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The development of orally administered protein drugs is challenging due to their intrinsic unfavourable features, including large molecular size and poor chemical stability, both of which limit gastrointestinal (GI) absorption efficiency. Nanoparticles can overcome the GI barriers effectively and improve the oral bioavailability of proteins in the GI tract. They possess large surface area to volume ratio, and can facilitate the GI absorption of nanoparticles via the paracellular and transcellular routes. Nanoparticles can be prepared by various fabrication techniques that can encapsulate the fragile therapeutic proteins via hydrophobic bonding and electrostatic interaction. A desirable technique should involve minimal harsh conditions and encapsulate therapeutic proteins with preserved functionalities. The current review examines the characteristics of each preparation technique, and illustrates the examples of insulin-loaded nanoparticles that have been developed in each fabrication method. The following techniques, which include nanoprecipitation, hydrophobic conjugation, flash nanocomplexation, double emulsion, ionotropic gelation, and layer-by-layer adsorption, have been used to formulate ligand-modified nanoparticles for targeted delivery of insulin. Other techniques, including reduction, complex coacervation (polyelectrolyte complexation), hydrophobic ion pairing and emulsion solvent diffusion method, and sol-gel technology, were also discussed in the latter part of the review due to their extensive use in fabrication of insulin nanoparticles. This review also discusses the strategies that have been utilised during the formulation process to improve the stability and bioactivity of therapeutic proteins.

Normative values of common sport-related concussion assessment tools may assist clinical diagnosis and management. However, current baseline normative values are not representative of athletic participants across international domains. This study develops healthy baseline norms on the Balance Error Scoring System (BESS), and King-Devick (K-D), providing baseline reference values for professional Zambian football athletes.

Of the 125 male participants (aged 24.48±5.41years) screened for this study, 9 (7.2%) reported a previous history of concussion, 98 (78.4%) completed the Balance Error Scoring System and 88 (70.4%) completed the King-Devick. Descriptive statistics calculated for the BESS and the K-D test included mean, standard deviation, median, interquartile range (IQR), and percentiles ranks.

Participants scored a mean ± standard deviation of 10.15±5.6 and a median [IQR] of 9 [6-12.25] errors on the total BESS and completed the K-D test in a mean ± standard deviation 56.85±10.55seconds and a median related concussion assessment resources.Introduction Acquired thrombotic thrombocytopenic purpura (aTTP) is a thrombotic microangiopathy caused by inhibitory autoantibodies against ADAMTS13 protein. Until recently, the combination of plasma exchange (PEX) and immunosuppression has been the standard front-line treatment in this disorder. However, aTTP-related mortality, refractoriness, and relapse are still a matter of concern. Areas covered The better understanding of the pathophysiological mechanisms of aTTP has allowed substantial improvements in the diagnosis and treatment of this disease. Recently, the novel anti-VWF nanobody caplacizumab has been approved for acute episodes of aTTP. Caplacizumab is capable to block the adhesion of platelets to VWF, therefore inhibiting microthrombi formation in the ADAMTS13-deficient circulation. In this review, the characteristics of caplacizumab together with the available data of its efficacy and safety in the clinical setting will be analyzed. Besides, the current scenario of aTTP treatment will be provided, including the role of other innovative drugs. Expert opinion With no doubt, caplacizumab is going to change the way we treat aTTP. In combination with standard treatment, caplacizumab can help to significantly reduce aTTP-related mortality and morbidity and could spare potential long-term consequences by minimizing the risk of exacerbation.The current study aimed to develop alendronate (ALN)-loaded chitosan nanoparticles (CS-ALN-NPs) for brain delivery via intranasal route. These CS-ALN-NPs reduced the peripheral side effects and released ALN directly to brain. These NPs were formulated through ionic gelation technique by mixing sodium tripolyphosphate (1.5 mg/ml) in ALN-CS (1.75 mg/ml) solution. CS-ALN-NPs attained 135.75 ± 5.80 nm, 0.21 ± 0.013, 23.8 ± 3.69 mV, 72.46 ± 0.879% and 30.92 ± 0.375% mean particle size, PDI, zeta potential, entrapment efficiency and loading capacity, respectively. Furthermore, the TEM and SEM analysis of CS-ALN-NPs, respectively, revealed the particle size in 200 nm range and spherical shape. The in vitro and ex vivo release profile revealed a sustained drug release through CS-ALN-NPs as compared to pure drug solution. Also these NPs acquired a high concentration in mice brain and better pharmacokinetic profile than ALN solution (intranasal) CS-ALN-NPs were then evaluated against intracerebroventricular-streptozotocal parameters in mice hippocampus.MicroRNA-24 (miR-24) has been identified to be related to the development of glioma. However, the exact molecular mechanism of miR-24 in glioma progression remains vague. The aim of the present study was to investigate the role of miR-24 in sepsis and to reveal the associated mechanisms. Quantitative real-time polymerase chain reaction was used to compare the levels of miR-24 in glioma and normal tissue. click here The miR-24 inhibitor or miR-24 mimic was transfected into glioma cells, and then the effects of miR-24 on cell proliferation and apoptosis were detected using CCK-8 (Cell Counting Kit-8) assay and flow cytometry, respectively. Western blot was used to examine the levels of CDX1 (caudal-type homeobox 1), PI3K, p-PI3K, Akt, p-Akt, Cyclin D1, p27, proliferating cell nuclear antigen, Bcl-2, Bax, and Cleaved-casp3. Luciferase assay was used to identify the target gene of miR-24. An animal model was established in mice to detect the role of miR-24 in vivo. These results suggested that miR-24 was elevated in glioma, and miR-24 could promote glioma progression by facilitating cell proliferation and inducing cell apoptosis through CDX1/PI3K/Akt signaling pathway, indicating a novel pathway underlying progression in glioma cells and providing a potential target for glioma treatment.