The severe respiratory distress syndrome (SRDS) has been a significant clinical issue in modern respiratory medicine. Its role in COVID-19 pandemic is not well defined. Outside-the-hospital SRDS is usually community-acquired septic pneumonia; however, in-hospitals incidences are complicated by co-infections. While SRDS is genetically selected in European and African origins, these are not clear in Middle East, particularly in COVID-19 backgrounds. There is a severe paucity in high quality data on correlations between COVID-19, ARDS, co-infectome, and patient demographics. We have conducted a comprehensive investigation on 298 patients for associations of SRDS, coinfections, and patient demographics on COVID-19 patients’ outcomes. Of these, 9.4% (n=28) had SRDS, and the rest (90.6%) had not. 54% of those with SRDS died while 84% survived; SRDS fatality was highly significant (Chi-square test P-value = 0.00000246). Irrespective of gender, the age of patients was significantly associated with SRDS (72.9 +/-8.9) compared to those without it (56.2 +/-15.1). However, there was no significant difference neither in the age of admitted patients before COVID-19 (58.5 +/-15.3) and during COVID-19 (57.2 +/-15.5) nor in the gender and COVID-19 fatality (Fisher Exact test 2-sided 1.000, 1-sided .546) ruling out that SRDS age-specificity were selected by virus susceptibility. A 100% of SRDS patients without bacterial co-infections survived while only 25% of those with co- infectome did not; this association was highly significant (P value= 0.00041). Co-infections alone without underlying SRDS was also associated with high fatality among patients (P value= 0.00000000076). Almost all COVID-19 patients without co-infectome (99.2%) survived while 28% of those with bacterial co-infection died. The major bacterial pathogens that potentially predisposed to SRDS, were Acinetobacter baumannii, and Escherichia coli either alone or in a mixed infection with Klebsiella pneumoniae were predominant species identified during SRDS attack. Thus, Gram-negative co-infectome potentially induced fatal SRDS aggravating COVID-19 outcome. These findings have significant clinical implications in specific differential diagnosis of SRDS syndromes for subsequent empiric therapy and patient management strategies. Future vertical investigation for similar mechanisms of cytokine-induced SRDS by Gram negative pathogens is imperative since hypervirulent strains are rapidly circulating in the region. The study is limited by a single center study confined to Ha’il hospitals; large scale investigation in major national hospitals would gain more insights.

Acute respiratory distress syndrome (ARDS) is one of the major problems in COVID-19 that is not well understood. ARDS is usually complicated by co-infections in hospitals. Although ARDS is inherited by Europeans and Africans, this is not clear for those from the Middle East. There are severe limitations in correlations made between COVID-19, ARDS, co-infectome, and patient demographics. We investigated 298 patients for associations of ARDS, coinfections, and patient demographics on COVID-19 patients’ outcomes. Of the 149 patients examined for ARDS during COVID-19, 16 had an incidence with a higher case fatality rate (CFR) of 75.0% compared to those without ARDS (27.0%) (p value = 0.0001). The co-infectome association showed a CFR of 31.3% in co-infected patients; meanwhile, only 4.8% of those without co-infections (p value = 0.01) died. The major bacteria were Acinetobacter baumannii and Escherichia coli, either alone or in a mixed infection with Klebsiella pneumoniae. Kaplan–Meier survival analysis of COVID-19 patients with and without ARDS revealed a significant difference in the survival time of patients with ARDS (58.8 +/− 2.7 days) and without ARDS (41.9 +/− 1.8 days) (p value = 0.0002). These findings prove that increased hospital time was risky for co-infectome-induced SDRS later on. This also explained that while empiric therapy and lethal ventilations delayed the mortality in 75% of patients, they potentially did not help those without co-infection or ARDS who stayed for shorter times. In addition, the age of patients (n = 298) was significantly associated with ARDS (72.9 +/− 8.9) compared to those without it (56.2 +/− 15.1) and was irrespective of gender. However, there were no significant differences neither in the age of admitted patients before COVID-19 (58.5 +/− 15.3) and during COVID-19 (57.2 +/− 15.5) nor in the gender and COVID-19 fatality (p value 0.546). Thus, Gram-negative co-infectome potentially induced fatal ARDS, aggravating the COVID-19 outcome. These findings are important for the specific differential diagnosis of patients with and without ARDS and co-infections. Future vertical investigations on mechanisms of Gram-negative-induced ARDS are imperative since hypervirulent strains are rapidly circulating. This study was limited as it was a single-center study confined to Ha’il hospitals; a large-scale investigation in major national hospitals would gain more insights.

Background/Objectives : Non-communicable diseases like obesity, diabetes mellitus (DM), and hypertension (HTN) impose major global burdens. Helicobacter pylori infection may worsen these conditions. This study examined the clinical, age-, and gender-specific profiles of H. pylori-infected inpatients and its association with dyslipidemia, obesity, HTN, DM, and other chronic conditions. Methods: Between September 2024 and February 2025, patients were tested using a stool antigen assay (SIMA CHECK–ACON BIOTEC). Demographic data, smoking status, and clinical diagnoses (including kidney, liver, and heart disease) were obtained from hospital records and confirmed with standard criteria. Associations were analyzed using chi-square/Fisher’s tests and logistic regression (adjusted for age, gender, and smoking). Results: Overall, 30.7% (64/208) of inpatients were H. pylori–positive, highest in middle-aged females (42.9%) and lowest in middle-aged males (20.9%). Dyslipidemia rose sharply in males (5.6%→77.1%) versus females (5.7%→58.3%), with infection modestly elevating rates (OR=1.648). Obesity declined with age (males: 36.1%→22.9%; females: 45.7%→20.8%) yet strongly correlated with H. pylori (OR=19.217). HTN (5.6 – 94.3% in males; 11.4 – 100% in females) and DM (16.7 – 80% vs. 17.1 – 95.8%) increased with age but showed no infection link reflecting inflammatory preference. Smoking peaked at 61.1% in younger males. Kidney and heart diseases appeared only in ages 60–85. Overall, the prevalence of comorbidities markedly increased with age. Conclusion: H. pylori infection is common among inpatients, particularly in middle-aged females, and is significantly linked to dyslipidemia and obesity. These findings support targeted screening, especially in females and individuals with metabolic abnormalities, while future studies should assess whether eradication therapy can mitigate chronic metabolic risks.

Objective: Lung cancer (LC) remains a leading cause of cancer mortality worldwide. Thymoquinone (TQ), a bioactive compound derived from Nigella sativa, possesses anti-inflammatory and antioxidant properties, but its precise mechanisms concerning miRNA regulation in LC are poorly defined. This study investigates the anti-cancer potential of TQ through modulation of microRNA signaling in LC. Methods: We employed an integrated approach combining bioinformatic predictions with rigorous experimental validation in A549 lung adenocarcinoma cells and SHP-77 human small-cell lung carcinoma (SCLC) cells. Bioinformatic analyses predicted miRNA targets, and experimental techniques included dual-luciferase reporter assays, miRNA inhibition, TaqMan RT-qPCR, cell-based ELISA, and Western blotting to dissect the molecular pathway. Results: We identified the transcription factor BACH1 as a direct and novel target of hsa-miR-155-5p. TQ potently suppressed interferon-γ-induced expression of both hsa-miR-155-5p and its target, BACH1. This TQ-mediated suppression led to subsequent downregulation of the key metastasis-promoter Matrix Metalloproteinase-9 (MMP-9). Genetic inhibition of miR-155-5p or direct BACH1 inhibition phenocopied the effects of TQ, confirming the functional significance of this axis. Thus, we define a novel oncogenic signaling cascade—the hsa-miR-155-5p/BACH1/MMP-9 axis that is effectively disrupted by TQ. Conclusions: This represents the first evidence that TQ exerts its anti-cancer effects in LC through the modulation of the critical signaling cascade (hsa-miR-155-5p → BACH1 → MMP-9). Our findings establish TQ as a multi-targeted agent capable of simultaneously inhibiting miRNA-mediated oncogenic signaling and protein-level effectors. The dual therapeutic action of TQ represents a novel therapeutic strategy and underscores its potential for synergistic combination therapies.

Background/Objectives: Effective thyroid-cancer care in Saudi Arabia demands local data on age-linked histology and nodule architecture—factors rarely studied beyond the worldwide dominance of papillary thyroid carcinoma (PTC). Methods: We retrospectively analysed 208-adult cases managed at King Salman Specialist Hospital, a Ha’il tertiary hospital (2022-2025). Extracted variables included age, sex, first-degree family history, smoking, obesity (BMI≥30 kg m⁻²), oral-contraceptive-pill (OCP) use, hypertension, diabetes, Hashimoto thyroiditis, nodule pattern (single vs multinodular) and final tumour subtype. Associations were tested with χ² or Fisher’s exact (α=0.05); effect size was expressed as odds ratios (ORs, 95% CI). Results: Patients were primarily female (70.2%) and aged 30–39 years (52.4%). Histology was dominated by papillary carcinoma (PTC, 87.5%), followed by follicular (8.2%), medullary (3.4%) and anaplastic (1.0%). Age strongly influenced subtype (χ²=30.7, p<0.001): PTC comprised 98.2% of tumours<40 years but only 72.5% were ≥50 years, where follicular and medullary cancers reached 27.5%. A positive family history markedly enriched for medullary carcinoma (11.4% vs 1.7%; χ²=8.95, p=0.030; OR=7.4). Smoking occurred exclusively in men (9.7% vs 0 %; χ²=14.5, p<0.001). Multinodularity was far more pronounced in males (43.5% vs 8.9%; χ²=33.6, p<0.001) and in women not using OCPs (32.7% vs 7.3%; χ²=21.5, p<0.001). Obesity, hypertension, and diabetes were correlated albeit no significant associations found in this study. Conclusions: Saudi thyroid cancer displays clear age-, sex- and heredity-linked heterogeneity patterns: non-PTC subtypes rise with age, medullary tumours cluster in families, multinodularity is predominantly male, and OCP exposure relates to single-nodule disease. These findings support age-stratified diagnostics, targeted RET proto-oncogene testing and consideration of hormonal influences in local management algorithms.