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עמוד בית
Fri, 05.12.25

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June 2005
April 2005
E. Bamberger, R. Madeb, J. Steinberg, A. Paz, I. Satinger, Z. Kra-0z, O. Natif and I. Srugo
Background: Although the current literature attributes most cases of hematospermia to an infectious agent, identification of the specific pathogens involved has been limited.

Objectives: To determine the prevalence of different pathogens in patients presenting to our sexually transmitted disease clinic with hematospermia.

Methods: Between January 1999 and January 2000, 16 patients presented to our STD[1] clinic with hematospermia after other non-infectious pathologies had been excluded by a referring physician. After obtaining informed consent, subjects completed a questionnaire addressing symptoms and sexual behavior. First void urine samples, as well as genitourinary and serum specimens were tested for Chlamydia trachomatis, Ureaplasma urealyticum and Herpes simplex virus. Standard bacterial cultures were also performed.

Results: Laboratory testing detected a pathogen in 12 of the 16 males presenting with hematospermia. The sexually transmitted pathogens detected were Herpes simplex virus in 5 patients (42%), Chlamydia trachomatis in 4 (33%), Enterococcus fecalis in 2 (17%), and Ureaplasma urealyticum in 1 (8%). In all cases in which a pathogen was identified, the appropriate antimicrobial agent was administered. Symptoms resolved for each patient following antimicrobial therapy. During a 1 year follow-up, all 12 patients remained free of disease.

Conclusions: Recent advances in microbiologic diagnostic techniques have facilitated the detection of pathogens in patients with hematospermia, thereby enhancing the efficacy of treatment.

____________________

[1] STD = sexually transmitted disease

E. Magen, D. Elbirt and Z. Sthoeger
Highly active antiretroviral therapy has dramatically improved the quality of life and life expectancy of patients with human immunodeficiency virus. However, the prolonged use of HAART[1] leads to severe metabolic adverse events. Both HIV[2]infection and HAART can cause changes in lipid and glucose metabolism as well as elevation of blood pressure, promoting the development of atherosclerosis. Cardiovascular diseases have become a major cause of mortality among HIV-infected subjects who respond well to antiretroviral therapy. Nevertheless, a proper lifestyle and pharmacologic intervention can improve cardiovascular risk factors in the HIV-treated population and significantly reduce healthcare investments in the treatment of future cardiovascular complications in this population. In this review we summarize the current knowledge of CVD[3] prevention and treatment in HIV patients.

________________

[1] HAART = highly active antiretroviral therapy

[2] HIV = human immunodeficiency virus

[3] CVD = cardiovascular disease
March 2005
R. Percik, J. Serr, G. Segal, S. Stienlauf, H. Trau, B. Shalmon, A. Shimoni and Y. Sidi
July 2004
E. Reinstein

The ubiquitin-proteasome pathway has a central role in selective degradation of intracellular proteins. Among the key proteins degraded by the system are those involved in the control of inflammation, cell cycle regulation and gene expression. With numerous important cellular pathways affected, derangements in the ubiquitin system were shown to result in a variety of human diseases including malignancies, neurodegenerative diseases and hereditary syndromes, and proteasome inhibition was implicated as a potential treatment for cancer and inflammatory conditions. Two proteasome inhibitors are currently under clinical evaluation for multiple myeloma and acute ischemic stroke. The ubiquitin system also has an important function in the immune and inflammatory response. It is involved in antigen processing and presentation to cytotoxic T cells, and the activation of nuclear factor-kappa B – the central transcription factor of the immune system. Since the proteasome is the central source of antigenic peptides that are presented to the immune system, some viruses, such as the Epstein-Barr virus, developed escape mechanisms that manipulate the ubiquitin-proteasome system in order to persist in the infected host. Understanding the mechanisms underlying the production of viral antigens by the ubiquitin-proteasome system may have therapeutic applications such as future development of vaccines.

April 2004
A. Ya'ari, C.L. Jaffe and B-Z. Garty

Background: Visceral leishmaniasis was first reported in Israel (then Palestine) in 1929. In the 1960s and 1970s, it was endemic to northern Israel, but only partial data about the disease have been gathered since then.

Objective: To investigate the epidemiologic trends of visceral leishmaniasis in Israel from 1960 to 2000, and to delineate some clinical features of the infection.

Methods: Data were collected from hospital charts, scientific publications, and reports of the Ministry of Health and the Kuvin Center for the Study of Infectious and Tropical Diseases.

Results: During the last four decades, 87 cases of visceral leishmaniasis were diagnosed in Israel, 76 of them (87%) in children. All 54 patients diagnosed in the 1960s occurred in the northern part of the country. The rate of infection declined significantly in the 1970s (5 cases) and then increased slightly in the 1980s (11 cases) and 1990s (17 cases). More than 50% of the cases in the 1990s were in central Israel. Children accounted for 100% of cases in the 1960s but only 58% in the 1990s. The main clinical features of the patients diagnosed in the last decade were fever, weight loss, hepatosplenomegaly and pancytopenia. Three of the adults were co-infected with human immunodeficiency virus.

Discussion: The decline in the incidence of visceral leishmaniasis in the 1970s and the slight increase in the 1980s and 1990s can be attributed to changes in the animal reservoir and vectors, and in the immunity status of part of the population exposed to Leishmania.

Conclusions: Visceral leishmaniasis has reemerged in Israel. This mandates better control of the animal reservoir and vectors and increased awareness of this infection.

December 2003
J-L. Touraine, K. Sanhadji and R. Sembeil

Background: The humanized SCID mouse model is an attractive tool for testing gene therapy to combat human immunodeficiency virus infection in vivo.

Objectives: To devise a more specific gene therapy directed against HIV, replacing the formerly used interferon with either soluble CD4 molecule immunoadhesin (sCD4-IgG) and/or anti-gp41 monoclonal antibody (2F5), or negative transdominants (Tat, Rev).

Methods: Human monocytoid cell line (U937) was transfected with IFNa[1], b or g genes. 3T3 murine fibroblastic cell line was transfected with sCD4-IgG or 2F5, or both genes, and a human T4 cell line (CEM) was grafted to SCID mice. Negative transdominant genes (Tat, Rev or both) were also transduced in CEM T cell line. Animals were then challenged with HIV-1[2]. Viral load was followed.

Results: IFNa or b were potent anti-HIV, reducing viral load in vivo and inhibiting reverse transcriptase activity in human-removed cells from animals. sCD4-IgG immunoadhesin and gp41 monoclonal antibody resulted in a dramatic reduction of HIV-1 cellular and plasmatic viral load in humanized SCID mice. The simultaneous introduction of negative Tat and Rev genes resulted in a synergistic inhibition of HIV-1 replication in vivo.

Conclusions: Despite the marked reduction of HIV-1 propagation by IFN genes or by negative Tat and Rev transdominants, the gene therapy using soluble CD4 immunoadhesin or anti-gp41 was a more efficient preventive treatment against HIV infection.






[1] IFN = interferon



[2] HIV = human immunodeficiency virus


September 2003
P.A. Feldman, J. Steinberg, R. Madeb, G. Bar, O. Nativ, J. Tal and I. Srugo

Background: Seroepidemeliogic surveys have provided valuable information on the prevalence and incidence of herpes simplex virus-2 infection in general and in selected populations.

Objective: To review the reliability of traditional diagnostic approaches in herpes simplex virus-2 infection.

Methods: In this cross-sectional study, 472 patients attending a clinic for sexually transmitted disease in 1998-1999 were evaluated for HSV-2 infection through collection of epidemiologic and clinical data.

HSV-2 infection was confirmed by the presence of specific Viral glycoprotein, gG-2, antibody in sera.

Results: The seroprevalence of HSV-2 among clinic attendees was 9.33%. Of these attendees only 22% presented with or reported a history of typical vesicular lesions in the genital area. Infection rate was  higher in patients with multiple sex partners (20.8% vs. 8.7%, P< ( 0.0023 in individuals aged 30 or older (12.6 vs. 6.4%, P = 0.03) and  in the Israeli Jewish population as compared to the Israeli Arab population (11.1% vs. 2.4%, P ~ 0.01). Females with multiple sex partners exhibited higher rates of infection than did their male counterparts (50 vs. 16.1%, P < 0.0275(.

Conclusion: The findings support the need for HSV-2 serologi  testing in patients presenting to STD clinics even when typical genital  lesions are not evident but where risk factors for HSV-2 infection are  identified.
 

September 2002
Dan Miron, MD, Yoseph Merzel, MD, Amiram Lev, MD, Jean-Jack Meir, MD and Yoseph Horowitz, MD
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