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עמוד בית
Thu, 30.05.24

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September 2022
David Segal MD MPH, Nitzan Shakarchy-Kaminsky MD MSc, Yair Zloof MD, Tomer Talmy MD, Galina Shapiro MD PHD, Irina Radomislensky BSc, Avishai M. Tsur MD MHA, Shaul Gelikas MD MBA, Erez Karp MD MHA, and Avi Benov MD MHA; Israel Trauma Group

Background: Medical organizations worldwide aim for equity and diversity in the medical profession to improve care quality. Data on whether the caregiver gender affects outcomes in the prehospital setting are essential but scarce compared to available in-hospital studies.

Objective: To analyze the rates of missed injuries in the prehospital setting and determine whether these rates were associated with the gender of the on-field physician or paramedic.

Methods: A retrospective record review was conducted, which included trauma records documented in two trauma registries, the prehospital Israel Defense Forces-Trauma Registry (IDF-TR), and the in-hospital Israeli National Trauma Registry (INTR). Missed injuries were defined as injuries documented in the INTR but not in the IDF-TR. A multivariable regression analysis was performed to assess the association between provider’s gender and missed injuries.

Results: Of 490 casualties, 369 (75.3%) were treated by teams that included only male paramedics or physicians. In 386 (78.8%) cases, a physician was a part of the prehospital team. In all, 94 (19.2%) casualties sustained injuries that were missed by the prehospital medical team. Missed injuries were not associated with the gender of the paramedic or physician (odds ratio 1.242, 95% confidence interval 0.69–2.193).

Conclusions: No association was found between the gender of the medical provider in the prehospital setting and the rate of missed injuries. These results should encourage prehospital emergency medical systems to aim for a balanced and diverse caregiver population.

April 2008
B. Kristal, R. Shurtz-Swirski, O. Tanhilevski, G. Shapiro, G. Shkolnik, J. Chezar, T. Snitkovsky, M. Cohen-Mazor and S. Sela

Background: Polymorphonuclear leukocyte priming and low grade inflammation are related to severity of kidney disease. Erythropoietin-receptor is present on PMNLs[1].

Objectives: To evaluate the effect of 20 weeks of EPO[2]-alpha treatment on PMNL characteristics in relation to the rate of kidney function deterioration in patients with chronic kidney disease.

Methods: Forty anemic chronic kidney disease patients, stage 4-5, were assigned to EPO and non-EPO treatment for 20 weeks. A group of 20 healthy controls was also studied. PMNL priming and PMNL-derived low grade inflammation were estimated, in vivo and ex vivo, before and after EPO treatment: The rate of superoxide release, white blood cells and PMNL counts, serum alkaline phosphatase and PMNL viability were measured. EPO-receptor on PMNLs was assayed by flow cytometry. The effect of 20 weeks of EPO treatment on kidney function was related to the estimated glomerular filtration rate.

Results: EPO treatment attenuated superoxide release ex vivo and in vivo and promoted PMNL survival ex vivo. Decreased low grade inflammation was reflected by reduced WBC[3] and PMNL counts and ALP[4] activity following treatment. EPO retarded the deterioration in GFR[5]. The percent of PMNLs expressing EPO-R[6] was higher before EPO treatment and correlated positively with the rate of superoxide release. After 20 weeks of EPO treatment the percent of PMNLs expressing EPO-R was down-regulated.

Conclusions: These non-erythropoietic properties of EPO are mediated by EPO-R on PMNLs, not related to the anemia correction. A new renal protection effect of EPO via attenuation of PMNL priming that decreases systemic low grade inflammation and oxidative stress is suggested.

[1] PMNL = polymorphonuclear leukocytes

[2] EPO = erythropoietin

[3] WBC = white blood cells

[4] ALP = alkaline phosphatase

[5] GFR = glomerular filtration rate

[6] EPO = EPO-receptor

November 2002
Shifra Sela, PhD, Revital Shurtz-Swirski, PhD, Jamal Awad, MD, Galina Shapiro, MSc, Lubna Nasser, MSc, Shaul M. Shasha, MD and Batya Kristal, MD

Background: Cigarette smoking is a well-known risk factor for the development of endothelial dysfunction and the progression of atherosclerosis. Oxidative stress and inflammation have recently been implicated in endothelial dysfunction.

Objectives: To assess the concomitant contribution of polymorphonuclear leukocytes to systemic oxidative stress and inflammation in cigarette smokers.

Methods: The study group comprised 41 chronic cigarette-smoking, otherwise healthy males aged 45.0 ± 11.5 (range 31–67 years) and 41 male non-smokers aged 42.6 ± 11.3 (range 31–65) who served as the control group. The potential generation of oxidative stress was assessed by measuring the rate of superoxide release from separated, phorbol 12-myristate 13-acetate-stimulated PMNL[1] and by plasma levels of reduced (GSH) and oxidized (GSSG) glutathione. Inflammation was estimated indirectly by: a) determining the in vitro survival of PMNL, reflecting cell necrosis; b) in vivo peripheral PMNL counts, reflecting cell recruitment; and c) plasma alkaline phosphatase levels, indicating PMNL activation and degranulation.

Results: PMA[2]-stimulated PMNL from cigarette smokers released superoxide at a faster rate than PMNL from the controls. Smokers had decreased plasma GSH[3] and elevated GSSG[4] levels. In vitro incubation of control and smokers' PMNL in sera of smokers caused necrosis, while control sera improved smoker PMNL survival. Smokers' PMNL counts, although in the normal range, were significantly higher than those of controls. Plasma ALP[5] levels in smokers were significantly higher than in controls and correlated positively with superoxide release and PMNL counts.

Conclusions: Our study shows that PMNL in smokers are primed in vivo, contributing concomitantly to systemic oxidative stress and inflammation that predispose smokers to endothelial dysfunction, and explains in part the accelerated atherosclerosis found in smokers.


[1] PMNL = polymorphonuclear leukocytes

[2] PMA = phorbol 12-myristate 13-acetate

[3] GSH = reduced glutathione

[4] GSSG = oxidized glutathione

[5] ALP = alkaline phosphatase

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