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Biomedical subjects

Arik Eisenkraft

Publications and source records attributed to Arik Eisenkraft.

11 recordsLinked to original sources
PubMed2006

MCP-1 in the cerebrospinal fluid of children with acute lymphoblastic leukemia.

BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) is a member of the CC chemokines. MCP-1 has been previously shown to have a major role in the migration of monocytes towards human leukemic cells, yet it cannot increase cytotoxic effects of monocytes on human leukemic cells. AIM: To determine levels of MCP-1 in the CSF of children during various stages of acute lymphoblastic leukemia (ALL). PATIENTS AND METHODS: A 19 children with ALL and without known CNS involvement were enrolled in the study. CSF samples were aliquoted at different stages of therapy (diagnosis, induction, and maintenance) and were frozen at -70 degrees C until use. MCP-1 was measured with a sandwich enzyme-linked immunoabsorbent assay. RESULTS: Mean MCP-1 levels in the CSF were 1762.38 pg/ml (range 522-5000 pg/ml). In children without CNS involvement at diagnosis, CSF MCP1 levels did not change over time and remained within this range throughout the diagnosis and treatment stages. CNS involvement was associated with an increased MCP-1 level following chemotherapy, in patients with CNS involvement from 840 to 3990 pg/ml (P<0.0001), and in patients without CNS involvement from 1134 to 1943 pg/ml (P-value of 0.0322). White blood cells found in the CSF at diagnosis have vanished after induction. CONCLUSIONS: CNS involvement in ALL is associated with significantly higher levels of MCP1 during therapy. This significant rise in MCP-1 levels might be one of the mechanisms involved in the regulation of CNS leukemia. Since chemokines target specific leukocyte subsets, inhibition of a single Chemokine ligand or receptor may have a circumscribed effect, endowing the inhibitor with a limited side effect profile. Chemokines should be considered as possible targets for therapeutic intervention.

Adolescent↗
PubMed2005

Clinical and molecular findings in a family with the carbonic anhydrase II deficiency syndrome.

Carbonic anhydrase II (CA2) deficiency syndrome is an autosomal recessive disorder leading to osteopetrosis, renal tubular acidosis, and cerebral calcifications. Affected members of an Arab family with the CA2 deficiency syndrome carried the "Egyptian mutation" in CA2, i.e., c.191 del A, H64fsX90. One affected member, homozygote for the mutation, developed primary pulmonary hypertension. Primary pulmonary hypertension was never described before in patients with this unique syndrome. The likelihood of both occurring randomly in a single individual is very low. We therefore speculate that there might be a possibility of an etiologic link between these entities.

Acidosis, Renal Tubular↗
PubMed2005

Inherited and acquired interactions between ACHE and PON1 polymorphisms modulate plasma acetylcholinesterase and paraoxonase activities.

The 5.5 Mb chromosome 7q21-22 ACHE/PON1 locus harbours the ACHE gene encoding the acetylcholine hydrolyzing, organophosphate (OP)-inhibitable acetylcholinesterase protein and the paraoxonase gene PON1, yielding the OP-hydrolyzing PON1 enzyme which also displays arylesterase activity. In search of inherited and acquired ACHE-PON1 interactions we genotyped seven polymorphic sites and determined the hydrolytic activities of the corresponding plasma enzymes and of the AChE-homologous butyrylcholinesetrase (BChE) in 157 healthy Israelis. AChE, arylesterase, BChE and paraoxonase activities in plasma displayed 5.4-, 6.5-, 7.2- and 15.5-fold variability, respectively, with genotype-specific differences between carriers of distinct compound polymorphisms. AChE, BChE and arylesterase but not paraoxonase activity increased with age, depending on leucine at PON1 position 55. In contrast, carriers of PON1 M55 displayed decreased arylesterase activity independent of the - 108 promoter polymorphism. Predicted structural consequences of the PON1 L55M substitution demonstrated spatial shifts in adjacent residues. Molecular modelling showed substrate interactions with the enzyme variants, explaining the changes in substrate specificity induced by the Q192R substitution. Intriguingly, PON1, but not BChE or arylesterase, activities displayed inverse association with AChE activity. Our findings demonstrate that polymorphism(s) in the adjacent PON1 and ACHE genes affect each other's expression, predicting for carriers of biochemically debilitating ACHE/PON1 polymorphisms adverse genome-environment interactions.

Acetylcholinesterase↗
PubMed2005

[Political poisoning with dioxins--a weapon of chemical "disgracefulness"].

The recent attempt to poison Ukrainian President, Viktor Yuschenko with dioxins, raised public concern regarding this toxic chemical. In industrial countries, there is a constitutive exposure of humans to dioxin compounds, which are formed as by-products in manufacturing processes of various chlorinated organic chemicals and in waste incinerators. Dioxins are extremely stable in the environment and have a low turnover rate in the body--sometimes they are detected years after the original exposure. Of the dioxins, the most notoriously famous is the TCDD (2,3,7,8 tetrachlorodibenzo-p-dioxin). Dioxins exhibit high acute toxicity in various animal species. Humans, however, are considered less susceptible and so far there were no reported deaths following acute dioxin poisoning. Nevertheless, numerous adverse health effects are attributed to dioxin exposure. The most prominent is the chloracne--an acute acneiform eruption, usually appearing on facial skin. There is a solid evidence base that some dioxins are carcinogens. Other long-term deleterious effects of dioxin include: immunosuppression, effects on reproduction, impairments in developmental, neurological and cognitive functions in infants, increased risk for diabetes and cardiovascular diseases and various hormonal alterations. The action of dioxins resembles that of hormones, since their toxicity is mostly receptor-mediated. Dioxins manifest their toxicity in extremely low concentrations. Although there are compounds that exhibit their biological activity at even lower dose range (e.g. nerve gases), this potency of dioxins is considered extraordinary, since there is an every-day exposure to dioxins through environmental vectors mostly via the food chain. Until now, there is no antidotal cure for dioxins, but only symptomatic treatment combined with techniques that accelerate its excretion rate from the body.

Animals↗
PubMed2003

[Using thalidomide against pathological neovascularization].

Thalidomide was first used during the 50's-60's, especially for morning sickness in pregnant women. It was found to be a powerful teratogen only years later and was banned from use. At the same time it was found to have anti-inflammatory and anti-angiogenic properties and was approved as treatment for leprosy. As such, thalidomide might be used against pathological neovascularization, as seen in mustard gas exposure. From past experience we know that the eyes are the most vulnerable organ to mustard gas exposure. In some of the casualties there is a late sequella including pathological corneal neovascularization. So far there is no specific effective treatment against this neovascularization. The purpose of this review is to examine current research about the potential use of thalidomide as an anti-angiogenic agent, including potential role in treating mustard gas eye injury.

Angiogenesis Inhibitors↗
PubMed2003

[Medical aspects of the lacrimator CS].

Since the 1960's, CS has become the main riot control agent in use by police and army forces throughout the world. The first post-exposure symptom is a burning sensation in the eyes, nose and throat. At a later stage, lacrimation, rhinorrhea, conjunctivitis, sore throat and salivation appear. These symptoms are followed by chest pain and dry cough, and if the substance is swallowed, it may cause nausea and vomiting. This article reviews the physical properties of CS, the main dispersing techniques, the clinical signs and symptoms of exposure, including information on mutagenicity, carcinogenesis, pregnancy safety, and will introduce guidelines for treatment after exposure.

Chest Pain↗
PubMed2002

Simulation-based training of medical teams to manage chemical warfare casualties.

With chemical warfare becoming an imminent threat, medical systems need to be prepared to treat the resultant mass casualties. Medical preparedness should not be limited to the triage and logistics of mass casualties and first-line treatment, but should include knowledge and training covering the whole medical spectrum. In view of the unique characteristics of chemical warfare casualties the use of simulation-assisted medical training is highly appropriate. Our objective was to explore the potential of simulator-based teaching to train medical teams in the treatment of chemical warfare casualties. The training concept integrates several types of skill-training simulators, including high tech and low tech simulators as well as standardized simulated patients in a specialized simulated setting. The combined use of multistimulation modalities makes this maverick program an excellent solution for the challenge of multidisciplinary training in the face of the looming chemical warfare threat.

Chemical Warfare↗
PubMed2002

Training Israeli medical personnel to treat casualties of nuclear, biologic and chemical warfare.

Recent events have significantly increased concern about the use of biologic and chemical weapons by terrorists and other countries. Since weapons of mass destruction could result in a huge number of casualties, optimizing our diagnostic and therapeutic skills may help to minimize the morbidity and mortality. The national demands for training in medical aspects of nuclear, biologic and chemical warfare have increased dramatically. While Israeli medical preparedness for non-conventional warfare has improved substantially in recent years especially due to extensive training programs, a standardized course and course materials were not available until recently. We have developed a core curriculum and teaching materials for a 1 or 2 day modular course, including printed materials.

Biological Warfare↗
PubMed2002

[Personal protection against biological warfare agents].

Exposure to biological warfare agents may occur in several ways, the most prominent being aerosol infection, droplet infection, common component infection and via physical contact. These agents may enter the body through the respiratory tract, mucous membranes and through the skin. The mechanism of exposure and the route of entry of the specific agent will dictate the appropriate protection required. Available protective equipment include respiratory protective devices, full face protective masks and surgical masks for respiratory protection, battle dress overgarments, protective gloves and overboots for skin protection. Full protection is needed when the agent has not been identified. When the biological agent is known, the protective measures should be determined by its characteristics. Protection may include several levels of precautions: standard risk, aerosol infection, droplet infection and contact infection. This paper describes the routes of exposure to biological warfare agents, the available protective equipment and the precautions needed when treating biowarfare casualties.

Biological Warfare↗
PubMed2002

[Viral encephalitis caused by biowarfare agents].

Many viruses may cause encephalitis. Three such viruses of the Alpha genus (Venezuelan equine encephalitis (VEE), Western equine encephalitis (WEE) and Eastern equine encephalitis (EEE)) may be used as biological warfare agents. The clinical course of the diseases caused by these viruses is not specific, and resembles a broad range of bacterial and viral diseases. Several attenuated and inactivated vaccines were developed, but their efficacy in the biological warfare scenario is questionable. There is no effective drug therapy for the treatment of these diseases, and treatment is mainly supportive. Several VEE outbreaks were reported in humans and horses in South America and southern United States. This virus usually causes a febrile illness, which might be complicated with encephalitis, mainly in the cases of children and elderly patients. The EEE virus causes the most severe form of disease, with severe encephalitis and high proportion of sequel. It is prevalent mainly in the eastern parts of Northern America. The WEE virus, which is hybridization between the Sindbis virus and the EEE virus, causes encephalitis mainly in children. The severity of the disease caused by WEE and the sequel rate is much lower than that of EEE.

Biological Warfare↗