Israel Medical Association Journal

In the grand theater of modern medicine, artificial intelligence (AI) has swiped the lead role, with a performance so riveting it deserves an Oscar, or at least a Nobel. From the intricate labyrinths of our arteries to the profound depths of our peepers, AI is the new maestro, conducting symphonies of data with the finesse of a seasoned virtuoso [1,2].

Over the last decade the use of artificial intelligence (AI) has reformed academic research. While clinical diagnosis of psoriasis and psoriatic arthritis is largely straightforward, the determining factors of a clinical response to therapy, and specifically to biologic agents, have not yet been found. AI may meaningfully impact attempts to unravel the prognostic factors that affect response to therapy, assist experimental techniques being used to investigate immune cell populations, examine whether these populations are associated with treatment responses, and incorporate immunophenotype data in prediction models. The aim of this mini review was to present the current state of the AI-mediated attempts in the field. We executed a Medline search in October 2023. Selection and presentation of studies were conducted following the principles of a narrative–review design. We present data regarding the impact AI can have on the management of psoriatic disease by predicting responses utilizing clinical or biological parameters. We also reviewed the ways AI has been implemented to assist development of models that revolutionize the investigation of peripheral immune cell subsets that can be used as biomarkers of response to biologic treatment. Last, we discussed future perspectives and ethical considerations regarding the use of machine learning models in the management of immune-mediated diseases.

Twenty-five years ago, we, the undersigned together with the chairman of the Israel Medical Association at the time, Prof. Yoram Blachar, and the Secretary General of the Israel Medical Association, Adv. Leah Wapner, joined forces to found an Israeli medical journal in English. The purpose of this journal was to present to the world Israeli clinical medicine and medical research. That journal is none other than the Israel Medical Association Journal (IMAJ), and in 2023 its 300th issue was published. In 2024 we keep going, taking pride in the fact that every one of those past 300 issues has been published and dispatched on time, without delay, regardless of any circumstances.

On 7 October 2023, a large-scale invasion by armed Hamas terrorists occurred in southern Israel. Approximately 1500 militants breached the Gaza security barrier using tractors, RPGs, and explosives. Concurrently, the terrorists utilized various means including armed vehicles, motorized paragliders, sea incursions, and a massive rocket attack launched toward Israel. On entering Israeli territory, the militants dispersed and targeted several towns, kibbutzim (collective communities), and Israel Defense Forces (IDF) military bases near Gaza. This strategy resulted in a death toll exceeded 1300 civilians and soldiers. In addition, more than 240 individuals were abducted. This attack occurred in one day. In this article, we introduce the Israeli National Institute of Forensic Medicine, which specialized in forensic analysis during mass casualty incidents, and pivotal role it played on 7 October. We present a detailed discussion on methods, challenges, and adaptations the institute took in response to the event of 7 October.

On Saturday, 7 October 2023, the Jewish holiday of Simchat Torah, our entire country woke to a reality of the worst terror attacks it has ever known, despite its long history of wars and terror. These horrific attacks included killing and burning babies, children, women, men, and the elderly; raping women; beheading babies; destroying settlements; and kidnapping more than 240 civilians and soldiers. The severe traumatic events created different circles of those exposed to trauma. In each group, the intensity of the trauma was different and had different characteristics.

Background: Data are scarce on the immunogenicity of coronavirus disease 2019 vaccines in patients with autoimmune rheumatic diseases (ARD).

Objectives: To measure the immunoglobulin G (IgG) response after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) immunization and to evaluate clinical characteristics associated with seropositivity.

Methods: Samples were collected after the second and third doses of the three different types of vaccines in ARD patients. Seroconversion rates and IgG antibody S1/S2 titers were measured.

Results: The type of ARD diagnosis and previous treatment had no significant impact on the serum IgG antibody levels measured after the second (P = 0.489 and P = 0.330, respectively) and boost dose (P = 0.441 and P = 0.446, respectively). What made a significant difference regarding serum IgG antibody levels after the second dose was the type of SARS-CoV-2 vaccine. The difference was highly statistically significant for all vaccine types (P = 0.001 with the highest odds ratio for the mRNA vaccine). After the boost with the mRNA vaccine, all patients achieved a high level of serum IgG antibody levels (t = 10.31, P = 0.001). No ARD patients experienced serious post-vaccinal reactions. Eight patients developed COVID-19 before the boost dose.

Conclusions: In ARDs patients, the highest level of serum IgG antibody against S1/S2 proteins was achieved with the mRNA vaccine, irrespective of the therapy applied or the type of the disease. We recommend a booster dose with mRNA vaccine in all ARDs for the highest SARS-CoV-2 protection without serious post-vaccinal reactions observed.

Background: While several studies have noted smell impairment in schizophrenia, it is unclear whether this impairment extends to acute psychosis and whether it is associated with more severe illness as expressed in extended hospitalization.

Objectives: To evaluate the olfactory function of patients in an acute psychotic state and correlate it with clinical symptomatology and length of hospitalization.

Methods: Olfactory function was assessed in 20 patients with schizophrenia in their first week of hospital admission for acute psychosis compared with matched controls. Olfaction was evaluated via three stages: threshold, discrimination, and identification of different odors utilizing the Sniffin' Sticks test battery.

Results: Schizophrenia patients scored significantly lower on total smell score, discrimination, and identification abilities. A significant association was observed between hospitalization duration and total smell score and smell discrimination. No significant associations between smell and clinical symptomatology were observed.

Conclusions: Study observations confirm impaired sense of smell in schizophrenia patients and suggest that smell impairment may be a potential marker of more serious illness as expressed in longer hospital stay.

Background: Fibromyalgia syndrome (FMS) is estimated to affect 2–4% of the general population. While FMS has some known environmental and genetic risk factors, the disorder has no clear etiology. A common coexisting disorder with FMS is small fiber neuropathy (SFN). High levels of serum immunoglobulin M (IgM) binding to trisulfated-heparin-disaccharide (TS-HDS) were recently found to be associated with SFN.

Objectives: To evaluate potential differences in anti-TS-HDS antibody titers in women with FMS compared to healthy controls.

Methods: In this cross-sectional study, we evaluated 51 female participants: 30 with a diagnosis of FMS and 21 healthy controls who had been recruited at the Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Israel. All of the participants were older than 18 years of age. Anti-TS-HDS IgM levels were measured in their sera using the enzyme immunoassay technique.

Results: The mean anti-TS-HDS IgM levels were significantly lower in the FMS group, compared with the control group (7.7 ± 5 vs. 13.2 ± 8.6 U/ml, respectively; P = 0.013).

Conclusions: There is a possible association between FMS and anti-TS-HDS IgM. This association might be the missing link for the coexistence of SFN and FMS, but further study should be performed to assess this association and this auto-antibody characteristic.

The interplay between post-traumatic stress disorder (PTSD) and autoimmunity is well known. One of the contributors leading to immune disorders is autonomic dysregulation, which is characterized by attenuated parasympathetic and elevated sympathetic systems. In this review, we described evidence regarding the relationship between stress, PTSD, autonomic dysfunction, and autoimmunity. Stress is a physiological response, which is functional for our being. The implication of dysfunction in stress response may be a cause of disease development. We described the fundamental role of the pathological high levels of stress in PTSD as a mediator factor that contributes to autonomic dysfunction, which as a result may lead to autoimmunity. Systemic lupus erythematosus, rheumatoid arthritis, and type 1 diabetes are some of the autoimmune diseases PTSD patients are at higher risk of developing. Notably, some autoimmune diseases are shown to increase the susceptibility to develop PTSD, which may indicate a bidirectional influence. In addition, we elaborated on stress as a major component in both fibromyalgia and PTSD, as there are overlaps between the pathogenesis of fibromyalgia and PTSD. Underlying chronic low-grade inflammation, which characterizes PTSD patients, may be a potential target and biomarker in treating PTSD patients. We believe that chronic low-grade inflammation, high concentrations of cytokines, and other inflammatory biomarkers, which characterize PTSD patients, may be potential targets and biomarkers in the treatment of PTSD patients and part of the PTSD diagnostic criteria.

The connection between physical exercise and the brain has long been studied. The evidence showing that physical exercise plays a significant role on neurogenesis and cognitive function has primarily been based on research examining aerobic exercise. In this review, we described three exercise modalities: aerobic, anaerobic, and resistance exercise and their impact on brain plasticity and cognitive function. While each of these exercise modalities have been demonstrated to positively influence brain plasticity and cognitive function, the specific mechanism that stimulates these changes appear to differ to some degree between these training modalities. The effect of aerobic and anaerobic exercise appears to be primarily mediated by changes in expression of brain-derived neurotrophic factor (BDNF), lactate, vascular endothelial growth factor (VEGF), and several additional proteins within the brain. However, resistance exercise appears to influence brain plasticity by myokines such as irisin, insulin-growth factor-1 (IGF1), and BDNF that are secreted from skeletal tissue and stimulate neurogenesis within the brain. In addition to the various training modes, manipulation of various acute program variables such as intensity, volume, and rest intervals leads to numerous possible training paradigms that can provide a different stimulus for neurogenesis. This review focuses on the three primary training modes and their connection to neurogenesis and cognitive function.