannot be treated with iron chelators. The therapy with L-Dopa is also not an option, as L-Dopa only leads to an initial slight improvement in symptoms in isolated cases.

Iron overload and liver function in patients with beta thalassemia major: A cross sectional study.

In thalassemia major, repeated blood transfusions result in iron overload causing organ damage. The objective of this study was assessment of liver enzymes in patients with Thalassemia major and to observe their association with ferritin. A cross-sectional study was performed, at Islamabad Medical and Dental College and its affiliated Akbar Niazi Teaching Hospital from November 2021 till August 2022. Serum ferritin, AST, ALT, and total bilirubin levels were determined, in 135 patients of beta thalassemia major receiving transfusions. Data analysis was performed using SPSS Version 20. For categorical variables, calculation of frequencies and percentages was performed. Mean (± standard deviation) was determined for quantitative variables. ANOVA with post hoc Tukey's test was used for determining association between liver enzymes and serum ferritin. A p-value of <0.05 was considered significant. The correlation between ferritin and LFTs was determined by Pearson's correlation coefficient. Patients had an age range of 7-30 years, and males constituted 51% of sample. Mean level of ferritin was 6062.61 + 3641.79 ng/ml, with an insignificant difference between the genders (p =0.366). The levels of AST, ALT and bilirubin were perceived to show a significant increase in patients with ferritin levels >5000ng/ml, when compared with patients having ferritin levels < 2,500 ng/ml. A significant positive correlation of increasing serum ferritin levels was observed with ALT (r= 0.682), to a lesser extent with AST (r = 0.532), and only a weak correlation with serum bilirubin (r = 0.350). Liver damage was caused by increased iron deposition. LFTs should be performed regularly to detect and reduce liver damage by increasing chelation therapy, thereby reducing morbidity and mortality due to thalassemia.

Petrographic and Diffractometric Analysis of Drill Samples from the Iron Ore Deposits of Zatua Hills, Haut Uélé Province, DRC

Seven samples were selected from various facies of geological formations intersected by the drill holes for petrographic analysis, supplemented by diffractometry. The goal was to identify the mineralogical composition of Banded Iron Formations (BIFs), the associated parageneses, and elements deleterious to the metallurgical processing of iron ore. Field tests, based on geophysical maps, were conducted to identify high-prospectivity sites characterized by low magnetic susceptibility and hematite richness, followed by sampling and drilling to confirm mineralization. Selected samples from characteristic facies in contact with iron ores underwent petrographic analysis using optical and scanning electron microscopy, supported by diffractometric analyses to ensure accurate mineralogical identification. The study revealed the presence of hematitic BIF, predominantly composed of weakly aggregated euhedral and subhedral martite grains, with evidence of some leaching. Magnetite, identified as the protore mineral, has been oxidized by fluid influence into martite (hematite), with a low presence of secondary supergene minerals. Variscite, kaolinite, and gibbsite were the main secondary minerals identified in both petrographic and diffractometric analyses, and are considered sources of phosphorus, aluminum, and silica—elements recognized as harmful in the metallurgical processing of iron and its alloys. These secondary minerals were precipitated within interstitial cavities leached between martite and hematite aggregates, forming a botryoidal texture. The BIFs of the Zatua Hills are primarily composed of hematitic iron ores associated with goethite, microplaty hematite, and secondary supergene minerals, likely formed through fluid circulation along fracture zones, shearing, and folding. Geochemical studies are recommended to complete the analysis, aiming to determine the content of these iron oxides, secondary minerals, and the degree of hydration through loss on ignition.

Iron Overload Cardiomyopathy

Iron overload cardiomyopathy is a condition of excessive iron accumulation in cardiomyocytes due to abnormal iron absorption or repeated blood transfusion. In the early stages, the patient may be asymptomatic with good ventricular systolic function. Iron deposit in ventricular cause dyspnea on effort due to left ventricular systolic dysfunction then in atrial cause atrioventricular block and supraventricular arrhythmic. For severe symptom due to dilated cardiomyopathy is characterized by left ventricular dilatation and risk of sudden cardiac death. Diagnosis of iron overload cardiomyopathy can be made if there is evidence of heart disease, the presence of iron overload (serum ferritin &gt; 300 ng/mL and transferrin saturation &gt; 55%) and cardiac siderosis with cardiac MRI T2 * &lt; 20 ms as gold standard. Patient management involves lowering systemic iron levels and preventing iron entry into cardiomyocytes. Therapy with phlebotomy or iron chelation as indicated. Administration of calcium channel blockers and resveratrol antioxidant therapy may be considered to reduce morbidity and mortality due to cardiac siderosis.

Advancing Skarn Iron Ore Detection through Multispectral Image Fusion and 3D Convolutional Neural Networks (3D-CNNs)

This study explores novel techniques to improve the detection accuracy of skarn iron deposits using advanced image-processing methodologies. Leveraging the capabilities of ASTER image, band ratio (BR) images, and principal component analysis (PCA) alongside the power of 3D convolutional neural networks (3D-CNNs), the research aims to enhance the precision and efficiency of ore detection in complex geological environments. The proposed method employs a specific 3D-CNN architecture accepting input as a 7 × 7 × C image patch, where C represents the combined number of selected ASTER image bands, principal component (PC) bands, and computed BR images. To evaluate the accuracy of the proposed method, five distinct image band combinations, including the proposed band combination, were tested and evaluated based on the overall accuracy (OA), average accuracy (AA), and kappa coefficient. The results demonstrated that while the incorporation of BR images alongside ASTER bands initially seemed promising, it introduced significant confusion in certain classifications, leading to unexpected misclassification rates. Surprisingly, utilizing solely ASTER bands as input parameters yielded higher accuracy rates (OA = 93.13%, AA = 91.96%, kappa = 90.91%) compared with scenarios involving the integration with band ratios (OA = 87.02%, AA = 79.15, kappa = 82.60%) or the integration of BR images to PC bands (OA = 87.78%, AA = 82.39%, kappa = 83.81%). However, the amalgamation of ASTER bands with selected PC bands showed slight improvements in accuracy (OA = 94.65%, AA = 92.93%, kappa = 93.45%), although challenges in accurately classifying certain features persisted. Ultimately, the proposed combination of ASTER bands, PC bands, and BR images (proposed band combination) presented the most visually appealing and statistically accurate results (OA = 96.95%, AA = 94.87%, kappa = 95.93%), effectively addressing misclassifications observed in the other combinations. These findings underscore the synergistic contributions of each of the ASTER bands, PC bands, and BR images, with the ASTER bands proving pivotal for optimal skarn classification, the PC bands enhancing intrusions classification accuracy, and the BR images strengthening wall rock classification accuracy. In conclusion, the proposed combination of input image bands emerges as a robust and comprehensive methodology, demonstrating unparalleled accuracy in the remote sensing detection of skarn iron minerals.