Publications by authors named "Tripti Halder"

Purpose: The current study was conducted to develop and evaluate sialic acid grafted cationic myricetin (MY) fabricated nanostructured lipid carrier (Sia-Cat-MY-NLC) for Alzheimer's disease (AD) management.

Methods: In-vitro amyloid beta aggregation inhibition and mitochondrial membrane potential of prepared NLCs were observed in SH-SY5Y cells. The transendothelial electrical resistance was measured through hCMEC/D3 cells.

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Biodegradable polymers, encompassing both natural and synthetic polymers, have demonstrated efficacy as carriers for synthetic drugs, natural bioactive molecules, and inorganic metals. This is due to their ability to control the release of these substances. As a result, various advanced materials, such as nanoparticle- loaded hydrogels, nanofibrous scaffolds, and nanocomposites, have been developed.

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Early mortality in sickle cell disease (SCD) is attributed to increased infections due to loss of splenic function. Marginal zone B cells are important for initial opsonization of pathogens and can be absent in spleen histopathology in SCD. The frequency of unswitched memory B cells (UMBC), the circulating correlate of marginal zone B cells, reflects the immunologic function of the spleen.

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Sialic acid (SA) serves a critical role in neuronal repair and cognitive functions. SA is a nine-carbon carboxylated sugar with a glycoconjugate cap that acts as a ligand and surface decoration with SA facilitates delivery to the target site. The present research aimed to develop SA surface modified AA nanostructured lipid carrier (NLCs) with carbodiimide conjugation method.

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Objectives: Preterm infants are born functionally pancreatic insufficient with decreased pancreatic production of lipase and proteases. Developmental pancreatic insufficiency (PI) may contribute to reduced nutrient absorption and growth failure. We sought to determine longitudinal fecal elastase (ELA1) levels in a cohort of preterm infants and whether levels are associated with growth outcomes.

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Article Synopsis
  • Asiatic acid (AA)
  • has potential neuroprotective effects against Alzheimer’s disease, and this study aimed to enhance its delivery to the brain using nanostructured lipid carriers (AAN).
  • Methodology
  • involved optimizing AAN through various factors affecting particle size, stability, and efficiency, followed by testing its effectiveness in protecting neurons and improving cognitive function in Alzheimer's model rats.
  • Results
  • showed that AAN had significantly improved targeting and neuroprotective capabilities compared to standard AA, and effectively reduced cognitive deficits in the AD model, suggesting its potential for further development in treating the disease.
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Aims: This research aimed to evaluate the potential of MY loaded nanostructured lipid carrier (MY-NLCs) to ameliorate the bioavailability in the brain and cognitive impairment in Aβ induced Alzheimer''s model.

Materials And Methods: MY-NLCs were prepared with precirol ATO 5, labrafac lipophile WL 1349, and tween 80 as solid lipid, liquid lipid, and surfactant respectively. The formulation was optimized with central composite design (CCD) and characterized by different parameters.

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Liver dysfunction, including coagulopathy, is a prominent feature of protein-energy malnutrition. To identify mechanisms underlying malnutrition-associated coagulopathy, we administered a low-protein low-fat diet to lactating dams and examined hepatic transcription and plasma coagulation parameters in young adult weanlings. Malnutrition impacted body composition to a greater extent in male versus female mice.

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Background: Slow gastrointestinal (GI) transit occurs in moderate-to-severe malnutrition. Mechanisms underlying malnutrition-associated dysmotility remain unknown, partially due to lack of animal models. This study sought to characterize GI dysmotility in mouse models of malnutrition.

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Background: An important limitation of gastrointestinal motility testing is high variability. Conditions that could contribute to variability, including the duration of pretest fasting and time of day, are rarely reported and have not been examined systematically. This study aimed to explore whether these conditions, as well as age, sex, and strain of mice, affect the results of a standard laboratory test of upper gastrointestinal motility.

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During aging, decreases in energy expenditure and locomotor activity lead to body weight and fat gain. Aging is also associated with decreases in muscle strength and endurance leading to functional decline. Here, we show that lifelong deletion of ghrelin prevents development of obesity associated with aging by modulating food intake and energy expenditure.

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Background: Cachexia and muscle atrophy are common consequences of cancer and chemotherapy administration. The novel hormone ghrelin has been proposed as a treatment for this condition. Increases in food intake and direct effects on muscle proteolysis and protein synthesis are likely to mediate these effects, but the pathways leading to these events are not well understood.

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Objectives: To identify novel approaches to improve innate immunity in the lung following trauma complicated by hemorrhagic shock (T/HS) for prevention of nosocomial pneumonia.

Methods: We developed a rat model of T/HS followed by Pseudomonas aeruginosa (PA) pneumonia to assess the effect of alveolar epithelial cell (AEC) apoptosis, and its prevention by IL-6, on lung surfactant protein (SP)-D protein levels, lung bacterial burden, and survival from PA pneumonia, as well as to determine whether AEC apoptosis is a consequence of the unfolded protein response (UPR). Lung UPR transcriptome analysis was performed on rats subjected to sham, T/HS, and T/HS plus IL-6 protocols.

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Cardiac hypertrophy, a major determinant of morbidity and mortality in hypertrophic cardiomyopathy (HCM), is considered a secondary phenotype and potentially preventable. To test this hypothesis, we screened 30 5- to 6-month-old beta-myosin heavy chain Q403 transgenic rabbits by echocardiography and selected 26 without cardiac hypertrophy. We randomized the transgenic rabbits to treatment with atorvastatin (2.

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