A comparative study of a new cardiotocography analysis program.

Cardiotocography (CTG) is a frequently used technique of fetal monitoring to evaluate the well being of the fetus during pregnancy and in labor. The surveillance technique depends on the analysis of characteristic fetal heart rate patterns and uterine contractions. Computerized analyses can mitigate the intra-observer and inter-observer variability of visual CTG recording explanation, decrease the examination time, and the need of additional tests for fetal health. Several studies also showed that the signal processing techniques could help to determine the fetal heart rate (FHR) patterns, but all of them were only suitable for physicians. Following the criteria and consensuses of National Institute of Child Health and Human Development in April 2008, we developed a LabVIEW based FHR and uterine contraction (UC) pattern analysis software. This software has great potential for home-care use. The signal processing methods utilized in this study are median filter and peak/valley detection method. The analysis performance was verified by nineteen pregnant women's data. The accuracy of FHR baseline, baseline variability, early deceleration, UC frequency and NST all reach 100%. The accuracy of acceleration frequency reaches 90%. The accuracy of late and variable decelerations reaches 95%.

The development and evaluation of the Citizen Telehealth Care service System: case study in Taipei.

Because of the rapid aging population in Taiwan and the trend of fewer children, people are looking into technical solutions for continuous/intermittent monitoring of vital signs in the home setting environment and the interactions between family members. In this study we developed a smart medical services system for managing chronic disease, called Citizen Telemedical Care service System (CTCS). The system integrates biosignal measurement, hypertension risk estimation expert system, clinic appointment service, video communication service, medical assistance referral, health frequency program record, and health/hygiene education. The demo version CTCS is exhibited in the center of INSIGHT opened for visit and trial use. In order to verify the demand and acceptability of the system and services, we have interviewed 251 volunteers with a questionnaire survey with the help from Taipei City Government. The results showed that people have positive expectation about the service program for health care and the capability of home devices. They also expressed high motivation on learning to use the system and to participate in the program. According to the evaluation results, the system is processing a small user test led by Taipei City Government, in order to further verify the acceptability and satisfaction of the system.

Immunohistochemical localization of the NM23 protein in salivary gland neoplasms with distinct biological behavior.

The NM23 protein was shown to be associated with metastasis suppression in human malignancies with various tissue origins. However, its association with the metastatic phenotype of salivary gland neoplasms (SGN) remains unknown. To evaluate the role of NM23 in SGN, the expression patterns of NM23 in the following were compared: benign (pleomorphic adenoma) vs malignant (adenoid cystic carcinoma and mucoepidermoid carcinoma) SGN, and primary malignancies with/without evidence of metastasis vs their metastatic implants (MI). The lesions were studied immunohistochemically. NM23 protein was found in the cytoplasm of 75% of benign SGN, 73.3% of primary SGN malignancies with no evidence of metastasis, 86.6% of primary SGN malignancies with evidence of metastasis, and 60% of MI. There was no statistically significant difference in the frequency of NM23-positive cells between benign and primary malignant tumors (p = 0.79), nor between primary malignancies with/without evidence of metastasis and MI (p = 0.51). However, nuclear NM23 protein was restricted to primary SGN malignancies with evidence of metastasis and MI. The presence of nuclear NM23 protein may be a good marker for predicting the metastatic potential of SGN malignancies.

Overexpression of Smad2 in Tgf-beta3-null mutant mice rescues cleft palate.

Transforming growth factor (TGF)-beta3 is an important contributor to the regulation of medial edge epithelium (MEE) disappearance during palatal fusion. SMAD2 phosphorylation in the MEE has been shown to be directly regulated by TGF-beta3. No phospho-SMAD2 was identified in the MEE in Tgf-beta3-null mutant mice (Tgf-beta3-/-), which was correlated with the persistence of the MEE and failure of palatal fusion. In the present study, the cleft palate phenotype in Tgf-beta3-/- mice was rescued by overexpression of a Smad2 transgene in Keratin 14-synthesizing MEE cells following mating Tgf-beta3 heterozygous mice with Keratin 14 promoter directed Smad2 transgenic mice (K14-Smad2). Success of the rescue could be attributed to the elevated phospho-SMAD2 level in the MEE, demonstrated by two indirect evidences. The rescued palatal fusion in Tgf-beta3-/-/K14-Smad2 mice, however, never proceeded to the junction of primary and secondary palates and the most posterior border of the soft palate, despite phospho-SMAD2 expression in these regions at the same level as in the middle portion of the secondary palate. The K14-Smad2 transgene was unable to restore all the functional outcomes of TGF-beta3. This may indicate an anterior-posterior patterning in the palatal shelves with respect to TGF-beta3 signaling and the mechanism of secondary palatal fusion.

TGF-beta3-dependent SMAD2 phosphorylation and inhibition of MEE proliferation during palatal fusion.

Transforming growth factor (TGF) -beta3 is known to selectively regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Previous studies suggested that the selective function of TGF-beta3 in MEE was conducted by TGF-beta receptors. Further studies were needed to demonstrate that the TGF-beta signaling mediators were indeed expressed and phosphorylated in the MEE cells. SMAD2 and SMAD3 were both present in the MEE, whereas SMAD2 was the only one phosphorylated during palatal fusion. SMAD2 phosphorylation was temporospatially restricted to the MEE and correlated with the disappearance of the MEE. No phosphorylated SMAD2 was found in MEE in TGF-beta3(-/-) mice, although nonphosphorylated SMAD2 was present. The results suggest that TGF-beta3 is required for initiating and maintaining SMAD2 phosphorylation in MEE. Phospho-SMAD3 was not detectable in palate during normal palatal fusion. Previous results suggested TGF-beta-induced cessation of DNA synthesis in MEE cells during palatal fusion in vitro. The present results provide evidence that inhibition of MEE proliferation in vivo was controlled by endogenous TGF-beta3. The number of 5-bromo-2'-deoxyuridine (BrdU) -labeled MEE cells was significantly reduced in TGF-beta3(+/+) compared with TGF-beta3(-/-) mice when the MEE seam formed (t-test, P < 0.05). This finding suggests that TGF-beta3 is required for inhibiting MEE proliferation during palatal fusion. The inhibition of MEE proliferation may be mediated by TGF-beta3-dependent phosphorylation of SMAD2.