Evaluating emergency response at a hospital near the Gaza border within 24 h of increased conflict.

BACKGROUND: Frontline hospitals near active hostilities face unique challenges in delivering emergency care amid threats to infrastructure and personnel safety. Existing literature focuses on individual aspects like mass casualty protocols or medical neutrality, with limited analysis of operating acute services directly under fire. OBJECTIVES: To describe the experience of a hospital situated meters from hostilities and analyze strategies implemented for triage, expanding surge capacity, and maintaining continuity of care during attacks with limited medical staff availability due to hazardous conditions. A focus will be placed on assessing how the hospital functioned and adapted care delivery models in the event of staffing limitations preventing all teams from arriving on site. METHODS: A retrospective case study was conducted of patient records from Barzilai University Medical Center at Ashkelon (BUMCA) Medical Center in Israel within the first 24 h after escalated conflict began on October 7, 2023. Data on 232 admissions were analyzed regarding demographics, treatment protocols, time to disposition, and mortality. Missile alert data correlated patient surges to attacks. Statistical and geospatial analyses were performed. RESULTS: Patients predominantly male soldiers exhibited blast/multisystem trauma. Patient surges at the hospital were found to be correlated with the detection of incoming missile attacks from Gaza within 60 min of launch. While 131 (56%) patients were discharged and 55 (24%) transferred within 24 h, probabilities of survival declined over time reflecting injury severity limitations. 31 deaths occurred from severe presentation. CONCLUSION: Insights gleaned provide a compelling case study on managing mass casualties at the true frontlines. By disseminating BUMCA's trauma response experience, strategies can strengthen frontline hospital protocols optimizing emergency care delivery during hazardous armed conflicts through dynamic surge capacity expansion, early intervention prioritization, and infrastructure/personnel protection measures informed by risks.

Early pathology in sleep studies of patients with familial Creutzfeldt-Jakob disease.

In this study, we aimed to assess sleep function in patients with recent-onset familial Creutzfeldt-Jakob disease (fCJD). The largest cluster of fCJD patients is found in Jews of Libyan origin, linked to the prion protein gene (PRNP) E200K mutation. The high index of suspicion in these patients often leads to early diagnosis, with complaints of insomnia being a very common presenting symptom of the disease. The study included 10 fCJD patients diagnosed by clinical manifestations, magnetic resonance imaging (MRI) scan of the brain, elevated tau protein in the cerebrospinal fluid (CSF) and positive PRNP E200K mutation. Standard polysomnography was performed after a brief interview confirming the presence of sleep disturbances. All patients showed a pathological sleep pattern according to all scoring evaluation settings. The sleep stages were characterized by (i) disappearance of sleep spindles; (ii) outbursts of periodic sharp waves and shallowing of sleep consisting in increased Stage 2 and wake periods during the night, as well as decrease of slow-wave sleep and rapid eye movement (REM) sleep. Recordings of respiratory functions reported irregular breathing with central and obstructive apnea and hypopnea. The typical hypotonia occurring during the night and atonia during REM sleep were replaced by hyperactive sleep consisting of multiple jerks, movements and parasomnia (mainly talking) throughout the night. In conclusion, we report unique pathological sleep patterns in early fCJD associated with the E200K mutation. Specific respiratory disturbances and lack of atonia could possibly serve as new, early diagnostic tools in the disease.

Passive transfer of narcolepsy: anti-TRIB2 autoantibody positive patient IgG causes hypothalamic orexin neuron loss and sleep attacks in mice.

Narcolepsy is a sleep disorder characterized by excessive daytime sleepiness and cataplexy (a sudden weakening of posture muscle tone usually triggered by emotion) caused by the loss of orexin neurons in the hypothalamus. Autoimmune mechanisms are implicated in narcolepsy by increased frequency of specific HLA alleles and the presence of specific autoantibody (anti-Tribbles homolog 2 (TRIB2) antibodies) in the sera of patients with narcolepsy. Presently, we passively transferred narcolepsy to naïve mice by injecting intra-cerebra-ventricularly (ICV) pooled IgG positive for anti-TRIB2 antibodies. Narcolepsy-IgG-injected mice had a loss of the NeuN (neuronal marker), synaptophysin (synaptic marker) and orexin-positive neurons in the lateral hypothalamus area in narcolepsy compared to control-IgG-injected mice and these changes were associated with narcolepsy-like immobility attacks at four weeks post injection and with hyperactivity and long term memory deficits in the staircase and novel object recognition tests. Similar behavioral and cognitive deficits are observed in narcoleptic patients. This is the first report of passive transfer of experimental narcolepsy to naïve mice induced by autoantibodies and supports the autoimmune pathogenesis in narcolepsy.

[Narcolepsy as an autoimmune disease].

Narcolepsy is a chronic sleep disorder characterized by excessive daytime sleepiness and irresistible sleep attacks that occur during the activities of daily living. Falling asleep in the middle of essential activities such as driving or crossing the street may lead to life-threatening situations. Narcolepsy is estimated to affect 0.002% of the Israeli population. By using animal models, human autopsies and brain biopsies, it has recently been shown that the destruction of the orexin-secreting neurons underlies the pathogenicity of this disease. Orexin is a neurotransmitter involved in the sleep arousal cycle and also in the development of hunger sensations. Based on circumstantial evidence, it is estimated that the autoimmune system is responsible for the destruction of the orexin-secreting neurons. There are several findings in the literature that might connect the autoimmunity with the narcolepsy existence. For instance: narcolepsy is associated with high frequency of specific HLA system alleles, especially DQB1*0602. Furthermore, polymorphism in the alpha chain of the T cell receptors was found among narcolepsy patients. A more direct connection is the discovery of the Trib--an autoantigen. This protein is presented by orexin-secreting neurons and was recently found in narcoleptic patients exclusively, and not in the healthy control group. Nevertheless, there is still no agreement within the scientific community since a direct link between the autoimmune mechanism and narcolepsy has not yet been proved. Several trials using immune modulator therapy did not show any significant improvement.

Assessment of Predictors for SARS-CoV-2 Antibodies Decline Rate in Health Care Workers after BNT162b2 Vaccination-Results from a Serological Survey.

Background: SARS-CoV-2 is a novel human pathogen causing Coronavirus Disease 2019 that has caused widespread global mortality and morbidity. Since health workers in Israel were among the first to be vaccinated, we had a unique opportunity to investigate the post-vaccination level of IgG anti-S levels antibodies (Abs) and their dynamics by demographic and professional factors. Methods: Prospective Serological Survey during December 2020−August 2021 at Barzilai Medical Center among 458 health care workers (HCW) followed for 6 months after the second BNT162b2 vaccine dose. Results: Antibody levels before the second dose, and 30, 90 and 180 days after were 57.1 ± 29.2, 223 ± 70.2, 172.8 ± 73.3 and 166.4 ± 100.7 AU/mL, respectively. From GEE analysis, females had higher Abs levels (ß = 26.37 AU/mL, p = 0.002). Age was negatively associated with Abs, with a 1.17 AU/mL decrease for each additional year (p < 0.001). Direct contact with patients was associated with lower Abs by 25.02 AU/mL (p = 0.009) compared to working with no such contact. The average decline rate overall for the study period was 3.0 ± 2.9 AU/mL per week without differences by demographic parameters and was faster during the first 3 months after vaccination than in the subsequent 3 months. Conclusions: All demographic groups experienced a decline in Abs over time, faster during the first 3 months. Findings of overall Abs lower in males, workers with direct contact with patients, and older workers, should be considered for policy-making about choosing priority populations for additional vaccine doses in hospital settings.

The influence of odorants on respiratory patterns in sleep.

To assess the feasibility of using odors as a potential mechanism for treating sleep apnea, we set out to test the hypothesis that odorants delivered during sleep would modify respiratory patterns without inducing arousal or wake in healthy sleepers. We used 2 mildly trigeminal odorants: the pleasant lavender and unpleasant vetiver oil and 2 pure olfactory odorants: the pleasant vanillin and unpleasant ammonium sulfide. During sleep, an olfactometer delivered a transient odorant every 9, 12, or 15 min (randomized), providing 21-37 odorant presentations per night. Each of 36 participants was studied for 1 night and with 1 of the 4 different odorants tested. In addition to standard overnight polysomnography, we employed highly accurate measurements of nasal and oral respiration. Odorants did not increase the frequency of arousals or wake but did influence respiration. Specifically, all 4 odorants transiently decreased inhalation and increased exhalation for up to 6 breaths following odor onset. This effect persisted regardless of odorant valence or stage of sleep. These results suggest that the olfactory system may provide a path to manipulate respiration in sleep.

Extrapyramidal signs in neurosarcoidosis versus multiple sclerosis: Is TNF alpha the link?

Specific inflammatory pathways and specifically Tumor Necrosis Factor alpha (TNF-α) have been associated with the neurodegeneration in Parkinson's disease (PD). TNFα is also known to play an important role in the pathogenesis of sarcoidosis and TNF blockers can ameliorate the disease. In contrast, multiple sclerosis (MS) is clearly exacerbated by anti- TNF-α medications. We have therefore hypothesized that Parkinson-like disease would be more common in neurosarcoidosis (NS) compared to MS. The aim of this case-control study was therefore to assess the frequency of extrapyramidal signs in patients with NS compared to MS patients. In order to do so the medical records of NS patients and of age and gender matched MS patients were reviewed and data regarding the clinical features, ancillary tests performed, treatment, and outcome were documented. Patients were then examined in a uniform manner for the presence of extrapyramidal signs. We found that in the NS group 8 patients had minor signs, one had mild functional disability and 3 subjects had significant extrapyramidal signs compatible with the diagnosis of Parkinson's disease. All extrapyramidal signs found in 5 of the MS group were minor. The proportional severity of extrapyramidal signs was significantly higher (p=0.045, chi square test) in the NS group compared to the MS group. We conclude that the specificity of extrapyramidal to NS raises the intriguing question of whether specific inflammatory pathways involving TNF-α play a role in the pathogenesis of PD and therefore may be a therapeutic target.

Characterization of sleep disorders in patients with E200K familial Creutzfeldt-Jakob disease.

The largest cluster of E200K familial Creutzfeldt-Jakob disease (fCJD) which occurs is in Jews of Libyan origin in Israel. Insomnia is a very common early complaint in those patients and may even be the presenting symptom. The aim of this study was to assess and characterize sleep pathology in E200K fCJD patients. To do so, sleep studies of 10 consecutive fCJD patients were compared with those of 39 age and gender-matched controls. All patients presented pathological sleep characterized by fragmentation of sleep, loss of sleep spindles and reduced REM sleep amount. Respiration was characterized by irregular rhythm, periodic breathing, apneas and hypopneas, either central or obstructive. EMG recordings revealed repeated movements in sleep, with loss of REM atonia. Comparing to controls, a significant decrease of total sleep time, sleep efficacy and slow-wave sleep as well as a significant increase in the number of awakenings, apnea-hypopnea index and mixed and central apneas were evident in CJD patients. Comparison of two sequential sleep studies in one patient revealed a 40 % reduction of the total sleep time, a 40 % reduction in sleep efficacy and a 40-fold increase of the number of arousals in the second study. A significant correlation was found between the disease severity, as reflected by the CJD Neurological Scale and Periodic leg movement index. These definite and characteristic sleep pathologies in patients with fCJD associated with the E200K mutation may serve as a new diagnostic tool in the disease.