Since amniocentesis made prenatal diagnosis feasible in 1967, the method has been remarkably instrumental in obstetrical practice. A recent study conducted between 1980 and 1997 collected 11,000 ...amniocentesis procedures done at 10 university hospitals and tertiary centers in Korea. The study indicated that the use of amniocentesis on patients has increased steadily since 1980; however, the number has increased sharply for patients in the mid 1990's. In the 1980's, amniocentesis had been used primarily for patients in advanced maternal age groups (at least 35 years or older). In 1995, amniocentesis had been implemented for the detection of abnormal serum markers (37.6%), and by 1997, amniocentesis was involved in such diagnosis even more frequently (44.8%). Of the total number of uses, 270 (2.5%) involved the detection of chromosomal anomaly. In autosomal disorders, 96 Down syndrome, 33 Edward syndrome, and 6 Patau syndrome were diagnosed. In sex chromosomal anomaly, 10 Turner syndrome, and 10 Klinefelter syndrome were diagnosed. Added to that, 83 translocations, and 15 mosaicisms were diagnosed. Of the 322 cases with abnormal ultrasonographic findings, 21 (6.5%) resulted in chromosomal anomaly. The use of genetic amniocentesis as a prenatal diagnostic test for Korean women has risen 10-fold between 1988 and 1998. As stated earlier, amniocentesis had earlier been used primarily for those in advanced maternal age groups. Today, maternal serum markers and highly sensitive ultrasonic technology can detect many fetal anomalies which eventually necessitate amniocentesis.
To determine the prevalence and clinical relevance of HGV infection in dialysis patients, we performed a cross-sectional study of 61 HD patients and 79 Continuous Ambulatory Peritoneal Dialysis ...(CAPD) patients. HGV-RNA was identified by reverse-transcription (RT) polymerase chain reaction (PCR) assay with primers from the 5'-untranslated region of the viral genome. The prevalence of HGV infection was similar in HD and CAPD patients (9.8% vs. 12.7%), while that of HCV infection was significantly higher in HD patients compared to CAPD patients (16.4% vs. 1.3%, p < 0.05). The mean age (49.2 +/- 13.4 vs. 46.7 +/- 13.0 years), male to female ratio (2.4:1 vs. 1.3:1), history of transfusion (62.3% vs. 49.4%), history of hepatitis (27.9% vs. 26.6%), mean ALT level during the previous 6 months (22.4 +/- 37.9 vs. 14.0 +/- 7.4 IU/L), and the prevalence of HBsAg (8.2% vs. 6.3%) showed no difference between HD and CAPD patients. In both HD and CAPD patients, the presence of HGV RNA was not related to age, sex, duration of dialysis, history of transfusion, history of hepatitis, or to the presence of HBV or HCV markers. There was no significant difference in the clinical and biochemical data between patients with isolated HGV infection (n = 12) and patients without viremia (n = 106). The clinical feature of patients coinfected with HGV and HBV (n = 2), or HGV and HCV (n = 2) seemed to be similar to those of patients with isolated HBV (n = 8) or HCV (n = 9) infection. In conclusion, the prevalence of HGV infection was not different between HD and CAPD patients, and HGV infections did not seem to be associated with clinically significant hepatitis. The routes of HGV transmission, other than transfusion or contamination during HD procedure, were suspected.
The intensive use of chemotherapeutic agents for the treatment of cancer has resulted in the cure or improved survival of many patients. But unfortunately, many cancers including human hepatocellular ...carcinoma (HCC) don't respond to chemotherapy. One of the major mechanisms for the drug resistance in the HCC is an elevated MDR1 RNA expression which makes cells become multidrug resistant. To overcome the multidrug resistance (MDR) phenotype, a high dose of verapamil is required both clinically and experimentally. Accordingly we have examined the MDR modulating effects with combinations of tamoxifen, cyclosporin A, and verapamil in vitro with the physiologically achievable concentrations of each agent, i.e., 2.0 microM/L for tamoxifen, 1.6 microM/L for cyclosporin A, and 2.5 microM/L for verapamil respectively in HCC lines. As expected, verapamil alone with the physiologically achievable concentration at which we tested didn't enhance the doxorubicin cytotoxicity in the HCC lines. Furthermore, any verapamil combination with cyclosporin A or tamoxifen was not effective in overcoming the doxorubicin resistance in the high MDR1 expressor (Hep-G2) line. However tamoxifen reduced the IC50 of doxorubicin by a factor of 1.9 in the low MDR1 expressor (SK-Hep1) and 1.1 in the high MDR1 expressor line (p < 10(-5) respectively). Of interest, combinations of tamoxifen and cyclosporin A showed a significant reduction in the IC50 of doxorubicin in both HCC lines. The IC50 of doxorubicin was reduced by a factor of 3.9 and 1.3, i.e., from 0.023943 micrograms/ml to 0.006157 micrograms/ml (p < 10(-5)) in the SK-Hep1 cell line, and 0.068819 micrograms/ml to 0.052442 micrograms/ml (p < 10(-5)) in Hep-G2 respectively when tamoxifen and cyclosporin A were administered together. Both the estrogen and progesterone receptors in the SK-Hep1 and Hep-G2 lines were less than 0.01 fmol/mg of cytosol protein, respectively. It is therefore suggested that the reversal of doxorubicin resistance is unrelated to their anti-estrogenic activity in the HCC lines. Three modulator combinations of tamoxifen, cyclosporin A, and verapamil were not more effective than the combination of tamoxifen and cyclosporin A on the sensitivity to doxorubicin. MDR modulators of tamoxifen, cyclosporin A, and verapamil didn't reduce the IC50 of cisplatin to the clinically achievable concentration range in HCC lines. In summary, the combination of tamoxifen and cyclosporin A at the concentrations normally seen after clinical administration of these modulators showed significant synergism on the sensitivity to doxorubicin in both low and high MDR1 expressor HCC lines. These data indicate the need for in vivo trials.
New architectures of the dual chain InCaP MMIC power amplifiers withouuwith automatic bias current control (ABC 2 ) have been developed for improving efficiency in the low-power region while ...maintaining the high linearity for all Pout regions. For low standby current less than 25 mA, the amplifiers initially operate using small HBT arrays. For small chip sue, high load impedance in low-power region, and efficient power combining in high-power region, phase-compensating L-C matching circuits using lowpass and high-pass networks are used. A new simple power detection and bias current control circuit is employed to the power amplifier, resulting in automatic gain control for Pout variation. The fabricated (ABC 2 ) power amplifier module shows good ACPR more -48 dBc over all Pouts, and high efficiency of 6 % PAE (conventional 3.5~4%) at Pout=9 dBm, and 37.5 % PAE at Pout=28 dBm.
The increase in pattern complexity due to optical proximity correction (OPC), the tight requirements for critical dimension (CD) control and the difficulties in defect inspections make IC manufacture ...more expensive. To alleviate the high cost, manufacturing requirements must be handled at the design stage to improve the quality and yield of ICs. We demonstrate the extraction of critical areas for detecting failures and a new lithography simulation method for full-chip level optical proximity corrected layout. The methodology has been used in our mask verification process that is called litho-friendly layout (LFL). For the critical area extraction, we present three approaches using process window, normalized image log-slope (NILS) and edge placement error (EPE). For full-chip level simulation, we introduce an automatic calibration method for simulation process parameters, a mask decomposition method and a selective simulation method. The verification process includes lithography process simulation, print-image based LVS (layout vs. schematic) and DRC (design rule check). We also demonstrate that LFL can provide guidelines for better OPC of sub-80 nm processes.
Lipopolysaccharide (LPS) endotoxin of Gram-negative bacteria compromises the integrity of the airway epithelial barrier and initiates migration of leukocytes across the epithelium. The goal of the ...present study was to identify the role of extracellular regulated kinase (ERK1/2) transduction pathways in these processes. The first aim was to determine whether LPS induces ERK1/2 activation and changes in epithelial permeability in epithelial cells alone or only in the presence of immune cells. The second aim was to determine whether the changes in the epithelial permeability were diminished by ERK1/2 blockade. The third aim was to investigate the role of protein kinase C (PKC) activation as an upstream event in activation of ERK1/2. In vitro 20 mu g/ml LPS challenge reduced epithelial barrier function, and induced ERK1/2 phosphorylation in primary cultures of bovine tracheal epithelium and in the transformed human airway epithelial cell line, Calu-3. LPS initiated migration of neutrophil-like and monocyte-like transformed HL-60 cell across sheets of Calu-3 cells. The migration rate and the associated changes in the electrical resistance, permeability to albumin, and ERK1/2 phosphorylation were all blocked by calphostin C, the specific blocker of PKC and by PD98059 (2'-amino-3'-methoxyflavone), a selective cell-permeable inhibitor of MAP kinase kinase. In rats, in vivo perfusion of the lumen of an isolated segment of trachea with LPS (0.1 mg/ml) initiated migration of neutrophils and increased the permeability to albumin. Again, these effects were markedly inhibited by PD98059 and calphostin C (by > 50%). We conclude that epithelial ERK1/2 is activated by endotoxin via PKC and is an important pathway in regulation of epithelial permeability.
In this paper, the performance of a pre-equalization technique which can be applicable for the B-WLL uplink is evaluated and compared to post-equalization under three kinds of rain attenuation ...channels such as rain, intermittent light rain and thundershower. The comparison of two algorithms (LMS and RLS) is investigated in the context of channel models and the length of training sequence. From the simulation results, it is shown that the post-equalization outperforms only at quite good channel conditions such as AWGN, while the pre-equalization can guarantee better BER performance at all channel conditions, especially performance gain increases as the severity of the channel increases. It is concluded that the pre-equalizer using the LMS algorithm is preferable at delay-tolerant situations where the complexity of the algorithm is not a strict factor, while one using RLS is suitable for fast burst transmission with a relatively short training sequence.
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