Age of Bottle Cessation and BMI-for-Age Percentile among Children Aged Thirty-Six Months Participating in WIC.

Background: Children's age at bottle weaning typically ranges from 12 to 24 months. The recommended age of bottle weaning varies. The American Academy of Pediatrics recommends weaning by 12 months; The American Academy of Pediatric Dentistry recommends 12-15 months; The US Department of Agriculture recommends 18 months. Prolonged bottle use is associated with dental caries, iron-deficiency anemia, and child overweight or obesity. We examined factors associated with age of bottle cessation, and the association between age of bottle cessation and BMI-for-age percentile at age 36 months among Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) participants. Methods: Data were from the WIC Infant and Toddler Feeding Practices Study-2 (ITFPS-2). The ITFPS-2, a longitudinal study of WIC participants (mothers and their children) began in 2013. We used Cox proportional hazards models to identify factors associated with bottle cessation and multivariate linear regression to examine the association between age of bottle cessation and BMI. Results: About 34% of children used a bottle longer than 12 months, and 13% longer than 18 months. Bottle cessation at older ages was associated with Hispanic ethnicity, multiparity, low income, low education, higher caregiver weight, and not initiating breastfeeding. The adjusted children's BMI-for-age percentile at age 36 months increased by 0.47 for each additional month of bottle use. Conclusion: Prolonged bottle use was associated with increased children's BMI-for-age percentile. Future research is warranted to determine the optimal age to recommend bottle cessation for WIC participants.

Suggesting 7,8-dihydroxyflavone as a promising nutraceutical against CNS disorders.

7,8-dihydroxyflavone (DHF), a naturally-occurring plant-based flavone, is a high-affinity tyrosine kinase receptor B (TrkB) agonist and a bioactive molecule of therapeutic interest for neuronal survival, differentiation, synaptic plasticity and neurogenesis. In the family of neurotrophic factors, this small BDNF-mimetic molecule has attracted considerable attention due to its oral bioavailability and ability to cross the blood-brain barrier. Recent evidences have shed light on the neuroprotective role of this pleiotropic flavone against several neurological disorders, including Alzheimer's disease, Parkinson's disease, cerebral ischemia, Huntington's disease, and other CNS disorders. DHF also elicits potent protective actions against toxins-induced insults to brain and neuronal cells. DHF shows promising anti-oxidant and anti-inflammatory properties in ameliorating the neurodegenerative processes affecting the CNS. This review provides an overview of the significant neuroprotective potentials of DHF and discusses how it exerts its multitudinous beneficial effects by modulating different pathways linked with the pathophysiology of CNS disorders, and thus proposes it to be a nutraceutical against a broad spectrum of neurological disorders.

Lycopene - A pleiotropic neuroprotective nutraceutical: Deciphering its therapeutic potentials in broad spectrum neurological disorders.

Lycopene is a naturally occurring carotenoid found abundantly in red fruits and vegetables. Myriads of literature documented potential health benefits of lycopene, owing to its sublime capacity of suppressing oxidative stress, inflammation, and modulation of various cell survival pathways. Due to its lipophilic nature, lycopene can reach brain adequately by traversing the blood-brain barrier thereby extending it's promising therapeutic benefits in neurological disorders. Lycopene efficiently assists in restoring the characteristic behavioural and pathophysiological changes associated with neurodegenerative disorders, epileptic conditions, aging, subarachnoid hemorrhage, spinal cord injury, and neuropathy. The detrimental impacts of environmental neurotoxins on brain and neuropathological consequences of consumption of high-lipid diet can also be mitigated by lycopene. Apart from its high antioxidant potency, lycopene confers neuroprotection by preventing proteinopathies, neuroinflammation, apoptosis, cerebral edema, and synaptic dysfunction. This review provides a lucid idea on the potential multi-faceted benefits of lycopene in disorders of the central nervous system and elucidates the molecular mechanisms and pathways of its action.

Natural Products and Their Therapeutic Effect on Autism Spectrum Disorder.

Autism is a complex neurodevelopmental disorder that is evident in early childhood and can persist throughout the entire life. The disease is basically characterized by hurdles in social interaction where the individuals demonstrate repetitive and stereotyped interests or patterns of behavior. A wide number of neuroanatomical studies with autistic patients revealed alterations in brain development which lead to diverse cellular and anatomical processes including atypical neurogenesis, neuronal migration, maturation, differentiation, and degeneration. Special education programs, speech and language therapy, have been employed for the amelioration of behavioral deficits in autism. Although commonly prescribed antidepressants, antipsychotics, anticonvulsants, and stimulants have revealed satisfactory responses in autistic individuals, adverse side effects and increased risk of several other complications including obesity, dyslipidemia, diabetes mellitus, thyroid disorders, etc. have compelled the researchers to turn their attention toward herbal remedies. Alternative approaches with natural compounds are on continuous clinical trial to confirm their efficacy and to understand their potential in autism treatment. This chapter aims to cover the major plant-based natural products which hold promising outcomes in the field of reliable therapeutic interventions for autism.

Neuroprotective attributes of L-theanine, a bioactive amino acid of tea, and its potential role in Parkinson's disease therapeutics.

Meta-analyses of tea consumption and reduced risk of Parkinson's disease have thrown light in the pathway of exploring beneficial properties of tea components. On the basis of dry mass, a typical black or green tea beverage contains approximately 6% of free amino acids, which impart high quality, taste and distinctive aroma to the tea infusion. L-theanine (chemically known as γ-glutamylethylamide) is a non-proteinogenic amino acid of tea that takes part in the biosynthesis of its polyphenols. Recently discovered neuroprotective effects of L-theanine can be attributed to its structural analogy with glutamate, the principal excitatory neurotransmitter in brain. This unique amino acid also bears a potential to ameliorate the pathophysiological changes associated with Parkinson's disease as it displays antioxidant and anti-inflammatory properties, improves motor behavioral abnormalities, increases dopamine availability and may cause a favorable downshift in neurodegeneration due to glutamate excitotoxicity. To gain an explicit understanding of the role of L-theanine, this review article is the first one to focus on its mechanism of neuromodulatory action and to critically evaluate the possibilities of employing this bioactive amide in the forage of anti-Parkinsonian medication. We also hypothesize the idea of L-theanine being a potent natural agent against L-DOPA induced dyskinesia, since long-term reliance on dopamine replacement therapy is linked with elevation in glutamate receptor activity.

Garcinol, a multifaceted sword for the treatment of Parkinson's disease.

Garcinol, the principal phytoconstituent of plants belonging to the genus Garcinia, is known for its anti-oxidant as well as anti-inflammatory properties, which can be extended to its possible neuroprotective role. Recent reports disseminate the capacity of garcinol to influence neuronal growth and survival, alter the neurochemical status in brain, as well as regulate memory and cognition. The concomitant neuro-rescue property of garcinol may render it as an effective compound in Parkinson's disease (PD) therapeutics since it is capable of ameliorating the related pathophysiological changes. Emerging pieces of evidence linking histone acetylation defects to the progression of neurodegenerative diseases provide an effective basis for targeting PD. Hyperacetylation of histones has been reported in Parkinsonian brain, which demands the use of pharmacological inhibitors of histone acetyltransferases (HAT). Garcinol serves as a potent natural HAT inhibitor and has unveiled promising results in molecular interaction studies against Monoamine oxidase B (MAO-B) and Catechol-O-Methyltransferase (COMT), as well as in L-DOPA induced dyskinesia. This review highlights the prospective implications of garcinol as a novel anti-Parkinsonian agent, and establishes a bridge between histone acetylation defects and the pathological aspects of PD.

Garcinol, an effective monoamine oxidase-B inhibitor for the treatment of Parkinson's disease.

Loss of dopamine containing neurons in the substantia nigra pars compacta of midbrain, and resultant depletion of dopamine in the striatum is the cause of Parkinson's disease (PD), which is associated with motor abnormalities. Replenishment of dopamine by oral supplementation of its precursor, the levodopa (L-DOPA), remains the primary mode of treatment of PD, despite its potential side-effects after prolonged use in patients. To reduce the daily dosing of L-DOPA in patients, inhibitors of dopamine catabolizing enzymes, particularly monoamine oxidase-B (MAO-B), are prescribed. The most widely used MAO-B inhibitor to maintain the bioavailability of dopamine in the brain of PD patients is L-deprenyl, despite of its potential side-effects. The present study identified Garcinol as a potential candidate in the treatment paradigm of PD by virtue of its exorbitant MAO-B inhibitory potential. The inhibitory potential is comparable to the known MAO-B inhibitors, which was evaluated using molecular docking technique. Owing to its known antioxidant, anti-inflammatory and catechol-o-methyl transferase inhibitory potential, the molecule would confer neuroprotection as well, and thus, the present study is of immense significance in the treatment paradigm of PD.

Neuroprotective potential of silymarin against CNS disorders: insight into the pathways and molecular mechanisms of action.

Silymarin, a C25 containing flavonoid from the plant Silybum marianum, has been the gold standard drug to treat liver disorders associated with alcohol consumption, acute and chronic viral hepatitis, and toxin-induced hepatic failures since its discovery in 1960. Apart from the hepatoprotective nature, which is mainly due to its antioxidant and tissue regenerative properties, Silymarin has recently been reported to be a putative neuroprotective agent against many neurologic diseases including Alzheimer's and Parkinson's diseases, and cerebral ischemia. Although the underlying neuroprotective mechanism of Silymarin is believed to be due to its capacity to inhibit oxidative stress in the brain, it also confers additional advantages by influencing pathways such as ß-amyloid aggregation, inflammatory mechanisms, cellular apoptotic machinery, and estrogenic receptor mediation. In this review, we have elucidated the possible neuroprotective effects of Silymarin and the underlying molecular events, and suggested future courses of action for its acceptance as a CNS drug for the treatment of neurodegenerative diseases.

Novel middle-type Kenyon cells in the honeybee brain revealed by area-preferential gene expression analysis.

The mushroom bodies (a higher center) of the honeybee (Apis mellifera L) brain were considered to comprise three types of intrinsic neurons, including large- and small-type Kenyon cells that have distinct gene expression profiles. Although previous neural activity mapping using the immediate early gene kakusei suggested that small-type Kenyon cells are mainly active in forager brains, the precise Kenyon cell types that are active in the forager brain remain to be elucidated. We searched for novel gene(s) that are expressed in an area-preferential manner in the honeybee brain. By identifying and analyzing expression of a gene that we termed mKast (middle-type Kenyon cell-preferential arrestin-related protein), we discovered novel 'middle-type Kenyon cells' that are sandwiched between large- and small-type Kenyon cells and have a gene expression profile almost complementary to those of large- and small-type Kenyon cells. Expression analysis of kakusei revealed that both small-type Kenyon cells and some middle-type Kenyon cells are active in the forager brains, suggesting their possible involvement in information processing during the foraging flight. mKast expression began after the differentiation of small- and large-type Kenyon cells during metamorphosis, suggesting that middle-type Kenyon cells differentiate by modifying some characteristics of large- and/or small-type Kenyon cells. Interestingly, CaMKII and mKast, marker genes for large- and middle-type Kenyon cells, respectively, were preferentially expressed in a distinct set of optic lobe (a visual center) neurons. Our findings suggested that it is not simply the Kenyon cell-preferential gene expression profiles, rather, a 'clustering' of neurons with similar gene expression profiles as particular Kenyon cell types that characterize the honeybee mushroom body structure.

SHP-2 tyrosine phosphatase inhibits p73-dependent apoptosis and expression of a subset of p53 target genes induced by EGCG.

Green tea polyphenol, epigallocatechin-3-gallate (EGCG) differentially regulates the cellular growth of cancer cells in a p53-dependent manner through apoptosis and/or cell cycle arrest. In an effort to further elucidate the mechanism of differential growth regulation by EGCG, we have investigated the role of the tyrosine phosphatase, SHP-2. Comparing the responses of mouse embryonic fibroblasts (MEFs), expressing either WT or functionally inactive/truncated SHP-2, we find that inactivation of SHP-2 remarkably sensitizes cells to EGCG-mediated killing. MEFs lacking functional SHP-2 undergo massive apoptosis upon treatment with EGCG. By comparing gene expression profiles, we have identified a set of transcriptional targets of p53 that are differentially modulated in cells undergoing apoptosis. Western blot and real-time PCR analyses of a select group of genes further confirm that the expression is SHP-2-dependent. Similar observations were made in MEFs lacking p53, confirming that the expression of these "p53 target genes" is p53-independent. In addition, EGCG treatment induced the expression of p73 mRNA and protein in both cell types, but not p63. Inactivation of p73 in cells expressing nonfunctional SHP-2 markedly inhibited apoptosis and p53 target gene expression. Although phosphorylation of JNK is differentially regulated by SHP2, it was found to be dispensable for EGCG-induced apoptosis and p53 target gene expression. Our results have identified SHP-2 as a negative regulator of EGCG-induced-apoptosis and have identified a subset of p53 target genes whose expression is paradoxically not mediated by p53 but by one of its family members, p73.