The Sister-Chromatid Exchange and Acetylcholine Esterase Enzyme Levels among Patients with Insecticide Intoxication in the Cukurova Region, Turkey.

This study included 45 patients with intentional insecticide intoxication and 21 with accidental intoxication who were treated at the First-Aid and Emergency Department of Balcali Hospital at the Faculty of Medicine in the Cukurova University, Adana, Turkey, while the control group consisted of 25 people selected from university personnel known to be healthy. Patients with a history of X-ray exposure in the last 6 months or of any virus disease as well as continuous drug users and smokers were excluded, leaving a total of 49 patients. Acetylcholine esterase (Pseudocholinesterase) enzyme (AchE), sister-chromatid exchanges (SCE), the mitotic index (MI), and the replication index (RI) were evaluated. Blood samples were cultured for SCE evaluation and sera separated for AchE levels. Insecticide exposure was generally intentional for suicide in adolescents and at older ages, but accidental for children. AchE levels were found to be significantly lower in organophosphorus (OP) and carbamated (CB) insecticide poisoning groups in comparison with the control group (p&#60;0.001), while the pyrethroid (PY) group was not statistically different for the AchE effect (p&#62;0.05). SCE was found to be significantly higher in OP and CB groups (p&#60;0.001), while the PY and control groups were statistically similar for SCE levels (p&#62;0.05). This study showed an increase in SCE in response to orally ingested insecticides. These findings indicate that insecticide exposure results in cell abnormalities, with resulting impediments to the division and replication of cells, as suggested by MI decreases and RI increases, while the speed of the division cycles of stimulated cells increases.</p

Cancer Pathways

A &#8221;cancer pathway&#8221; is a cellular regulatory system whose activation or inactivation by a genetic or epigenetic mutation is essential for the development of at least one human canver. Typically, cancer pathways become evident by alterations in different components of the same regulatory system in individual cases of one cancer type or in distinct cancers. By this latter criterion, several regulatory systems can be regarded as prototypic cancer pathways. These comprise the MAPK pathway, the TP53 regulatory system, and the cell cycle regulatory net work centered around RB1. These pathways all interact with each other. Further pathways and proteins are also connected to them, such as the PI3K pathway, the PKC kinases, the STAT pathway, the NF&#954;B pathway, and the TGF&#946; response pathway. The third group of cancer pathways comprises the WNT and Hedgehog response pathways and the NOTCH regulatory system. [Archives Medical Review Journal 2011; 20(4.000): 187-229

Genetics of Cancer

Uncontrolled cell proliferation causes cancer in many cases. There are many biological control systems to ensure that cell division is implemented when required by specific cells. There are a number of different ways that cell proliferation can be initiated. Quiescent cells are activated by various signal transduction pathways entailing cascades of protein phosphorylations that activate successive intermediary proteins and, in the end promote the expression of genes that encode cell division proteins. When necessary, apoptosis is triggered and cells are selectively destroyed. Usually cancer formation requires mutations in somatic cells that affect diverse aspects of the cell proliferation process and apoptosis. [Archives Medical Review Journal 2003; 12(4.000): 328-339

Evaluation of the cytogenetical results of 4707 cases diagnosed with amniocentesis.

PURPOSE: Amniocentesis is a very crucial diagnostic procedure for preventing the birth of genetically defective fetuses in order to decrease the prevalence of genetic diseases in populations. METHODS: The karyotyping of 4707 fetuses was carried out in our department during the years of 2000-2009 from the samples of amniotic fluids, CVS, fetal tissues and urines which were sent from departments of Gynecology and Obstetrics of Balcali Hospital and other regional hospitals. RESULTS: The mean maternel and gestational age of pregnant women evaluated for prenatal diagnosis were 29.1 years of age and 18.8 months respectively. Among 4707 fetuses that were karyotyped; 2284 fetuses were males and 2205 fetuses were females and 218 (4.63%) fetuses had various chromosomal abnormalities. Consequently, male to female ratio of fetuses that were examined was 1.03. The advanced maternal age pregnancies followed by positive triplescreening were related to the highest rate of chromosomal abnormalities. The mean age of pregnant women having fetuses with chromosomal abnormalities was found to be 33 years of age which suggest that fetal chromosomal abnormalities were associated with maternal age. Numerical chromosomal abnormalities predominated the structural chromosomal abnormalities (55.5% vs to 44.5%). The numerical chromosomal abnormalities with an incidence of 47.9% trisomy 21, 14.1% trisomy 18, 8.7% Klinefelter Syndrome, 7% monosomy X, 6.6% trisomy 13, 1.7% trisomy X, 1.7% XYY Syndrom, 10% mosaics and the others represented the remaining. Of the structural abnormalities 35% were balanced while the 4% were unbalanced. The frequent structural abnormalities were 25.3% 46,XX/XY, inv(9)(p11;q12) and 19.5% 46,XX/XY, inv(9)(p11;q13). Balanced and unbalanced translocations, deletions and duplications were alsocontributed to chromosomal abnormalities in lesser extent. CONCLUSIONS: Corollary to literature and our findings revealed that the advanced maternal age and certain environmental factors can increase the risk of fetal chromosomal abnormalities. Fetal chromosomal abnormalities representing 4.63% in our study group is crucial and underlines the importance of prenatal diagnosis for healthier pregnancies. [Cukurova Med J 2011; 36(1): 8-14