Iron Status Research Articles

A circular economy approach for utilization of tannery fleshing hydrolysate and kitchen wastes into organic fertilizer through enzymatic decomposition

This study presents a sustainable method for converting tannery fleshing waste (FH) into organic fertilizer using enzymatic decomposition with crude protease. After extracting fat from the enzymatic hydrolysis, the enzyme-rich residue was mixed with dried kitchen waste (KW) and allowed to decompose for 45 days, producing nutrient-rich fertilizer. FT-IR spectroscopy confirmed the presence of important functional groups, including hydroxyl, aliphatic hydrocarbons, esters, and amide-I linkages. The organic fertilizers had higher nutrient content, with nitrogen (1.08-1.67%), phosphorus (0.78–0.98 %), potassium (0.1–0.76 %), and magnesium (239–259.5 ppm) which is higher than commercial fertilizers. FESEM-EDX analysis revealed a dense, porous structure with a high surface concentration of calcium, which enhances nutrient release in the soil. Dissolution tests showed that nutrients from the organic fertilizer were released gradually over 36 hours, whereas commercial NPK fertilizers released nutrients within 150 minutes in simulated soil-water conditions. Field trials with a Randomized Complete Block Design (RCBD) demonstrated improved growth in Malabar spinach, particularly with fertilizer sample S-5, which had an optimal flesh to kitchen waste (FH to KW) ratio of 1:10. Although S-5 had a lower nitrogen content (1.08 %), it contained higher levels of phosphorus (0.98 %), potassium (0.765 %), and magnesium (259.5 ppm), contributing to enhanced plant growth. The organic fertilizer resulted in a shoot length of 38.8 ± 2.0 cm, root length of 16.33 cm, 31 ± 3 leaves, and 95.12 % dry matter of the plant. Heavy metal analysis of the plant confirmed that levels of chromium (Cr), iron (Fe), nickel (Ni), cadmium (Cd), copper (Cu), and lead (Pb) were within WHO safety limits. Phytotoxicity tests of the fertilizer also showed no negative impact on Malabar spinach seed germination.

A-159 Re-evaluating Ferritin Cutoffs for the Diagnosis of Iron Deficiency and Iron Deficiency Anemia

Abstract Background Iron deficiency (ID) is the most common nutrient deficiency in the world and iron deficiency anemia (IDA) is estimated to affect 1.24 billion people. Serum ferritin is an iron storage protein commonly used as a biomarker for ID and IDA. The ferritin lower limit of normal (LLN) defined in many clinical laboratories is lower than evidence-based cutoffs and may not detect ID and IDA with adequate sensitivity, particularly when sex-based reference intervals (RIs) are used. This may be due in part to the use of asymptomatic, iron-depleted individuals for RI studies. Recent efforts have been made to increase the LLN for ferritin to at least 30 ng/mL and re-evaluate sex based RIs to improve diagnosis of ID and IDA. In this study, we aimed to investigate LLN ferritin cutoffs for ID and IDA in our patient population. Methods Patient data from June 2022-May 2023 were collected with approval from the Institutional Review Board (IRB), including age, sex, and values for ferritin, iron, transferrin saturation, and hemoglobin. Patients were classified as iron replete (IR), ID, or IDA based on measurements for iron, transferrin saturation, and hemoglobin. IR patients were defined as having iron and transferrin saturation values within current RIs, while those below the cutoff were grouped as ID. ID and IDA were further classified based on hemoglobin values. A range of ferritin concentrations between 1 and 100 ng/mL were used to calculate true and false positive rates (TPR and FPR) and diagnostic accuracy (DA). Receiver operator characteristic (ROC) curve and J index analysis were used to define optimal ferritin cutoffs for ID and IDA. Results Data from 26,455 patients (65% female) were used in this study. Conclusions These findings highlight the need to re-examine ferritin RIs in the context of ID/IDA, especially for those patients assigned female at birth.

Lactylation of nuclear receptor coactivator 4 promotes ferritinophagy and glycolysis of neuronal cells after cerebral ischemic injury.

Ischemic stroke remains a major cause of disability and mortality. Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy is involved in cerebral ischemic injury. Additionally, lactylation regulates the progression of ischemia injury. This study aimed to investigate the impact of NCOA4 on ferritinophagy and glycolysis of hippocampal neuron cells and its lactylation modification. Middle cerebral artery occlusion (MCAO) mouse and oxygen-glucose deprivation (OGD)-treated HT22 cell models were generated. Ferritinophagy was evaluated via detecting ferrous iron (Fe 2+ ), glutathione, malondialdehyde, and protein levels. Glycolysis was assessed by examining the glucose consumption, lactate production, and extracellular acidification rate. The lactylation was evaluated using immunoprecipitation and immunoblotting. Brain injury in vivo was analyzed by measuring brain infarct and neurological function. The results showed that NCOA4 expression was increased in the blood of patients with acute ischemia stroke, the peri-infarct region of the brain in MCAO mice (increased percentage: 142.11%) and OGD-treated cells (increased percentage: 114.70%). Knockdown of NCOA4 inhibited ferritinophagy and glycolysis of HT22 cells induced by OGD. Moreover, OGD promoted the lactylation of NCOA4 at lysine (K)450 sites, which enhanced NCOA4 protein stability. Additionally, interfering with NCOA4 attenuated brain infarction and neurological dysfunction in MCAO mice. Lactylation of NCOA4 at K450 sites promotes ferritinophagy and glycolysis of hippocampal neuron cells, thereby accelerating cerebral ischemic injury. These findings suggest a novel pathogenesis of ischemic stroke.

Distinct regional vulnerability to Aβ and iron accumulation in post mortem AD brains.

The paramagnetic iron, diamagnetic amyloid beta (Aβ) plaques and their interaction are crucial in Alzheimer's disease (AD) pathogenesis, complicating non-invasive magnetic resonance imaging for prodromal AD detection. We used a state-of-the-art sub-voxel quantitative susceptibility mapping method to simultaneously measure Aβ and iron levels in post mortem human brains, validated by histology. Further transcriptomic analysis using Allen Human Brain Atlas elucidated the underlying biological processes. Regional increased paramagnetic and diamagnetic susceptibility were observed in medial prefrontal, medial parietal, and para-hippocampal cortices associated with iron deposition (R=0.836, p=0.003) and Aβ accumulation (R=0.853, p=0.002) in AD brains. Higher levels of gene expression relating to cell cycle, post-translational protein modifications, and cellular response to stress were observed. These findings provide quantitative insights into the variable vulnerability of cortical regions to higher levels of Aβ aggregation, iron overload, and subsequent neurodegeneration, indicating changes preceding clinical symptoms. The vulnerability of distinct brain regions to amyloid beta (Aβ) and iron accumulation varies. Histological validation was performed on stained sections of ex-vivo human brains. Regional variations in susceptibility were linked to gene expression profiles. Iron and Aβ levels in ex-vivo brains were simultaneously quantified.

Hepatocyte activation and liver injury following cerebral ischemia promote HMGB1-mediated hepcidin upregulation in hepatocytes and regulation of systemic iron levels

We previously reported that high mobility group box 1 (HMGB1), a danger-associated molecular pattern (DAMP), increases intracellular iron levels in the postischemic brain by upregulating hepcidin, a key regulator of iron homeostasis, triggering ferroptosis. Since hepatocytes are the primary cells that produce hepcidin and control systemic iron levels, we investigated whether cerebral ischemia induces hepcidin upregulation in hepatocytes. Following middle cerebral artery occlusion (MCAO) in a rodent model, significant liver injury was observed. This injury was evidenced by significantly elevated Eckhoff’s scores and increased serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Additionally, total iron levels were significantly elevated in the liver, with intracellular iron accumulation detected in hepatocytes. Hepcidin expression in the liver, which is primarily localized in hepatocytes, increased significantly starting at 3 h after MCAO and continued to increase rapidly, reaching a peak at 24 h. Interestingly, HMGB1 levels in the liver were also significantly elevated after MCAO, with the disulfide form of HMGB1 being the major subtype. In vitro experiments using AML12 hepatocytes showed that recombinant disulfide HMGB1 significantly upregulated hepcidin expression in a Toll-like receptor 4 (TLR4)- and RAGE-dependent manner. Furthermore, treatment with a ROS scavenger and a peptide HMGB1 antagonist revealed that both ROS generation and HMGB1 induction contributed to hepatocyte activation and liver damage following MCAO–reperfusion. In conclusion, this study revealed that cerebral ischemia triggers hepatocyte activation and liver injury. HMGB1 potently induces hepcidin not only in the brain but also in the liver, thereby influencing systemic iron homeostasis following ischemic stroke.

Association Between Homocysteine Levels and Ovarian Reserve in Subfertile Women.

To evaluate the relationship between homocysteine levels and anti-mullerian hormone (AMH) levels, a biomarker of ovarian reserve, and the effect of high homocysteine levels on ovarian reserve in subfertile women. Observational case-control study. Place and Duration of the Study: Samsun Training and Research Hospital, Samsun, Turkiye, from October to December 2023. Seventy-nine subfertile women and 35 healthy fertile women were included in this study. AMH, homocysteine, thyroid stimulating hormone (TSH), free T3 (fT3), free T4 (fT4), iron, and ferritin levels of subfertile and fertile women were compared. Logistic regression, receiver operating characteristic, and Kaplan-Meier analyses were performed for homocysteine levels. AMH, fT4, iron, and ferritin levels were lower in subfertile women than in fertile women (p <0.001). Homocysteine and TSH levels were higher in subfertile women than in fertile women (p <0.001). The sensitivity for homocysteine levels was 94.90% and the specificity was 94.30%. In the Kaplan-Meier analysis, homocysteine levels of 12.90 μmol/L and above were found to be risky in terms of fertility. Homocysteine levels, AMH, and ferritin levels were negatively correlated and TSH levels were positively correlated in subfertile women (p <0.001). However, these correlations were not observed in fertile women (p >0.05). High homocysteine levels can be considered as a risk factor affecting ovarian reserve in subfertile women. Anti-mullerian hormone, Female subfertility, Homocysteine, Hyperhomocysteinaemia, Ovarian reserve.

Exploring the Link between Iron Status and Catalase Activity in Type 2 Diabetes Mellitus

خلفية البحث:تتزايد حالات الاصابة بداء السكري من النوع الثاني على مستوى العالم، وقد اصبح عبئا صحيا خطيرا حيث يساهم في 90% من جميع حالات مرضى السكري . يرتبط مرض السكري بالتغيير في تواون الحديد في اابلازما لدى الاشخاص والذي لديه القدرة على توليد انواع الاوكسجين التفاعلية الناجمة عن المرض. الكاتلاز هو انزيم موجود في كل مكان تقريبا في جميع الكائنات الحية ويحفز تحلل بيروكسيد الهيدروجين الى الماء والاوكسجين. وهو انزيم مهم في حماية الخلايا من الاضرار التأكسدية التي تسببها انواع الاوكسجين التفاعلية. الهدف: هدفت الدراسة الحالية الى معرفة حالة الحديد وعلاقتها بنشاط الكاتلاز لدى المرضى العراقيين المصابين بداء السكري من النوع الثاني. المرضى وطرق البحث: اجمالي 150 مشاركا، من بينهم 100 مريض T2DM تم تقسيمهم الى ثلاث مجموعات وفقا لمدة المرض: A1 (38 مريضا ، اقل من 5 سنوات)، A2 (37 مريضا ، 5-10 سنوات) و A3 (25 مريضا، اكثر من 10 سنوات) بالاضافة الى 50 شخصا سليما كمجموعة سيطرة. تم تقييم مستويات الجلوكوز في دم الصائم (FBG) ، والهيموغلوبين الغليكوزيلاتي (HbA1c) ، الحديد، TIBC ، UIBC، الفيريتين، والترانسفيرين وتشبع الترانسفيرين (S.Trans) ، ونشاط الكاتالايز (CAT). النتائج: ارتفاع مستويات FBG، HbA1c، الفيريتين بينما انخفض الحديد و UIBC TIBC S.Trans بشكل ملحوظ في المرضى مقارنة بمجموعة السيطرة. كان مستوى الترانسفيرين للمجموعة A2 اقل من مجموعة السيطرة. لوحظ انخفاض كبير في نشاط الكاتالايز في جميع مجموعات المرضى قيد الدراسة. كانت هناك علاقة ايجابية بين مستوى الحديد ونشاط الكاتالايز في جميع مجموعات المرضى. الاستنتاج: قد يكون ارتفاع مستوى الفيريتين في الدم احد عوامل الخطر لمرضى السكري من النوع الثاني. تشير بياناتنا ايضا الى وجود علاقة بين انخفاض مستويات الحديد ونشاط الكاتاليز والذي قد يكون مؤشرا محتملا لحدوث مرض السكري وشدته.

Evaluation of Oxidative Stress, Anti-Oxidant, Vitamins and Co-Factor Elements in The Sera of Gastric Cancer in Iraqi Patients.

The objective of this study is to analyze oxidative stress markers Total Oxidant Status (TOS) and total Antioxidant Status (TAS), assess antioxidant levels (vitamin C, E), and evaluate co-factor element profiles zinc (Zn), copper (Cu), iron (Fe) in the serum of Iraqi gastric cancer patients. By elucidating these relationships, the research aims to enhance knowledge on oxidative stress, dietary factors, and potential therapeutic approaches for managing nutritional imbalances in this cohort. The study included 60 gastric cancer patients and 60 matched controls. Blood samples were collected and serum was extracted for analysis of TOS, TAS, Vitamin C, Vitamin E, copper, zinc, and iron levels. Measurements were conducted using spectrophotometry and ELISA kits from various companies. Statistical analysis was performed with IBM SPSS 25.0, presenting results as means ± SD, and differences between groups were assessed via independent samples t-test at p < 0.05 and p ≤ 0.01. The study results indicated statistically significant differences between gastric cancer patients and controls in various biomarkers, with all comparisons showing p-values less than 0.001. This suggests strong evidence for the observed differences between the two groups in (TOS), (TAS), vitamins C and E, Cu, Zn, and Fe levels. These relationships underscore the intricate connections among biomarkers in gastric cancer pathophysiology. The study underscores the intricate relationship between oxidative stress, antioxidant depletion, and micronutrient imbalances in gastric cancer. These findings offer valuable insights into the disease's pathophysiology, indicating potential diagnostic biomarkers. Further research is warranted to unravel underlying mechanisms and explore clinical applications for early gastric cancer diagnosis.

Role of ferroptosis in mitochondrial damage in diabetic retinopathy

Diabetic retinopathy is driven by oxidative stress-mitochondrial damage. Activation of ROS producing cytosolic NADPH oxidase 2 (Nox2) in diabetes precedes retinal mitochondrial damage, initiating a vicious cycle of free radicals. Elevated ROS levels peroxidize membrane lipids increasing damaging lipid peroxides (LPOs). While glutathione peroxidase 4 (GPx4) neutralizes LPOs, an imbalance in its generation-neutralization leads to ferroptosis, which is characterized by increased LPOs, free iron and decreased GPx4 activity. Mitochondria are rich in polyunsaturated fatty acids and iron and have mitochondrial isoform of GPx4. Our aim was to investigate mitochondrial ferroptosis in diabetic retinopathy, focusing on Nox2 mediated ROS production. Using human retinal endothelial cells, incubated in 5mM or 20mM D-glucose for 12 to 96 hours, with or without Nox2 inhibitors (100μM apocynin, 5μM EHop-016 or 5μM Gp91 ds-tat), or ferroptosis inhibitors (1μM ferrostatin-1, 50μM deferoxamine) or activator (0.1μM RSL3), cytosolic and mitochondrial ROS, LPOs, iron, GPx4 activity, mitochondrial integrity (membrane permeability, oxygen consumption rate, mtDNA copy numbers) and cell death were quantified. High glucose significantly increased ROS, LPOs and iron levels and inhibited GPx4 activity in cytosol, and while Nox2 and ferroptosis inhibitors prevented glucose-induced increase in ferroptosis markers, mitochondrial damage and cell death, RSL3, further worsened them. Furthermore, high glucose also increased ferroptosis markers in the mitochondria, which followed their increase in the cytosol, suggesting a role of cytosolic ROS in mitochondrial ferroptosis. Thus, targeting Nox2-ferroptosis should help break down the self-perpetuating vicious cycle of free radicals, initiated by the damaged mitochondria, and could provide novel therapeutics to prevent/retard the development of diabetic retinopathy.

NDRG1 regulates iron metabolism and inhibits pathological cardiac hypertrophy

BackgroundCardiac pathological hypertrophy, a pathological physiological alteration in many cardiovascular diseases, can progress to heart failure. The cellular biology underlying myocardial hypertrophy remains to be fully elucidated. While NDRG1 has been reported to participate in cellular proliferation, differentiation, and cellular stress responses, its role in cardiac diseases remains unexplored. Here, we investigated the role of NDRG1 in pathological hypertrophy. MethodCardiomyocyte-specific-NDRG1 knockout (KO) transgenic mice and NDRG1-AAV9 were used in mice. Angiotensin II (AngII) stimulation were applied to induce hypertrophy. Histological, molecular, and RNA-sequencing analyses were performed, and ferroptosis markers and iron levels were studied. We used co-IP and application of iron chelator to further studied the mechanisms of NDRG1 in cardiac hypertrophy. ResultsWe found that NDRG1 expression is decreased in pathological hypertrophy induced by AngII stimulation. Conditional knockout of NDRG1 in mouse cardiomyocytes led to progressive cardiac hypertrophy and heart failure. Cardiomyocyte-specific overexpression of NDRG1 via AAV9 significantly reversed AngII-induced ventricular hypertrophy and fibrosis. Mechanistically, NDRG1-deficient cardiomyocytes exhibited iron overload and increased ferroptosis, accompanied by elevated levels of reactive oxygen species (ROS) and lipid peroxidation. Subsequently, we confirmed the involvement of NDRG1 in regulating ferroptosis and iron metabolism in myocardial cells. Finally, we identified an interaction between NDRG1 and transferrin in cells. The iron chelator Dp44mT effectively reduced myocardial iron overload and ventricular remodeling induced by NDRG1 deficiency. ConclusionThese findings highlight NDRG1's critical role in iron metabolism and ferroptosis in cardiomyocytes, suggesting that NDRG1 or iron metabolism may serve as therapeutic targets for cardiac hypertrophy.

Comparative intrafollicular and plasma iron, ferritin, and transferrin concentrations in cycling mares

Background and Aim: In females of various species and experimental animals, iron (Fe) status in follicular fluid (FF) is associated with local physiological reproductive events related to follicle development, steroidogenesis, and oocyte maturation. However, these mechanisms remain unknown. This study aimed to determine and compare the intrafollicular and plasma concentrations of Fe, ferritin (Ferr), and transferrin (TRF) in cycling mares. Materials and Methods: Sixty ovaries were collected during the breeding season from 30 clinically normal mares raised for slaughterhouse meat production. Blood samples were collected before slaughter. Follicles were classified into three categories according to size: Small (20–30 mm; n = 20), medium (≥31–40 mm; n = 20), and large (≥41 mm; n = 20). The FF samples, after collection, were immediately taken to the laboratory for processing and were centrifuged, and the Fe and Ferr concentrations in the supernatant and plasma were determined by spectrophotometry. Results: Although intrafollicular Fe and Ferr were similar to plasma, TRF was significantly higher in FF than in systemic circulation (p &lt; 0.05). Follicular development does not modify the status of Fe in the mare. Conclusion: Based on this evidence, it is possible that the acquisition of this molecule possibly originated from a local de novo source, whereas their diffusion through ultrafiltration does not play a relevant role. These results provide new scientific insights into the status of follicle Fe, suggesting its involvement in normal ovarian functions in mares. Keywords: ferritin, follicular fluid, iron, mare, transferrin.

The effect of norepinephrine on ovarian dysfunction by mediating ferroptosis in mice model.

Studies have shown that stress is associated with ovarian dysfunction. Norepinephrine (NE), a classic stress hormone involved in the stress response, is less recognized for its role in ovarian function. In this study, an NE-treated mouse model is induced by intraperitoneal injection of NE for 4 weeks. Compared with normal control mice, NE-treated mice show disturbances in the estrous cycle, decreased levels of anti-Mullerian hormone (AMH) and estradiol (E2), and increased level of follicle-stimulating hormone (FSH). Additionally, the numbers of primordial follicles, primary follicles, secondary follicles, and antral follicles are decreased, whereas the number of atretic follicles is increased in NE-treated mice, indicating NE-induced ovarian dysfunction. RNA sequencing further reveals that genes associated with ferroptosis are significantly enriched in NE-treated ovarian tissues. Concurrently, the levels of reactive oxygen species (ROS), ferrous ions, and malondialdehyde (MDA) are increased, whereas the expression level of glutathione peroxidase 4 (GPX4) is decreased. To elucidate the mechanism of NE-induced ferroptosis in ovaries and the potential reversal by Coenzyme Q10 (CoQ10), an antioxidant, we conduct both in vitro and in vivo experiments. In vitro, the granulosa cell line KGN, when treated with NE, shows decreased cell viability, reduced expression of GPX4, elevated levels of ferrous ion and ROS, and increased MDA level. However, these NE-induced changes are reversed by the addition of CoQ10. Compared with the NE group, the NE-treated mice supplemented with CoQ10 present increased GPX4 level and decreased iron, ROS, and MDA levels. Moreover, the differential expression of genes associated with ferroptosis induced by NE is ameliorated by CoQ10 in NE-treated mice. Additionally, CoQ10 improves ovarian function, as evidenced by increased ovarian weight, more regular estrous cycles, and an increase in follicles at various stages of growth in NE-treated mice. In conclusion, NE induces ovarian dysfunction by triggering ferroptosis in ovarian tissues, and CoQ10 represents a promising approach for protecting reproductive function by inhibiting ferroptosis.

Petrogenesis and tectonic setting of granitic pegmatites in the Beishan orogenic Belt, Northwest China: Evidence from geology, geochronology and geochemistry

The Weiboshan (Li-, Cs- and Ta-enriched) LCT-type Nb–Ta deposit located in Ejin Banner, Inner Mongolia, represents a newly discovered pegmatite-type rare metal deposit of significant interest. In this paper, we describe the petrography and present new mineralogical and whole-rock geochemical data and zircon U–Pb ages of ore-related granitic pegmatites in this deposit. Pegmatite dikes can be divided into three distinct zones on the basis of their contents: the K-feldspar graphic granite pegmatite zone (Kf), microcline graphic granite pegmatite zone (Mic), and albite–muscovite granite pegmatite zone (Ab). The pegmatite dikes and associated mineralization formed during the Mesozoic. Granite pegmatites in various zones display distinctive geochemical features characterized by high silicon contents, substantial alkali enrichment, and relatively low iron, calcium, and magnesium levels. These pegmatites are classified as peraluminous or quasialuminous and exhibit low total rare earth element concentrations. Notably, these pegmatites are enriched in large ion lithophile elements (LILEs), such as Rb, K, and U, but depleted in high field strength elements (HFSEs), such as P and Ti. The progression from the Kf to Mic to Ab zones signifies the thorough evolution of the granitic magma, where the late-stage near-hydrothermal system assumed a crucial role in the mineralization of rare metals during magma differentiation. The Weiboshan pegmatites, which exhibit syncollisional attributes, are A-type granites formed through crustal partial melting induced by decompression. This process occurred against the background of postorogenic extension driven by asthenospheric mantle upwelling resulting from lithospheric delamination due to crustal collision and thickening.

Environmental impact assessment of SONARA's oil sludge landfill in BATOKE, south-west Cameroon

The focus of this study was to assess the environmental impact of the BATOKE oil sludge dump. A field visit was conducted to evaluate the condition of the site, followed by the sampling of oil sludge, BATOKE river water, soil, and locally grown manioc and macabo tubers. Subsequent physico-chemical characterization revealed parameters such as pH, electrical conductivity, total hydrocarbons, COD, BOD5, TSS, major cations and anions, as well as heavy metals including iron, copper, zinc, nickel, chromium, lead, cadmium, mercury, arsenic, calcium, potassium, titanium, zirconium, and rubidium. The environmental impact was assessed using the Contamination Index calculation and the Correlation Matrix. Results indicated that most physical parameters met standards, except for the electrical conductivity of water and soil. However, elevated levels of iron, chromium, lead, cadmium, mercury, arsenic, and ammonium ion were found in the BATOKE River water. The soil showed heavy contamination with various metals, and cassava and macabo tubers were also found to be contaminated. The contamination index calculations confirmed severe pollution in the BATOKE environment, with a risk of further escalation without remediation efforts.

Unusual holopelagic Sargassum mass beaching in Northwest Africa: Morphotypes, chemical composition, and potential valorisation

The rapid proliferation of holopelagic Sargassum spp. in the tropical Atlantic Ocean presents environmental challenges and economic opportunities. In 2022, Senegal witnessed its first significant holopelagic Sargassum beaching event, triggering widespread concern and interest from civil society, industrial sectors, and government. This study represents the first analysis of stranded holopelagic Sargassum's morphotypes and chemical composition in Northwest Africa. We highlight the nature of Sargassum stranding, dominated by S. fluitans III, and describe a putative new morphotype. Compared to most of the studies in the tropical Atlantic, Senegalese Sargassum displayed lower arsenic concentrations (9–29 ppm), higher cadmium levels (9–15 ppm), and increased mercury content (0.47–0.57 ppm). In addition, Senegalese Sargassum showed higher levels of iron (237–1017 ppm) and phosphorus (1300–1772 ppm). The biochemical analysis revealed high total protein levels (15–40 % DW) in Senegalese samples, though further analysis is required to confirm this. Furthermore, variations in biochemical composition within various parts of the Sargassum thallus were observed. The low arsenic content makes the beached Senegalese Sargassum attractive for valorisation and sets it apart from holopelagic Sargassum from all other regions where it occurs. However, caution should be taken regarding the high concentrations of cadmium. Our study highlights promising applications in Senegal and neighbouring countries, particularly in animal feed and agriculture. Noteworthy is the notable palladium content (2 ppm), valuable phenolic compounds, and mannitol, which present additional opportunities for the chemical industry. Our interdisciplinary approach enhances the global scientific understanding of the Sargassum issue. With the anticipation of more frequent Sargassum beaching events and, more generally, for seaweed exploitation, we advocate for inter-governmental African organisations to establish standardised norms for their exploitation. We recommend that the Food and Agriculture Organization/World Health Organization consider incorporating more seaweed in the Codex Alimentarius to facilitate their uses particularly when states deal with algal blooms.

Increased Mortality Risk Is Associated with Abnormal Iron Status in Japanese Patients on Hemodialysis: A Nationwide Cohort Study

Increased Mortality Risk Is Associated with Abnormal Iron Status in Japanese Patients on Hemodialysis: A Nationwide Cohort Study

A Randomized Crossover Trial of Acceptability of Quadruple-Fortified Salt in Women and their Households in Southern India

BackgroundDouble-fortified salt (DFS; iron, iodine) improved iron status in randomized trials and was incorporated into India’s social safety net programs, suggesting opportunities to address other micronutrient deficiencies. ObjectivesTo evaluate acceptability of quadruple-fortified salt (QFS; iron, iodine, folic acid, vitamin B12) in women and their households, using a randomized crossover trial design and triangle tests. MethodsWomen 18-49y (n=77) and their households were randomized to receive QFS or DFS in a randomized crossover design over a 3-week period (week 1: QFS/DFS, 2: iodized salt, 3: DFS/QFS). Each week, participants completed a 9-point hedonic questionnaire (1=dislike extremely to 9=like extremely) to evaluate five sensory domains (color, odor, taste, texture, overall acceptability) of the intervention, and remaining salt was weighed using a digital scale. Triangle tests were conducted among women to evaluate sensory discrimination of salt consumed in rice dishes prepared using standardized recipes. Mixed models were used to examine hedonic ratings and salt use; salt type, sequence, and period were included as fixed effects, and household was included as a random effect. Binomial tests were used to evaluate sensory discrimination of salt type in triangle tests. ResultsMean hedonic ratings for most of the five sensory domains were ≥7 (like moderately) and did not differ by salt type (overall acceptability mean [SD]: QFS: 7.8 [0.7] vs. DFS: 7.7 [1.2]; p=0.68). Household salt use (weighed) did not differ by salt type. During the 3-week intervention period, weighed salt use and hedonic ratings significantly increased, indicating a period effect independent of salt type or sequence. In triangle tests, rice samples prepared with QFS, DFS, or iodized salt were not distinguishable. ConclusionAcceptability of QFS was high, based on individual hedonic ratings and weighed household salt use. Rice dishes prepared with DFS, QFS, and iodized salt were not distinguishable. Findings informed the design of a randomized trial of QFS in this population. Registration numbersNCT03853304 and REF/2019/03/024479.

Ferritin and Iron Levels Inversely Associated With Lymphoma Risk: A Mendelian Randomization Study.

Current knowledge on iron's role in lymphoma development is very limited, with studies yielding inconsistent findings. To address this gap, we conducted a rigorous two-sample mendelian randomization study, aiming to elucidate the potential associations between iron storage and the risk of developing lymphoma. This study leveraged extensive genetic data derived from a comprehensive genome-wide association study (GWAS) comprising 257,953 individuals. The primary objective was to pinpoint single-nucleotide polymorphisms (SNPs) that are significantly associated with iron storage. Subsequently, this genetic information was analyzed in conjunction with summary-level data pertaining to lymphoma cases and controls, sourced from the IEU open GWAS project, which included a sample size of 3,546 lymphoma cases and 487,257 controls. To evaluate the relationship between iron storage and lymphoma risk, an inverse variance-weighted method with random effects was employed, complemented by rigorous sensitivity analyses. Genetic predisposition to high ferritin and serum iron status was causally associated with lower odds of lymphoma. Ferritin exhibited an odds ratio (OR) of 0.777 (95% confidence interval (CI): 0.628 - 0.961, P = 0.020), indicating 22.3% reduced odds of lymphoma associated with a one standard deviation increase in ferritin levels. Similarly, serum iron demonstrated an OR of 0.776 (95% CI: 0.609 - 0.989, P = 0.040), corresponding to 22.4% decreased odds of lymphoma for a one standard deviation increase in serum iron. This study suggests that individuals with genes linked to higher iron storage levels have a lower risk of developing lymphoma, but further research is necessary before making any clinical recommendations.

Unusual Confluence: Exploring the Association of Biliary Atresia, Wilson Disease, and Iron Overload

ABSTRACT The case involves a 33-year-old man with biliary atresia, Wilson disease (WD), and iron overload. Biliary atresia, a cholangiodestructive disease, leads to cirrhosis if untreated. WD, caused by ATP7B gene mutations, results in copper accumulation affecting the liver and brain. Iron overload can be seen in cases of WD and with hereditary hemochromatosis gene mutations. The patient's concurrent presentation of these conditions poses a unique clinical challenge. Elevated iron levels may worsen WD outcomes. A detailed history and physical examination, genetic testing, and close follow-up are crucial. The case highlights the need for increased awareness and vigilant monitoring of patients with overlapping liver diseases.

In-depth cerebrovascular lipidomics profiling for discovering novel biomarkers and mechanisms in moyamoya and intracranial atherosclerotic disease.

Despite considerable research efforts, the precise etiology and underlying pathways contributing to Moyamoya Disease (MMD) remain poorly understood. Moreover, the overlapping vascular pathologies shared between MMD and Intracranial Atherosclerotic Disease (ICAD) pose challenges in clinical differentiation, even with gold-standard cerebral angiography. An in-depth exploration of lipidomic alterations in cerebral intracranial MMD vessels could offer valuable insights into the pathogenesis of MMD-related mechanisms, encompassing MMD and ICAD, and unveil novel biomarkers and potential therapeutic targets. However, to date, comprehensive lipidomic profiling has been lacking. To discover novel biomarkers and unravel the pathophysiological mechanisms underlying MMD, we conducted a lipidomics analysis to characterize various lipid species in matched human extracranial and intracranial artery tissues from patients diagnosed with MMD (n=99) and ICAD (n=12). Our analysis identified 569 lipid species and delineated a robust panel of lipidomic biomarkers capable of effectively distinguishing MMD from ICAD (area under curve=0.98), as determined by receiver operating characteristic curve analysis. Notably, we observed a significantly more pronounced positive correlation of diacylglycerols and a negative association of triglycerides in intracranial artery tissues of MMD patients compared to those with ICAD, suggesting a potential role of dysregulated diacylglycerol-induced signaling in MMD pathogenesis. Furthermore, our investigation into the correlations of critical differential intracranial artery vessel lipid species between MMD and ICAD and clinical parameters revealed negative associations with plasma iron levels, implying a potential link between plasma iron metabolism and artery lipid homeostasis during MMD pathogenesis. These findings offer promising prospects for advancing clinical diagnosis for enhanced differentiation between the two disease conditions. Additionally, they shed light on the fundamental mechanisms implicated in MMD pathogenesis and suggest potential therapeutic avenues through targeting artery vessel lipids or plasma iron levels.