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This study employs a mathematical model to analyze and forecast the severe outbreak of SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2), focusing on the socio-economic ramifications within the Thai population and among foreign tourists. Specifically, the model examines the impact of the disease on various population groups, including susceptible (S), exposed (E), infected (I), quarantined (Q), and recovered (R) individuals among tourists visiting the country. The stability theory of differential equations is utilized to validate the mathematical model. This involves assessing the stability of both the disease-free equilibrium and the endemic equilibrium using the basic reproduction number. Emphasis is placed on local stability, the positivity of solutions, and the invariant regions of solutions. Additionally, a sensitivity analysis of the model is conducted. The computation of the basic reproduction number (R0) reveals that the disease-free equilibrium is locally asymptotically stable when R0 is less than 1, whereas the endemic equilibrium is locally asymptotically stable when R0 exceeds 1. Notably, both equilibriums are globally asymptotically stable under the same conditions. Through numerical simulations, the study concludes that the outcome of COVID-19 is most sensitive to reductions in transmission rates. Furthermore, the sensitivity of the model to all parameters is thoroughly considered, informing strategies for disease control through various intervention measures.

In this paper, 100 nm-thick zinc oxide (ZnO) films were deposited as a seed layer on Corning glass substrates via a radio frequency (RF) magnetron sputtering technique, and vertical well-aligned Fe-doped ZnO (FZO) nanorod (NR) arrays were then grown on the seed layer-coated substrates via a low-temperature solution method. FZO NR arrays were annealed at 600 °C and characterized by using field emission scanning microscopy (FE-SEM) and X-ray diffraction spectrum (XRD) analysis. FZO NRs grew along the preferred (002) orientation with good crystal quality and hexagonal wurtzite structure. The main ultraviolet (UV) peak of 378 nm exhibited a red-shifted phenomenon with Fe-doping by photoluminescence (PL) emission. Furthermore, FZO photodetectors (PDs) based on metal–semiconductor–metal (MSM) structure were successfully manufactured through a photolithography procedure for UV detection. Results revealed that compared with pure ZnO NRs, FZO NRs exhibited a remarkable photosensitivity for UV PD applications and a fast rise/decay time. The sensitivities of prepared pure ZnO and FZO PDs were 43.1, and 471.1 for a 3 V applied bias and 380 nm UV illumination, respectively.

Dengue disease is found in tropical and subtropical regions around the world. Dengue virus is the cause of dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. It consists of 4 serotypes: DEN-1, DEN-2, DEN-3, and DEN-4. There are two modes of transmission for dengue virus in mosquito: horizontal transmission and vertical transmission. The mosquito can be infected when it bites an infectious human by horizontal transmission, but there can also be vertical transmission through sexual contact with an infected mosquito. This research presents a control mechanism based on our previously developed dengue model with vertical transmission. The two policies, namely vaccination and insecticide administration (Policy 1) and isolation and insecticide administration (Policy 2) are considered. The use of Pontryargin’s maximum principle allowed necessary and optimality conditions, thus facilitating the optimal control to be developed. Numerical solutions of our control systems and the conclusions of our two policies are presented.

Adjuvant radiotherapy has been shown to halve the risk of biochemical progression for patients with high-risk disease after radical prostatectomy. Early salvage radiotherapy could result in similar biochemical control with lower treatment toxicity. We aimed to compare biochemical progression between patients given adjuvant radiotherapy and those given salvage radiotherapy. We did a phase 3, randomised, controlled, non-inferiority trial across 32 oncology centres in Australia and New Zealand. Eligible patients were aged at least 18 years and had undergone a radical prostatectomy for adenocarcinoma of the prostate with pathological staging showing high-risk features defined as positive surgical margins, extraprostatic extension, or seminal vesicle invasion; had an Eastern Cooperative Oncology Group performance status of 0–1, and had a postoperative prostate-specific antigen (PSA) concentration of 0·10 ng/mL or less. Patients were randomly assigned (1:1) using a minimisation technique via an internet-based, independently generated allocation to either adjuvant radiotherapy within 6 months of radical prostatectomy or early salvage radiotherapy triggered by a PSA of 0·20 ng/mL or more. Allocation sequence was concealed from investigators and patients, but treatment assignment for individual randomisations was not masked. Patients were stratified by radiotherapy centre, preoperative PSA, Gleason score, surgical margin status, and seminal vesicle invasion status. Radiotherapy in both groups was 64 Gy in 32 fractions to the prostate bed without androgen deprivation therapy with real-time review of plan quality on all cases before treatment. The primary endpoint was freedom from biochemical progression. Salvage radiotherapy would be deemed non-inferior to adjuvant radiotherapy if freedom from biochemical progression at 5 years was within 10% of that for adjuvant radiotherapy with a hazard ratio (HR) for salvage radiotherapy versus adjuvant radiotherapy of 1·48. The primary analysis was done on an intention-to-treat basis. This study is registered with ClinicalTrials.gov, NCT00860652. Between March 27, 2009, and Dec 31, 2015, 333 patients were randomly assigned (166 to adjuvant radiotherapy; 167 to salvage radiotherapy). Median follow-up was 6·1 years (IQR 4·3–7·5). An independent data monitoring committee recommended premature closure of enrolment because of unexpectedly low event rates. 84 (50%) patients in the salvage radiotherapy group had radiotherapy triggered by a PSA of 0·20 ng/mL or more. 5-year freedom from biochemical progression was 86% (95% CI 81–92) in the adjuvant radiotherapy group versus 87% (82–93) in the salvage radiotherapy group (stratified HR 1·12, 95% CI 0·65–1·90; pnon-inferiority=0·15). The grade 2 or worse genitourinary toxicity rate was lower in the salvage radiotherapy group (90 [54%] of 167) than in the adjuvant radiotherapy group (116 [70%] of 166). The grade 2 or worse gastrointestinal toxicity rate was similar between the salvage radiotherapy group (16 [10%]) and the adjuvant radiotherapy group (24 [14%]). Salvage radiotherapy did not meet trial specified criteria for non-inferiority. However, these data support the use of salvage radiotherapy as it results in similar biochemical control to adjuvant radiotherapy, spares around half of men from pelvic radiation, and is associated with significantly lower genitourinary toxicity. New Zealand Health Research Council, Australian National Health Medical Research Council, Cancer Council Victoria, Cancer Council NSW, Auckland Hospital Charitable Trust, Trans-Tasman Radiation Oncology Group Seed Funding, Cancer Research Trust New Zealand, Royal Australian and New Zealand College of Radiologists, Cancer Institute NSW, Prostate Cancer Foundation Australia, and Cancer Australia.

Neutrophil extracellular traps (NETs) are critical for anti-bacterial activity of the innate immune system. We have previously shown that mitochondrial damage-associated molecular patterns (mtDAMPs), including mitochondrial DNA (mtDNA), are released into the circulation after injury. We therefore questioned whether mtDNA is involved in trauma-induced NET formation. Treatment of human polymorphoneutrophils (PMN) with mtDNA induced robust NET formation, though in contrast to phorbol myristate acetate (PMA) stimulation, no NADPH-oxidase involvement was required. Moreover, formation of mtDNA-induced NETs was completely blocked by TLR9 antagonist, ODN-TTAGGG. Knowing that infective outcomes of trauma in elderly people are more severe than in young people, we measured plasma mtDNA and NET formation in elderly and young trauma patients and control subjects. MtDNA levels were significantly higher in the plasma of elderly trauma patients than young patients, despite lower injury severity scores in the elderly group. NETs were not visible in circulating PMN isolated from either young or old control subjects. NETs were however, detected in PMN isolated from young trauma patients and to a lesser extent from elderly patients. Stimulation by PMA induced widespread NET formation in PMN from both young volunteers and young trauma patients. NET response to PMA was much less pronounced in both elderly volunteers' PMN and in trauma patients' PMN. We conclude that mtDNA is a potent inducer of NETs that activates PMN via TLR9 without NADPH-oxidase involvement. We suggest that decreased NET formation in the elderly regardless of higher mtDNA levels in their plasma may result from decreased levels of TLR9 and/or other molecules, such as neutrophil elastase and myeloperoxidase that are involved in NET generation. Further study of the links between circulating mtDNA and NET formation may elucidate the mechanisms of trauma-related organ failure as well as the greater susceptibility to secondary infection in elderly trauma patients.

Prostate cancer is the second leading cause of cancer-related death in men, with metastatic castration-resistant prostate cancer (mCRPC) and bone metastases representing a critical clinical challenge. Although radium-223 (Ra-223) is approved for treating mCRPC with bone metastases, its efficacy remains limited, necessitating the development of more effective therapies. This study investigates the therapeutic potential of [sup.177]Lu-PSMA-617, a PSMA-targeted radiopharmaceutical, in a murine model of prostate cancer bone metastases. To our knowledge, this is the first study to systematically evaluate [sup.177]Lu-PSMA-617 in an orthotopic bone metastatic prostate cancer model, providing a clinically relevant preclinical platform to assess both imaging and therapeutic performance. We conducted comprehensive preclinical evaluations, including synthesis, stability analysis, cell binding assays, nuclear imaging, in vivo biodistribution, pharmacokinetics, and antitumor efficacy. The synthesis of [sup.177]Lu-PSMA-617 demonstrated high radiochemical yield (99.2%), molar activity (25.5 GBq/μmol), and purity (>98%), indicating high product quality. Stability studies confirmed minimal release of free Lutetium-177, maintaining the compound’s integrity under physiological conditions. In vitro assays showed selective binding and internalization in PSMA-positive LNCaP prostate cancer cells, with negligible uptake in PSMA-negative PC-3 cells. In vivo biodistribution studies demonstrated efficient tumor targeting, with peak uptake in LNCaP tumors (23.31 ± 0.94 %IA/g) at 4 h post-injection. The radiopharmaceutical exhibited favorable pharmacokinetics, with high tumor-to-background ratios (tumor-to-blood, 434.4; tumor-to-muscle, 857.4). Therapeutic efficacy was confirmed by significant survival extension in treated mice (30.7% for 37 MBq and 53.8% for 111 MBq), with median survival times of 34 and 40 days, respectively, compared to 26 days in the control group. Radiation dosimetry analysis indicated a favorable safety profile with a calculated effective dose of 0.127 mSv/MBq. These findings highlight the novelty and translational relevance of using [sup.177]Lu-PSMA-617 in a clinically relevant bone metastasis model, reinforcing its potential as a dual-purpose agent for both targeted therapy and molecular imaging in advanced prostate cancer.

This article addresses the critical need for understanding the dynamics of COVID-19 transmission and the role of booster vaccinations in managing the pandemic. Despite widespread vaccination efforts, the emergence of new variants and the waning of immunity over time necessitate more effective strategies. A fractional-order mathematical model using Caputo-Fabrizio derivatives was developed to analyze the impact of booster doses, symptomatic and asymptomatic infections, and quarantine measures. The model incorporates real epidemic data from Thailand and includes a sensitivity analysis of parameters influencing disease spread. Numerical results indicate that booster vaccinations significantly reduce transmission rates, and the model’s predictions align well with the observed data. The basic reproduction number was determined to evaluate disease control, showing that a sustained vaccination campaign, including booster doses, is essential to maintaining immunity and controlling future outbreaks. The findings underscore the importance of ongoing vaccination efforts and provide a robust framework for policymakers to design effective strategies for pandemic control.

A molecularly imprinted polymer (MIP) and a nanocomposite prepared from gold nanoparticles (AuNP) and poly(3,4-ethylenedioxythiophene)/poly(styrene sulfonate) (PEDOT:PSS) were deposited on a screen-printed carbon electrode (SPCE). The nanocomposite was prepared by one-pot simultaneous in-situ formation of AuNPs and PEDOT:PSS and was then inkjet-coated onto the SPCE. The MIP film was subsequently placed on the modified SPCE by co-electrodeposition of o -phenylenediamine and resorcinol in the presence of the antibiotic nitrofurantoin (NFT). Using differential pulse voltammetry (DPV), response at the potential of ~ 0.1 V (vs. Ag/AgCl) is linear in 1 nM to 1000 nM NFT concentration range, with a remarkably low detection limit (at S/ N  = 3) of 0.1 nM. This is two orders of magnitude lower than that of the control MIP sensor without the nanocomposite interlayer, thus showing the beneficial effect of AuNP-PEDOT:PSS. The electrode is highly reproducible (relative standard deviation 3.1% for n  = 6) and selective over structurally related molecules. It can be re-used for at least ten times and was found to be stable for at least 45 days. It was successfully applied to the determination of NFT in (spiked) feed matrices and gave good recoveries. Graphical abstract Schematic representation of a voltammetric sensor for the determination of nitrofurantoin. The sensor is based on a screen-printed carbon electrode (SPCE) modified with an inkjet-printed gold nanoparticles-poly(3,4-ethylenedioxythiophene):poly(styrene sulfonate) nanocomposite and a molecularly imprinted polymer.

Recent toxicology studies suggest that nanosized aggregates of fullerene molecules can enter cells and alter their functions, and also cross the blood–brain barrier. However, the mechanisms by which fullerenes penetrate and disrupt cell membranes are still poorly understood. Here we use computer simulations to explore the translocation of fullerene clusters through a model lipid membrane and the effect of high fullerene concentrations on membrane properties. The fullerene molecules rapidly aggregate in water but disaggregate after entering the membrane interior. The permeation of a solid-like fullerene aggregate into the lipid bilayer is thermodynamically favoured and occurs on the microsecond timescale. High concentrations of fullerene induce changes in the structural and elastic properties of the lipid bilayer, but these are not large enough to mechanically damage the membrane. Our results suggest that mechanical damage is an unlikely mechanism for membrane disruption and fullerene toxicity. Computer simulations suggest that high concentrations of fullerenes can change the mechanical properties of the lipid membrane in cells. However, these changes are not large enough to damage the membrane, which suggests that other mechanisms are responsible for membrane disruption and fullerene toxicity.

Lipid peroxidation plays an important role in cell membrane damage. We investigated the effect of lipid peroxidation on the properties of 1-palmitoyl-2-linoleoyl- sn-glycero-3-phosphatidylcholine (PLPC) lipid bilayers using molecular dynamics simulations. We focused on four main oxidation products of linoleic acid with either a hydroperoxide or an aldehyde group: 9- trans, cis-hydroperoxide linoleic acid, 13- trans, cis-hydroperoxide linoleic acid, 9-oxo-nonanoic acid, and 12-oxo-9-dodecenoic acid. These oxidized chains replaced the sn-2 linoleate chain. The properties of PLPC lipid bilayers were characterized as a function of the concentration of oxidized lipids, with concentrations from 2.8% to 50% for each oxidation product. The introduction of oxidized functional groups in the lipid tail leads to an important conformational change in the lipids: the oxidized tails bend toward the water phase and the oxygen atoms form hydrogen bonds with water and the polar lipid headgroup. This conformational change leads to an increase in the average area per lipid and, correspondingly, to a decrease of the bilayer thickness and the deuterium order parameters for the lipid tails, especially evident at high concentrations of oxidized lipid. Water defects are observed in the bilayers more frequently as the concentration of the oxidized lipids is increased. The changes in the structural properties of the bilayer and the water permeability are associated with the tendency of the oxidized lipid tails to bend toward the water interface. Our results suggest that one mechanism of cell membrane damage is the increase in membrane permeability due to the presence of oxidized lipids.