The interaction of serum testosterone levels and androgen receptor CAG repeat polymorphism on the risk of erectile dysfunction in aging Taiwanese men.

Testosterone has been found to play important roles in men's sexual function. However, the effects of testosterone can be modulated by androgen receptor (AR) CAG repeat polymorphism. It could also contribute to the risk of erectile dysfunction (ED). The aim of this study is to evaluate the interaction of serum testosterone levels and AR CAG repeat polymorphism on the risk of ED in aging Taiwanese men. This cross-sectional data of Taiwanese men older than 40 years were collected from a free health screening held between August 2010 and August 2011 in Kaohsiung city, Taiwan. All participants completed a health questionnaires included five-item version of the International Index of Erectile Function (IIEF-5) and the International Prostate Symptoms Score, received a detailed physical examination and provided 20 cm3 whole blood samples for biochemical and genetic evaluation. The IIEF-5 was used to evaluate ED. Serum albumin, total testosterone (TT), and sex hormone-binding globulin levels were measured. Free testosterone level was calculated. AR gene CAG repeat polymorphism was determined by direct sequencing. Finally, 478 men with the mean age of 55.7 ± 4.8 years were included. When TT levels were above 330 ng/dL, the effect of testosterone level on erectile function seemed to reach a plateau and a significantly negative correlation between AR CAG repeat length and the score of IIEF-5 was found (r = -0.119, p = 0.034). After adjusting for other covariates, the longer AR CAG repeat length was still an independent risk factor for ED in subjects with TT above 330 ng/dL (p = 0.006), but not in TT of 330 ng/dL or below. In conclusion, both serum testosterone levels and AR CAG repeat polymorphism can influence erectile function concomitantly. In subjects with normal TT concentration, those with longer AR CAG repeat lengths have a higher risk of developing ED.

The impact of metabolic syndrome on the responsiveness to α1-blocker in men with BPH/LUTS.

AIMS: Increasing evidence has proposed the components of metabolic syndrome (MtS) as risk factors for the development of benign prostate hyperplasia (BPH); therefore, it is thought that MtS may play a role in lower urinary tract symptoms related to BPH (BPH/LUTS) aetiology. Considering the closed relationships between MtS and BPH/LUTS, it is possible that patients with MtS might have different drug responsiveness in men with BPH/LUTS. We prospectively investigated the impact of MtS on responsiveness to α1-blocker in men with BPH/LUTS. METHODS: We enrolled a total of 109 patients with a mean (SD) age of 59.8 (9.0) years, having a prostate volume of 20 cm(3) or greater with moderate to severe LUTS. All patients received doxazosin GITS (gastrointestinal therapeutic system) 4 mg once daily for a 12-week period of treatment. The efficacy measurement was assessed by the changes from baseline in the total IPSS, maximum urinary flow rate and postvoid residual urine volume. The drug responders were defined as those who had a total IPSS decrease of more than 4 points from baseline after 12 weeks of treatment. RESULTS: Using multiple logistic regression analysis, our results showed that MtS was an independent factor for drug non-responder (OR = 4.26, p = 0.002). The rate of drug responder and total IPSS improvements in patients with MtS significantly decreased as the number of MtS components increased (p = 0.012 and p = 0.026). Among the MtS components, abnormal fasting blood glucose (FBG) was the most significantly independent factor for drug non-responder (OR = 3.17, p = 0.020). CONCLUSION: This study suggested that the presence of MtS had a significantly negative impact on the responsiveness to α1-blocker in men with BPH/LUTS. Our results are important for BPH/LUTS patients who did not initially respond to α1-blocker or who strive to reduce these metabolic risk factors.

Shortened menstrual cycles in LCD manufacturing workers.

BACKGROUND: Many chemical agents used in liquid crystal display (LCD) manufacturing have been evaluated in animal studies of female reproductive toxicity. Knowledge of their reproductive toxicity in humans is scant. AIMS: To determine the effect of organic solvents on menstrual cycle characteristics of workers in LCD manufacturing. METHODS: Cross-sectional study of female premenopausal workers in an LCD plant in Taiwan. Menstrual cycle characteristics were assessed from self-administered questionnaires, and chemical exposure was assessed using hand-held volatile organic compound (VOC) monitors with 24h canister sampling. RESULTS: There was a response rate of 94%, and the final study population after exclusions was 288. Canister sampling found many chemical compounds with potential reproductive effects in the fabrication areas of the plant. Concentrations of total VOC were higher in the panel and module fabrication areas than in other areas of the plant. The prevalence of short menstrual cycles (>24 days) was higher in panel workers (adjusted odds ratio [OR]: 7.68; 95% confidence interval [CI]: 1.51-39.15) and module workers (adjusted OR: 8.38; 95% CI: 1.72-40.95) than in array fabrication workers and office workers. CONCLUSIONS: We found evidence for a possible link between repeated exposure to multiple organic solvents such as ethanol and acetone and increased prevalence of short menstrual cycles in premenopausal women.

Correlation between In content and emission wavelength of In(x)Ga(1-x)N/GaN nanowire heterostructures.

GaN nanowire ensembles with axial In(x)Ga(1-x)N multi-quantum-wells (MQWs) were grown by molecular beam epitaxy. In a series of samples we varied the In content in the MQWs from almost zero to around 20%. Within the nanowire ensemble, the MQWs fluctuate strongly in composition and size. Statistical information about the composition was obtained from x-ray diffraction and Raman spectroscopy. Photoluminescence at room temperature was obtained in the range of 2.2 to 2.5 eV, depending on In content. Contrary to planar MQWs, the intensity increases with increasing In content. We compare the observed emission energies with transition energies obtained from a one-dimensional model, and conclude that several mechanisms for carrier localization affect the luminescence of these three-dimensional structures.

Regulation of glucose/lipid metabolism and insulin sensitivity by interleukin-4.

OBJECTIVE: Abundant evidence has demonstrated that long-term cytokine-mediated inflammation is a risk factor for obesity and type 2 diabetes mellitus (T2DM). Our previous study reveals a significant association between promoter polymorphisms of Th2-derived cytokine interleukin-4 (IL-4) and T2DM, which suggests possible roles of IL-4 in metabolism. In this study, we focused on examining the putative regulation of glucose and lipid metabolism by IL-4. METHODS: C57BL/6 mice were intraperitoneally injected with either adenovirus containing full-length IL-4 encoding gene (AdIL-4) or recombinant IL-4 for mimicking the status of transient and long-term IL-4 overexpression, respectively, and the effects of the overexpressed IL-4 to glucose/lipid metabolism and insulin sensitivity were subsequently investigated. RESULTS: Our results reveal that IL-4 improves insulin sensitivity and glucose tolerance through upregulating Akt phosphorylation while attenuating GSK-3ß activities. IL-4 is also involved in lipid metabolism by inhibiting lipid accumulation in fat tissues, which lead to decreased weight gain and fat mass. CONCLUSIONS: Our results suggest that IL-4 regulates glucose and lipid metabolism by promoting insulin sensitivity, glucose tolerance and inhibiting lipid deposits. This study uncovers the novel roles of IL-4 in metabolism and provides new insights in the interaction between cytokines/immune responses, insulin sensitivity and metabolism.

Genetic polymorphisms in androgen receptor-binding sites predict survival in prostate cancer patients receiving androgen-deprivation therapy.

BACKGROUND: Activated androgen receptor binds to androgen-responsive elements (AREs) in genome to regulate target gene transcription and, consequently, mediates physiological or tumorigenic processes of the prostate. Our aim was to determine whether genetic variants in AREs are associated with clinical outcomes after androgen-deprivation therapy (ADT) in prostate cancer patients. PATIENTS AND METHODS: We systematically investigated 55 common single-nucleotide polymorphisms (SNPs) in the genome-wide insilico-predicted AREs in a cohort of 601 men with advanced prostate cancer treated with ADT. The prognostic significance of these SNPs on disease progression, prostate cancer-specific mortality (PCSM) and all-cause mortality (ACM) after ADT was assessed by Kaplan-Meier analysis and Cox regression model. RESULTS: In univariate analysis, two, five, and four SNPs were associated with disease progression, PCSM, and ACM, respectively. After adjusting for known prognostic factors, ARRDC3 rs2939244, FLT1 rs9508016, and SKAP1 rs6504145 remained as significant predictors for PCSM and FBXO32 rs7830622 and FLT1 rs9508016 remained as significant predictors for ACM in multivariate analysis. Moreover, strong combined genotype effects on PCSM and ACM were also observed (P(trend) < 0.001). CONCLUSION: Our results suggest that SNPs in AREs influence prostate cancer survival and may further advance our understanding of the disease progression.

Genetic polymorphisms in oestrogen receptor-binding sites affect clinical outcomes in patients with prostate cancer receiving androgen-deprivation therapy.

BACKGROUND: Accumulating evidence indicates that oestrogens have significant direct effects on normal prostate development and carcinogenesis. The majority of the biological activities of oestrogens are mediated through the oestrogen receptor (ER), which functions as a hormone-inducible transcription factor to regulate target gene expression by binding to oestrogen response elements (EREs) in the regulatory regions of target genes. Sequence variants in EREs might affect the ER-ERE interaction and subsequent physiological activities. Therefore, we tested whether common single-nucleotide polymorphisms (SNPs) inside EREs are related to the clinical outcomes of androgen-deprivation therapy (ADT) in men with prostate cancer. METHODS: We systematically evaluated 49 ERE SNPs predicted using a genome-wide database in a cohort of 601 men with advanced prostate cancer treated with ADT. The prognostic significance of these SNPs on disease progression, prostate cancer-specific mortality (PCSM) and all-cause mortality (ACM) after ADT was assessed using Kaplan-Meier analysis and a Cox regression model. RESULTS: Based on multiple hypothesis testing, BNC2 rs16934641 was found to be associated with disease progression; in addition, TACC2 rs3763763 was associated with PCSM, and ALPK1 rs2051778 and TACC2 rs3763763 were associated with ACM. These SNPs remained significant in multivariate analyses that included known clinicopathological predictors. Moreover, a combined genotype effect on ACM was observed when ALPK1 rs2051778 and TACC2 rs3763763 were analysed in combination. Patients with a greater number of unfavourable genotypes had a shorter time to ACM during ADT (P for trend <0.001). CONCLUSION: The incorporation of ERE SNPs into models with known predictors might improve outcome prediction in patients with prostate cancer receiving ADT.

Increased expression and secretion of interleukin-6 in human parvovirus B19 non-structural protein (NS1) transfected COS-7 epithelial cells.

Human parvovirus B19 (B19) has been associated with a variety of autoimmune diseases, including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). We have demonstrated previously that B19 non-structural protein (NS1) induced apoptosis through the mitochondria cell death pathway in COS-7 epithelial cells and that B19 NS1 may play a role in the pathogenesis of autoimmune diseases. In order to examine the expression profiles of cytokines and chemokines in B19 NS1 transfected COS-7 cells, we constructed the NS1 gene in the pEGFP-C1 vector named enhanced green fluorescence protein gene (EGFP)-NS1. COS-7 cells were transfected with EGFP or EGFP-NS1 plasmid. The expression profiles of cytokines and chemokines, including interleukin (IL)-1beta, IL-5, IL-6, IL-8, IL-10, tumour necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta, granulocyte-macrophage colony-stimulating factor (GM-CSF), growth-related oncogene alpha (GROalpha), interferon gamma-inducible protein (IP)-10, stromal cell derived factor (SDF)-1, macrophage inflammatory protein (MIP)-1beta, monocyte chemoattractant protein (MCP)-1, regulated upon activation normal T cell expressed and secreted (RANTES), Fractalkine, CX3CR1, CCR2, CCR5 and CCR11 were examined in COS-7 cells, EGFP and EGFP-NS1 transfected cells using enzyme-linked immunosorbent assay (ELISA) or reverse transcription-polymerase chain reaction (RT-PCR). Increased expression and levels of IL-6 were found in EGFP-NS1 transfected cells using RT-PCR and ELISA. There were no significant increases in the expression of IL-1beta, IL-8, IP-10, SDF-1, RANTES, Fractalkine, CX3CR-1, CCR2, CCR5, CCR11, TNF-alpha, GM-CSF and TGF-beta using RT-PCR. There were no significantly increased levels of IL-5, IL-10, TNF-alpha, TGF-beta, GROalpha, MIP-1beta and MCP-1 found by ELISA in this study. Our results show that increased expression and secretion of IL-6 in B19 NS1 transfected epithelial cells may play a role in the pathogenesis of autoimmune diseases.

The anti-tumor effect and mechanisms of action of penta-acetyl geniposide.

Gardenia, the fruit of Gardenia jasminoides Ellis, has been widely used to treat liver and gall bladder disorders in Chinese medicine. It has been shown recently that geniposide, the main ingredient of Gardenia Fructus, exhibits the anti-tumor effect. In this review, we discuss the anti-tumor effect and possible mechanisms of a derivative from Gardenia Fructus, penta-acetyl geniposide ((Ac)5GP). It has been demonstrated that (Ac)5GP plays more potent roles than geniposide in chemoprevention. (Ac)5GP decreased DNA damage and hepatocarcinogenesis induced by aflatoxin B1 (AFB1) by activating the phase II enzymes glutathione S-transferase (GST) and GSH peroxidase (GSH-Px). It reduced the growth and development of inoculated C6 glioma cells especially in pre-treated rats. In addition to the preventive effect, (Ac)5GP exerts its actions on apoptosis and growth arrest. Treatment of (Ac)5GP caused DNA fragmentation of glioma cells. (Ac)5GP induced sub- G1 peak through the activation of apoptotic cascades PKCdelta/JNK/Fas/caspase8 and caspase 3. Besides, p53/Bax signaling was suggested to be involved in (Ac)5GP-induced apoptosis, though its downstream cascades needs further clarified. (Ac)5GP has also been shown to inhibit DNA synthesis of tumor cells. It arrested cell cycle at G0/ G1 by inducing the expression of p21, thus suppressing the cyclin D1/cdk4 complex formation and the phosphorylation of E2F. The phosphorylation status of p53 on serine 392 correlated with the process of growth arrest. Evidences from the in vivo experiments showed that (Ac)5GP is not harmful to liver, heart and kidney. In conclusion, (Ac)5GP is highly suggested to be an anti-tumor agent for development in the future.

Anti-nuclear antibody, anti-DNA, and aCL in Graves' disease patients treated with propyluracil or methimazole.

One hundred and forty patients with Graves' disease [32 new patients, 54 treated with propylthiouracil (PTU) for a mean of 27.2 months and 54 treated with methimazole (MMI) for a mean of 48.6 months] were tested for anti-thyroid microsomal antibody (AMA), anti-thyroglobulin antibody (ATA), thyroid binding inhibitory immunoglobulin (TBII), and the non organ specific autoantibodies [i.e., anti-nuclear antibody (ANA), anti-double stranded DNA antibody (anti-dsDNA Ab), anti-cardiolipin antibody (aCL Ab) and anti-beta2-glycoprotein I antibody (IgG beta2GPI)]. Treatment with MMI or PTU produced a significant difference in IgG aCL Ab production but not in ANA, dsDNA Ab, IgM aCL or IgG beta2GPI. For those treated with MMI but not those treated with PTU, ANA and anti-dsDNA Ab were positively correlated. IgG and IgM aCL Ab were positively correlated overall and for those on MMI but not PTU treatment. No significant difference was found for any of the four non organ specific antibodies in AMA positive or negative patients but there was a significant difference in IgG aCL positivity rates for ATA positive and negative patients. On the other hand, ANA negative patients were significantly more likely to have higher TBII values. These results suggest that the appearance of the non organ specific autoantibodies is probably largely a coincidental effect of polyclonal activation - except, perhaps, for IgG aCL, which may be related to treatment.

TNF-alpha polymorphisms and type 2 diabetes mellitus in Taiwanese patients.

Type 2 diabetic mellitus (type 2 DM) comprises more than 95% of all Taiwanese patients with DM. Tumor necrosis factor-alpha (TNF-alpha) expression is linked with insulin resistance, and is under strong genetic control. The correlation between TNF promoter genotypes and type 2 DM is still controversial, because discrepancies among different studies exist. Ethnic differences play certain roles in these conflicting results, because the distribution of TNF promoter polymorphisms is different among study subjects with different racial origins. Therefore, we examined the relationship between the incidence of type 2 diabetes in Taiwanese and two polymorphisms of the TNF-alpha promoter region (positions -238 and -308) as well as the correlation between these polymorphisms and the patients' biochemical manifestations. Genomic DNA was extracted from peripheral blood cells of 261 Taiwanese patients with type 2 DM and 189 non-diabetic control study subjects, and their TNF promoter G-238A and G-308A polymorphisms were analyzed by PCR-RFLP analysis. No significant association between TNF-alpha G-238A and G-308A polymorphisms with type 2 diabetic incidence was observed. However, associations between TNF-alpha G-238A and low-density lipoprotein-cholesterol and between G-308A promoter polymorphism and high-fasting plasma glucose levels, using multiple linear regression analysis with adjustment for the subjects' age, sex, body mass index and diabetic status, were found. Our results suggested that though TNF-alpha G-238A and G-308A polymorphisms were not involved in the pathogenesis of type 2 DM, type 2 diabetic patients carrying TNFA-A or TNF-308*2 genotype might be more susceptible to diabetic complications such as atherosclerosis.

The clinical implications of telomerase activity in upper tract urothelial cancer and washings.

OBJECTIVE: To measure telomerase activity in upper tract urothelial carcinomas (as renal pelvic tumours comprise nearly half of all kidney tumours in Taiwan, a much higher percentage than in other countries) and to determine whether telomerase activity could be used as an additional diagnostic marker in exfoliated cancer cells present in upper tract urothelial washing fluids, thus providing earlier diagnosis and treatment. Materials and methods Telomerase activity was assessed using the telomeric repeat amplification protocol assay in tissue samples from 31 upper tract urothelial carcinomas (from 29 patients). The feasibility of identifying cancer using telomerase activity in exfoliated cancer cells in 17 upper tract urothelial washing samples was also investigated. RESULTS: Telomerase activity was found in 30 (97%) of the 31 upper tract urothelial cancer tissue samples; telomerase activity was detectable in 95% of superficial cancers and in all 11 invasive tumours. The sensitivity of measuring telomerase activity was 100% for grade 1, 93% for grade 2 and 100% for grade 3 tumours. In contrast, telomerase activity was detected in only two (8%) of 26 normal adjacent tissue samples. When the telomerase activity of urothelial washing fluid was compared with that in the corresponding tumours, there was compatible telomerase activity in 15 of the 17 samples. Telomerase activity was more sensitive than voided urine cytology (15%) and washing fluid cytology (53%). In addition, the telomerase activity was high in metastatic lesions. CONCLUSION: Telomerase activity is present in most upper tract urothelial cancer tissues and may be present at an early stage of carcinogenesis. Telomerase activity can be detected in exfoliated cells in urothelial washing fluids in a high proportion of patients with upper tract urothelial cancer. These results suggest that measuring telomerase activity in the exfoliated cancer cells obtained from urothelial washing could be a potentially useful addition to the conventional diagnostic tools used to identify patients with upper tract urothelial carcinoma.

[Torsion of the appendix testis].

The differential diagnosis of an acute scrotum includes spermatic cord torsion, torsion of a testicular appendage, torsion of spermatocele, epididymitis, orchitis, trauma, hernia, testicular segmental infraction and tumor. Among these, torsion of appendix testis could got dramatic improvement if accurately diagnosed and treated. 5 patients of torsion of appendix testis have been identified in our hospital in the recent 5 years. Ages ranged from 9 to 13 years old (mean age 11). The lesions were on the right side in 2 cases and left side in 3 cases. Duration of scrotal pain ranged from 2 to 7 days (mean of 4 days). The urine analyses were normal in all cases. The white blood counts were all within normal limits with mean of 5.72 x 10(3)/ul. No abnormality in passing urine or other infectious sign could be detected. Doppler ultrasonography or nuclear medicine testicular scan were performed selectively due to clinical availability. The result was equivocal and did not support a definite diagnosis. All 5 cases received surgical treatment. The necrotic testicular appendix was excised and reactive hydrocele treated. All the patients were discharged from the hospital the day after operation and recovered quickly. The pathological report revealed congestion and extensive hemorrhagic necrosis of the testicular appendix. Advances in technology have been helpful in improving the accuracy of diagnosis but technology is not infallible and an over reliance on it can also result in misdiagnosis. Various reports supporting the use of scrotal ultrasound in evaluating cases of acute scrotum pain. Ultrasonography has definitely helped in detecting scrotal pathology but its limitations need to be appreciated. Because of the difficulty of making an accurate diagnosis in acute scrotum, misdiagnosis and delayed operation offer result in disappointment of testis salvage rates. We have supported a policy of early scrotal exploration in any case suspicious of torsion of appendix testis.

Quantitative sensory testing and risk factors of diabetic sensory neuropathy.

The goal of this study was to identify risk factors for diabetic peripheral sensory neuropathy in type 2 diabetes mellitus in a Chinese population. Peripheral sensory neuropathy was detected by quantitative sensory testing (5.07/10 g monofilament, neurometer and 128-Hz Riedel Seiffert graduated tuning fork). Those who had two or more abnormal quantitative sensory testings were defined as having diabetic sensory neuropathy. Of the 558 non-insulin dependent diabetes mellitits subjects, 62 (11.1%) had peripheral neuropathy. In 59 (10.6%) detection was by monofilament testing, 45 (8.1%) by graduated tuning fork, and 189 (33.9%) by neurometer. In a multivariate logistic regression model, age and insulin therapy were significantly associated with peripheral neuropathy. Age, serum triglyceride, height, and fasting plasma glucose were independently associated with large fiber neuropathy. Our results confirm the previously identified multiple risk factors of diabetic neuropathy. Different quantitative sensory testings detect different nerve fiber defects. The weak correlation between these tests indicates the need to use more than one test in screening for diabetic neuropathy.

Sera from patients with scleroderma inhibit fibroblast micromotions monitored electrically.

OBJECTIVE: To investigate scleroderma fibroblast behavior, and the effect of different human sera on fibroblast behavior, we established a model using the newly developed electrical biosensor, electrical cell-substrate impedance sensing (ECIS). METHODS: Cellular locomotion, defined as cellular micromotion, measured by ECIS indicates the dynamic vertical motion of a given group of cells. The junctional resistance (Rb) between adjacent cells and the average height (h) between basal cell surface and substratum derived from ECIS were quantified for dermal fibroblasts obtained from patients with scleroderma and normal controls. The cellular micromotions of both scleroderma and normal control fibroblasts were compared in the presence of different human sera, including those from patients with scleroderma, systemic lupus erythematosus (SLE), and Sjögren's syndrome (SS) and from normal individuals. RESULTS: The Rb and h levels for scleroderma and normal fibroblasts were 2.7 omega.cm2, 150 nm and 0.8 omega.cm2, 303 nm respectively. The micromotions of scleroderma fibroblasts were more active than those of normal fibroblasts. Sera from patients with scleroderma can inhibit the micromotions of normal fibroblasts but not those of scleroderma fibroblasts, while sera from patients with SLE and SS have no inhibitory effect on either normal or scleroderma fibroblast micromotions. CONCLUSION: We have demonstrated the previously unrecognized characteristics of dermal fibroblasts and sera derived from patients with scleroderma. It is possible that in vivo activities cause scleroderma fibroblasts to display active cellular micromotions, while sera from patients with scleroderma inhibit the micromotions of normal fibroblasts. The use of ECIS technology has also provided a new approach to the study of scleroderma.

Emphysematous pyelonephritis: imaging diagnosis and follow-up.

We conducted the study to evaluate the efficacy and roles of different imaging modalities in the diagnosis and follow-up of emphysematous pyelonephritis (EPN) and to correlate imaging findings with clinical outcome. Retrospective analysis of the imaging studies and clinical outcome were performed in 28 consecutive patients with EPN. They were all initially treated with CT-guided percutaneous drainage (PCD). The imaging studies performed included plain abdominal radiography (KUB) (n = 28), sonography (US)(n = 24), intravenous urography (IVU)(n = 5), retrograde pyelography (RP)(n = 20) and computed tomography (CT)(n = 28). Follow-up imaging studies included CT(n = 23) and renal scintigraphy (n = 15). The sensitivities of detecting abnormal gas in EPN on KUB and US were 66% and 88%. The mortality rate was 11%, not associated with different types, stages or renal involvement. On the follow-up CT performed within one month of PCD, type I EPN evolved into type II in 86% of the cases. On the long-term follow-up CT, renal atrophy and focal scarring were revealed in the diffuse and focal renal involvement of EPN. The mean split renal function shown on the follow-up scintigraphy was 30%. We concluded KUB and US were valuable for screening EPN, although CT was the most specific and sensitive. Follow-up CT studies not only demonstrate the response of treatment but also depict the different courses and the results of different types and renal involvement of EPN, although not associated with mortality rate.

Screening for the Gly40Ser mutation in the glucagon receptor gene among patients with type 2 diabetes or essential hypertension in Taiwan.

As a major counterregulatory hormone of insulin, glucagon plays an important role in regulating glucose homeostasis through its binding to the glucagon receptor. Recently a missense mutation in the glucagon-receptor gene (Gly40Ser) was found to be associated with type 2 diabetes in France and Sardinia, with a frequency as high as 4.6% and 8.3%, respectively. This mutation was also found to be associated with essential hypertension in the white population with a frequency of 5.4%. To investigate the role of this mutation in the pathogenesis of type 2 diabetes and essential hypertension in Taiwanese population, we screened 121 normal controls, 213 unrelated subjects with type 2 diabetes, and 107 unrelated subjects with essential hypertension by use of polymerase chain reaction/restriction fragment length polymorphism (PCR-RFLP). None of the Taiwanese subjects recruited in the study had this receptor mutation. Our results demonstrate a strong genetic heterogeneity among the ethnic group and suggest that the Gly40Ser mutation of the glucagon receptor gene plays little role, if any, in the pathogenesis of type 2 diabetes and essential hypertension in the Taiwanese population.

[Studies on the application of antifreeze proteins in cryopreservation of rice suspension cells].

AFP from winter flounder was utilized in cryopreservation of plant cells. During cryopreservation of rice suspension cells by two-step method, AFP at 0.01 mg/ml damaged the cells extremely. The data obtained at relatively high concentration, however, decreased the variability of survival rate. During vitrification of rice cells, AFP at 0.2 mg/ml enhanced the viability. However, high concentration AFP (> 5 mg/ml) decreased the recovery rate. Studies indicated that the results of application of AFP in cryopreservation were closely related to the concentration of cryoprotectant. The amount of ice crystal in environment, the concentration of AFP and cryoprotectant, and the composition of plasma membrane were several key factors affecting the results of AFP application. In mechanism analysis, the authors suggested that on one hand AFP can interact with ice crystal, which inhibits ice recrystallization and prevent the cells from devitrification. On the other hand, AFP also can interact with cell membrane, resulting in the ice growth around the plasma membrane.