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עמוד בית
Mon, 06.05.24

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May 2010
H. Rosenblum, Y. Bar-Dayan, Z. Dovrish, S. Lew, N. Weisenberg, A. Neumann, T. Klein and H. Amital

Background: Obstruction of urine outflow can result from mechanical blockade as well as from functional defects. In adults, urinary tract obstruction is due mainly to acquired defects, such as pelvic tumors, calculi, and urethral stricture. In childhood it is mostly due to congenital malformations. In this article we present two rare cases of acute obstructive renal failure that presented with hydronephrosis. These cases underline the wide range of causes that may lead to this clinical feature. 

December 2009
November 2009
A. Amital, D. Shitrit, B.D. Fox, Y. Raviv, L.Fuks, I. Terner and M.R. Kramer

Background: Blunt chest trauma can cause severe acute pulmonary dysfunction due to hemo/pneumothorax, rib fractures and lung contusion.

Objectives: To study the long-term effects on lung function tests after patients' recovery from severe chest trauma.

Methods: We investigated the outcome and lung function tests in 13 patients with severe blunt chest trauma and lung contusion.

Results: The study group comprised 9 men and 4 women with an average age of 44.6 ± 13 years (median 45 years). Ten had been injured in motor vehicle accidents and 3 had fallen from a height. In addition to lung contusion most of them had fractures of more than three ribs and hemo/pneumothorax. Ten patients were treated with chest drains. Mean intensive care unit stay was 11 days (median 3) and mechanical ventilation 19 (0–60) days. Ten patients had other concomitant injuries. Mean forced expiratory volume in the first second was 81.2 ± 15.3%, mean forced vital capacity was 85 ± 13%, residual volume was 143 ± 33.4%, total lung capacity was 101 ± 14% and carbon monoxide diffusion capacity 87 ± 24. Post-exercise oxygen saturation was normal in all patients (97 ± 1.5%), and mean oxygen consumption max/kg was 18 ± 4.3 ml/kg/min (60.2 ± 15%). FEV1[1]. was significantly lower among smokers (71.1 ± 12.2 vs. 89.2 ± 13.6%, P = 0.017). There was a non-significant tendency towards lower FEV1 among patients who underwent mechanical ventilation.

Conclusions: Late after severe trauma involving lung contusion, substantial recovery is demonstrated with improved pulmonary function tests. These results encourage maximal intensive care in these patients. Further larger studies are required to investigate different factors affecting prognosis.

 

 






[1] FEV1 = forced expiratory volume in the first second


October 2009
G. Goldenberg, A. Eisen, N. Weisenberg and H. Amital
January 2008
Y. Shoenfeld, B. Gilburd, M. Abu-Shakra, H. Amital, O. Barzilai, Y. Berkun, M. Blank, G. Zandman-Goddard, U. Katz, I. Krause, P. Langevitz, Y. Levy, H. Orbach, V. Pordeus, M. Ram, Y. Sherer, E. Toubi and Y. Tomer
Y. Shoenfeld, G. Zandman-Goddard, L. Stojanovich, M. Cutolo, H. Amital, Y. Levy, M. Abu-Shakra, O. Barzilai, Y. Berkun, M. Blank, J.F. de Carvalho, A. Doria, B. Gilburd, U. Katz, I. Krause, P. Langevitz, H. Orbach, V. Pordeus, M. Ram, E. Toubi and Y. Sherer
Y. Shoenfeld, M. Blank, M. Abu-Shakra, H. Amital, O. Barzilai, Y. Berkun, N. Bizzaro, B. Gilburd, G. Zandman-Goddard, U. Katz, I. Krause, P. Langevitz, I.R. Mackay, H. Orbach, M. Ram, Y. Sherer, E. Toubi and M.E. Gershwin
E. Zifman and H. Amitai

Medical screening is not a tangible existent tool in autoimmune disorders as it is in other illnesses. Numerous attempts are made to identify individuals destined to develop an autoimmune disease, including analysis of the genetic background, which along with the immunological profile, may assist in identifying those individuals. If these efforts turn out to be successful they may lead to the possibility of proactive measures that might prevent the emergence of such disorders. This review will summarize the attempts made to pursue autoantibodies specific for the central nervous system as potential predictors of autoimmune neurological disorders.

N. Bassi, D. Amital, H. Amital, A. Doria and Y. Shoenfeld

Chronic fatigue syndrome is a heterogeneous disorder with unknown pathogenesis and etiology, characterized by disabling fatigue, difficulty in concentration and memory, and concomitant skeletal and muscular pain. Several mechanisms have been suggested to play a role in CFS[1], such as excessive oxidative stress following exertion, immune imbalance characterized by decreased natural killer cell and macrophage activity, immunoglobulin G subclass deficiencies (IgG-1[2], IgG-3) and decreased serum concentrations of complement component. Autoantibodies were also suggested as a possible factor in the pathogenesis of CFS. Recent studies indicate that anti-serotonin, anti-microtubule-associated protein 2 and anti-muscarinic cholinergic receptor 1 may play a role in the pathogenesis of CFS. It has been demonstrated that impairment in vasoactive neuropeptide metabolism may explain the CFS symptoms







[1] CFS = chronic fatigue syndrome

[2] IgG = immunoglobulin G


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