Introduction: recently studies have shown an association between thyroid antibody and spontaneous abortion. The aim of present study was to evaluate the relation between thyroid antibody and thrombophylia and C activated protein c resistance (APCR) with recurrent spontaneous miscarriage.Materials and Methods: from April 2007 to March 2008 (in a case control study).74 woman with a history of recurrent abortion and 80 matched woman without previews abortion enrolled in this study. APCR, thyroglobolin (TG), thyroid peroxides antibodies (TPO). Thyroid stimulation hormone (TSH) and free thyroxin (FT) and lupus anticoagulant levels were assessed. The data were analyzed by student t-test. Man Whitney, chi square and fisher exact.Results: A total 154 patient with mean age ±SD of 33.6±6.4, range=13-52years old) in case and 33.4±5.9 in control group assessed.There is a significant relation between APCR, TG, TPO, TSH, FT and recurrent spontaneous miscarriage (all p<0.05) but not relation with lupus anticoagulant levels.Conclusion: Based on the currently available evidence, it appears that the presence of thyroid antibodies and APCR is associated with an increased risk for spontaneous miscarriage in subfertile women this index may be considered as a potential diagnostic factor for miscarriage especially spontaneous abortion.

Background: Activated protein C (APC) inactivates factor V (FV) by cleavage of its heavy chain at Arg306, Arg506, Arg679, and Lys994. Mutational changes, which abolish APC cleavage sites, may predispose thrombosis by altering the inactivation process of FV. FV Leiden (FVL) (Arg506Glu) has been demonstrated as a strong risk factor for thrombosis. In the current study, we have studied whether mutations in the cleavage sites of FV for APC, not due to FVL, would have a role in presenting APC resistance (APCR) and initiation of a cerebral thrombotic event. Methods: A group of 22 patients with a history of cerebral venous thrombosis (CVT), who were not carriers of FVL enrolled in the study. The patients who had conditions associated with acquired APCR were excluded from the study. APCR test was performed on the remaining 16 patients, which showed APCR in 4 plasma samples. DNA sequencing was performed on four exons of FV of APCR patients, encoding Arg306, Arg506, Arg679, and Lys994. Results: Mutations were not found within nucleotides encoding the cleavage sites; neither was found within their close upstream and downstream sequences. Conclusion: Our results show that polymorphisms affecting cleavage sites of FV other than Arg506Glu it would be less likely to be the basis for APCR and its increased thrombosis susceptibility. In addition, it emphasizes on the importance of screening for APCR in the patients diagnosed with CVT.

The targets that either have low radar cross-section typically, or their return signal has been deliberately reduced are referred to as weak targets in radar terminology. There are several algorithms for detection of a weak moving target. When such a target is in the vicinity of a large target, the side lobes of the matched filter output due to the large target mask or hide the weak target. The adaptive pulse compression filter that uses the RMMSE estimator has the ability to detect the masked weak target. However, there are at least three factors (computational load, Doppler robustness and pulse eclipsing) which limit the practical application of RMMSE. In this paper, an optimized and integrated algorithm based on adaptive post-processing is proposed to detect targets and to overcome the challenges of RMMSE in electronic defense systems. The FFL-APCR proposed algorithm when compared qualitatively to other algorithms indicates better performance for different SNRs and various target velocities, showing that it is more suitable for implementation in real-time systems. The FFL-APCR algorithm can detect high speed and pulse eclipsed weak targets with lower computational load.

The matched filter in the radar receiver is only adapted to the transmitted signal version and its output will be wasted due to non-matching with the received signal from the environment. The sidelobes amplitude of the matched filter output in pulse compression radars are depended on the transmitted coded waveforms that extended as much as the length of the code on both sides of the target location. In order to detect a weak target in vicinity of strong target, the sidelobes of the matched filter output resulting from the strong target masked the weak target and didn’ t detect its. Generally, the radar dynamic range is defined by the maximum power ratio to the minimum detectable power that is depended on the level of the threshold and the sidelobe levels. Adaptive algorithms suppress the sidelobe levels to noise level with condition of maintain the range resolution and therefore increase the dynamic range. In this paper, an improved algorithm (in terms of computational cost and Doppler robustness) is proposed based on the minimum mean square error (MMSE) estimator denoted as Flexible Filter Length-Adaptive Pulse Compression Repair (FFL-APCR), which filter length depends on the length of transmitted code. It is also shown that the length of the code is influenced by determining the asymptotic peak sidelobe level and the dynamics range. In addition, the influence of the high-speed target on main lobe broadening and the performance degradation of adaptive filters is investigated. Finally, extending of radar dynamic range with the proposed FFL-APCR algorithm is shown in various conditions and its performance evaluated by mean square error criteria. Where return signals coincide with the transmission of a pulse, pulse eclipsing can occur which results in detection performance loss. The mismatches (Doppler phase shift and pulse eclipsing) degrades performance of sidelobes suppression algorithms. The FFL-APCR algorithm suppresses range sidelobes by using a smaller filter length and reduces the computational cost. Consequently, this algorithm should be computationally efficient (real-time) to enable the practical application of RMMSE.

APCR-ELISA was used for semiquantification of Streptococcus pneumoniae DNA in cerbrospinal fluid (CSF) due to meningitis. The PCR-ELISA was based on universal bacterial primers from 16s ribosomal RNA gene and specific probes for detection, identification and semiquantification. Only one specimen out of 45 control group specimens was positive and the optical density of the PCR-ELISA for the rest of them was below 1.5. All of the 38 positive CSF samples (positive culture of S. pneumoniae) were positive with the optical density of greater than 2.0(ranging 2.0 to 3.8). The sensitivity of the universal bacterial primers for S. pneumoniae was 5*103 CFU/ml. The clinical sensitivity and specificity for the test were 100% and 97.7% respectively.

Background: Thrombosis is the most common reason of death in the United States causing more than two million people die from arterial or venous thrombosis every year. Thrombotic episodes may be due to congenital abnormality or to acquired alteration. The term thrombophilia is used to describe any disorder associated with an increased tendendency to venous thromboembolism (VTE), either inherited or acquired. Clinical risk factors that predispose individuals to venous thrombosis include: 1- Venous stasis 2- Vessel wall damage 3- Factor V leiden and activated protein C resistance 4- Deficiency of circulating protease inhibitors 5- Elevated prothrombin levels 6- Antiphospholipid antibodies 7- Hyperhomocysteinemia 8- Decreased fibrinolytic activity 9- Malignancy.In venous thrombophilic processes multiple acquired and inherited factors are involved. Among genetic factors mutation in factor V leiden, prothrombin G20210A and C677T MTHFR plus HR2 haplotype have been described. Anti-phospholipid antibodies are the most prominent acquired form. Regarding the importance of factor V Leiden mutation, we decided to investigate the frequency of this mutation in thrombophilic patients who had referred to Tehran Blood Transfusion Organization.Thrombin activates protein c. which inhibits coagulation by inactivating factor va and factor Villa. A novel mechanism for familial thrombophilia was recognized in 1993 with the description of a syndrome characterized by inherited resistance to activated protein c, (APCR). Multiple genetical defects in F.V are reported, and it is thought that Leiden mutation (R506Q) leads to APC resistance, and genetical susceptibility to hyperquagulablity conditions. Material and Methods: In this research 300 Thrombophilic patients were selected who underwent APC-R screening test. As a result, APC resistance was observed in 23 patients. Next, DNA from positive samples was extracted through chelex method. PCR-RFLP with specific primers was chosen as a confirmatory test for factor V Leiden mutation. Short after amplification, PCR products were digested by Mull restriction enzyme. Hence, a different pattern of homozygote, heterozygote and wild type appeared.Results: From 300 patients participating in this study, 131 were male and169 were female (with the age mean of 42 (SD=±8.67). Leiden mutation was observed in 10 patients with the prevalence of 3.3%.Conclusion: In previous studies, the frequency of F.V Leiden in thrombophilic patients was reported 40-65%. Thus, it is likely that the mutation of F.V Leiden as a predisposing factor for thrombosis in our patients is not very important, and there may be other significant genetic mutations which must be investigated in further studies.