Effect of vitamin A on maternal, fetal, and neonatal outcomes: An overview of deficiency, excessive intake, and intake recommendations.

Vitamin A imbalance during pregnancy and lactation is a global public health concern with potentially negative consequences for fetuses and neonates. Inadequate vitamin A intake during this critical period can lead to anemia, weakened immune function, night blindness, and increased susceptibility to infections. Conversely, excessive intake of vitamin A can result in birth defects, hypercalcemia, and psychiatric symptoms. This review aims to identify risk factors contributing to vitamin A deficiency in pregnant women and its impact on maternal, fetal, and neonatal outcomes. It also examines the effects of high-dose vitamin A supplementation during pregnancy on offspring health. By analyzing existing literature and recommendations, the review emphasizes the significance of vitamin A in the development of various body systems and organs. It provides a comprehensive overview of the effects of vitamin A during pregnancy and lactation, encompassing deficiencies, excessive intake, and supplementation guidelines. The need for further research in this field is highlighted. In conclusion, maintaining a balanced vitamin A status is crucial during pregnancy to promote better outcomes for fetuses and newborns. Effective monitoring and intervention strategies are essential to address vitamin A deficiency and excess in pregnant women, thereby improving fetal and neonatal health.

Dietary replacement of soybean meal with black soldier fly larvae meal in juvenile Labeo rohita and Catla catla: Effects on growth, nutritional quality, oxidative stress biomarkers and disease resistance.

This experiment aimed to investigate the effects of partial substitution of crude protein from soybean meal (SBM) with black soldier fly (Hermetia illucens) larvae meal (BSFLM) in juvenile rohu (Labeo rohita) and catla (Catla catla). Four isonitrogenous diets (23% crude protein) were formulated to replace 0% (T0), 40% (T40), 80% (T80) and 100% (T100) crude protein from SBM with BSFLM. Triplicate groups of each species (10 fish per replicate) were fed in an eight week growth experiment. After final sampling (n = 20 fish per dietary group), the remaining fish were exposed to bacterial (Staphylococcus aureus) challenge (0.80 CFU/ml) for 15 days. Rohu fed with BSFLM substituted diets showed significantly higher growth and feed conversion ratio as compared to those in T0. Catla fed with BSFLM substituted diets showed slightly higher growth indices. The growth response of rohu to BSFLM substitution was better than that noted in catla in all groups. The chemical composition, amino acids and fatty acids profile, haematological and biochemical parameters, levels of liver function enzymes measured in T0, T40, T80 and T100 were similar between four dietary groups in both species. However, the maximum value of cholesterol and triglycerides were noted in T100 both in catla and rohu. The values of lauric acid, α-linolenic acid, decosahexanoic acid, n3:n6 fatty acids ratio progressively increased with dietary increase of BSFLM in both species. At end of the growth experiment, the levels of catalase, superoxide dismutase and lysozyme increased linearly with the inclusion of BSFLM in both species while malondialdehyde showed similar values between different groups. However, catalase, and superoxide dismutase increased (T0

Concern for Increased Prevalence of Heyde's Syndrome in Patients on Hemodialysis.

The association between aortic stenosis and increased gastrointestinal arteriovenous malformations is known as Heyde's syndrome. An acquired von Willebrand deficiency mediates the connection between these two seemingly dispersed pathologies. As von Willebrand factor passes through a stenosed aorta, it is broken down and can no longer inhibit angiogenesis, leading to angiodysplasias. Heyde's syndrome can manifest with chronic, refractory anemia requiring multiple hospitalizations for symptomatic gastrointestinal bleeding and transfusion. Hitherto, Heyde's syndrome has been considered exceptionally rare, with 1-3% of populations with aortic stenosis. However, given that 31.7% of patients with gastrointestinal angioplasty have aortic stenosis and gastrointestinal arteriovenous malformations are not screened for in patients without anemia, the prevalence of Heyde's syndrome is most likely higher than currently reflected in the literature. Also, the prevalence of Heyde's syndrome in populations who are predisposed to angiodysplasias, such as those on hemodialysis, is understudied. We aim to impart a need for increased research on the prevalence of Heyde's syndrome, especially in high-risk patients. This case report presents a patient with severe Heyde's syndrome on hemodialysis, showing an unconsidered risk factor for Heyde's syndrome in need of further research.

A Case of Legionnaires' Disease Manifesting as Heat Exhaustion.

A 69-year-old male with a history of prior admissions of heat exhaustion presented with non-specific symptoms including fatigue, diarrhea, and dehydration. The workup revealed a positive legionella urine antigen. He was treated with levofloxacin with symptom resolution within 48 hours.

Potassium silicate and zinc oxide nanoparticles modulate antioxidant system, membranous H+-ATPase and nitric oxide content in faba bean (Vicia faba) seedlings exposed to arsenic toxicity.

Current research focused on the potential role of zinc oxide nanoparticles (ZnONPs) and potassium (K+ ) in mitigation of arsenic (As) toxicity in Vicia faba L. seedlings. Faba bean seedlings were grown for 30days in potted soil. As stress curtailed root and shoot length, chlorophyll (Chl) content and net photosynthetic rate in V. faba seedlings. However, ZnONPs and K+ curtailed As stress in faba bean seedling through enhanced activity of superoxide dismutase (SOD), ascorbate peroxidase (APX), catalase (CAT) and peroxidase (POD) enzyme. Furthermore, ZnONPs and K+ significantly enhanced cysteine (Cys) content and serine acetyletransferase (SAT) activity in faba bean seedling exposed to As-toxificated soil. Application of ZnONPs and K+ curtailed superoxide ionic content and hydrogen peroxide (H2 O2 ) accumulation in V. faba seedlings exposed to As-polluted soil. Nitric oxide (NO) content also increased in faba bean seedlings treated with ZnONPs and K+ in normal and As-polluted soil. As stress alleviation was credited to reduce As uptake in faba bean seedlings treated with synergistic application of ZnONPs and K+ . It is proposed that K+ interaction with nanoparticles can be exploited at molecular level to understand the mechanisms involved in abiotic stress tolerance.

Synergistic Effect of Zinc Oxide Nanoparticles and Moringa oleifera Leaf Extract Alleviates Cadmium Toxicity in Linum usitatissimum: Antioxidants and Physiochemical Studies.

Among heavy metals, cadmium (Cd) is one of the toxic metals, which significantly reduce the growth of plants even at a low concentration. Cd interacts with various plant mechanisms at the physiological and antioxidant levels, resulting in decreased plant growth. This research was conducted to exploit the potential of synergistic application of zinc oxide nanoparticles (ZnO NPs) and Moringa oleifera leaf extract in mitigation of Cd stress in linseed (Linum usitatissimum L.) plants. The main aim of this study was to exploit the role of M. oleifera leaf extract and ZnO NPs on Cd-exposed linseed plants. Cd concentrations in the root and shoot of linseed plants decreased after administration of MZnO NPs. Growth parameters of plants, antioxidant system, and physiochemical parameters decreased as the external Cd level increased. The administration of MZnO NPs to the Cd-stressed linseed plant resulted in a significant increase in growth and antioxidant enzymes. Furthermore, the antioxidative enzymes superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX) exhibited a considerable increase in the activity when MZnO NPs were applied to Cd-stressed seedlings. The introduction of MZnO NPs lowered the levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2) in the linseed plant grown in Cd-toxic conditions. The NPs decreased electrolyte leakage (EL) in Cd-stressed linseed leaves and roots. It was concluded that synergistic application of ZnO NPs and M. oleifera leaf extract alleviated Cd stress in linseed plants through enhanced activity of antioxidant enzymes. It is proposed that role of MZnO NPs may be evaluated for mitigation of numerous abiotic stresses.

Assessment of anoxia tolerance and photoperiod dependence of GABAergic polarity in the pond snail Lymnaea stagnalis.

The pond snail Lymnaea stagnalis is reported to be anoxia-tolerant and if the tolerance mechanism is similar to that of the anoxia-tolerant painted turtle, GABA should play an important role. A potentially confounding factor investigating the role of GABA in anoxia tolerance are reports that GABA has both inhibitory and excitatory effects within L. stagnalis central ganglion. We therefore set out to determine if seasonality or photoperiod has an impact on: 1) the anoxia-tolerance of the intact pond snail, and 2) the response of isolated neuroganglia cluster F neurons to exogenous GABA application. L. stagnalis maintained on a natural summer light cycle were unable to survive any period of anoxic exposure, while those maintained on a natural winter light cycle survived a maximum of 4h. Using intracellular sharp electrode recordings from pedal ganglia cluster F neurons we show that there is a photoperiod dependent shift in the response to GABA. Snails exposed to a 16h:8h light:dark cycle in an environmental chamber (induced summer phenotype) exhibited hyperpolarizing inhibitory responses and those exposed to a 8h:16h light:dark cycle (induced winter phenotype) exhibited depolarizing excitatory responses to GABA application. Using gramicidin-perforated patch recordings we also found a photoperiod dependent shift in the reversal potential for GABA. We conclude that the opposing responses of L. stagnalis central neurons to GABA results from a shift in intracellular chloride concentration that is photoperiod dependent and is likely mediated through the relative efficacy of cation chloride co-transporters. Although the physiological ramifications of the photoperiod dependent shift are unknown this work potentially has important implications for the impact of artificial light pollution on animal health.

The cellular mechanisms of neuronal swelling underlying cytotoxic edema.

Cytotoxic brain edema triggered by neuronal swelling is the chief cause of mortality following brain trauma and cerebral infarct. Using fluorescence lifetime imaging to analyze contributions of intracellular ionic changes in brain slices, we find that intense Na(+) entry triggers a secondary increase in intracellular Cl(-) that is required for neuronal swelling and death. Pharmacological and siRNA-mediated knockdown screening identified the ion exchanger SLC26A11 unexpectedly acting as a voltage-gated Cl(-) channel that is activated upon neuronal depolarization to membrane potentials lower than -20 mV. Blockade of SLC26A11 activity attenuates both neuronal swelling and cell death. Therefore cytotoxic neuronal edema occurs when sufficient Na(+) influx and depolarization is followed by Cl(-) entry via SLC26A11. The resultant NaCl accumulation causes subsequent neuronal swelling leading to neuronal death. These findings shed light on unique elements of volume control in excitable cells and lay the ground for the development of specific treatments for brain edema.

Microglial CR3 activation triggers long-term synaptic depression in the hippocampus via NADPH oxidase.

Complement receptor 3 (CR3) activation in microglia is involved in neuroinflammation-related brain disorders and pruning of neuronal synapses. Hypoxia, often observed together with neuroinflammation in brain trauma, stroke, and neurodegenerative diseases, is thought to exacerbate inflammatory responses and synergistically enhance brain damage. Here we show that when hypoxia and an inflammatory stimulus (lipopolysaccharide [LPS]) are combined, they act synergistically to trigger long-term synaptic depression (LTD) that requires microglial CR3, activation of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), and GluA2-mediated A-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) internalization. Microglial CR3-triggered LTD is independent of N-methyl-D-aspartate receptors (NMDARs), metabotropic glutamate receptors (mGluRs), or patterned synaptic activity. This type of LTD may contribute to memory impairments and synaptic disruptions in neuroinflammation-related brain disorders.

Regenerative glutamate release by presynaptic NMDA receptors contributes to spreading depression.

Spreading depression (SD) is a slowly propagating neuronal depolarization that underlies certain neurologic conditions. The wave-like pattern of its propagation suggests that SD arises from an unusual form of neuronal communication. We used enzyme-based glutamate electrodes to show that during SD induced by transiently raising extracellular K(+) concentrations ([K(+)]o) in rat brain slices, there was a rapid increase in the extracellular glutamate concentration that required vesicular exocytosis but unlike fast synaptic transmission, still occurred when voltage-gated sodium and calcium channels (VGSC and VGCC) were blocked. Instead, presynaptic N-methyl-D-aspartate (NMDA) receptors (NMDARs) were activated during SD and could generate substantial glutamate release to support regenerative glutamate release and propagating waves when VGSCs and VGCCs were blocked. In calcium-free solutions, high [K(+)]o still triggered SD-like waves and glutamate efflux. Under such a condition, glutamate release was blocked by mitochondrial Na(+)/Ca(2+) exchanger inhibitors that likely blocked calcium release from mitochondria secondary to NMDA-induced Na(+) influx. Therefore presynaptic NMDA receptor activation is sufficient for triggering vesicular glutamate release during SD via both calcium entry and release from mitochondria by mitochondrial Na(+)/Ca(2+) exchanger. Our observations suggest that presynaptic NMDARs contribute to a cycle of glutamate-induced glutamate release that mediate high [K(+)]o-triggered SD.

Adenosinergic modulation of neuronal activity in the pond snail Lymnaea stagnalis.

Adenosine has been termed a retaliatory metabolite and its neuroprotective effects have been implicated in the hypoxia tolerance of several species; however, its role in the invertebrate CNS remains unclear. To determine if adenosine modulates neuronal activity in invertebrate neurons, we conducted whole-cell recordings from neurons in the central ring ganglia of the anoxia-tolerant pond snail Lymnaea stagnalis during exposure to adenosine and pharmacological compounds known to modulate the type I subclass of adenosine receptors (A(1)R). Action potential (AP) frequency and membrane potential (V(m)) were unchanged under control conditions, and addition of adenosine decreased AP frequency by 47% (from 1.08+/-0.22 to 0.57+/-0.14 Hz) and caused significant hyperpolarization of V(m). The A(1)R agonist cyclopentyladenosine (CPA) mimicked the results obtained with adenosine whereas antagonism of the A(1)R with 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) had no effect on AP frequency or V(m) but prevented the adenosine and CPA-mediated decreases in neuronal activity. Furthermore, Ca(2+) measurements with fluo-4 revealed that A(1)R activation led to a 12% increase in intracellular Ca(2+) concentration and this elevation was also antagonized by DPCPX. Our results suggest that adenosine acting via the adenosine receptor (type I subclass) depresses neuronal activity in the adult L. stagnalis CNS and this depression is correlated with an increase in cytosolic Ca(2+) levels.