Nanostructurally Engineering Covalent Organic Frameworks for Boosting CO2 Photoreduction.

Herein, a series of imine-linked covalent organic frameworks (COFs) are developed with advanced ordered mesoporous hollow spherical nanomorphology and ultra-large mesopores (4.6 nm in size), named OMHS-COF-M (M = H, Co, and Ni). The ordered mesoporous hollow spherical nanomorphology is revealed to be formed via an Ostwald ripening mechanism based on a one-step self-templated strategy. Encouraged by its unique structural features and outstanding photoelectrical property, the OMHS-COF-Co material is applied as the photocatalyst for CO2-to-CO reduction. Remarkably, it delivers an impressive CO production rate as high as 15 874 µmol g-1 h-1, a large selectivity of 92.4%, and a preeminent cycling stability. From in/ex situ experiments and density functional theory (DFT) calculations, the excellent CO2 photoreduction performance is ascribed to the desirable cooperation of unique ordered mesoporous hollow spherical host and abundant isolated Co active sites, enhancing CO2 activation, and improving electron transfer kinetics as well as reducing the energy barriers for intermediates *COOH generation and CO desorption.

Copolymerization of Parylene C and Parylene F to Enhance Adhesion and Thermal Stability without Coating Performance Degradation.

Parylene C has been widely used in the fields of microelectromechanical systems (MEMS) and electronic device encapsulation because of its unique properties, such as biocompatibility and conformal coverage. However, its poor adhesion and low thermal stability limit its use in a wider range of applications. This study proposes a novel method for improving the thermal stability and enhancing the adhesion between Parylene and Si by copolymerizing Parylene C with Parylene F. The successful preparation of Parylene copolymer films containing different ratios of Parylene C and Parylene F was confirmed using Fourier-transform infrared spectroscopy and surface energy calculations. The proposed method resulted in the copolymer film having an adhesion 10.4 times stronger than that of the Parylene C homopolymer film. Furthermore, the friction coefficients and cell culture capability of the Parylene copolymer films were tested. The results indicated no degradation compared with the Parylene C homopolymer film. This copolymerization method significantly expands the applications of Parylene materials.

Manipulation of Particle/Cell Based on Compressibility in a Divergent Microchannel by Surface Acoustic Wave.

The mechanical properties (compressibility or deformability) of cells are closely related to their death, migration, and differentiation. Accurate separation and manipulation of bioparticles based on these mechanical properties are still a challenging in the field of acoustofluidics. In this work, based on surface acoustic waves (SAW) and divergent microchannels, we developed a new method for separating and detecting particles or cells with different compressibility. The difference in acoustic radiation force (Fr) caused by compressibility are gradually amplified and accumulated by decreasing the flow velocity, and they are finally reflected in the particle migration distance. During the transverse migration process, the alternating dominance of the acoustic radiation force and the Stokes resistance force (Fs) drives the particles to create three typical migration patterns: intermittent migration, compound migration, and near-wall migration. In the present tilted SAW device, a 91% separation success rate of ∼10 µm polystyrene (PS) and polydimethylsiloxane (PDMS) particles can be achieved by optimizing the acoustic field input power and the fluid velocity. The application potential of the present divergent microchannel is validated by separating the myelogenous leukemia cell K562 and the natural killer cell NK92 that have similar densities and sizes (∼15 µm) but different compressibility. The results of this work are expected to provide valuable insights into the acoustofluidics separation and detection of the cells that are with different compressibility.

The risk of falls among the aging population: A systematic review and meta-analysis.

Aim: This study aims to clarify the risk factors for falls to prevent severe consequences in older adults. Methods: We searched the PubMed, Web of Science, Embase, and Google Scholar databases using the terms "risk factors" OR "predicting factors" OR "predictor" AND "fall" OR "drop" to identify all relevant studies and compare their results. The study participants were divided into two groups, the "fall group" and the "control group", and differences in demographic characteristics, lifestyles, and comorbidities were compared. Results: We included 34 articles in the analysis and analyzed 22 factors. Older age, lower education level, polypharmacy, malnutrition, living alone, living in an urban area, smoking, and alcohol consumption increased the risk of falls in the aging population. Additionally, comorbidities such as cardiac disease, hypertension, diabetes, stroke, frailty, previous history of falls, depression, Parkinson's disease, and pain increased the risk of falls. Conclusion: Demographic characteristics, comorbidities, and lifestyle factors can influence the risk of falls and should be taken into consideration.

Blood Th17 cells and IL-17A as candidate biomarkers estimating the progression of cognitive impairment in stroke patients.

BACKGROUND: T helper (Th) cells regulate immunity and inflammation to engage in cognitive impairment in several neurological diseases, while their clinical relevance in stroke patients is not clear. The current study intended to assess the relationship of Th1 cells, Th17 cells, interferon-gamma (IFN-γ), and interleukin (IL)-17A with cognitive function in stroke patients. METHODS: One hundred twenty stroke patients and 40 controls were enrolled in this muticenter study. Th1 and Th17 cells in peripheral blood were assessed by flow cytometry; meanwhile, IFN-γ and IL-17A in serum were detected by enzyme-linked immunosorbent assay. Cognitive function of stroke patients was evaluated by Mini-Mental State Examination (MMSE) score at enrollment (baseline), year 1, year 2, and year 3. RESULTS: Th1 cells (p = 0.037) and IFN-γ (p = 0.048) were slightly increased, while Th17 cells (p < 0.001) and IL-17A (p < 0.001) were greatly elevated in stroke patients compared with controls. Th17 cells (rs  = -0.374, p < 0.001) and IL-17A (rs  = -0.267, p = 0.003) were negatively correlated with MMSE score at baseline, but Th1 cells and IFN-γ were not. Meanwhile, Th17 cells (p = 0.001) and IL-17A (p = 0.024) were increased in patients with cognitive impairment compared to those without cognitive impairment. Notably, Th17 cells were positively associated with 1-year (rs  = 0.331, p < 0.001), 2-year (rs  = 0.261, p = 0.006), and 3-year (rs  = 0.256, p = 0.011) MMSE decline; IL-17A was positively correlated with 1-year (rs  = 0.262, p = 0.005), 2-year (rs  = 0.193, p = 0.045), but not 3-year MMSE decline. However, both Th1 cells and IFN-γ were not linked with MMSE decline. CONCLUSION: Th17 cells and IL-17A estimate the progression of cognitive impairment in stroke patients.

In Situ Electroporation on PERFECT Filter for High-Efficiency and High-Viability Tumor Cell Labeling.

Labeling-assisted visualization is a powerful strategy to track circulating tumor cells (CTCs) for mechanism study (e.g., tumor metastasis). Due to the rarity of CTCs in the whole blood, efficient simultaneous enrichment and labeling of CTCs are needed. Hereby, novel in situ electroporation on a previously-developed micropore-arrayed filter (PERFECT filter) is proposed. Benefiting from the ultra-small-thickness and high-porosity of the filter plus high precision pore diameter, target rare tumor cells were enriched with less damage and uniform size distribution, contributing to enhanced molecular delivery efficiency and cell viability in the downstream electroporation. Various biomolecules (e.g., small molecule dyes, plasmids, and functional proteins) were used to verify this in situ electroporation system. High labeling efficiency (74.08 ± 2.94%) and high viability (81.15 ± 3.04%, verified via live/dead staining) were achieved by optimizing the parameters of electric field strength and pulse number, ensuring the labeled tumor cells can be used for further culture and down-stream analysis. In addition, high specificity (99.03 ± 1.67%) probing of tumor cells was further achieved by introducing fluorescent dye-conjugated antibodies into target cells. The whole procedure, including cell separation and electroporation, can be finished quickly (<10 min). The proposed in situ electroporation on the PERFECT filter system has great potential to track CTCs for tumor metastasis studies.

Atomically Dispersed NiN3 Sites on Highly Defective Micro-Mesoporous Carbon for Superior CO2 Electroreduction.

Direct electrochemical conversion of CO2 to CO product powered by renewable electricity is widely advocated as an emerging strategy for alleviating CO2 emissions while addressing global energy issues. However, the development of low-cost and efficient electrocatalysts with high Faradaic efficiency for CO production (FECO ) and high current density remains a grand challenge. Herein, a robust single nickel atomic site electrocatalyst, which features isolated and dense single atomic NiN3 sites anchored on highly defective hierarchically micro-mesoporous carbon (Ni-SAs/HMMNC-800), to enable enhanced charge transport and more exposed active sites for catalyzing electrochemical CO2 -to-CO conversion, is reported. The Ni-SAs/HMMNC-800 catalyst achieves excellent activity and selectivity with high FECO values of >90% throughout a wide potential range (the FECO reaches 99.5% at -0.7 V vs reversible hydrogen electrode) and a CO partial current density as high as 13.0 mA cm-2 at -0.7 V versus reversible hydrogen electrode, as well as a far outstanding durability during long-term continuous operation, indicating a superior CO2 electroreduction performance than that of other reference samples and most of previously reported carbon-based single atom electrocatalysts. Experimental and density functional theory calculations reveal that atomic NiN3 coordination sites coupled adjacent defects are favorable to significantly enhancing the formation of COOH* reaction intermediates while suppressing the competing hydrogen evolution reaction, thereby enhancing the electrocatalytic activity for CO2 -to-CO reduction. Notably, this work provides a valuable new prospect for designing and synthesizing efficient and cost-effective single atom CO2 electroreduction catalysts for practical applications.

Changes of Necroptosis in Irbesartan Medicated Cardioprotection in Diabetic Rats.

BACKGROUND: Diabetic cardiomyopathy (DCM) is strongly linked to microvascular disease, renin-angiotensin system (RAS) activation, cardiac inflammation and cell apoptosis. Irbesartan is an angiotensin II (Ang II) receptor antagonist in RAS system, which inhibited the conversion of Ang I into Ang II, while the specific mechanism is still obscure. OBJECTIVE: This study aims to investigate the expressions necroptosis RIP1-RIP3-MLKL pathway in myocardium of diabetic rats, and the protective action of irbesartan on myocardial damage. MATERIALS AND METHODS: In our study, 30 Sprague-Dawley rats were divided into 5 groups: CON4W, high glucose and high caloric (HC4W), diabetes mellitus 4 weeks (DM4W group), diabetes mellitus 8 weeks (DM8W group), and irbesartan diabetes 8 weeks (Ir DM8W group). RESULTS: We discovered that as diabetes progresses, the rats gradually lost weight, the HW/BW ratio were increased gradually, and the cardiac function became worse accompanied with the aggravation of inflammatory injury. Meanwhile, the myocardial fibers and cells were disordered, and the expression of positive substances, RIP1 and RIP3 increased significantly. The mRNA and protein levels of myocardial RIP1, RIP3 and MLKL were all increased with the progression of DM. After the intervention of irbesartan in diabetic rats, the cardiac function was improved, whereas inflammatory injury and HW/BW ratio were decreased. Also, the myocardial fibrosis injury was attenuated, and the PAS positive substances, RIP1 and RIP3 were significantly decreased. The curative effect of irbesartan was related to decreased myocardial RIP1, RIP3 and MLKL mRNA and protein levels. CONCLUSION: In conclusion, irbesartan has a cardioprotective effect on the diabetic rats, and its mechanism may be connected with inhibition of RIP1-RIP3-MLKL pathway.

Flavonoids composition and antioxidant potential assessment of extracts from Gannanzao Navel Orange (Citrus sinensis Osbeck Cv. Gannanzao) peel.

The antioxidant effect of 95% ethanol extract and its three subfractions, PE (petroleum ether), EtOAc (ethyl acetate), and water extracts, from Gannanzao navel orange peel, were evaluated by ABTS (2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid)), DPPH (1,1-diphenyl-2-picryl-hydrazyl) and FRAP (ferric reducing/antioxidant potential) methods for the first time. Furthermore, the TPC (total polyphenol content), TFC (total flavonoid content), and primary individual flavonoids of the four extracts were analyzed and compared. The results indicated that: (1) the EtOAc extract exhibited the best antioxidant potential among these four extracts in all three antioxidant bioassay platforms; (2) Corresponding to the antioxidant potential, the EtOAc extract contained the highest contents of both TPC and TFC; (3) Compared with other extracts, the EtOAc extract was significantly (p < 0.01) rich in the contents of narirutin, sinensetin, nobiletin, 4',5,6,7-tetramethoxyflavone, and 3,3',4',5,6,7-hexamethoxyflavone, which might be the main bioactive compounds responsible for the excellent antioxidant potential of EtOAc extract.

MiR-324-3p Regulates Fibroblast Proliferation via Targeting TGF-ß1 in Atrial Fibrillation.

Atrial fibrillation (AF), one of the common clinical arrhythmias, lacks effective treatment manners. Cardiac fibroblasts play an essential role in myocardial fibrosis and cardiac remodeling, which are involved in AF progression. Reportedly, MicroRNAs (miRNAs) regulate the myocardial fibrosis in AF. However, whether miR-324-3p involves myocardial fibrosis in AF and the tentative molecular mechanisms of miR-324-3p regulating cardiac fibroblasts during AF remains unknown. In the present study, miR-324-3p was found to be decreased in patients with AF and AF rat model. Next, we investigated the effect of miR-324-3p on myocardial fibroblast proliferation through miR-324-3p overexpression and found that miR-324-3p inhibited fibroblast proliferation in vitro. Furthermore, we found that miR-324-3p directly targeted transforming growth factor ß1 in fibroblast, which may be involved in the development of myocardial fibrosis during AF. Meanwhile, miR-324-3p mimics treatment suppressed the PI3K/AKT signaling pathway in fibroblast. These results demonstrated a molecular mechanism of miR-324-3p regulating fibroblast proliferation in vitro, which might provide a novel potential treatment manner in AF in clinic.

Effects of irbesartan on myocardial injury in diabetic rats: The role of NLRP3/ASC/Caspase-1 pathway.

To observe the mechanism of myocardial injury in diabetic rats after irbesartan intervention and analyze the role of nucleotide binding oligomerization domain-like receptor protein 3 (NLRP3) inflammatory pathway. The experiment was divided into four groups: normal control group (CON), high glucose and high caloric diet group (HC), diabetes group (DM) and diabetes+irbesartan group (DM+Ir). Compared with CON group, in HC group, triglyceride, total cholesterol and fasting blood glucose levels were increased; however, there was no significant difference of the cardiac function, the degree of myocardial fibrosis, NLRP3, ASC, Caspase-1 mRNA and protein expressions and the releasing of inflammatory factors interleukin (IL)-1ß and IL-18. Compared with HC group, in DM group, triglyceride, total cholesterol, fasting blood glucose, IL-1ß and IL-18 levels, NLRP3, ASC, Caspase-1 mRNA and protein expressions and the degree of myocardial fibrosis were increased, but the cardiac function was decreased. Compared with DM group, there were no changes in total cholesterol and fasting blood glucose, the degree of myocardial fibrosis cardiac function was attenuated, NLRP3, ASC, Caspase-1 expressions, IL-1ß and IL-18 levels were reduced in DM+Ir group. The results suggested that irbesartan may exert myocardial protection by inhibiting the expression of the NLRP3/ASC/Caspase-1 pathway in diabetic rats.

MicroRNA-143-5p modulates pulmonary artery smooth muscle cells functions in hypoxic pulmonary hypertension through targeting HIF-1α.

This paper explores the potential mechanism of microRNA-143-5p regulation effects on pulmonary artery smooth muscle cells (PASMCs) functions in hypoxic pulmonary hypertension (HPH) via targeting HIF-1a, which may offer a new idea for HPH therapy. PASMCs were transfected with mimics control/miR-143-5p mimics or inhibitor control/miR-143-5p inhibitor. We used Western blotting and RT-qPCR to detect the protein and mRNA expressions, CCK-8 assay to detect cellular viability, Annexin V-FITC/PI staining and caspase- 3/cleaved caspase-3 protein to evaluate cellular apoptosis, transwell migration experiment for cellular migration measurement and Dual luciferase reporter gene assay to prove the target of miR-143-5p. Cells under hypoxic condition presented the decreased protein and mRNA expressions of α-smooth muscle actin (SM-α-actin), Myocardin, smooth muscle myosin heavy chain (SMMHC), and smooth muscle-22α (SM22α), Calponin1 and Hypoxia-inducible factor-1α(HIF-1α), the increased cell viability and miR-143-5p level; Overexpression of miR-143-5p obviously reduced vascular smooth muscle-specific contraction marker protein levels and cellular apoptosis, increased cellular migration of PASMCs with hypoxia stimulation; Low-expression of miR-143-5p caused the opposite changes, while co-transfected with Si HIF-1 α blocked the beneficial effects of miR-143-5p inhibition on PASMCs under hypoxia. MicroRNA-143-5p can promote the phenotype conversion, proliferation and migration of pulmonary artery smooth muscle cells under hypoxic condition through direct targeting of HIF-1α.

MicroRNA-362-3p Targets PAX3 to Inhibit the Development of Glioma through Mediating Wnt/ß-Catenin Pathway.

BACKGROUND: Glioma is identified as a broad category of brain and spinal cord tumors. MiR-362-3p is important in regulating the genesis of different cancers; however, the mechanism of miR-362-3p in the progression of glioma remains largely unknown. OBJECTIVES: This study aimed to elucidate pathobiological functions of miR-362-3p by targeting PAX3 in glioma. METHOD: qRT-PCR and western blotting were used to examine miR-362-3p and PAX3 expression in glioma tissues and cells. CCK-8 assay and transwell assays were used to examine the functions of miR-362-3p on human glioma. Two bioinformatics analysis software and luciferase reporter assay were performed to analyze the relationship between miR-362-3p and PAX3. RESULTS: MiR-362-3p was downregulated, and PAX3 was upregulated in glioma tissues and cells. Functional assays revealed that ectopic expression of miR-362-3p inhibited glioma cell proliferation and migration. Further, PAX3 was confirmed as direct target gene of miR-362-3p, and downregulation of PAX3 reversed the suppressive effects of miR-362-3p in glioma. In addition, miR-362-3p also exhibited suppressive effect on epithelial-mesenchymal transition and Wnt/ß-catenin pathway. CONCLUSIONS: MiR-362-3p downregulation or PAX3 overexpression predicted poor prognosis in glioma. MiR-362-3p played a role in the suppressive effect on glioma by targeting PAX3 through suppressing Wnt/ß-catenin pathway.

[Effects of mitochondrial aldehyde dehydrogenase 2 on autophagy-associated proteins in neonatal rat myocardial fibroblasts cultured in high glucose].

OBJECTIVE: To investigate whether autophagy mediates the effects of aldehyde dehydrogenase 2 (ALDH2) on the proliferation of neonatal rat cardiac fibroblasts cultured in high glucose. METHODS: Cardiac fibroblasts were isolated from neonatal (within 3 days) SD rats and subcultured. The fibroblasts of the third passage, after identification with immunofluorescence staining for vimentin, were treated with 5.5 mmol/L glucose (control group), 30 mmol/L glucose (high glucose group), or 30 mmol/L glucose in the presence of Alda-1 (an ALDH2 agonist), daidzin (an ALDH2 2 inhibitor), or both. Western blotting was employed to detect ALDH2, microtubule-associated protein 1 light chain 3B subunit (LC3B) and Beclin-1 in the cells, and a hydroxyproline detection kit was used for determining hydroxyproline content in cell culture medium; CCK- 8 kit was used for assessing the proliferation ability of the cardiac fibroblasts after the treatments. RESULTS: Compared with the control cells, the cells exposed to high glucose exhibited obviously decreased expressions of ALDH2, Beclin-1 and LC3B and increased cell number and hydroxyproline content in the culture medium. Treatment of the high glucose-exposed cells with Alda-1 significantly increased Beclin-1, LC3B, and ALDH2 protein expressions and lowered the cell number and intracellular hydroxyproline content, whereas the application of daidzin resulted in reverse changes in the expressions of ALDH2, Beclin-1 and LC3B, viable cell number and intracellular hydroxyproline content in high glucose-exposed cells. CONCLUSIONS: Mitochondrial ALDH2 inhibits the proliferation of neonatal rat cardiac fibroblasts induced by high glucose, and the effect is possibly mediated by the up-regulation of autophagy-related proteins Beclin-1 and LC3B.

Circ 0001434 RNA reduces inflammation in acute lung injury model through Wnt/ß-catenin and NF-κB by miR-625-5p.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common and complicated inflammatory lung diseases. Circ RNAs have emerged as a novel class of gene regulatory molecules that play vital roles in multiple complex diseases, including ALI. In this study, we aimed to identify potential regulators of Circ 0001434 on acute lung injury (ALI) and to explore their roles in lipopolysaccharide (LPS)-induced ALI. In a mouse ALI model, Circ 0001434 expression was effectively down-regulated, compared with the control group. Up-regulation of Circ 0001434 effectively decreased the inflammation of ALI in an in vitro model. Down-regulation of Circ 0001434 effectively promoted inflammation in ALI in an in vitro model. Over-expression of Circ 0001434 induced Wnt and ß-catenin protein expression, and suppressed NF-κB p65 protein expression in the ALI in vitro model by miR-625-5p. Down-regulation of Circ 0001434 significantly suppressed Wnt and ß-catenin, and induced NF-κB p65 protein expression in the ALI in vitro model by miR-625-5p. Wnt reduced the function of Circ 0001434 on inflammation in ALI in an in vitro model. The inhibition of miR-625-5p reversed the function of anti-Circ 0001434 on inflammation in ALI vitro model. Taken together, Circ 0001434 mediates ALI-induced lung inflammation through Wnt/ß-catenin and NF-κB activation by miR-625-5p.

Neuroprotective effects of diallyl trisulfide in SOD1-G93A transgenic mouse model of amyotrophic lateral sclerosis.

Diallyl trisulfide (DATS) is one of the major constituents in garlic oil and has been documented to transcriptionally activate phase II enzymes. The purpose of this study is to evaluate the effects of DATS in prolonging disease duration and survival in a transgenic mouse model of amyotrophic lateral sclerosis (ALS). SOD1-G93A transgenic mice were randomly divided into DATS-treated group (80mg/kg/d, p.o.) and vehicle-treated group at disease onset stage. Oral administration of DATS beginning at clinical onset stage significantly prolonged disease duration and extended life span for about one week. DATS treatment induced HO-1 and reduced GFAP expression in the lumbar spinal cord of SOD1-G93A transgenic mice. This study indicates that DATS has multifunctional neuroprotective effects in SOD1-G93A transgenic mice.

[Effects of ferrous sulfate supplementation on bone marrow hemopoiesis in rats].

OBJECTIVE: To explore the influences of different dosage ferrous sulfate supplements on bone marrow hemopoiesis in rats. METHODS: Female weaning Wistar rats were fed with an iron deficient diet (< 10 mg/kg diet) until the level of hemoglobin of rats was lower than 100 g/L. Rats (n = 50) were randomly divided into five groups according to the levels of hemoglobin and body weight, iron deficiency control (ID), daily low iron diet supplement (LDs), daily high iron diet supplement (HDs), weekly low iron supplement (LWs), and weekly high iron supplement (HWs). RESULTS: After 12 weeks, bone marrow stainable iron was seldom in ID group, and ample in supplement groups. The proportions of iron staining of bone marrow smear in supplement groups were more than 30%. Bone marrow cells in all rats were hyperplastic or active hyperplastic. CONCLUSIONS: Daily high iron supplement or once weekly high iron supplement were safe to bone marrow hemopoiesis in rats.

[Protection of zinc and selenium content of brain and blood on learning and memory exposed to lead in growing rats].

OBJECTIVE: The purpose of this paper was to explore the relations between lead levels of brain and blood on learning and memory, and to determine the antagonization of selenium and zinc on lead toxicity in brain and blood. METHODS: The growing rats were fed with diet added with different levels of selenium, zinc and lead for 12 weeks. RESULTS: (1) The lead levels of brain and blood of rats exposed to lead was higher than that of the control group; the lead levels of brain and blood administrated lead decreased following the increased in selenium and zinc levels in the diet. (2) Error frequencies and total time in water-maze significantly reduced in the groups exposed to lead. (3) Error frequencies and total time in water-maze and lead levels of brain and blood presented positive relation. CONCLUSION: The present study indicated that supplementary suitable zinc or/and selenium could alleviate the lead toxicity on the brain and blood of rats.

[Study on the effect of micronutrients supplementation on health status of children].

To study the effect of multi-micronutrients supplementation on nutritional status of children, 220 students aged 8-12 years were observed for 6 months. A half of them were given the supplements, another half placebo. The results showed that in comparison with the placebo, the supplemented children had a higher urine excretion of vitamin B2 and vitamin C after loading; a higher concentration of serum 25-OH-D3, a high content of hydroxy-proline and hydroxy-proline/creatinine ratio in fast urine, and a higher bone mineral content and bone mass density of the mid-ulna. The supplemented children performed significantly better than the placebo in reading speed, learning capacity and arithmetic examinations. It is concluded that micronutrients supplementation played a notable rule in resulting better nutritional status and learning ability of school children.