Sediment analysis and water quality assessment in the Pixquiac basin: drinking water supply of Xalapa city (Veracruz, Mexico).

Fluvial sediment analysis and water quality assessment are useful to identify anthropic and natural sources of pollution in rivers. Currently, there is a lack of information about water quality in the Pixquiac basin (Veracruz state, Mexico), and this scarcity of data prevents authorities to take adequate measures to protect water resources. The basin is a crucial territory for Xalapa, the capital city of Veracruz state, as it gets 39% of its drinkable water from it. This research analyzed 10 physicochemical parameters and 12 metal concentrations in various rivers and sources during two seasons. Dissolved metals presented average concentrations (µg/L): Al (456.25) > Fe (199.4) > Mn (16.86) > Ba (13.8) > Zn (7.6) > Cu (1.03) > Pb (0.27) > As (0.12) > Ni (0.118) (Cd, Cr and Hg undetectable). Metals in sediment recorded average concentrations (ppm): Fe (38575) > Al (38425) > Mn (460) > Ba (206.2) > Zn (65.1) > Cr (29.8) > Ni (20.9) > Cu (16.4) > Pb (4.8) > As (2.1) (Cd and Hg undetectable). During the rainy season, Water Quality Index (WAWQI) classified stations P17 and P18's water as "unsuitable for drinking" with values of 110.4 and 117.6. Enrichment factor (EF) recorded a "moderate enrichment" of Pb in sediment in P24. Pollution was mainly explained by wastewater discharges in rivers but also because of erosion and rainfall events. Statistical analysis presented strong relationships between trace and major metals which could explain a common natural origin for metals in water and sediment: rock lixiviation.

Histological and neurotrophic changes triggered by varying models of bladder inflammation.

PURPOSE: We determined whether bladder inflammation causes elevated expression of nerve growth factor by bladder parenchymal cells, leading to alterations in neurons innervating the bladder. To answer this question biochemical, histological and neuronal size data were obtained in rats following various experimental models of bladder inflammation. MATERIALS AND METHODS: Chemical (2.5% formalin), immune (lipopolysaccharide 2 x 104 cfu/ml.) and mechanical (chromic catgut) inflammation was evaluated at various times and compared to control bladders. Hematoxylin and eosin, and Giemsa staining was done to characterize inflammation and quantify mast cells in the bladder. Nerve growth factor protein and messenger RNA were assayed in the bladder and major pelvic ganglion using 2-site enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction, respectively. Retrograde axonal tracing was done to size bladder neurons in the major pelvic and dorsal root ganglia. RESULTS: All forms of inflammation increased bladder weight and produced diffuse hyperplasia, intramural edema, acute and chronic inflammatory cells, infiltration and mastocytosis. Generally bladder inflammation resulted in a 50% increase in nerve growth factor and 52% to 58% enlargement of peripheral neurons. CONCLUSIONS: Inflammation results in altered nerve growth factor content of the bladder, and morphological changes in sensory and motor neurons innervating the bladder. Such neuroplasticity may be a possible explanation for the association of bladder inflammation with long-term symptoms and pain after inflammation subsides.

Anterior flap extraperitoneal cystoplasty.

PURPOSE: We report on our initial experience with the anterior flap extraperitoneal cystoplasty for refractory voiding symptoms secondary to detrusor hyperactivity. MATERIALS AND METHODS: A total of 27 patients underwent anterior flap extraperitoneal cystoplasty, the principles of which include a Pfannenstiel skin incision, a small peritoneotomy with minimal manipulation of the bowel, extraperitoneal bowel resection with ileovesical anastomosis and creation of an anterior bladder wall flap. RESULTS: Convalescence was uneventful in 25 patients (92%). Oral intake resumed on postoperative day 3 or 4, and the patient was discharged home on postoperative day 5 or 6. Voiding symptoms resolved or improved significantly in 92% of patients, who were dry or used 1 or no pads a day. Two complications required prolonged hospitalization. CONCLUSIONS: Anterior flap extraperitoneal cystoplasty is a safe and effective treatment that has the potential to decrease postoperative complications and recovery time.

Diagnosis of stress urinary incontinence. An overview.

This article represents an overview of the evaluation and diagnosis of stress urinary incontinence. Lower urinary tract anatomy in women is reviewed with particular attention to the salient features contributing to stress incontinence. Also discussed is the relevance of the distinction between anatomic incontinence and intrinsic sphincter deficiency in the classification of stress urinary incontinence. Various diagnostic techniques are described with emphasis on the importance of urodynamic evaluation in complex cases.

Transvaginal correction of pelvic prolapse.

Pelvic prolapse has a myriad of clinical manifestations ranging from urethral incontinence to total vault prolapse. The evaluation and treatment of these conditions is facilitated by dividing them into three anatomic regions. Anterior vaginal wall prolapse is the most common type and includes simple urethral hypermobility as well as severe cystocele. Surgical treatment includes the modified anterior vaginal wall sling, six-corner bladder neck suspension, and formal cystocele repair. Posterior vaginal wall prolapse, manifested by rectocele and perineal relaxation, is corrected by plication of the prerectal and pararectal fascia, reconstruction of the levator hiatus, and repair of the perineal body. Vault prolapse includes enterocele, uterine prolapse, and generalized vault prolapse. The choice of treatment depends on the presence of anterior vaginal wall prolapse, the degree of vault prolapse, and the patient's desire to remain sexually active. It is important to remember that urethral incontinence is only one manifestation of pelvic prolapse, and must be treated in conjunction with other prolapse to avoid recurrence or poor results.

Erosion of an inflatable penile prosthesis reservoir into the bladder, presenting as bladder calculi.

We report a case of erosion of an inflatable penile prosthesis reservoir int the bladder 4 years after implantation for organic impotence. In contrast to previously reported cases this complication was not associated with incontinence, urinary tract infection or a revision procedure. Microscopic hematuria was present but there was no pyuria. Diagnosis evaded radiographic and cystoscopic confirmation. Bladder erosion of the reservoir was discovered incidentally during treatment of bladder calculi.

Inhibition of fungal and mammalian sterol biosynthesis by 2-aza-2,3-dihydrosqualene.

2-Aza-2,3-dihydrosqualene (I) and a quaternary ammonium derivative (II) inhibited ergosterol biosynthesis in cells and cell-free extracts of the pathogenic yeast Candida albicans as measured by incorporation of radiolabelled precursors. The compounds inhibited squalene epoxidase and 2,3-oxidosqualene cyclase to varying degrees in microsomes from C. albicans and from rat liver. The rat liver epoxidase was 50% inhibited by I at 2.4 microM. In C. albicans cells, but not in cell-free extracts, I also inhibited lanosterol demethylation and led to accumulation of an unidentified polar product.

Ergosterol biosynthesis inhibition by the thiocarbamate antifungal agents tolnaftate and tolciclate.

The thiocarbamate antimycotics tolnaftate and tolciclate blocked sterol biosynthesis in fungal cells and cell extracts, with accumulation of squalene. This point of action was confirmed by the direct inhibition of microsomal squalene epoxidase from Candida albicans. There was no inhibition of other steps in ergosterol biosynthesis. In whole Candida cells, ergosterol biosynthesis inhibition was not complete at drug concentrations up to 100 mg/liter, whereas full inhibition occurred in a cell-free test system. Rat liver cell-free cholesterol biosynthesis was much less sensitive to the drugs. The biochemical action of tolnaftate and tolciclate is thus similar to that of the allylamine antimycotics naftifine and terbinafine.

Inhibition of squalene epoxidase by allylamine antimycotic compounds. A comparative study of the fungal and mammalian enzymes.

The inhibition of squalene epoxidase by the allylamine antimycotic agents naftifine and compound SF 86-327 was investigated, with particulate enzyme preparations from the pathogenic yeasts Candida albicans and Candida parapsilosis and from rat liver. Both naftifine and compound SF 86-327 were potent inhibitors of the Candida epoxidases and showed apparently non-competitive kinetics with respect to the substrate squalene. The Ki values for naftifine and compound SF 86-327 in the C. albicans system were 1.1 microM and 0.03 microM respectively. The C. parapsilosis enzyme was slightly more sensitive to inhibition. Varying the concentrations of cofactors or the soluble cytoplasmic fraction (S200) had no effect on the inhibition. The epoxidase from rat liver was much less sensitive (Ki for compound SF 86-327 was 77 microM). The inhibition was also qualitatively different from that in Candida, being competitive with respect to squalene and also with respect to the S200 fraction. S200 fraction derived from C. albicans also antagonized the inhibition of the epoxidase from liver, but the liver S200 fraction did not affect inhibition of the Candida enzyme by compound SF 86-327. There was no evidence for an irreversible or mechanism-based inhibition of either the fungal or the mammalian epoxidase. The selective inhibition of squalene epoxidase was sufficient to account for the known antimycotic action of the compounds.

Properties of a particulate squalene epoxidase from Candida albicans.

The properties and requirements of squalene epoxidase and effects of some inhibitors were investigated in the pathogenic yeast Candida albicans. A washed 'microsomal' fraction converted radiolabelled squalene to 2,3-oxidosqualene and lanosterol. Minimum requirements for activity were molecular oxygen, NADH or NADPH, and FAD. Epoxidase activity was stimulated by up to 100% by addition of the soluble cytoplasmic fraction, which itself contained negligible epoxidase activity. This stimulation was most powerful at low concentrations of enzyme, or high concentrations of squalene. Divalent cations did not stimulate activity and EDTA was not inhibitory. An apparent Km for squalene of 50 microM was determined in the presence of soluble cytoplasm. Epoxidase activity was destroyed by Triton X-100, deoxycholate or Cu2+, and partially inhibited by thiol reagents, rotenone and antimycin A. The enzyme was not inhibited by cyanide or by several inhibitors of cytochrome P-450.

Antimicrobial activity of econazole and miconazole in vitro and in experimental candidiasis and aspergillosis.

The antibacterial and antimycotic activity of econazole base, an imidazole derivative, was examined in vitro and in experimental infections of mice. Comparative minimal inhibitory concentration (MIC) determinations indicate econazole as well as miconazole to be of moderate activity against gram-positive bacteria (MICs: 0.78-25mug/ml) and yeasts (MICs: 1.56-25 mug/ml). Against filamentous fungi, econazole exhibits better in vitro activity than miconazole and - with the exception of Rhizopus oryzae and Absidia corymbifera - MICs are markedly lower than against yeasts. No effect of nutrient media and no effect of the inoculum were observed with the four drugs. A strong influence of bovine serum on MIC values, however, suggested a strong protein binding. In experimental candidiasis of mice, no therapeutic effect with econazole base administered orally or intraperitoneally could be observed (ED50 and 'minimum life-prolonging dose': great than 200 mg/kg). In experimental aspergillosis of mice, a slight effect, as demonstrated by the 'minimum life-prolonging dose' of 100 mg/kg, was found. The in vitro and in vivo results are discussed in the light of the available pharmacokinetic and toxicological data. It is concluded that more studies, especially on the pharmacology of econazole and about the clinical efficacy, are needed to come to a definite judgement.