Complete mitochondrial genome of the crinoid Poliometra prolixa (Crinoidea: Comatulida: Antedonidae).

Poliometra prolixa Sladen, 1881, is a comatulid crinoid found in the Arctic deep sea. In this study, we report the complete mitochondrial genome sequence of P. prolixa (Comatulida: Antedonidae). The complete mitogenome of P. prolixa was 15,916 bp long and comprised 13 protein-coding genes (PCGs), 22 transfer RNA genes, and 2 ribosomal RNA genes. The base composition of the P. prolixa mitogenome was 24.0% A, 44.9% T, 19.0% G, and 12.1% C. Phylogenetic analysis using all PCGs of the complete mitogenome confirmed the inclusion of P. prolixa within the Comatulida.

Chronic exposure to environmental concentrations of harmful algal bloom-forming dinoflagellates induces oxidative stress and reduces immune and hepatic functions in red seabream.

Harmful algal blooms (HABs) caused by dinoflagellates can be detrimental to aquaculture and fisheries. However, little is known regarding their ichthyotoxic effects on fish, particularly after chronic exposure to sublethal levels. In this study, significant modulations in physiology, immunity, antioxidant components, and hepatic indicators owing to non-toxin-producing dinoflagellate strains (Alexandrium affine and Cochlodinium polykrikoides) were analyzed in juvenile red seabream, Pagrus major, exposed to sublethal concentrations (0, 1, and 100 cells mL-1) for 60 days. At 60 days, higher mortality was induced by A. affine than by C. polykrikoides. Significant increases in respiration rate and plasma cortisol were observed in red seabream exposed to 100 cells mL-1 of the two dinoflagellates. Intracellular reactive oxygen species and malondialdehyde levels were significantly elevated in the gill and liver tissues in response to 100 cells mL-1 of either dinoflagellate. Immunity parameters such as alternative complement activity, lysozyme activity, and total immunoglobulin content were significantly decreased during exposure to 100 cells mL-1 of the two dinoflagellates. Although no significant change was observed in the gonadosomatic index, the hepatosomatic index was significantly decreased by exposure to 100 cells mL-1 of the two dinoflagellates on day 60. The significant decrease in enzymatic activities of ethoxyresorufin-O-deethylase, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase upon exposure to 100 cells mL-1 of either dinoflagellate suggested impaired hepatic function through prolonged exposure. Our results suggest that consistent exposure to sublethal concentrations of HAB-forming dinoflagellates is detrimental to fish physiology and biochemical defenses.

Characterization and phylogenetic analysis of the complete mitochondrial genome of the rainbow krib, Pelvicachromis pulcher (Perciformes: Cichlidae).

We report the complete mitochondrial genome information of the rainbow krib, Pelvicachromis pulcher (Boulenger 1901). Illumina HiSeq genome sequencing allowed the assembly of a circular mitogenome of 17,196 base pairs (bp) from P. pulcher consisting of 47% GC nucleotides, 13 protein-coding genes (PCGs), 2 ribosomal RNA (rRNA) genes, 22 transfer RNA (tRNA) genes, and a putative control region in the typical teleost gene composition. The gene order of the P. pulcher mitogenome was identical to that of other cichlid species. A maximum likelihood phylogenetic tree based on mitochondrial PCGs showed a relationship of P. pulcher with a cichlid Tylochromis polylepis (Boulenger 1900), suggesting that more complete mitogenomes are needed to explore mitogenome evolution in West African tribes and riverine cichlids, as this genomic information is the first complete mitogenome in the tribe Chromidotilapiini.

Complete mitochondrial genome of the six-line wrasse Pseudocheilinus hexataenia (Labriformes, Labridae).

Here, we report the complete mitogenome information of the six-line wrasse Pseudocheilinus hexataenia (Bleeker, 1857). Genome sequencing using the Illumina HiSeq platform allowed the assembly of a circular mitochondrial genome of 17,111 bp from P. hexataenia, consisting of 54% AT nucleotides, 13 protein-coding genes (PCGs), two ribosomal RNA (rRNA) genes, 22 transfer RNA (tRNA) genes, and a putative control region in the typical Labriformes gene composition. The gene order of the P. hexataenia mitochondrion was identical to that of the Labridae mitogenomes. Phylogenetic reconstruction places P. hexataenia with a close relationship with the mitogenome of the goldsinny wrasse, Ctenolabrus rupestris.

Chronic exposure to sublethal concentrations of saxitoxin reduces antioxidant activity and immunity in zebrafish but does not affect reproductive parameters.

Saxitoxin produced by dinoflagellates and cyanobacteria can be transferred to humans through intoxicated organisms such as fish, but limited research has addressed the adverse effects of this toxin on aquatic organisms. In this study, we measured the potential effects of a 90-day exposure to saxitoxin (0.1 or 1 µg·L - 1) on body weight and length, antioxidant defense system, immunity, sex hormones, and genes involved in associated key metabolic pathways in zebrafish (Danio rerio). Significant impairments in body weight and length were observed in response to 1 µg·L - 1 saxitoxin in both male and female zebrafish. A significant increase in the levels of malondialdehyde, together with decreased enzymatic activities of catalase and superoxide dismutase, was observed in fish of both sexes exposed to 1 µg·L - 1 saxitoxin, indicating the occurrence of lipid peroxidation and oxidative stress. Immune parameters such as alternative complement activity, lysozyme activity, and immunoglobulin content were also significantly reduced. However, exposure of male and female zebrafish to saxitoxin for 90 days did not significantly affect reproductive parameters such as the gonadosomatic index and plasma concentrations of vitellogenin, estradiol, and 11-keto testosterone. Transcriptional responses showed similar trends to those of the biochemical parameters, as genes involved in the antioxidant defense system and immunity were downregulated, whereas the transcription of genes related to reproductive metabolism showed no significant change upon treatment with 1 µg·L - 1 saxitoxin. Our findings indicate that long-term exposure to a sublethal concentration of saxitoxin can inhibit growth through induction of oxidative stress and immunosuppression, while the reproductive parameters of zebrafish are not a main target of this toxin at sublethal concentrations.

The complete mitochondrial genome of Lamprologus signatus (Perciformes: Cichlidae).

In this study, the complete 16,583 bp mitochondrial genome of Lamprologus signatus (Poll, 1952) was determined from a specimen sourced from Lake Tanganyika. The mitogenome contains 37 genes [13 protein-coding genes (PCGs), two ribosomal RNA (rRNA) genes, and 22 transfer RNA (tRNA) genes] and a putative control region, which consists of 27.1% A, 27.0% T, 29.9% C, and 16.0% G, with a total G + C content of 45.9%. A maximum likelihood phylogenetic tree based on mitochondrial PCGs suggested that L. signatus is clustered with members of the tribes Haplochromini and Tropheini. As this is the first report of the entire mitogenome in the tribe Lamprologini, the complete mitochondrial sequence information of L. sigantus will be useful in determining phylogenetic relationships of Pseudocrenilabrinae tribes.

The complete mitochondrial genome of the terebellid polychaete Thelepus plagiostoma (Terebellida; Terebellidae).

Here, we report the complete mitogenome information of the terebellid polychaete, Thelepus plagiostoma (Schmarda, 1861). Genome sequencing by Illumina HiSeq platform permitted assembly of a circular mitochondrial genome of 15,628 bp from T. plagiostoma consisting of 67% AT nucleotides, 13 protein-coding genes (PCGs), 2 ribosomal RNA (rRNA) genes, 22 transfer RNA (tRNA) genes, and a non-coding region in the typical annelid gene composition. Gene order of the T. plagiostoma mitochondrion is identical to those of the Terebelliformia mitogenomes. Phylogenetic reconstruction places T. plagiostoma within the monophyletic subclass Sedentaria, a sister to Pista cristata in the suborder Terebelliformia.

Complete mitochondrial genome of the marine polychaete Hediste japonica (Phyllodocida, Nereididae).

To date, only five species are registered in the genus Hediste, and complete mitochondrial genome is reported in one species, Hediste diadroma. In this study, a complete 15,783 bp genome for the marine polychaete H. japonica mitochondrion was assembled through Illumina HiSeq platform. The complete mitochondrial genome of H. japonica contained 13 protein-coding genes (PCGs), 22 transfer RNA (tRNA) genes, two ribosomal RNA (rRNA) genes, and one control region. Overall genomic structure and gene orientation of H. japonica mitogenome are identical to those of H. diadroma. Phylogenetic analysis using the maximum likelihood method validated the sister relationship between Hediste sp. and other polychaetes. This information will be useful to understand geographical distribution, phylogenetic relationship, and evolutionary history of marine polychates.

Complete mitochondrial genome of the crinoid echinoderm, Florometra species (Echinodermata, Crinoidea).

In this study, we report the sequence of the mitochondrial genome (mitogenome) of the crinoid echinoderm, Florometra species (Echinodermata, Crinoidea). The complete mitogenome of Florometra sp. was 15,792 base pairs long and was composed of 13 protein-coding genes (PCGs), two ribosomal RNA (rRNA) genes, 22 transfer RNA (tRNA) genes, and three regions of unassigned sequence (UAS) including one putative control region. Unique nucleotide composition, a clear positive bias for T with an apparent loss of C in PCGs as observed in the Crinoidea mitogenomes, was also seen in the Florometra sp. mitogenome (45% T, 12% C). Phylogenetic analysis with the concatenated nucleotide sequences of entire PCGs of echinoderms confirmed that Florometra sp. is highly related to F. serratissima within the family Crinoidea.

Prolonged exposure to hypoxia inhibits the growth of Pacific abalone by modulating innate immunity and oxidative status.

In aquatic animals, hypoxia is associated with growth retardation, impaired immunity, susceptibility to pathogens, oxidative stress, and mortality. However, the relative long-term effects of hypoxia on bivalves, including abalone, are not well understood. In this study, we examined the effects of exposure to hypoxic (2.5 and 4 mg O2 L-1) and normoxic (8 mg O2 L-1) conditions on the growth, survival, and immune and antioxidant responses of the economically important Pacific abalone Haliotis discus hannai over a 4 month period. We observed that exposure to 2.5 mg O2 L-1 resulted in marked reductions in assessed shell parameters, average meat weight, and survival compared with exposure to 4 and 8 mg O2 L-1. There were also significant reductions in oxygen consumption and ammonia-N excretion in abalone exposed to 2.5 mg O2 L-1. We also detected initial immunosuppression in the 2.5 mg O2 L-1-treated abalone, as evidenced by a significant reduction in total hemocytes and inhibition of antibacterial and lysozyme activities. Furthermore, intracellular malondialdehyde concentrations were significantly elevated at 1 month in the 2.5 mg O2 L-1 treatment group, whereas there were reductions in the levels of glutathione and enzymatic activities of catalase and superoxide dismutase, thereby indicating potential hypoxia-induced oxidative stress and a depression of antioxidant capacity. After 4 months of treatment, severe hypoxia (2.5 mg O2 L-1) had significantly modulated all measured parameters, whereas exposure to 4 and 8 mg O2 L-1 had induced no significant effects. Collectively, our observations indicate that under long-term exposure to hypoxia, Pacific abalone failed to maintain an effective antioxidant defense system and adequate immunity, with the observed biochemical disruptions leading to a reduction in growth and survival.

Constant and intermittent hypoxia modulates immunity, oxidative status, and blood components of red seabream and increases its susceptibility to the acute toxicity of red tide dinoflagellate.

Hypoxia is an increasing threat to aquatic ecosystems and its impact on economically and ecologically important marine fish species needs to be studied. Especially, the consequences of hypoxia when occurring along with harmful algal blooms (HABs) are currently not well documented. In this study, we investigated the effect of constant and intermittent (daily and weekly) hypoxia on respiration, immunity, hematological parameters, and oxidative status of red seabream for 2, 4, and 6 weeks. Under constant and daily intermittent hypoxia, respiration rate significantly increased in 2 weeks compared to the control. Constant and daily intermittent hypoxia caused significant decreases in the activity of alternative complement pathway, lysozyme, and the level of total immunoglobulin (Ig), as well as significant increases in the concentrations of cortisol, hemoglobin, red blood cells, and white blood cells. A significantly higher level of malondialdehyde was measured for all hypoxia-exposed groups, indicating lipid peroxidation and oxidative stress. At 4 and 6 week, the level of glutathione and enzymatic activities of glutathione reductase and glutathione peroxidase were significantly decreased after constant and daily intermittent hypoxia challenge. The enzymatic activities of superoxide dismutase and catalase were significantly increased at 2 and 4 weeks, but they were decreased after 6 weeks by constant and daily intermittent hypoxia. Constant and daily intermittent hypoxia with subsequent non-toxin producing dinoflagellate Cochlodinium polykrikoides treatment significantly reduced the respiration rate in 3 and 24 h exposure and survival rate of red seabream. Taken together, the red seabream can be vulnerable to HABs under hypoxia condition through inhibition of immunity and antioxidant defense ability. Our findings are helpful in better understanding of molecular and physiological effects of hypoxia, which can be used in aquaculture and fisheries management.

[Effects of a video education program for patients with benign uterine tumors receiving high-intensity focused ultrasound treatment]. / ê³ ê°•ë„ 집속 초음파 치료를 받는 ìžê¶ì–‘ì„±ì¢ ì–‘ 환자의 동영상 교육프로그램 효과.

Purpose: The purpose of this study was to examine the effects of a video education program in women receiving high-intensity focused ultrasound (HIFU) treatment. Methods: This was a quasi-experimental study with a nonequivalent control group non-synchronized design. The participants were 54 patients who had benign uterine tumors and adenomyosis. The data were collected from June to August 2018. A 10-minute video education program on HIFU and post-procedural care was developed based on the literature. The experimental group was provided the video education program with a question-and-answer session for 10 minutes after viewing the video. The control group received usual care (i.e., verbal instructions on post-procedural self-care). The questionnaire survey was conducted twice: before the educational program and before being discharged from the hospital. Differences in uncertainty, emotions, and self-efficacy among patients were analyzed. Data were analyzed using the chi-square test, Shapiro-Wilk test, paired t-test, and t-test with SPSS version 23.0. Results: The participants in the experimental group showed a decrease in uncertainty(t=4.33, p<.001), improvements in anxiety(t=-4.07, p<.001) and depression (t=-3.55,p<.001), and an enhancement ofself-efficacy (t=-4.39,p<.001) compared to the control group. Conclusion: This nursing intervention was effective at reducing uncertainty, improving emotions, and enhancing self-efficacy. This intervention is feasible for use in nursing practice as an aid for patients when considering treatment methods.

Hypoxia induces glucose uptake and metabolism of adipose­derived stem cells.

It has previously been demonstrated that hypoxia has diverse stimulatory effects on adipose­derived stem cells (ASCs), however, metabolic responses under hypoxia remain to be elucidated. Thus, the present study aimed to investigate the glucose uptake and metabolism of ASCs under hypoxic conditions, and to identify the underlying molecular mechanisms. ASCs were cultured in 1% oxygen, and experiments were conducted in vitro. As determined by proteomic analysis and western blotting, GAPDH and enolase 1 (ENO1) expression were upregulated under hypoxia. In addition, lactate production was significantly increased, and mRNA levels of glycolytic enzymes, including GAPDH, ENO1, hexokinase 2 (HK2), and lactate dehydrogenase α (LDHα) were upregulated. Hypoxia­inducible factor 1­α (HIF­1α) expression was increased as demonstrated by western blotting, and a pharmacological inhibitor of HIF­1α significantly attenuated hypoxia­induced lactate production and expression of glycolytic enzymes. It was also observed that hypoxia significantly increased glucose uptake in ASCs, and glucose transporter (GLUT)1 and GLUT3 expression were upregulated under hypoxia. Pharmacological inhibition of the HIF­1α signaling pathways also attenuated hypoxia­induced GLUT1 and GLUT3 expression. These results collectively indicate that hypoxia increases glucose uptake via GLUT1 and GLUT3 upregulation, and induces lactate production of ASCs via GAPDH, ENO1, HK2, and LDHα. Furthermore, HIF­1α is involved in glucose uptake and metabolism of ASCs.

Deferoxamine Improves Alveolar and Pulmonary Vascular Development by Upregulating Hypoxia-inducible Factor-1α in a Rat Model of Bronchopulmonary Dysplasia.

Fetal lung development normally occurs in a hypoxic environment. Hypoxia-inducible factor (HIF)-1α is robustly induced under hypoxia and transactivates many genes that are essential for fetal development. Most preterm infants are prematurely exposed to hyperoxia, which can halt hypoxia-driven lung maturation. We were to investigate whether the HIF-1α inducer, deferoxamine (DFX) can improve alveolarization in a rat model of bronchopulmonary dysplasia (BPD). A rat model of BPD was produced by intra-amniotic lipopolysaccharide (LPS) administration and postnatal hyperoxia (85% for 7 days), and DFX (150 mg/kg/d) or vehicle was administered to rat pups intraperitoneally for 14 days. On day 14, the rat pups were sacrificed and their lungs were removed and examined. A parallel in vitro study was performed with a human small airway epithelial cell line to test whether DFX induces the expression of HIF-1α and its target genes. Alveolarization and pulmonary vascular development were impaired in rats with BPD. However, DFX significantly ameliorated these effects. Immunohistochemical analysis showed that HIF-1α was significantly upregulated in the lungs of BPD rats treated with DFX. DFX was also found to induce HIF-1α in human small airway epithelial cells and to promote the expression of HIF-1α target genes. Our data suggest that DFX induces and activates HIF-1α, thereby improving alveolarization and vascular distribution in the lungs of rats with BPD.

FBXO11 represses cellular response to hypoxia by destabilizing hypoxia-inducible factor-1α mRNA.

The transcriptional factor hypoxia-inducible factor-1α (HIF-1α) is induced under hypoxia and plays crucial roles in cancer progression and angiogenesis. Protein arginine methyltransferases (PRMTs), 11 isoforms of which have been identified so far, modulates the functions of diverse proteins by catalyzing arginine methylation in post-translational level. PRMT9 (alternatively named FBXO11) and PRMT11 (FBXO10) are expected to have the E3 ubiquitin ligase activity through their F-box domains as well as the methyltrasferase activity. Given previous studies examining roles of 8 PRMT isoforms (PRMT1-8) in the HIF-1 signaling pathway, PRMT1 and PRMT5 were demonstrated to regulate HIF-1α expression in opposite ways. We herein examined if FBXO10 and FBXO11 participate in the HIF-1 signaling pathway. Consequently, the siRNA-mediated knockdown of FBXO11 facilitated HIF-1α expression in various cancer cells and HIF-1-driven gene expressions, but the FBXO10 knockdown did not. Mechanistically, FBXO11 was found to inhibit de novo synthesis of HIF-1α protein by destabilizing HIF-1α mRNA. Since a FBXO11 mutant lacking F-box failed to reverse the HIF-1α expression by FBXO11 knockdown, the FBXO11 regulation of HIF-1α may be attributed to the ubiquitination of some proteins controlling HIF-1α mRNA stability. Considering the oncogenic roles of HIF-1α, FBXO11 is suggested to act as a tumor suppressor and also to be a potential target for cancer therapy.

Oleanolic acid suppresses resistin induction in adipocytes by modulating Tyk-STAT signaling.

Oleanolic acid, a naturally occurring triterpenoid widely distributed in foods and medicinal plants, has anticancer, antioxidant, and antiaging properties. We hypothesized that oleanolic acid would suppress the production of the inflammatory adipokine resistin during adipogenic differentiation of 3T3-L1 adipocytes. 3T3-L1 adipocytes were cultured in adipogenic media with and without 1 to 25 µM oleanolic acid for up to 8 days to stimulate adipocyte differentiation. Adipocyte production of resistin was markedly enhanced during differentiation and was dose dependently attenuated by 1 to 25 µM oleanolic acid. This study further investigated whether Tyk2-Stat1/3 signaling was responsible for cellular production of resistin. Signal transducer and activator of transcription factor (STAT) 1 and STAT3 were activated during differentiation in a disparate temporal fashion; STAT1 was maximally phosphorylated on day 5 after initiating differentiation, whereas STAT3 was rapidly activated within 1 day of differentiation. When oleanolic acid was supplied to differentiating adipocytes, STAT1 and STAT3 phosphorylation was substantially suppressed. Upstream Tyk2 was rapidly activated in a manner similar to STAT3 and reactivated on days 3 to 5 after initiating differentiation, which was attenuated by incubating adipocytes with oleanolic acid. In addition, cellular expression of suppressor of cytokine signaling 3 (SOCS3), which inhibits Tyk2 activity, was markedly promoted from day 5 of adipocyte differentiation. Oleanolic acid attenuated SOCS3 expression, which was highly enhanced during the late phase of differentiation. Taken together, oleanolic acid suppressed adipocyte differentiation-associated resistin and adipogenesis production by disturbing the Tyk2-STAT1/3 signaling pathway and promoting SOCS3 expression. Therefore, oleanolic acid may be a possible bioactive agent that blunts adipogenesis and adipokine inflammation.

Sildenafil alleviates bronchopulmonary dysplasia in neonatal rats by activating the hypoxia-inducible factor signaling pathway.

Bronchopulmonary dysplasia (BPD) is a major cause of morbidity in premature infants receiving oxygen therapy. Currently, sildenafil is being examined clinically to improve pulmonary function in patients with BPD. Based on the pharmacological action of sildenafil, the elevation of cyclic guanosine 3',5'-monophosphate (cGMP) in lung tissue is considered to underlie its beneficial effects, but this mechanism is not understood at the molecular level. Here, we examined the possibility that sildenafil helps the pulmonary system adapt to hyperoxic stress. To induce BPD, fetal rats were exposed to LPS before delivery, and neonates were exposed to hyperoxia, followed by intraperitoneal injections of sildenafil. Alveolarization was impaired in rats exposed to hyperoxia, and alveolarization significantly recovered with sildenafil. An immunohistochemical examination revealed that sildenafil effectively increased vascular distribution in lung tissue. Furthermore, the oxygen sensor hypoxia-inducible factor (HIF)-1/2α and the angiogenic factor vascular endothelial growth factor (VEGF) were highly expressed in the lungs of sildenafil-treated rats. In human small-airway epithelial cells, HIF-1/2α and its downstream genes, including VEGF, were confirmed to be induced by sildenafil at both the protein and mRNA levels. Mechanistically, cGMP in airway cells accumulated after sildenafil treatment because of interfering phosphodiesterase Type 5, and subsequently cGMP activated HIF-mediated hypoxic signaling by stimulating the phosphoinositide 3-kinase (PI3K)-v-akt murine thymoma viral oncogene homolog 1 (AKT)-mammalian target of rapamycin (mTOR) pathway. This study provides a better understanding about the mode of action for sildenafil, and suggests that HIF can be a potential target for treating patients with BPD.

Red ginseng and 20(S)-Rg3 control testosterone-induced prostate hyperplasia by deregulating androgen receptor signaling.

Since prostate growth is governed by the androgen signaling pathway, blockade of the pathway is regarded as an appropriate strategy for the treatment of benign prostatic hyperplasia (BPH). Panax ginseng is known to have various pharmacological activities. Of several products of its root, red ginseng, having many bioactive ginsenosides, is most popularly used in Korea, and recently has been reported to control the proliferation of cancer cells. We here tested the effect of a water extract of Korean red ginseng (WKRG) on testosterone-induced prostate hyperplasia. WKRG (daily intraperitoneal injection) prevented prostate overgrowth and epithelial thickening induced by testosterone in rats, and suppressed a rat prostate kallikrein-S3. In human prostate cells, WKRG inhibited testosterone-induced cell proliferation, arrested cell cycle by inducing p21 and p27, and induced apoptosis. Testosterone-induced expression of human kallikrein-3 mRNA and activation of androgen receptor (AR) were effectively inhibited by WKRG. Of the major ginsenosides included in WKRG, 20(S)-Rg3 was identified to repress AR activity and to attenuate prostate cell growth during testosterone stimulation. Moreover, 20(S)-Rg3 downregulated AR by facilitating the degradation of AR protein. WKRG and 20(S)-Rg3 were found to have new pharmacological activities against testosterone-induced prostate overgrowth. Given that red ginseng has been used safely in Asia for 1000 years, red ginseng and 20(S)-Rg3 could be potential therapeutic regimens for treating BPH.

Effects of a problem-solving counseling program to facilitate intensified walking on Koreans with type 2 diabetes.

AIM: This study aimed to evaluate the immediate and long-term effects of a 12 week problem-solving (PS) counseling program to facilitate intensified walking with machinery monitoring on persons with type 2 diabetes mellitus in Korea. METHODS: The study used a quasi-experimental design. The participants were 57 patients with diabetes from three endocrinology or internal medicine clinics in an urban city of South Korea. Moderate-intensity walking and PS counseling were recommended to both groups. The difference between the two groups was whether the intensity of the exercise was monitored by an ambulatory heart rate monitor (experimental group) or was self-regulated (comparison group). Those programs were evaluated in relation to BMI, glycemic control (blood glucose level, glycosylated hemoglobin [HbA1c]), a vascular complication index (total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, tissue plasminogen activator [t-PA], plasminogen activator inhibitor-1 [PAI-1], Parma Cardiovascular Risk Index), and coping strategies at 3 and 6 months. RESULTS: The experimental group members showed dramatic decreases in their glucose and HbA1c levels at 3 months. The values of t-PA decreased significantly at baseline, compared to at 3 months. The levels of PAI-1 continuously declined and the Parma Cardiovascular Risk Index score did not change significantly from baseline to at 3 months, but showed significant effects at 6 months. CONCLUSION: A combined program of intensified walking, using a heart rate monitor, with PS counseling is more helpful to prevent complications than self-regulated exercise for persons with type 2 diabetes in Korea.

[Quality of sleep and serum lipid profile in patients with restless legs syndrome].

PURPOSE: The purpose of this study was to compare the quality of sleep with the serum lipid profile in patients who have restless legs syndrome (RLS). METHODS: The data were obtained from 116 patients with RLS through questionnaires and blood sampling. RESULTS: The results of this study showed correlations between lower quality of sleep and serum lipid profile (LDL Cholesterol) in patients with RLS (r=.19, p=.040). There were correlations for scores of quality of sleep from the, Pittsburgh Sleep Quality Index (PSQI) sub-region between lower subjective sleep quality and serum lipid profile (LDL Cholesterol) (r=.20, p=.026), between fewer hours of sleep duration and serum lipid profile (Total Cholesterol) (r=-.21, p=.024), and, between higher daytime dysfunction and serum lipid profile (LDL Cholesterol) (r=.42, p<.001) of patients with RLS. CONCLUSION: Patients with RLS have sleep disorders with lower quality of sleep and changes in the serum lipid profile for total cholesterol and LDL cholesterol. That is, patients with RLS have lower quality of sleep and dyslipidemia compared to persons without RLS. Further research is needed to monitor serum the lipid profile in early stage symptoms of midlife adult patients with RLS and especially older women.