Saudi patients' preferred modes of receiving radio imaging reports from radiologists, their impact, and determinants - a survey.

OBJECTIVE: To review patients' perspectives regarding getting imaging reports from radiologists and the factors affecting their desired mode of receiving reports. SUBJECTS AND METHODS: This cross-sectional survey was conducted in 2022 at a tertiary hospital in Saudi Arabia. Patients undergoing imaging investigations were surveyed regarding real-time communication and delayed communication for normal and abnormal reports. We also asked about the impact of receiving reports and their timing. We used a five-point graded Likert scale for responses. The scores of responses were correlated by age group, gender, and type of report. RESULTS: We surveyed 377 patients. 37.4% (141) of participants and 40% (181) of participants expressed a strong desire or a desire to receive reports on the same day. The scores for receiving same-day abnormal reports were higher than for normal reports (p-value = 0.03). 259 (68.7%) patients wanted to get the report from their physician. Significantly more patients with abnormal reports wanted to review them with their physicians than patients with normal reports (p-value < 0.001). Getting reports quickly positively affected the mental health of patients. 57% of patients preferred receiving reports on abnormal findings within two hours, while 45.9% preferred receiving routine or normal reports within the same time frame. The value of radiologists' prompt reporting is appreciated by patients regardless of the type of results. Females reported a more positive impact on mental health from getting a radiology report sooner than males (p-value = 0.028). Age group did not correlate with real-time communication, delayed reporting, or the impact on mental health. CONCLUSIONS: The desire to quickly receive investigative radio-imaging reports by Saudi patients was complemented by reviewing the outcome with the attending physician, and it had a more positive impact on mental health in females than in males.

DOX and MET treatment induces cognitive impairment through downregulation of IL-1-alpha and IRS-1 in the rat brain.

OBJECTIVE: Chemotherapeutic drugs are effective in the treatment of various types of cancers. However, the secondary side effects of chemotherapy, such as cardiotoxicity, hepatotoxicity, and cognitive impairment, limit its clinical effectiveness in cancer treatment. The present study was aimed at investigating the effects of doxorubicin (DOX) on cognitive impairment through its effects on interleukin (IL)-1, insulin receptor substrate 1 (IRS-1), IL-6, Akt, and tumor necrosis factor (TNF)-alpha expression. MATERIALS AND METHODS: Rats were treated with DOX, metformin (MET), and DOX+MET, and IL-1, IRS-1, IL-6, Akt, and TNF-alpha expression levels were assessed using Enzyme-Linked Immunosorbent Assay kits. RESULTS: The DOX-treated rats showed significantly decreased IL-1 and IRS-1 expression in the brain, and the expression of these proteins was rescued on MET administration. On the other hand, IL-6, protein kinase B (PKB/Akt), and TNF-alpha expression was unaltered in the brain of DOX- and MET-treated rats. CONCLUSIONS: Our findings showed that DOX induces cognitive impairment by modulating IL-1-alpha and IRS-1 expression and that MET administration failed to rescue the DOX-mediated memory impairment.

Playing polo during mitosis: PLK1 takes the lead.

Polo-like kinase 1 (PLK1), the prototypical member of the polo-like family of serine/threonine kinases, is a pivotal regulator of mitosis and cytokinesis in eukaryotes. Many layers of regulation have evolved to target PLK1 to different subcellular structures and to its various mitotic substrates in line with its numerous functions during mitosis. Collective work is starting to illuminate an important set of substrates for PLK1: the mitotic kinases that together ensure the fidelity of the cell division process. Amongst these, recent developments argue that PLK1 regulates the activity of the histone kinases Aurora B and Haspin to define centromere identity, of MPS1 to initiate spindle checkpoint signaling, and of BUB1 and its pseudokinase paralog BUBR1 to coordinate spindle checkpoint activation and inactivation. Here, we review the recent work describing the regulation of these kinases by PLK1. We highlight common themes throughout and argue that a major mitotic function of PLK1 is as a master regulator of these key kinases.

Repeated exposure to whole cigarette smoke promotes primary human gingival epithelial cell growth and modulates keratin expression.

BACKGROUND AND OBJECTIVE: The gingiva is the first oral tissue directly exposed to cigarette smoke (CS). Exposure to CS compromises the structure and function of gingival tissue. Damaging or altering the gingival epithelium leads to a compromised protective barrier of the periodontium, resulting in several diseases. The aim of this study was to assess the effect of repeated exposure to CS on gingival epithelial cell growth and on expression of apoptotic protein and keratin. MATERIAL AND METHODS: Primary human gingival epithelial cells were seeded on a collagen scaffold for 5 d to allow growth and stratification. The cells were then exposed for 5 min to whole CS for 3, 6 and 9 d. At the end of each exposure period, cell proliferation [using (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) (MTT) and 5-bromo-2'-deoxyuridine (BrdU) assays], gene expression [by quantitative reverse transcription polymerase chain reaction (qRT-PCR)] and protein production (by western blot analysis) were investigated. RESULTS: Higher metabolic activity was found in the CS-exposed cells than in the nonexposed cells, specifically after 3 and 6 d of exposure to CS. At 9 d there was no significant difference between CS-exposed and nonexposed cells. Metabolic activity was supported by the BrdU cell-proliferation analyses, which showed increased cell growth at 3 d compared with the control. However, at 6 and 9 d, cell proliferation in the CS-exposed culture was comparable to that in the nonexposed culture. Interestingly, the Bax/Bcl-2 protein ratios decreased with increased CS exposure, suggesting cell resistance. Moreover, protein analyses showed that CS decreased expression of keratin(K) 5 at 3, 6 and 9 d, and increased expression of K14 at 6 and 9 d. Finally, mRNA analyses showed significant decreases of K1, K6, K10 and K16 in CS-exposed cultures, correlating, at times, with a decrease of protein production. CONCLUSION: CS was shown to increase epithelial cell proliferation, which may involve cell resistance to apoptosis. This is supported by the modulation of expression of different keratin genes and proteins. Altogether, these data may explain the hyperplasia reported in gingival tissue, as well as periodontal disease, in smokers.