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Objectives This study aims to describe the common myths and misconceptions in addition to the perception and attitudes toward coronavirus disease 2019 (COVID-19) vaccines in the Saudi Arabian community. Methods This is a cross-sectional study that included adults (18 years and older) residing in the Kingdom of Saudi Arabia. Participants were asked to complete an online survey that evaluated their perception and attitudes toward the available COVID-19 vaccines in Saudi Arabia. Statistical comparison between two groups and more was done using chi-square, independent t-test, and one-way ANOVA. Results A total of 471 responses were analyzed with a majority (83.2%) believing that vaccinations are important. The vaccine preferred among the Saudi Arabian population was Pfizer (65.4%). More than half of our respondents (54.8%) strongly agreed that COVID-19 vaccines can reduce the severity of the COVID-19 infection. Respondents in the healthcare sector were significantly more likely to have a more positive view on vaccines compared to those in non-healthcare sectors (p 0.001). Conclusion The Saudi Arabian population has shown substantial awareness about COVID-19 vaccines; however, public health officials need to further increase awareness measures on COVID-19 vaccines to limit myths and misconceptions, especially among certain populations that are more prone to it.

Iodinated contrast agents, which are routinely used to improve contrast in x-ray diagnostic radiography, have been successfully proven to enhance radiation effects in kilovoltage x-ray radiation therapy beams. The studies determined the influence of iodine on the level of radiation biotoxicity to cells as an indicator of the radiation dose enhancement. The use of other high-atomic-number materials such as gold nanoparticles (AuNPs) may also provide advantages in terms of radiation dose enhancement. In this work AuNPs have been used for the enhancement of radiation effects on bovine aortic endothelial cells of superficial x-ray radiation therapy and megavoltage electron radiation therapy beams. Results reveal an increase of cell damage with increasing concentration of AuNPs. At 1 mM concentration of AuNPs, enhancement of radiation peaked at 25 times for a kilovoltage x-ray beam. AuNPs showed similar effects on electron beams but to a lesser extent. This study showed that AuNPs can be used to enhance the effect of radiation doses from kilovoltage x-ray radiation therapy and megavoltage electron radiation therapy beams. In the prevailing clinical circumstances, wherein radiation therapy dose is constrained by normal tissue tolerance, this enhancement could in the future be used to improve local control in superficial x-ray treatments, megavoltage electron beam radiation therapy, microbeam radiation therapy, and intraoperative irradiation using kilovoltage x-rays or megavoltage electron beams. Moreover, the value of this work also stems from the fact that the damage to the endothelial cells lining the highly vasculature structure of tumors deprives tumors of their oxygen and nutrients supply and enhances the efficiency of radiation therapy treatment, where it has been proven that more of the AuNPs injected into animals ends up into the blood than in the tumor.

Endothelial cells possess multiple mechanisms for the control of Ca2+ influx during agonist and mechanical stimulation. Increased intracellular Ca2+ during such events is important in the production of vasoactive substances including NO, prostacyclin, and, possibly, endothelium-derived hyperpolarizing factor(s). The present studies examined the effect of arachidonic acid on cellular Ca2+ entry and the underlying mechanisms by which this fatty acid regulates entry. Studies were conducted in cultured bovine aortic endothelial cells (passages 3 to 6) with changes in intracellular Ca2+ determined using the fluorescent Ca2+-sensitive indicator fura 2. Arachidonic acid (1 to 50 microM) stimulated Ca2+ entry from the superfusate without affecting Ca2+ release from intracellular stores. 2-aminoethoxydiphenyl borate (2APB) (100 microM) added at the peak of Ca2+ entry did not inhibit arachidonic acid-induced Ca2+ entry but, in contrast, significantly inhibited entry stimulated by ATP (1 microM). Arachidonic acid-induced Ca2+ entry was inhibited by econazole (1 microM), but not indomethacin (10 microM) or nordihydroguairetic acid (10 microM), suggesting the involvement of cytochrome P450 monooxygenase metabolite of arachidonic acid. Oleic acid (10 microM) was ineffective in inducing Ca2+ entry, whereas linoleic acid (10 microM) stimulated Ca2+ entry but by a mechanism insensitive to econazole. Collectively the data demonstrate that primary cultured aortic endothelial cells possess a Ca2+ entry mechanism modulated by arachidonic acid. This mode of Ca2+ entry appears to operate independently of store depletion-mediated mechanisms.

Studies have shown diabetes to be associated with alterations in composition of extracellular matrix and that such proteins modulate signal transduction. The present studies examined if non-enzymatic glycation of fibronectin or a mixed matrix preparation (EHS) alters endothelial cell Ca 2 + signaling following agonist stimulation. Endothelial cells were cultured from bovine aorta and rat heart. To glycate proteins, fibronectin (10 μg/ml), or EHS (2.5 mg/ml) were incubated (37°C, 30 days) with 0.5 M glucose-6-phosphate. Matrix proteins were coated onto cover slips after which cells (10 5 cells/ml) were plated and allowed to adhere for 16 h. For measurement of intracellular Ca 2 + , cells were loaded with fura 2 (2 pM) and fluorescence intensity monitored. Bovine cells on glycated EHS showed decreased ability for either ATP (10 6 M) or bradykinin (10 7 M) to increase Ca 2 + i . In contrast, glycated fibronectin did not impair agonist-induced increases in Ca 2 + i . In the absence of extracellular Ca 2 + , ATP elicited a transient increase in Ca 2 + i consistent with intracellular release. Re-addition of Ca 2 + resulted in a secondary rise in Ca 2 + i indicative of store depletion-mediated Ca 2 + entry. Both phases of Ca 2 + mobilization were reduced in cells on glycated mixed matrix; however, as the ratio of the two components was similar in all cells, glycation appeared to selectively impair Ca 2 + release from intracellular stores. Thapsigargin treatment demonstrated an impaired ability of cells on glycated EHS to increase cytoplasmic Ca 2 + consistent with decreased endoplasmic reticulum Ca 2 + stores. Furthersupport for Ca 2 + mobilization was provided by increased baselin IP 3 levels in cells plated on glycated EHS. Impaired ATP-induced Ca 2 + release could be induced by treating native EHS with laminin antibody or exposing cells to H 2 O 2 (20-200 μM). Glycated EHS impaired Ca 2 + signaling was attenuated by treatment with aminoguanidine or the antioxidant α-lipoic acid. The results demonstrate that matrix glycation impairs agonist-induced Ca 2 + i increases which may impact on regulatory functions of the endothelium and implicate possible involvement of oxidative stress.

1. Agonists increase endothelial cell intracellular Ca(2+), in part, by capacitative entry, which is triggered by the filling state of intracellular Ca(2+) stores. It has been suggested that depletion of endoplasmic reticulum (ER) Ca(2+) stores either leads to a physical coupling between the ER and a plasma membrane channel, or results in production of an intracellular messenger which affects the gating of membrane channels. As an axis involving the IP(3) receptor has been implicated in a physical coupling mechanism the aim of this study was to examine the effects of the putative IP(3) receptor antagonists/modulators, 2 aminoethoxydiphenyl borate (2APB) and xestospongin C, on endothelial cell Ca(2+) entry. 2. Studies were conducted in fura 2 loaded cultured bovine aortic endothelial cells and endothelial cells isolated from rat heart. 3. 2APB (30 - 300 microM) inhibited Ca(2+) entry induced by both agonists (ATP 1 microM, bradykinin 0.1 microM) and receptor-independent mechanisms (thapsigargin 1 microM, ionomycin 0.5 and 5 microM). 2APB did not diminish endothelial cell ATP-induced production of IP(3) nor effect in vitro binding of [(3)H]-IP(3) to an adrenal cortex binding protein. Capacitative Ca(2+) entry was also blocked by disruption of the actin cytoskeleton with cytochalasin (100 nM) while the initial Ca(2+) release phase was unaffected. 4. Similarly to 2APB, xestospongin C (3 - 10 microM) inhibited ATP-induced Ca(2+) release and capacitative Ca(2+) entry. Further, xestospongin C inhibited capacitative Ca(2+) entry induced by thapsigargin (1 microM) and ionomycin (0.5 microM). 5. The data are consistent with a mechanism of capacitative Ca(2+) entry in vascular endothelial cells which requires (a) IP(3) receptor binding and/or an event distal to the activation of the ER receptor and (b) a spatial relationship, dictated by the cytoskeleton, between Ca(2+) release and entry pathways.

1. An exact understanding of signal transduction pathways within intact and functional arteriolar smooth muscle is made difficult by limited access to the intracellular environment due to the cell membrane. The aim of the present studies was to determine the feasibility of using polycationic lipids and reverse permeabilization for the introduction of peptide inhibitors into smooth muscle cells of the intact arteriolar wall. 2. Isolated cannulated arterioles were exposed to polycationic lipid preparations together with varying concentrations of the protein beta-galactosidase (30-90 microg/mL). Similar experiments were also performed using cultured smooth muscle cells. Staining for the chromogenic substrate of beta-galactosidase (5-bromo-4-chloro-3-indolyl-beta-d-galactosidase; X-gal) demonstrated incorporation of the protein into cultured cells but not intact arteriolar smooth muscle. Similarly, polycationic lipid treatment did not enable loading of arteriolar smooth muscle (as assessed by cAMP-mediated vasodilation) with the protein kinase (PK) A inhibitory peptide PKI. 3. In contrast, reverse permeabilization, using high ATP concentrations in the presence of EGTA enabled introduction of PKI and inhibition of forskolin-mediated vasodilatation. Furthermore, arterioles maintained full viability following reverse permeabilization, as demonstrated by an ability to develop spontaneous myogenic tone. 4. Reverse permeabilization provides a method for introducing peptide inhibitors into functional arteriolar smooth muscle and manipulating signal transduction. Protein transfection using polycationic lipids appears to be limited by the barrier provided by the adventitia or inherent differences between cells under cultured conditions compared within the intact arteriole.

Purpose: Microbeam radiotherapy(MRT) is a technique that use array parallel thin (

Purpose: To investigate the radiosensitization of superficial kilovoltage range of x‐ray energy and megavoltage electron beams due to the presence of goldnanoparticles (AuNps) using cell survival curves and normoxic polyacrymide gel (nPAG). Method and Materials: Bovine aortic endothelial cells (BAECs) with and without AuNps were irradiated with kilovoltage superficial x‐ray beams and megavoltage electron beams. Cell survival at various concentrations of AuNps (0.25mMol–1mMol) was measured using colorimetric assay. Level of dose enhancement for x‐ray and electron beams was also quantified using AuNps doped nPAG. Results: AuNps enhanced the cells killing up to 21 fold for 1mMol of AuNps irradiated with 80 kVp x‐ray beams. Maximum dose enhancement factor (DEF) of 4.63 was measured for 12 MeV electron beams in the presence of 1mMol AuNps. 80 kVp which represents effective beam energy of around 40 keV was the optimum energy found that yield highest enhancement ratio. Measurements using AuNps doped nPAG also exhibit higher polymerization resulting from increased photoelectric interactions, Auger electrons and characteristic x‐ray generation. The experimental dose enhancements obtained were also in agreement with theoretical calculation and those previously documented for iodine atoms. Conclusion: Both experiments with cell culture and nPAG confirm that AuNps are able to enhance the radiationdose for x‐ray and electron superficial therapy. Lower doses from external sources are required to produce the same radiation effect with AuNps compared without application of AuNps. This will lead to improvement in superficial radiotherapy techniques of both x‐ray and electron. The use of this technique with microbeam radiotherapy technique and kilovoltage type intraoperative radiotherapy techniques are now under investigation in our group.