Changes in hydration of the stratum corneum are the most suitable indicator to evaluate the irritation of surfactants on the skin.

BACKGROUND/PURPOSE: Irritancy levels of surfactants on human skin have not been clarified completely. The relationships between skin damage and changes of skin properties caused by various surfactants were investigated using non-invasive measurements. METHODS: Aqueous solutions of seven kinds of anionic, non-ionic, and amphoteric surfactants were exposed to the inside of forearm skin of 20 human subjects in two separate studies using the cup method. Hydration of the stratum corneum (SC), transepidermal water loss (TEWL), pH, skin surface roughness, and contents of the SC were measured before and after one exposure and after five and nine consecutive exposures to various surfactants. The discontinuation ratio of subjects for testing in each surfactant was determined by skin irritation symptoms and was defined as the degree of skin damage. RESULTS: Significant changes were observed only in hydration, TEWL, and natural moisturizing factors (NMF) content in the SC following surfactant exposure. A significant correlation was observed between the discontinuation ratio of each surfactant and the changes of hydration, TEWL, and NMF. Especially, the change of SC hydration showed an excellent correlation with the discontinuation ratio both for single (r = 0.942, P < 0.001) and for chronic exposures (r = 0.934, P < 0.001). CONCLUSION: Our results indicate that the change of hydration of the SC is equivalent to the skin damage caused by surfactants, and therefore is the most suitable indicator to evaluate the irritation of surfactants on the skin.

Long-term mild exercise training enhances hippocampus-dependent memory in rats.

Although exercise training improves hippocampus-related cognition, the optimum exercise intensity is still disputed. Based on the lactate threshold (LT, approximately 20 m/min on treadmill) of rats, we have shown that 2 weeks of training with stress-free mild exercise (ME, LT), comprising exercise stress, promotes adult hippocampal neurogenesis (Okamoto et al., PNAS, 2012), a potential substrate for memory improvement. These results led us to postulate that long-term ME, but not IE, training leads to improved hippocampal function as assessed with a Morris water maze (MWM) task. To test this hypothesis, we investigated the changes in physiological stress levels and MWM task performance in rats assigned to 6 weeks of sedentary control (CONT), ME-training or IE-training conditions. Results showed that, compared to the other conditions, only IE causes general adaptive syndrome (GAS), including adrenal hypertrophy, thymic atrophy and hypercorticosteronemia. In the MWM, ME led to enhanced memory, but not learning, compared with CONT, while IE produced no change in either capacity, probably due to GAS. These findings support the hypothesis that 6 weeks of continuous ME training leads to enhanced hippocampus-related memory, which may have implications for both healthy adults and subjects with low physical capacity.

Relationship between clinical factors and severity of esophageal candidiasis according to Kodsi's classification.

Severe Candida esophagitis (CE) may lead to development of strictures, hemorrhage, esophagotracheal fistula, and a consequent decrease in quality of life. Although the severity of CE has been classified based on macroscopic findings on endoscopy, the clinical significance remains unknown. The aim of the study was to elucidate the predictive clinical factors for endoscopic severity of CE. Patients who underwent upper endoscopy and answered questionnaires were prospectively enrolled. Smoking, alcohol, human immunodeficiency virus (HIV) infection, diabetes mellitus, chronic renal failure, liver cirrhosis, systemic steroids use, proton pump inhibitor use, H2 blocker use, and gastrointestinal (GI) symptoms were assessed on the same day of endoscopy. GI symptoms including epigastric pain, heartburn, reflux, hunger cramps, nausea, dysphagia, and odynophagia were assessed on a 7-point Likert scale. Endoscopic severity was classified as mild (Kodsi's grade I/II) or severe (grade III/IV). Of 1855 patients, 71 (3.8%) were diagnosed with CE (mild, n = 48; severe, n = 23). In the CE patients, 50.0% (24/48) in the mild group and 23.1% (6/23) in the severe group did not have any GI symptoms. In HIV-infected patients (n = 17), a significant correlation was found between endoscopic severity and declining CD4 cell count (Spearman's rho = -0.90; P < 0.01). Multivariate analysis revealed that GI symptoms (odds ratio [OR], 3.32) and HIV infection (OR, 3.81) were independently associated with severe CE. Patients in the severe group experienced more epigastric pain (P = 0.02), reflux symptoms (P = 0.04), dysphagia (P = 0.05), and odynophagia (P < 0.01) than those in the mild group. Of the GI symptoms, odynophagia was independently associated with severe CE (OR 9.62, P = 0.02). In conclusion, the prevalence of CE in adults who underwent endoscopy was 3.8%. Silent CE was found in both mild and severe cases. Endoscopic severity was associated with characteristic GI symptoms and comorbidity of HIV infection. A decline in immune function correlated with CE disease progression.

Circulating Insulin-Like Growth Factor I Regulates Its Receptor in the Brain of Male Mice.

The role of IGF-1 and its receptor (IGF-1R) in brain pathology is still unclear. Thus, either reduction of IGF-IR or treatment with IGF-1, two apparently opposite actions, has proven beneficial in brain diseases such as Alzheimer's dementia. A possible explanation of this discrepancy is that IGF-1 down-regulates brain IGF-1R levels, as previously seen in a mouse Alzheimer's dementia model. We now explored whether under normal conditions IGF-1 modulates its receptor. We first observed that in vitro, IGF-1 reduced IGF-1R mRNA levels in all types of brain cells including neurons, astrocytes, microglia, endothelial cells, and oligodendrocytes. IGF-1 also inhibited its own expression in neurons and brain endothelium. Next, we analyzed the in vivo actions of IGF-1. Because serum IGF-1 can enter the brain, we injected mice with IGF-1 ip. As soon as 1 hour after the injection, decreased hippocampal IGF-1 levels were observed, followed by increased IGF-1 and IGF-1R mRNAs 6 hours later. Because environmental enrichment (EE) stimulates the entrance of serum IGF-1 into the brain, we analyzed whether a physiological entrance of IGF-1 also produced changes in brain IGF-1R. Stimulation of IGF-1R by EE triggered a gradual decrease in hippocampal IGF-1 levels. After 6 hours of EE exposure, IGF-1 levels reached a significant decrease in parallel with increased IGF-1R expression. After longer times, IGF-1R mRNA levels returned to baseline. Thus, under nonpathological conditions, IGF-1 regulates brain IGF-1R. Because baseline IGF-1R levels are rapidly restored, a tight control of brain IGF-1R expression seems to operate under physiological conditions.

Exercise and cerebrovascular plasticity.

Aging impairs cerebrovascular plasticity and subsequently leads cerebral hypoperfusion, which synergistically accelerates aging-associated cognitive dysfunction and neurodegenerative diseases associated with impaired neuronal plasticity. On the other hand, over two decades of researches have successfully demonstrated that exercise, or higher level of physical activity, is a powerful and nonpharmacological approach to improve brain function. Most of the studies have focused on the neuronal aspects and found that exercise triggers improvements in neuronal plasticity, such as neurogenesis; however, exercise can improve cerebrovascular plasticity as well. In this chapter, to understand these beneficial effects of exercise on the cerebral vasculature, we first discuss the issue of changes in cerebral blood flow and its regulation during acute bouts of exercise. Then, how regular exercise improves cerebrovascular plasticity will be discussed. In addition, to shed light on the importance of understanding interactions between the neuron and cerebral vasculature, we describe neuronal activity-driven uptake of circulating IGF-I into the brain.

Hair cycle-dependent changes in skin immune functions: anagen-associated depression of sensitization for contact hypersensitivity in mice.

To assess whether hair follicle cycling influences skin immunity, we examined the association between highly synchronized hair follicle cycling and experimental contact hypersensitivity in C57BL/6 mice. Hair cycle synchronization was performed by depilation of hair shafts on the back with telogen skin. Mice were sensitized on the lower back skin with picryl chloride between 0 and 25 d, after anagen induction by depilation, and challenged on the earlobes with picryl chloride 5 d later. The magnitude of contact hypersensitivity was significantly decreased in mice sensitized on day 1, was minimal on day 3 (early anagen), and slowly increased thereafter, reaching level comparable to day 0 on day 25 (telogen). The significantly depressed contact hypersensitivity response in anagen skin was confirmed in mice with spontaneously developed follicles. Lymph node cells taken from mice sensitized with picryl chloride on days 0, 1, and 3 after depilation were cultured in vitro in the presence of syngeneic, haptenized, Langerhans cell-enriched epidermal cells. Marked proliferative responses of lymph node cells to haptenized cells were found in mice not only of day 0, but also of days 1 and 3, suggesting that immune T cells exist even lymph node cells of the low-responsive mice. Flow cytometric analyses demonstrated that the number of intraepidermal Langerhans cells and their functions, including the expression of major histocompatibility complex class II, CD54, and CD86, and mixed epidermal cell lymphocyte reactions, were not changed in skin on days 0,1, and 3. These findings demonstrated that contact hypersensitivity is induced most effectively via skin with telogen hair follicles and that the depressed response in early anagen skin is not simply due to failure in Langerhans cell function or sensitization of T cells.

Altered permeability and disordered cutaneous immunoregulatory function in mice with acute barrier disruption.

In vivo and in vitro T-cell-activating ability of murine epidermal cells (EC) was investigated in acutely barrier-disrupted skin by extraction of epidermal lipids with acetone or removal of corneocytes by tape stripping. Contact sensitivity (CS) to 2,4-dinitrofluorobenzene (DNFB) and picryl chloride (PCl) and contact photosensitivity (CPS) to tetrachlorosalicylanilide (TCSA) were significantly augmented when challenged or sensitized at sites treated with acetone 24 h before, compared with the intact skin. CS to DNFB was also enhanced by tape stripping, but not by water rubbing, suggesting that physical stress or a toxic effect of acetone was not responsible for the augmentation. Semi-quantification of TCSA-EC photoadducts showed markedly increased permeability of hapten in the epidermis 24 h after acetone treatment. Bioactive IL-1alpha was more pronounced in barrier-disrupted than in intact skin. Lymph node T cells from PCl-sensitized mice proliferated significantly more in a hapten-specific and co-stimulatory molecule-dependent manner in response to trinitrophenylated (TNP) EC from acetone-treated skin than to those from untreated skin. Immunofluorescence staining of epidermal sheets and flow cytometric analysis of dispersed EC showed that subpopulations of Langerhans cells (LC) in acetone-rubbed or tape-stripped skin expressed major histocompatibility complex class II CD54 and CD86 molecules at levels higher than the rest of LC and LC from water-treated or untreated epidermis. Therefore, not only increased permeability of hapten through the epidermis but also altered immune functions of EC potentiate T-cell activation in acute barrier disruption. Such augmentation of immune reactivity may be critical to elimination of environmental noxious agents that penetrate easily into the barrier-disrupted epidermis.

Pulsatility of brachial artery pressure is associated with an increased risk of coronary artery disease in men.

OBJECTIVES: The purpose of this study was to evaluate whether the pulsatility of brachial artery pressure is related to an increased risk of coronary artery disease (CAD). On the basis of vascular mechanics, we recently reported that relative pulse pressure can predict the occurrence of restenosis after percutaneous transluminal coronary angioplasty. We also hypothesized that relative pulse pressure of the brachial arterial pressure waveform is associated with an increased risk of CAD. DESIGN: A cross-sectional study. PATIENTS: We enrolled 172 men who had the same cardiac performances. MAIN OUTCOME MEASURES: We measured their brachial artery pressures with a sphygmomanometer. To quantify the relative magnitude of the pulsatility to diastolic pressure, we made use of the ratio of pulse pressure to diastolic pressure (PP/DP). We investigated the effects of the PP/DP in relation to the risk of CAD. RESULTS: PP/DP was associated with an increased risk of CAD. The prevalence rates of significant stenosis were 28.1% for the lowest, 43.1% for the middle and 49.1% for the highest tertile of PP/DP levels. The age-adjusted odds ratio of CAD was 2.23 (95% confidence interval 0.98-5.04) for the middle tertile of the PP/DP level and 2.55 (1.10-5.93) for the highest tertile compared with the lowest tertile. CONCLUSIONS: The pulsatility of the brachial artery pressure was associated with an increased risk of CAD.

Photohapten TCSA painting plus UVA irradiation of murine skin augments the expression of MHC class II molecules and CD86 on Langerhans cells.

Hapten painting of skin is known to augment the expression of major histocompatibility complex (MHC) class II, CD54, and CD86 on Langerhans cells. We investigated whether painting with 3,3',4',5-tetrachlorosalicylanilide (TCSA), the representative photohapten, and subsequent irradiation with ultraviolet A (UVA) alter the expression of these surface molecules on epidermal Langerhans cells (LC). BALB/c mice were painted with 5 microl of 0.1% TCSA on the earlobes and irradiated with 16 J/cm2 (at 365 nm) of UVA. Epidermal cells were prepared from these earlobes 24 h later, and the levels of MHC class II, CD54, CD80, and CD86 on these cells were analyzed by flow cytometry. As compared with untreated earlobes, the levels of MHC class II and CD86 on LC were markedly augmented and those of CD54 and CD80 were slightly elevated in earlobes treated with TCSA/UVA. Since neither TCSA painting nor UVA exposure alone enhanced the expression, both treatments were essential for enhancement. A dot plot analysis showed the presence of subpopulations of LC expressing MHC class II and CD86 at high levels. The percentage of these highly expressing LC was increased with increasing concentrations of TCSA and doses of UVA up to 1% and 24 J/cm2, respectively. In addition, keratinocyte expression of CD54 was also augmented by TCSA plus UVA. These results suggest that photohaptens, with following UVA exposure, augment the expression of immunologically functional molecules on LC as do ordinary haptens, leading to effective sensitization and elicitation of contact photoallergy.

Pulsatility of ascending aortic blood pressure waveform is associated with an increased risk of coronary heart disease.

BACKGROUND: Although it was reported that pulse pressure of the peripheral artery could differentiate patients with coronary heart disease (CHD) from those without CHD, it is not known whether pulsatility of the ascending aortic pressure waveform differentiates patients with CHD from those without CHD. The purpose of this study was to evaluate whether the pulsatility of ascending aortic pressure is associated with an increased risk of CHD. METHODS: For this study, we enrolled 293 subjects who had chest pain, normal contractions, no local asynergy, and no history of myocardial infarction. We measured the ascending aortic pressure using a fluid-filled system. To quantify the relative magnitude of the pulsatile to mean artery pressure, we normalized the pulse pressure to the mean pressure and referred to this value as the fractional pulse pressure (PPf). We investigated the association between the PPf and the risk of CHD. RESULTS: The PPf of the ascending aorta was associated with an increased risk of CHD. The multiple-adjusted odds ratio of CHD was 2.93 (95% CI, 1.44 to 5.94) for the middle tertile of the PPf level and was 3.93 (95% CI, 1.74 to 8.85) for the highest tertile compared with the lowest tertile. CONCLUSION: Ascending aortic pulsatility is related to an increased risk of CHD.

Active-site-directed inactivation of Aspergillus oryzae beta-galactosidase with beta-D-galactopyranosylmethyl-p-nitrophenyltriazene.

beta-D-Galactopyranosylmethyl-p-nitrophenyltriazene (beta-GalMNT), a specific inhibitor of beta-galactosidase, was isolated as crystals by HPLC and its chemical and physicochemical characteristics were examined. Aspergillus oryzae beta-galactosidase was inactivated by the compound. We studied the inhibition mechanism in detail. The inhibitor was hydrolyzed by the enzyme to p-nitroaniline and an active intermediate (beta-galactopyranosylmethyl carbonium or beta-galactopyranosylmethyldiazonium), which inactivated the enzyme. The efficiency of inactivation of the enzyme (the ratio of moles of inactivated enzyme to moles of beta-GalMNT hydrolyzed by the enzyme) was 3%; the efficiency of Escherichia coli beta-galactosidase was 49%. In spite of the low efficiency, the rate of inactivation of A. oryzae enzyme was not very different from that of the E. coli enzyme, because the former hydrolyzed beta-GalMNT faster than the latter did. A. oryzae beta-galactosidase was also inactivated by p-chlorophenyl, p-tolyl, and m-nitrophenyl derivatives of beta-galactopyranosylmethyltriazene. However, E. coli beta-galactosidase was not inactivated by these triazene derivatives. The results showed that the inactivation of A. oryzae and E. coli beta-galactosidases by beta-GalMNT was an enzyme-activated and active-site-directed irreversible inactivation. The possibility of inactivation by intermediates produced nonenzymatically was ruled out for E. coli, but not for the A. oryzae enzyme.

Increases in levels of brain-derived neurotrophic factor mRNA and its promoters after transient forebrain ischemia in the rat brain.

Expression of brain-derived neurotrophic factor (BDNF) may play a role in the mechanism of neuronal cell death after cerebral ischemia. We investigated the changes in levels of mRNAs encoding BDNF and its promoters in the rat brain after transient forebrain ischemia. Transient forebrain ischemia was induced by occlusion of bilateral common carotid arteries and systemic hypotension for 8 min. The alterations in BDNF gene expression in the hippocampus and in the cerebral cortex were examined by in situ hybridization using a mouse BDNF cDNA probe and cDNA probes including exon-specific promoters. BDNF transcripts were rapidly enhanced after the ischemic insult, both in the hippocampus and the cerebral cortex. NBQX suppressed the enhanced gene expression of BDNF markedly in the dentate gyrus (DG). In contrast, MK-801 had little effect on BDNF expression. In the piriform cortex, MK-801 or NBQX reduced the expression only moderately. After the ischemic insult, promoter specific BDNF 5'-exon I and exon III were increased remarkably in the DG. The increase in exon I in DG was suppressed partially by MK-801 and NBQX, while the increase in exon III in CA3 was suppressed by MK-801 but that in DG was not suppressed by either antagonist. In the piriform cortex, exon III was increased remarkably and this increase was not influenced by either agonist. These results suggest that the gene expression of BDNF was enhanced by transient ischemia both in the hippocampus and the cerebral cortex and that the cerebral ischemia stimulated at least two different promoter- and neuron type-specific pathways regulating expression of the BDNF gene mediated by glutamate receptors of non-NMDA type and NMDA type.

AS-924, a novel, orally active, bifunctional prodrug of ceftizoxime: physicochemical properties, oral absorption in animals, and antibacterial activity.

AS-924 is an oral prodrug of the antibiotic ceftizoxime (CTIZ), a parenteral use cephalosporin. This novel prodrug, produced by esterifying CTIZ with a lipophilic pivaloyloxymethyl (POM) group and introducing a water soluble L-alanyl group, is expected to increase the bioavailability and thereby, augment the antibacterial activity of CTIZ in vivo compared with existing prodrugs. To study the effect of the L-alanyl group in AS-924 on its bioavailability, the plasma concentration profiles of CTIZ in dogs were examined following the dosing of AS-924 and CTIZ-POM, in powder form, after pretreatment with the antacid ranitidine, and following the dosing of AS-924 after pretreatment with a gastrointestinal motility stimulant metoclopramide or suppressant scopolamine butylbromide. The absorption rate of AS-924 was constant under these different conditions due to its unique balance of lipophilicity and water solubility. CTIZ is as antibacterially active as pre-existing oral cephalosporins against Gram-positive clinical isolates, while being more active against all Gram-negative isolates-particularly Enterobacteriaceae and Haemophilus influenzae. A simulation model for the eradication profile of bacteria in computer programmed pharmacokinetic (PK) system was carried out to study the antibacterial action of CTIZ in human. CTIZ was proven to eradicate Streptococcus pneumoniae and H. influenzae effectively, while cefpodoxime (CPOD), the active moiety of CPOD proxetil, eradicated S. pneumoniae, but not H. influenzae. These results confirm that, AS-924 is a potent oral antibiotic and would be expected to be clinically effective and efficient.

The role of brain-derived neurotrophic factor in transient forebrain ischemia in the rat brain.

Brain-derived neurotrophic factor (BDNF) may play a role in the pathophysiology of neuronal cell death after cerebral ischemia. We investigated alterations in BDNF gene expression and the effect of BDNF on neuronal death after transient forebrain ischemia in the rat brain. Transient forebrain ischemia was induced by occlusion of the bilateral common carotid arteries and by producing systemic hypotension for 8 minutes. The alterations in the BDNF messenger ribonucleic acid content in the hippocampus and the cerebral cortex were examined by Northern blot analysis, using a phosphorus-32-labeled mouse BDNF complementary deoxyribonucleic acid probe. Recombinant Chinese hamster ovary cells with BDNF-secreting capacity were established by expression vector transfection with BDNF complementary deoxyribonucleic acid. The effect of BDNF on neuronal death in the hippocampal CA1 region after ischemia was then examined by using a continuous intraventricular infusion of 200 microliters of normal (Group II, n = 6) or 30-times concentrated recombinant Chinese hamster ovary cell culture medium containing BDNF (Group IV, n = 6). Normal (Group I, n = 6) or 30-times concentrated (Group III, n = 6) Chinese hamster ovary cell culture medium, not including BDNF complementary deoxyribonucleic acid, was infused into the same ischemic brains, which served as controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Photohaptenic properties of fluoroquinolones.

Although quinolone antibacterial agents have both phototoxicity and photoallergenicity, the latter's potency has been poorly investigated compared with the former's. Some of the photoallergic chemicals serve as photohaptens, which lead to T-cell-mediated immune reactions after photobinding to protein by UVA radiation. We examined the photohaptenic potential of fluoroquinolones, including lomefloxacin (LFLX), ciplofloxacin, norfloxacin, ofloxacin, levofloxacin, fleroxacin, enoxacin and sparfloxacin (SPFX). The absorption spectra of the quinolones were altered by UVA irradiation, with an exception of SPFX that seems to be photostable toward UVA. Bovine serum albumin and murine epidermal cells were coupled with these fluoroquinolones other than SPFX by exposure to UVA. Subcutaneous inoculation of fluoroquinolone-photomodified epidermal cells induced and elicited a delayed-type hypersensitivity reaction in mice. However, epidermal cells incubated with LFLX without UVA exposure also induced and elicited a significant hypersensitivity reaction to a lesser degree than LFLX-photomodified epidermal cells. Furthermore, there was cross-reactivity between LFLX-photomodified epidermal cells and simply LFLX-incubated cells. This suggests that cells can be weakly modified with LFLX even in the dark and that UVA irradiation promotes this modification. Our study demonstrated that fluoroquinolones have photohaptenic properties to which their photoallergenicity is probably ascribed.

[Clinical study of carfecillin in chronic urinary tract infection (author's transl)].

1. Ten patients with chronic urinary tract infection by Pseudomonas aeruginosa or Proteus species were treated with carfecillin. Excellent response was seen in one case, fairly good in 5 cases and clinical effective rate was 60%. 2. The recurrence suppression effect of carfecillin was examined in two patients suffering from complicated urinary tract infection. In both cases, recurrence was not found when carfecillin was administered for a week after the effective pretreatment of carbenicillin, but found when administered for two weeks. 3. Side effects were observed in 3 cases (itching, tinnitus, diarrhea).

[Minocycline diffusion into prostatic tissue].

We evaluated the concentration of minocycline in human prostatic tissue. Twenty-six patients undergoing transurethral resection of prostate, two patients undergoing open prostatectomy for benign prostatic hyperplasia and two patients undergoing radical cystoprostatectomy for bladder cancer were studied. Prostatic tissue and blood were sampled at 1, 2 or 3 hours after the intravenous administration of 200 mg of minocycline. The concentration of minocycline was 2.95 +/- 1.39 micrograms/ml (mean +/- SD) in serum and 1.97 +/- 0.79 cg/g (mean +/- SD) in the prostatic tissue. The ratio of the prostatic concentration/serum concentration was 0.76 +/- 0.33 (mean +/- SD).

[Myelolipoma of the adrenal gland: report of a case].

A 50-year-old male was admitted to our municipal hospital because of his right suprarenal tumor which had been found by ultrasonography by chance at National Toneyama Hospital. His physical examination was normal except for obesity. Hematological examination and blood chemistry were normal and no endocrine disorder was found. Excretory urogram revealed neither deformity of the collecting system nor displacement of the right kidney. Computed tomography visualized sharp marginated in homogeneous structured mass of different densities within the negative range. Angiography revealed hypovascularity of the tumor. Right adrenalectomy was performed and the specimen weighed 72 g. Histopathologically is consisted of adult fat tissue and hematopoietic tissue. In addition to our case, 17 cases of surgically removed myelolipoma reported in the Japanese literature are reviewed.

[Clinical study on 15 cases of torsion of the spermatic cord].

We experienced fifteen cases of torsion of the spermatic cord during the past 10 years. The age distribution was from 10 to 40 years old and the average age was 21.1 years. All cases except one case of right undescended testis occurred on the left side. To our interest, the onset in 12 of the 13 cases with known onset time were during sleep or within one hour after waking up. All cases except one case in the undescended testis complained of pain of the testis and some of them were accompanied with pain in the inguinal and lower abdominal region. Swelling and tenderness of the testis were observed in most cases and shortness of the spermatic cord probably caused by torsion and secondary inflammation seemed to be important findings. Prehn's sign and fever up were observed in few cases but leukocytosis was seen in 10 cases. Eleven cases of surgical treatment consisting of 10 orchiopexy and one orchiectomy were performed. Four cases of spontaneous detorsion were included in our experience. Orchiopexy of the contralateral intact testis was not done, but, we have never experienced relapse of torsion.

[A clinical study on transitional cell carcinoma of renal pelvis and ureter].

During the 9 years between 1983 and 1992, 36 patients with renal pelvic and ureteral tumors were treated in our hospital. There were 24 males and 12 females. The most common chief complaint was macrohematuria. Intravenous pyelography (IVP) revealed the finding of non-visualized kidney, filling defects and hydronephrosis in 99%. Histologically, 26 were found to have transitional cell carcinoma, one squamous cell carcinoma and one adenocarcinoma. The 5-year survival rate of this study was 54.5% according to the Kaplan-Meier's method. In our study the most important prognostic factor was histopathological grading.