Comparison between a new electronic bidet and conventional sitz baths: a manometric evaluation of the anal resting pressure in normal healthy volunteers.

BACKGROUND: A bidet has been proposed as a replacement for the sitz bath. Like a sitz bath, it brings water into contact with the perineum. However, the high force of water from commercially used electronic bidets may harm the anus. We developed a new electronic bidet and evaluated its effects on anal resting pressure compared with a warm sitz bath. METHODS: Forty volunteers used the electronic bidet and sitz bath on separate days. The electronic bidet was newly designed with warm (38 °C) water and very low force (10 mN) with a fountain type of flow. Anal resting pressure at the high-pressure zone was measured before (control) and after the electronic bidet and sitz bath. Pressure changes after bidet or sitz bath were expressed as percentages compared with control. Water temperatures and rectal temperatures were also recorded. RESULTS: The anal resting pressures before the electronic bidet and sitz bath were 90.2 ± 24.6 and 88.1 ± 16.8 mmHg, respectively. At 3 min after the electronic bidet and sitz bath, the anal resting pressures were 71.3 ± 23.4 and 69.6 ± 19.8 mmHg, respectively. The pressure changes compared with the control were 78.2 ± 12.9 and 78.1 ± 12.5%, respectively, which were not significantly different. The maximal increase and minimal decrease were not significantly different. The rectal temperature was not elevated, and the water temperature decreased significantly with the sitz bath (p < 0.001). CONCLUSIONS: Our new electronic bidet may reduce the anal resting pressure much like a warm sitz bath does.

Efficient association study design via power-optimized tag SNP selection.

Discovering statistical correlation between causal genetic variation and clinical traits through association studies is an important method for identifying the genetic basis of human diseases. Since fully resequencing a cohort is prohibitively costly, genetic association studies take advantage of local correlation structure (or linkage disequilibrium) between single nucleotide polymorphisms (SNPs) by selecting a subset of SNPs to be genotyped (tag SNPs). While many current association studies are performed using commercially available high-throughput genotyping products that define a set of tag SNPs, choosing tag SNPs remains an important problem for both custom follow-up studies as well as designing the high-throughput genotyping products themselves. The most widely used tag SNP selection method optimizes the correlation between SNPs (r(2)). However, tag SNPs chosen based on an r(2) criterion do not necessarily maximize the statistical power of an association study. We propose a study design framework that chooses SNPs to maximize power and efficiently measures the power through empirical simulation. Empirical results based on the HapMap data show that our method gains considerable power over a widely used r(2)-based method, or equivalently reduces the number of tag SNPs required to attain the desired power of a study. Our power-optimized 100k whole genome tag set provides equivalent power to the Affymetrix 500k chip for the CEU population. For the design of custom follow-up studies, our method provides up to twice the power increase using the same number of tag SNPs as r(2)-based methods. Our method is publicly available via web server at http://design.cs.ucla.edu.

An ion optics study for KSTAR neutral beam injector development.

Ion optics of three accelerator geometries was studied in terms of an analytic linear optics analysis, a numerical simulation using the IGUN program, an optical multichannel measurement of Doppler-shifted H(alpha) lines, and a water-flow calorimetry on the beam absorbing target. In general, there was a reasonable agreement observed between the four analysis methods and thus the theoretical analyses can be utilized with confidence for design iteration.

Identification of a previously unrecognized production site of human renin.

We found expression of the renin gene in the intestine of human, mouse and the transgenic mouse in which the 3' flanking sequences of the human renin gene function as a tissue-specific promoter. A cotransfection analysis showed that the promoter is activated by the product of adenovirus E1A 13S mRNA in cells originated from extrarenal tissues.

SELENBP1 expression in the prefrontal cortex of subjects with schizophrenia.

Selenium binding protein 1 (SELENBP1) messenger RNA (mRNA) has previously been shown to be upregulated in the brain and blood from subjects with schizophrenia. We aimed to validate these findings in a new cohort using real-time PCR in Brodmann's Area (BA) 9, and to determine the disease specificity of increased SELENBP1 expression by measuring SELENBP1 mRNA in subjects with major depressive disorder and bipolar disorder. We then extended the study to include other cortical regions such as BA8 and BA44. SELENBP1 mRNA was higher in BA9 (P = 0.001), BA8 (P = 0.003) and BA44 (P = 0.0007) from subjects with schizophrenia. Conversely, in affective disorders, there was no significant difference in SELENBP1 mRNA in BA9 (P = 0.67), suggesting that the upregulation may be diagnosis specific. Measurement of SELENBP1 protein levels showed that changes in mRNA did not translate to changes in protein. In addition, chronic treatment of rats with antipsychotics did not significantly affect the expression of Selenbp1 in the cortex (P = 0.24). Our data show that elevated SELENBP1 transcript expression is widespread throughout the prefrontal cortex in schizophrenia, and confirm that this change is a consistent feature of schizophrenia and not a simple drug effect.

Renin gene expression in the adrenal and kidney of patients with primary aldosteronism.

mRNA levels for renin in the adrenal gland and kidney were measured by ribonuclease protection assay (RPA). Renin mRNA was not detected by RPA in aldosteronoma and kidney tissues obtained from two patients with primary aldosteronism (PA). In these patients, the PRA values, plasma concentrations of active renin (ARC), and total renin (TRC = ARC + prorenin) were below the assay limit (less than 0.03 ng/L.s, 2.5 ng/L, and 10 ng/L, respectively). On the other hand, renin mRNA was recognized by RPA in aldosteronoma and kidney tissues obtained from two other patients with PA treated with 50 mg/day spironolactone for more than 2 months. Their TRC values were 49.8 and 16.6 ng/L, but their PRA and ARC were undetectable. Renin mRNA content was greater in normal adrenocortical tissue and in the normal kidneys obtained from three hypertensive patients with renal cell carcinoma. In these patients, the mean values of PRA, ARC, and TRC were 0.28 +/- 0.03 (mean +/- SD) ng/L.s, 18.4 +/- 7.8 ng/L, and 110 +/- 15 ng/L, respectively. This is the first report of the lack of renin gene expression in aldosteronoma and kidney tissues obtained from untreated patients with PA. Furthermore, treatment with spironolactone resulted in an increase in the levels of renin mRNA in the aldosteronoma and kidney tissues of patients with PA.

Expression of rat BTG(3) gene, Rbtg3, is regulated by redox changes.

The Rbtg3 gene was isolated by PCR (polymerase chain reaction) cloning from the cDNA library of Rat1 fibroblasts that were stimulated with TPA (12-O-tetradecanoylphorbol-13-acetate) or various growth factors for 3h and was found to be a rat homologue of mouse BTG3 and human ANA genes. The Rbtg3 gene had unique DNA sequences in the 5'-UTR and 3'-UTR that contained four ATTTA and one TTATTTA(T/A)(T/A) nonamer motif, and also a polyA addition site. Nucleotide homology of Rbtg3 with BTG3 and ANA was 88.5 and 76.6%, respectively. Expression of Rbtg3 was investigated in SD rats as well as cell lines derived from mouse--SW3T3, NIH3T3 fibroblasts--and rat--Rat1, 3Y1 fibroblasts and PC12--cells. Rbtg3 was highly expressed in brain but barely in lung, kidney, thymus and spleen. The constitutive expression level was high in SW3T3, Rat1 and 3Y1 fibroblasts, but very low in NIH3T3 fibroblast and PC12 cells. However, in all cells tested, Rbtg3 was proved to be one of the primary response genes superinduced by TPA (50ng/ml)+cycloheximide (CHX, 10 microgram/ml). Expression of Rbtg3 was induced by H(2)O(2) (500mM) up to fourfold in PC12 cells and was blocked by pretreatment of NAC (N-acetyl-L-cysteine, 10mM). The induction was ninefold in 3Y1 fibroblasts by menadione (25mM) treatment for 1h, whereas it was reduced to a third of the control level in SW3T3 fibroblast by the same treatment. Rbtg3 was not expressed in NIH3T3 cells but minimally regulated by redox changes as compared with rapid and strong induction of TIS21/BTG2 mRNAs after TPA or H(2)O(2) stimulation. The above results indicate that Rbtg3 is one of many redox-regulated genes as well as a primary response gene.

Adenosine triphosphate-induced heterologous desensitization of endothelin-1- and glutamate-evoked calcium increases in cultured rat cortical astrocytes.

In rat cortical astrocytes, we investigated the occurrence of cross-talks between purinoceptor and endothelin (ET) receptor, or glutamate receptor. The treatments of adenosine triphosphate (ATP), ET-1, and glutamate induced the increase of intracellular calcium level in the astrocytes. In repetitive additions of ATP to astrocytes, the second application of ATP exhibited comparable amplitude of calcium response, but the stimulation with ATP completely blocked subsequent ET-1- or glutamate-evoked calcium responses showing complete heterologous desensitization. In contrast, ET-1 and glutamate failed to desensitize the response elicited by ATP. Preincubation with sphingosine, a protein kinase C (PKC) inhibitor, reversed the ATP-induced desensitization of ET-1- and glutamate-evoked calcium responses. Taken together, these results demonstrate the resistance of purinoceptor to homologous desensitization, and unidirectional desensitization between ATP and other receptors such as ET and glutamate receptors, suggesting a dominant role of purinoceptor in modulating calcium signal of astrocytes.

Cellular distribution of isozymes of protein kinase C in septal olfactory epithelium of mice.

To determine the presence of protein kinase C (PKC) isozymes in the septal olfactory epithelium of mice (mSOE), western blotting and immunohistochemistry were performed using antibodies against PKC isozymes. With the exception of PKC-betaI, all of the PKC isozymes were detected in the whole lysate of septal tissue layer and apparent molecular weights for each isoform were found. PKC-alpha, PKC-gamma and PKC-epsilon were detected in the olfactory glandular cells of the lamina propria, and PKC-betaI and PKC-betaII were located in the microvillar cells. Neither novel PKC nor atypical PKC was detected in olfactory glandular cells or microvillar cells, except for PKC-epsilon. PKC-lambda was localized in the mucous layer of the mSOE. Meanwhile, PKC-delta and PKC-xi were distributed in the receptor cells in the mSOE. These data demonstrate the isoform-specific expression of PKC in mSOE and suggest a role for the novel and atypical types of PKC in olfactory transduction.

Triangular transchamber suture.

A 64-year-old woman with a fibrous membrane at the lens plane after traumatic loss of all the iris and massive intraocular hemorrhage had posterior chamber intraocular lens (PCIOL) implantation anterior to the fibrous membrane with a triangular transchamber suture to prevent possible PCIOL-corneal touch and enhance the stability of the PCIOL. After 3 years, the PCIOL remained in a good position and visual rehabilitation was satisfactory and without complications.

Activation of telomerase by silica in rat lung.

By measuring the activity of telomerase in a silica-instilled rat lung, the study found a significant increase in telomerase activity compared to that of the control. Pneumoconiosis displays the characteristics of fibroblast-proliferation and accumulation of collagen, which finally causes the pathologic changes of irreversible and progressive fibrosis of the lung. On the basis of the hypothesis that cellular proliferation may trigger telomerase-activity, the experiment was carried out with telomerase-activation in silicosis. Silica-instilled rat lungs showed increased activity of telomerase, which was measured by TRAP (telomeric repeat amplification protocol) assay, at the time of the 1st, 5th and 8th week after intratracheal instillation of silica in vivo. However, no activity was shown in silica-co-cultured fibroblast in vitro. By summarizing these results, the activity of telomerase is thought to be a very sensitive marker for the evaluation of pathogenicity, showing cellular immortalization in an experimental silicosis model.

Purification and characterization of iron superoxide dismutase and copper-zinc superoxide dismutase from Acanthamoeba castellanii.

Two superoxide dismutases (SOD I and SOD II) were purified from Acanthamoeba castellanii and characterized for several biochemical properties. Analysis of the primary structure and inhibition studies revealed that SOD I is iron SOD (Fe-SOD), with a molecular mass of 50 kDa, and SOD II is copper-zinc SOD (Cu,Zn-SOD), with a molecular mass of 38 kDa. Both enzymes have a homodimeric structure consisting of 2 identical subunits, each with a molecular mass of 26 and 19 kDa for SOD I and SOD II, respectively. The isoelectric points of SOD I and SOD II were 6.4 and 3.5, respectively, and there were no isoenzyme forms detected. Both enzymes show a broad optimal pH of 7.0-11.0. Because no differences were observed in the apparent molecular weight of SOD I after addition of the reducing agent 2-mercaptoethanol, the subunits do not appear to be linked covalently by disulfide bonds. However, the subunits of SOD II were covalently linked by intra- and interdisulfide bonds. Western blot analyses showed that the 2 enzymes have different antigenicity. Both enzymes occur as cytoplasmic and detergent-extractable fractions. These enzymes may be potential virulence factors of A. castellanii by acting both as antioxidants and antiinflammatory agents. These enzymes may be attractive targets for chemotherapy and immunodiagnosis of acanthamoebiasis.

Recurrent unilateral frosted branch angiitis.

In the left eye of a 27-year-old man we found perivascular creamy sheathing of retinal veins with retinal hemorrhages and, on fluorescein angiography, delayed filling of veins with late leakage. Dramatic recovery of visual acuity and healing of retinal lesions followed intravenous corticosteroid therapy. However, the condition recurred several times within a few months. Fluorescein angiography showed delayed filling of arteries and veins and arteriovenous anastomoses with a widespread capillary nonperfusion area. Eventually, neovascular glaucoma resulted. It is suggested that frosted branch angiitis is related to vascular occlusion. Systemic corticosteroid therapy seems to affect the course of this disease.

A new technique for repositioning a posteriorly dislocated intraocular lens.

Pars plana vitrectomy was performed to treat a complete posterior dislocation of an intraocular lens in seven patients. The method that the authors have developed appears to be safer and simpler than those previously described. The haptics are externalized for a secure tie at the proper site, and are then reinternalized back through the pars plana sclerotomies. Only two small needle perforations are made for the scleral fixation of the intraocular lens in the ciliary sulcus. Perfluorocarbon liquid is used to prevent intraoperative retinal damage.

Axial length in branch retinal vein occlusion.

To determine the effects of axial length on the development of branch retinal vein occlusion (BRVO), determination of the affected eye, development of surgical complications, and visual prognosis, axial length was measured in 27 eyes each in surgical, non-surgical and control group and in 54 eyes each in occlusion (surgical + non-surgical group), non-affected eye (non-affected eyes of occlusion group), and non-occlusion group (both eyes of the control group). The average axial length was 22.61 mm in surgical, 22.48 mm in non-surgical, 23.09 mm in control, 22.55 mm in occlusion, 22.56 mm in non-affected eye, and 23.11 mm in non-occlusion group. The axial length showed a statistically significant difference between surgical and control group (p = 0.018), between non-surgical and control group (p = 0.002), and between occlusion and non-occlusion group (p < 0.001); however, no statistically significant difference was seen between surgical and non-surgical group, between non-affected eyes of surgical and non-surgical group, and between occlusion and non-affected eye group. Also, in such as BRVO groups as surgical, non-surgical, and occlusion groups, no correlation was present between axial length and degree of visual acuity recovery and final visual acuity. Although the possibility of developing BRVO is higher in those with short axial length, the axial length may have no relationship with the determination of the affected eye, visual prognosis and development of surgical complications.

Dapsone maculopathy.

After the injection of about 10 gm of dapsone, a 38-year-old male showed a whitish-yellow patch in the macular region of both eyes, with decreased visual acuity of the counting finger in the right and 0.04 in the left eye. Two weeks after the start of systemic steroid therapy the patch disappeared, and on follow-up at 11 months, visual acuity was 0.02 in the right and 0.08 in the left eye, with macular degeneration and foveal nonperfusion. This retinal damage seems to be ischemic in origin and to be caused by a combination of acute severe peripheral hypoxemia and the vascular obstructive effect of red cell fragmentation resulting from massive hemolysis.

Intravitreal cysticercosis.

Examination of a 36-year-old man with naked visual acuity of 20/20 revealed a floating, conspicuous cyst of Cysticercus cellulosae in the vitreous cavity of the right eye. A vitreous traction band from the vitreous base and the optic disc was connected to the lodging bulb of the cyst. In the superonasal area, an ovoid retinal break surrounded by a white retinal lesion with two elliptical retinal hemorrhages was found, and this seems to be the previous lodging site of the cyst. A pars plana vitrectomy was performed to remove the parasite, and laser photocoagulation was carried out around the retinal break. Four months after the operation, the patient was satisfied with naked visual acuity of 25/20 without any complication in the affected eye.

Management of posteriorly dislocated intraocular lens using pars plana vitrectomy.

In order to evaluate the results of pars plana vitrectomy (PPV) for the treatment of posteriorly dislocated intraocular lens (PC-IOL), we retrospectively examined and analyzed the hospital records of patients who had undergone PPV to exchange or reposition a PC-IOL dislocated into the vitreous cavity. Of 20 eyes in 20 patients, IOL exchange was performed in 6 eyes, and IOL repositioning in 14 eyes. Posteriorly dislocated IOL occurred in 14 eyes during or within 2 days, and in 6 eyes 6 months after the IOL implantation. Thirteen eyes were surgically treated early after the occurrence, within 3 days, while 7 eyes were treated later, between 5 to 7 days. Compared with preoperative best-corrected visual acuity, the final visual acuity improved more than 2 lines in 12 eyes. With no significant difference on the statistics, earlier visual rehabilitation seemed to be shown in late-treated patients than in early-treated. Accordingly, a posterior dislocation of IOL can be successfully treated with PPV, and barring any serious complications such as retinal detachment, there is no need for surgery immediately following the occurrence.

Changes in refraction and axial length according to the viscosity of intraocular silicone oil.

We performed this study to evaluate the changes in refraction and axial length induced by intraocular silicone oil, and to compare with various clinical parameters between 1,000 and 5,000 cSt silicone oil. The refraction length was measured with an autorefractometer, and the axial length was measured with A-scan ultrasonography. These measurements were performed before and after removal of the silicone oil, using a clear cornea technique in which the silicone oil was injected in combination with pars plana vitrectomy. The mean age of the 25 patients was 38.73 years. On average the intraocular retention after the removal of the silicone oil lasted 5.13 months, and the follow-up time following silicone oil removal was 4.37 months. The changes in refraction and axial length were 6.32 diopters and 12.02 mm, respectively. Eyes injected with 5,000 cSt (11 eyes) tended to have higher changes in the refraction (5.84 vs 6.86 diopters) and axial length (11.70 vs 12.34 mm) than did eyes injected with 1,000 cSt silicone oil (14 eyes). Statistically significant differences were shown for the changes in refraction (p = 0.010) and intraocular pressure (0.63 vs 2.00 mmHg; p = 0.006), whereas but not for the changes in axial length (p = 0.306) and visual acuity (14/100 vs 15/100; p = 0.125). Intraocular silicone oil induced changes in refraction and axial length, and these changes seemed to vary with different viscosities.

Decreased cortical muscarinic M1 receptors in schizophrenia are associated with changes in gene promoter methylation, mRNA and gene targeting microRNA.

Many studies have shown decreased cortical muscarinic M1 receptors (CHRM1) in schizophrenia (Sz), with one study showing Sz can be separated into two populations based on a marked loss of CHRM1 (-75%) in -25% of people (Def-Sz) with the disorder. To better understand the mechanism contributing to the loss of CHRM1 in Def-Sz, we measured specific markers of gene expression in the cortex of people with Sz as a whole, people differentiated into Def-Sz and people with Sz that do not have a deficit in cortical CHRM1 (Non-Def-Sz) and health controls. We now report that cortical CHRM1 gene promoter methylation and CHRM1 mRNA are decrease in Sz, Def-Sz and Non-Def-Sz but levels of the micro RNA (miR)-107, a CHRM1 targeting miR, are increased only in Def-Sz. We also report in vitro data strongly supporting the notion that miR-107 levels regulate CHRM1 expression. These data suggest there is a reversal of the expected inverse relationship between gene promoter methylation and CHRM1 mRNA in people with Sz and that a breakdown in gene promoter methylation control of CHRM1 expression is contributing to the global pathophysiology of the syndrome. In addition, our data argues that increased levels of at least one miR, miR-107, is contributing to the marked loss of cortical CHRM1 in Def-Sz and this may be a differentiating pathophysiology. These latter data continue to support the hypothesis that microRNAs (miRNA) have a role in the underlying neurobiology of Sz but argue they are differentially affected in subsets of people within that syndrome.