Simeon Ikechukwu Egba

The accumulation of non‐biodegradable plastics is driving the search for environmentally friendly, low‐cost alternatives. This study investigated the production of biodegradable bioplastics using starch extracted from Ipomoea batatas and Manihot esculenta tubers. The tubers were pulverized, and starch was extracted. Bioplastic was produced by reacting the starch with ethanoic, methanoic, and propanoic acids in the presence of glycerol and water at 80°C for 25 min. The starch yield and the physicochemical, mechanical, and degradability properties of the bioplastics were determined. The results showed starch yields (57.5%; 52.26%), moisture content (12.38%; 13.74%), pH (6.9; 6.7), amylose content (20.4%; 20.67%) and amylopectin content (79.6%; 80.2%) for Ipomoea batatas and Manihot esculenta tubers, respectively. The mass of bioplastic produced was directly proportional to starch content and the number of carbon chains present in the organic acid. The mechanical properties showed that tensile strength was significantly ( p < 0.05) higher than that of the control, except for the 15 g bioplastic produced. Shear strength also showed a trend similar to tensile strength. The elongation/break properties significantly ( p < 0.05) increased in the methanoic acid‐derived bioplastic. The bioplastic degradation rates were (0.0059, 0.0056 and 0.0043 mg/ml/h) for Ipomoea batatas and (0.0099, 0.0098 and 0.0091 mg/ml/h) for Manihot esculenta‐derived biodegradable plastic, respectively , using Pseudomonas aeruginosa . The results of this study show that starches from Ipomoea batata and Manihot esculenta tubers could be a good source for bioplastic production because they are inexpensive, renewable, and readily biodegradable when disposed of in the environment.

Sickle cell disease (SCD) is a hereditary haemoglobin abnormality due to a point mutation in the β-globin gene resulting in the production of haemoglobin S. Polymerization of deoxygenated hemoglobin S results in red cell sickling, hemolysis, endothelial injury, ischemia-reperfusion damage, vaso-occlusion, and, in addition to being a hemolytic anaemia and vaso-occlusive condition, SCD is now considered a chronic inflammatory disease with significant immunological abnormalities. This review explores the pathophysiological and immunological basis of SCD, with particular emphasis on how hemolysis, inflammation, innate and adaptive immunity, vulnerability to infection and their implications for current and emerging therapeutics. SCD is characterised by sustained innate and adaptive immune responses, including leukocytosis; neutrophil and monocyte activation; changes in cytokine profiles; complement activation; and T- and B-cell dysfunction. Danger-associated molecular patterns released during hemolysis, including activate inflammasomes, oxidative stress, and endothelial dysfunction through toll-like receptors. Repeat vaso-occlusion maintains sterile inflammation and facilitates coagulation, immune regulation, and vascular damage. Also present are functional asplenia and defective humoral immunity, which predisposes to infection, particularly that caused by encapsulated bacteria. These disruptions help cause vaso-occlusive crises, acute chest syndrome, stroke, pulmonary hypertension, leg ulcers, nephropathy and long-term organ damage. Immunological dysregulation lies at the core of the pathophysiology and complications of SCD. A more detailed understanding of the immune landscape can enhance disease management and inform treatment, including drug administration, transfusion, hematopoietic stem cell transplantation, and gene-based therapies.

This study examines the role and function of the specific signaling molecules that are associated with the binding of sex hormone receptors, including estrogen receptor (ER) and progesterone receptor (PR), in relation to cell proliferation, differentiation, and survival. The present work focuses on the mutual relationship between signaling pathways of sex hormone receptors and MAPK and PI3K/AKT pathways, as well as the involvement of these molecules in the development of breast cancer. The review systemizes the present knowledge regarding genetic changes related to breast cancer, including the effects of changes on sex hormone signaling, biochemical pathways influencing sex hormone availability, and epigenetic modifications. The focus is made on genetic changes the researchers observed in breast cancer, like ERBB2/HER2 amplification and TP53 mutations, which cooperate with sex hormone signaling to advance tumor growth. The changes in the metabolism of sex hormones are as follows: High aromatase leading to high estrogen and more. Furthermore, the impact of sex steroids on the tumor microenvironment, including angiogenesis, immune regulation, and matrix, is consequently discussed. The effects of sex hormones on DNA methylation, histone modifications, and noncoding RNA with regard to breast cancer development are reviewed. The study also demonstrates how genetic changes, metabolism, and epigenetics work in concert with sex hormones to modulate breast cancer development. SERMs, aromatase inhibitors, and the endocrine approach are described, as well as novel directions to develop inhibitors of androgen and other hormone signaling pathways.

Multiple sclerosis (MS) is a chronic autoimmune disorder of CNS with demyelination, neurodegeneration and compartmentalized inflammatory disorder. Excessive T-helper cell (CD4⁺) activation and unregulated cytokine signaling play a key role in its onset and progression. These changes impair communication between peripheral immune cells and CNS resident microglia, astrocytes and oligodendrocytes. This review provides an overview on the contribution of specific subsets of T-helper cells to MS pathology/immunity. Th1 cells release interferon-γ and lymphotoxin, that stimulate activation of myeloid cells/antigen presentation. Activated by IL-23, the Th17 cells produce IL-17A/F that lowers the blood–brain barrier (BBB) integrity, recruit neutrophils and monocytes, and enhance microglial killing. Activation of CD4⁺ T cells leads to activation of B cells via T follicular helper cells which couple these processes through the production of IL-21 and CXCR5. This leads to the development of tissue-like aggregates and intrathecal antibody production. T-cell plasticity adds to epitope spreading as well as chronic inflammation, IL-22, IL-9, IL-1β, IL-6, and TGF-β (these are additional mediators involved in the regulation of effector phenotypes). In MS, the regulation of dendritic cell co-stimulation and of glial activation often does not work. This is due to the lack of control of dendritic-cells co-stimulation and the lack of regulation of glial activation by regulatory pathways such as FOXP3⁺ regulatory T cells and Tr1 cells that secrete IL-10 and TGF-Beta. The review also explores the cytokine network biomarkers, CSF and serum signatures and single-cell immune states, as well as existing and new drugs. These include migration blockade, targeting of S1P-receptors, anti-CD20 therapy, targeting of Th17/GM-CSF and JAK–STAT pathways, low-dose IL-2, approaches of targeting antigens and engineered Tregs. Investigating the areas of stage and compartment-specific CD4⁺ T-cell circuits can help to advance targeted immunomodulation in progressive MS and neuro-repair.

Objectives: To evaluate the therapeutic potential of Uvaria chamae extracts in mitigating paracetamol-induced hepatic injury in rats. Methods: Rats were administered paracetamol to induce hepatic toxicity and subsequently treated with Uvaria chamae extracts. Biochemical markers of liver and kidney function, oxidative stress, and lipid profile were measured. Antioxidant enzyme activities and electrolyte levels were also assessed. Liver tissues were examined histologically to evaluate structural integrity. Results: Treatment with Uvaria chamae extracts produced significant reductions ( p < 0.05) in markers of hepatic and renal injury, including AST, ALT, ALP, GGT, MDA, total and direct bilirubin, total cholesterol, LDL, TAG, urea, and creatinine. Treated groups also showed a significant decrease in final body weight compared with the induced but untreated group. Antioxidant parameters—including SOD, catalase, and GPx—were significantly elevated ( p < 0.05). Total protein, albumin, HDL, and potassium levels also increased following treatment. Histological examination revealed normal liver architecture in treated groups, with no observed lesions. Conclusions: Uvaria chamae extracts ameliorated biochemical and structural indicators of paracetamol-induced hepatic injury in rats. These findings support its potential as a therapeutic candidate for liver damage associated with paracetamol toxicity.

Rheumatoid factor (RF), which is an autoantibody that is predominantly targeted at the Fc region in IgG, has been a key point of diagnosis and prognostication of rheumatoid arthritis (RA). There is, however, an emergent body of evidence that RF positivity, including in persons with preexisting autoimmune disease as well as asymptomatic seropositive persons, can indicate more global immune dysregulation with consequences of cardiometabolic and hepatic health. RF is involved in the development of circulating immune complexes, which increases inflammation through complement activation, Fc receptor interaction and cytokine release. These routes are becoming well-known mechanistic causes of cardiometabolic diseases, such as atherosclerosis, insulin resistance, metabolic syndrome, and heart failure. Similarly, the immune-complex deposition and chronic inflammatory signaling also play a role in hepatic injury, metabolic dysfunction-associated fatty liver disease (MAFLD) and fibrosis. The present review summarizes the existing information about the role of RF as a predictor and a possible mediator of cardiometabolic and hepatic dysfunction in chronic diseases. We searched scientific databases for epidemiologic relationships, possible biological pathways, and clinical implications for risk stratification and integrated care. RF could serve as an accessible biomarker of systemic inflammatory risk, complementing its traditional role in rheumatology and, within the framework of precision medicine, helping to guide early detection and preventive strategies across diverse clinical populations.

Background: This study explored the phytochemical composition, Gas Chromatography-Mass Spectrometry (GC-MS), Fourier Transform Infrared spectroscopy (FT-IR), and antioxidant properties of the crude methanol extract (CRUME) and its fractions from Uvaria chamae in search of potential hepatoprotective drug candidates. Methods: Qualitative and quantitative phytochemical analyses were performed on CRUME and its methanol (MEFUC), ethyl acetate (EAFUC), and dichloromethane (DIFUC) fractions. Antioxidant assays, including Thiobarbituric reacting substance (TBARS), 2,2-diphenyl-1-picrylhydrazyl (DPPH), ferric reducing antioxidant power (FRAP), and total antioxidant capacity (TAC), were conducted. FTIR analysis was used to identify functional groups, and GC-MS analysis identified bioactive compounds in the methanol fraction. Molecular docking and drug-likeness assessments were conducted to evaluate hepatoprotective potential and safety profiles. Results: Phytochemical screening revealed diverse classes in varying concentrations. Antioxidant assays showed maximum TBARS scavenging activity for CRUME (73.67 ± 4.16% at 250 µg/mL), DIFUC (91.67 ± 0.16% at 250 µg/mL), EAFUC (81.33 ± 0.16% at 125 µg/mL), and MEFUC (69.33 ± 0.58% at 500 µg/mL), comparable to BHT (74.33 ± 0.16% at 15.53 µg/mL). DPPH activity peaked at 500 µg/mL for CRUME (98.00 ± 0.70%), DIFUC (68.33 ± 2.08%), and EAFUC (61.67 ± 5.51%), while MEFUC showed peak activity at 15.53 µg/mL (89.33 ± 1.16%), similar to ascorbic acid (64.19 ± 1.34% at 31.25 µg/mL). FTIR revealed multiple functional groups; GC-MS identified 39 bioactive compounds. Docking studies highlighted 10 compounds with strong hepatoprotective potential. Drug-likeness and ADMET profiling indicated no signs of hepatotoxicity, immunotoxicity, cytotoxicity, or mutagenicity. Conclusion: The methanol leaf extract of Uvaria chamae and its fractions demonstrate potent antioxidant activities and contain bioactive compounds with significant potential as hepatoprotective drug candidates for the management of liver-related diseases.

The integration of phytochemicals with nanotechnology represents a promising approach to enhance nasal drug delivery, improving therapeutic efficacy and targeted brain delivery. This review explores recent advances in phytochemical–nanotechnology formulations and their applications in managing neurodegenerative diseases, respiratory disorders, and cancers. Phytochemicals such as curcumin, resveratrol, and quercetin exhibit potent pharmacological properties but suffer from poor solubility and limited bioavailability. Nanotechnology-based systems-including nanoparticles, liposomes, and nanoemulsions-overcome these drawbacks by improving stability, absorption, and controlled release. However, challenges such as nasal mucosa irritation, formulation complexity, regulatory barriers, and scalability still impede clinical translation. Notably, encapsulation of curcumin in polymeric nanoparticles has been shown to enhance its solubility and bioavailability, producing improved therapeutic outcomes in preclinical Alzheimer’s models. Overall, this review underscores the synergistic potential of phytochemicals and nanotechnology in developing innovative nasal delivery platforms capable of providing targeted, effective, and patient-friendly treatment options for a range of medical conditions.