Serological and molecular prevalences and phylogenetic analysis of in dogs in Al-Qadisiyah and Baghdad Provinces, Iraq.

Background And Aim: is a highly contagious zoonotic bacterial micro-organism. This study aimed to estimate the prevalence of in dogs using serological and molecular methods. Furthermore, a sequencing analysis of dog isolates was conducted.

Should left- and right-sided unilateral cleft lip and palate patients be grouped together when reporting the outcomes?

Objectives: Investigate associations between cleft laterality in patients with non-syndromic unilateral cleft lip and palate (UCLP) and oral-health, dental-arch, speech, audiological, psychological and nasolabial-aesthetic outcomes.

Methods: Secondary data analysis of the outcomes of 5-year-old children with non-syndromic complete UCLP identified from three studies: Cleft Collective (n = 155), Cleft Care UK (CCUK) (n = 266) and Clinical Standards Advisory Group (CSAG) study (n = 238). Outcome measures included occlusal assessment using the 5-year-old's index score, speech intelligibility rating using the CAPS-A Audit tool, audiological assessment using pure tone audiometry, nasolabial aesthetic assessment using the Asher-McDade tool, oral-health assessment using decayed, missing, filled teeth scores and parent-reported outcomes.

Unveiling the Crystal Ball: Predictors of Adverse Outcomes in Intracerebral Hemorrhage Patients.

Introduction: Intracerebral hemorrhage (ICH) is a severe form of stroke with substantial morbidity and mortality worldwide. Despite its impact, research has often focused on ischemic strokes, making ICH an essential area to explore.

Methods: A retrospective cohort study spanning 5 years was conducted in an Oman-based tertiary care teaching hospital's emergency room.

Chronic granulomatous disease in the United Arab Emirates: clinical and molecular characteristics in a single center.

Background: Chronic granulomatous disease (CGD) is a genetic disorder caused by defective oxidative burst within phagocytes, manifesting as recurrent, severe infections as well as hyperinflammation.

Objective: This is the first report from the United Arab Emirates (UAE) to describe the demographic, clinical, laboratory, radiological, and genetic characteristics of patients with CGD.

Methods: This is a retrospective study that was conducted at Tawam Hospital in the UAE on patients with confirmed CGD between 2017 and 2022.

Clinical Outcomes of COVID-19 in Newborns and Infants: A Multicenter Experience of 576 Cases.

Background: The literature describing clinical presentation, disease course and outcomes of SARS-CoV-2 in infants remains scarce.

Methods: We conducted a retrospective study across 2 major pediatric referral centers evaluating the demographics, clinical and laboratory characteristics, management and outcomes of COVID-19 among newborns and infants in the United Arab Emirates (UAE). Clinical and biochemical markers were evaluated for their accuracy in predicting intensive care unit (ICU) transfer and death.

Clinical course of COVID-19 among immunocompromised children: a clinical case series.

Infection with SARS-CoV-2 represents a great source of concern and a new threat for immunocompromised patients. Limited studies are available on COVID-19 in immunocompromised children. This case series aimed to evaluate the clinical and laboratory characteristics, management and outcomes of COVID-19 in five children immunocompromised due to different underlying conditions.

HEM1 deficiency disrupts mTORC2 and F-actin control in inherited immunodysregulatory disease.

Immunodeficiency often coincides with hyperactive immune disorders such as autoimmunity, lymphoproliferation, or atopy, but this coincidence is rarely understood on a molecular level. We describe five patients from four families with immunodeficiency coupled with atopy, lymphoproliferation, and cytokine overproduction harboring mutations in , which encodes the hematopoietic-specific HEM1 protein. These mutations cause the loss of the HEM1 protein and the WAVE regulatory complex (WRC) or disrupt binding to the WRC regulator, Arf1, thereby impairing actin polymerization, synapse formation, and immune cell migration.

Phenotyping acute and chronic atopic dermatitis-like lesions in Stat6VT mice identifies a role for IL-33 in disease pathogenesis.

The Stat6VT mouse model of atopic dermatitis (AD) is induced by T-cell-specific expression of a constitutively active form of the protein signal transducer and activator of transcription 6 (STAT6). Although AD-like lesions are known to develop in Stat6VT mice, this study was designed to determine if these mice develop acute and chronic phases of disease similar to humans. To address this, AD-like lesions from Stat6VT mice were harvested at two different timepoints relative to their onset.

Chemotherapeutic agents subvert tumor immunity by generating agonists of platelet-activating factor.

Oxidative stress suppresses host immunity by generating oxidized lipid agonists of the platelet-activating factor receptor (PAF-R). Because many classical chemotherapeutic drugs induce reactive oxygen species (ROS), we investigated whether these drugs might subvert host immunity by activating PAF-R. Here, we show that PAF-R agonists are produced in melanoma cells by chemotherapy that is administered in vitro, in vivo, or in human subjects.

Platelet-activating factor receptor agonists mediate xeroderma pigmentosum A photosensitivity.

To date, oxidized glycerophosphocholines (Ox-GPCs) with platelet-activating factor (PAF) activity produced non-enzymatically have not been definitively demonstrated to mediate any known disease processes. Here we provide evidence that these Ox-GPCs play a pivotal role in the photosensitivity associated with the deficiency of the DNA repair protein xeroderma pigmentosum type A (XPA). It should be noted that XPA-deficient cells are known to have decreased antioxidant defenses.

Progression of toxic epidermal necrolysis after tanning bed exposure.

Background: In addition to recreational tanning bed use, UV radiation exposures are sometimes sought to self-treat skin conditions. The ability of tanning bed radiation exposure to trigger toxic epidermal necrolysis has not been reported.

Observations: A young woman attempted to treat a self-limiting drug hypersensitivity reaction via tanning bed radiation exposure, which resulted in a systemic toxic epidermal necrolysis-like reaction.

Infected atopic dermatitis lesions contain pharmacologic amounts of lipoteichoic acid.

Background: Bacterial infection with Staphylococcus aureus is a known trigger for worsening of atopic dermatitis (AD); the exact mechanisms by which bacterial infection worsens dermatitis are unknown.

Objective: We sought to characterize the amounts of the biologically active bacterial lipoprotein lipoteichoic acid (LTA) in infected AD lesions.

Methods: Eighty-nine children with clinically impetiginized lesions of AD were enrolled in this study.

Epidermal platelet-activating factor receptor activation and ultraviolet B radiation result in synergistic tumor necrosis factor-alpha production.

Ultraviolet B radiation (UVB) is a potent stimulator of epidermal cytokine production which has been implicated in photoaggravated dermatoses. In addition to cytokines such as tumor necrosis factor-alpha (TNF-alpha), UVB generates bioactive lipids including platelet-activating factor (PAF). Our previous studies have demonstrated that UVB-mediated production of keratinocyte TNF-alpha is in part due to PAF.

Ultraviolet B radiation generated platelet-activating factor receptor agonist formation involves EGF-R-mediated reactive oxygen species.

Recent studies have implicated the lipid mediator platelet-activating factor (PAF) in UVB-mediated systemic immunosuppression known to be a major cause for skin cancers. Previously, our group has demonstrated that UVB irradiation triggers the production of PAF and oxidized glycerophosphocholines that act as PAF-receptor (PAF-R) agonists. The present studies explored the mechanisms by which UVB generates PAF-R agonists.

Involvement of platelet-activating factor in ultraviolet B-induced hyperalgesia.

Ultraviolet B (UVB) radiation causes cutaneous inflammation. One important clinical consequence of UVB-induced inflammation is increased pain or hyperalgesia, which is likely mediated by enhanced sensitivity of cutaneous sensory neurons. Previous studies have demonstrated that UVB radiation generates the lipid mediator, platelet-activating factor (PAF), as well as oxidized phospholipids that act as PAF-mimetics.

Augmentation of UVB radiation-mediated early gene expression by the epidermal platelet-activating factor receptor.

UVB radiation (UVB) is a known inducer of many biological changes in human skin, and triggers the production of glycerophosphocholines that act as platelet-activating factor (PAF) agonists. To gain a better insight into the role of the epidermal PAF receptor (PAF-R) in UVB-mediated gene expression, Affymetrix oligonucleotide microarrays were used to compare mRNA expression in the PAF-R-negative epithelial cell line KB-expressing PAF-Rs (KBP) with that in KB cells transduced with a vector control (KBM). Total RNA was isolated from KB cells 1 hour after treatment with a PAF-R agonist or UVB irradiation.

Staphylococcal lipoteichoic acid inhibits delayed-type hypersensitivity reactions via the platelet-activating factor receptor.

Staphylococcus aureus infections are known triggers for skin inflammation and can modulate immune responses. The present studies used model systems consisting of platelet-activating factor receptor-positive and -negative (PAF-R-positive and -negative) cells and PAF-R-deficient mice to demonstrate that staphylococcal lipoteichoic acid (LTA), a constituent of Gram-positive bacteria cell walls, acts as a PAF-R agonist. We show that LTA stimulates an immediate intracellular Ca2+ flux only in PAF-R-positive cells.

Augmentation of chemotherapy-induced cytokine production by expression of the platelet-activating factor receptor in a human epithelial carcinoma cell line.

In addition to their known cytotoxic effects, chemotherapeutic agents can trigger cytokine production in tumor cells. Moreover, many chemotherapeutic agents are potent pro-oxidative stressors. Although the lipid mediator platelet-activating factor (PAF) is synthesized in response to oxidative stress, and many epidermal carcinomas express PAF receptors (PAF-R) linked to cytokine production, it is not known whether PAF is involved in chemotherapeutic agent-induced cytokine production.

The epidermal platelet-activating factor receptor augments chemotherapy-induced apoptosis in human carcinoma cell lines.

Most chemotherapeutic agents exert their cytotoxic effects in part through the induction of apoptosis. In addition, many chemotherapeutic agents are potent pro-oxidative stressors. Although the lipid mediator platelet-activating factor (PAF) is synthesized in response to oxidative stress, and many epidermal carcinomas express PAF receptors, it is not known whether PAF is involved in chemotherapeutic agent-induced apoptosis.