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Background/Objectives: Asthma is a chronic inflammatory disorder of the airways affecting over 10% of the global population. It is characterized by airway inflammation, mucus hypersecretion, and bronchial hyperresponsiveness, driven predominantly by type 2 helper T cells (Th2) and type 2 innate lymphoid cells (ILC2s) in a subset of patients. However, a significant portion of asthmatic individuals present with "type 2-low" asthma that is often refractory to standard inhaled corticosteroid (ICS) therapy. Therefore, developing innovative therapeutic strategies has become essential. Recent studies have highlighted cannabidiol (CBD) as a promising anti-inflammatory agent capable of modulating immune responses. This study investigates the therapeutic potential of a high-CBD extract (CBD-X) in asthma. Methods: We evaluated the effects of CBD-X on cells involved in asthma pathogenesis using primary human Th2 cells, neutrophils, and asthma mouse model. Results: Our findings indicate that CBD-X extract inhibits Th2 differentiation and reduces the secretion of IL-5 and IL-13, which are crucial cytokines in asthma. Additionally, CBD-X significantly reduces pro-inflammatory cytokines IL-8 and IL-6 in neutrophils and impairs their migration, a critical step in airway inflammation. In a murine asthma model, CBD-X administration led to marked downregulation of IgE and pro-asthmatic cytokines, along with reduced leukocyte, eosinophil, and neutrophil infiltration in lung tissues. Conclusions: These results suggest that CBD-X extract could offer a novel and complementary approach to managing both type 2-high and type 2-low asthma by targeting key inflammatory pathways and modulating immune cell behavior. [ABSTRACT FROM AUTHOR]

Introduction: Venous thromboembolism (VTE) events are a significant risk factor for morbidity and mortality among hospitalized patients and 50-75% of the events occur in internal medicine wards. Despite the proven efficiency of prophylactic treatments, their usage in hospitals is underutilized. Multiple studies have shown that only 30-50% of the high risk VTE patients are treated prophylactically. Interventional programs were shown to significantly increase the awareness and hence, the percent of patients treated. However, there are no official guidelines for prophylaxis implementation among hospital personnel in Israel., Methods: We conducted a prospective study of patients hospitalized in internal medicine wards to estimate the risk of VTE events and the prophylaxis rate. Patients were randomly selected and evaluated for VTE risk and treatment provided. During daily staff meetings on random sampling days, an open inquiry was conducted for each patient's management regarding VTE prophylaxis. This supervision was carried out for 3 consecutive months and 6 months later, to evaluate the implementation of the process., Results: A total of 205 patients were sampled during the study. During the first month, 35% of the patients with indications for prophylaxis were treated. This percent increased to 50% in the second month, 60% in the third, and to 86% after six months (p<0.0001)., Conclusions: The awareness of VTE prophylaxis was low, and only a third of the patients with indications for prophylaxis were treated. The awareness implementation was slow and incremental, and increased from 35% to 86%. We conclude that the supervision and training on VTE prophylaxis is efficient and essential.

Spontaneous bacterial empyema, a complication of hepatic hydrothorax in cirrhotic patients, is a rare but nevertheless important medical entity. The diagnosis, treatment and prognosis of spontaneous bacterial empyema differs from the "usual" empyema, and avoiding proper diagnosis or treatment delay may have far reaching consequences. We report on a patient who was diagnosed in our department with spontaneous bacterial empyema, review the main current literature on the subject and elaborate on the specific therapeutic considerations related to the case management.

Pharyngeal collapsibility during sleep is believed to increase due to a decline in dilator muscle activity. However, genioglossus electromyogram (EMG) often increases during apnoeas and hypopnoeas, often without mechanical effect. 17 patients with obstructive sleep apnoea were anaesthetised and evaluated from termination of propofol administration to awakening. Genioglossus EMG, flow and pharyngeal area (pharyngoscopy) were monitored. Prolonged hypopnoeas enabled evaluation of the relationships between genioglossus EMG and mechanical events, before and after awakening. Additional dilator muscle EMGs were recorded and compared to the genioglossus. Electrical stimulation of the genioglossus was used to evaluate possible mechanical dysfunction. Prolonged hypopnoeas during inspiration before arousal triggered an increase in genioglossus EMG, reaching mean ± SD 62.2 ± 32.7% of maximum. This augmented activity failed to increase flow and pharyngeal area. Awakening resulted in fast pharyngeal enlargement and restoration of unobstructed flow, with marked reduction in genioglossus EMG. Electrical stimulation of the genioglossus under propofol anaesthesia increased the inspiratory pharyngeal area (from 25.1 ± 28 to 66.3 ± 75.5 mm(2); p<0.01) and flow (from 11.5 ± 6.5 to 18.6 ± 9.2 L · min(-1); p<0.001), indicating adequate mechanical response. All additional dilators increased their inspiratory activity during hypopnoeas. During propofol anaesthesia, pharyngeal occlusion persists despite large increases in genioglossus EMG, in the presence of a preserved mechanical response to electrical stimulation.

Background: Sleep spindles (SS) are conducted by the thalamus during sleep and have an inhibitory effect on information rising through the thalamus to the cortex, probably representing the mechanism called Arousal Inhibitory Mechanism. They appear during sleep stage 2 but also in stages 3, 4 and REM (Rapid Eye Movements). Patients with post traumatic stress disorder (PTSD) complain of insomnia, although objective studies have revealed that their sleep is deeper and their awakening threshold is higher. The relationships between PTSD or selective serotonin reuptake inhibitors (SSRI) to SS density are not described in the literature., Goals: This study aimed to examine the hypothesis that the higher awakening threshold reflects an active defense process which would be manifested in increased sleep spindles in patients with PTSD., Methods: A total of 15 PTSD patients (36.3 +/- 11.4 years) comprised the research group and 15 healthy students (27.3 +/- 2.18 years) comprised the control group. Participants underwent a polysomnography study in the sleep laboratory at 'Rambam' Hospital, Haifa, Israel., Results: There was no difference in the sleep spindles density per minute during stage 2 between the research group (2.54 +/- 1.14) and the control group (2.86 +/- 1.3). However, sleep spindles density was highly affected by selective serotonin reuptake inhibitors, such that PTSD patients treated with SSRI's had significantly higher spindles density than the remaining PTSD patients (3.25 +/- 1.1 vs 1.72 +/- 0.46, p=0.0044). Stage 2 was shorter in the research group (47% +/- 8.75%) compared to the control group (58% +/- 8.5%, p=0.0014), while stages 3, 4 were longer (32% +/- 8% vs 18% +/- 6.26%, p<0.001)., Conclusions: Sleep spindle density was generally not increased in patients with PTSD, thus other mechanisms are probably responsible for their stabilization of sleep. SSRI's were found to have an important role in spindles density, which supports a serotonergic mechanism in the stabilization of sleep, although it requires further research.