Cost Saving by Heat Recovery. 1 – Stenters

From Mr T A Weaver Sir, I read with interest the above publication [J. S. D. C., 96 (June 1980) 305], and feel that observations arising from our own experience in supplying stenters over a number of years may be appropriate.     

Vesicoureteral reflux associated with intact orthotopic ureterocele

Two cases of vesicoureteral reflux into intact, orthotopic ureteroceles are described. A review of the literature failed to reveal any similar reports. Insufficient submucosal ureteral length was thought to be the cause in each of the cases. Both patients were satisfactorily managed with standard ureteroneocystostomy after resection of the ureterocele.     

Chromosomal anomalies in stage D1 prostate adenocarcinoma primary tumors and lymph node metastases detected by fluorescence in situ hybridization

We previously reported a HPLC assay method using fluorimetric detection for the simultaneous determination of urinary N2-(3-aminopropyl)biopterin (oncopterin, a natural pteridine newly found in urine from cancer patients), biopterin and neopterin. We now have observed that an unknown substance, which may be derived from methotrexate, in urine from a patient with stomach cancer interfered with the assay of oncopterin and demonstrated that oncopterin could be completely separated from the unidentified substance by HPLC using a Nucleosil 100-5SA strong cation-exchange column. Furthermore, oncopterin was not detectable by this HPLC-fluorimetric method in urine samples from patients with stomach cancer who were not treated with methotrexate. The content of urinary oncopterin from cancer patients is supposed to be very low, with less than 1 mumol/mol creatinine. The present results indicate that the peak found with elution from the C18 column was a methotrexate-derived compound and co-eluted with the analyte oncopterin.     

Mitochondrial respiratory enzyme function and superoxide dismutase activity following brain glutathione depletion in the rat

In substantia nigra from patients with Parkinson's disease, there are decreased levels of reduced glutathione (GSH) and diminished activities of mitochondrial complex I and alpha-ketoglutarate dehydrogenase (alpha-KGDH), along with increased activity of superoxide dismutase (SOD). However, the interrelationship among these events is uncertain. We now report the effect of decreased brain GSH levels on SOD and mitochondrial respiratory enzyme activity in rat brain. In addition, we have investigated the ability of thioctic acid, an endogenous antioxidant, to alter these parameters. Unilateral or bilateral intracerebroventricular (ICV) administration of buthionine sulphoximine (BSO; 1 x 3.2 mg or 2 x 1.6 mg) over a 48-hr period reduced cortical GSH by 55-70%. There was no change in the activity of complex I, II/III, or IV or of citrate synthase in cortex. Similarly, there was no alteration of mitochondrial or cytosolic SOD activity. Thioctic acid (50 or 100 mg/kg IP) alone had no effect on cortical GSH levels in control animals and did not reverse the decrease in GSH levels produced by unilateral or bilateral ICV BSO administration. Thioctic acid (50 or 100 mg/kg IP) had no overall effect on complex I, II/III, or IV or on citrate synthase activity in control animals. Thioctic acid also did not alter cortical mitochondrial respiratory enzyme activity in BSO-treated rats. At the lower dose, thioctic acid tended to increase mitochondrial and cytosolic SOD activity in control animals and in BSO-treated rats. However, at the higher dose, thioctic acid tended to decrease mitochondrial SOD activity. Overall, there was no consistent effect of thioctic acid (50 or 100 mg/kg IP) on SOD activity in control or BSO-treated animals. This study shows that BSO-induced glutathione deficiency does not lead to alterations in mitochondrial respiratory enzyme activity or to changes in SOD activity. GSH depletion in Parkinson's disease therefore may not account for the alterations occurring in complex I and mitochondrial SOD in substantia nigra. Thioctic acid did not alter brain GSH levels or mitochondrial function. Interestingly, however, it did produce some alterations in SOD activity, which may reflect either its antioxidant activity or its ability to act as a thiol-disulphide redox couple.     

Cutaneous leishmaniasis in Egypt (review and comment)

Leishmania is primarily characterized by existing in two stages in its life cycle, each occurs in a distinct host. The amastigote stage found in the cytoplasm of the reticulo- endothelial cells, monocytes and other phagocytic cells of the vertebrate host. The promastigote stage found in the gut of its insect vector. The leishmaniasis comprise several diseases of wide diversity of manifestations caused by different species of the genus Leishmania. Because of the virtual morphological identity of the organisms throughout the genus, they are classified according to the clinical conditions which they produce in man, under three main headings: (1) Cutaneous leishmaniasis (CL.), (2) Mucocutaneous leishmaniasis (MCL.), (3) Visceral leishmaniasis (VL). Generally speaking, leishmaniasis is an example of a zoonosis that reaches man through an insect vector. The great majority of the Leishmania species are maintained by mammalian reservoir hosts in natural foci of infection. Rodents, dogs, wild cats, jackals, foxes, sloths, hyraxes and other carnivores are the animal reservoirs which maintain the infection in nature. The insect vectors are over 50 species of the genus Phlebotomus in the Old World and genus Lutzomyia in the New World.     

Analytical development of electrospray and nanoelectrospray mass spectrometry in combination with liquid chromatography for the characterization of proteins

Microbial pathogens may be transmitted to humans via food animals and food animal products. A quick reference table is presented to provide easy access to food safety information related to the major food animal product areas. Included in the table are the pathogens, mode of transmission, public health impact, and control and prevention strategies for poultry, beef, dairy products, and pork.     

Activated protein C resistance, thrombophilia, and inflammatory bowel disease

Thromboembolic events frequently complicate the clinical course of patients with inflammatory bowel disease (IBD). Hereditary thrombophilia may contribute to this tendency. Resistance to activated protein C is the most recently described thrombophilic state and may account for up to 40% of patients with thrombophilia. Thirty-seven patients with IBD were studied (mean age 44 years, range 18-82 years). Three patients had a history of thrombotic episodes. The 37 controls included 23 men and 17 women (mean age 48 years, range 16-89 years). Disease activity was assessed using the Harvey Bradshaw index for patients with Crohn's disease and the Truelove and Witts grading system for patients with ulcerative colitis. Levels of fibrinogen, antithrombin III (ATIII), protein C, protein S, activated protein C resistance (APCR), and the presence of a lupus anticoagulant (LA) were determined. Median ATIII levels in patients with IBD were significantly lower than controls (98% vs 106%, P = 0.007), while fibrinogen was elevated (4.2 vs 3.3 g/liter, P = 0.026) despite quiescent disease activity. LA was detected in 7/37 patients in the IBD group compared to 0/37 controls. (chi2 = 5.68, P = 0.017). No significant difference was observed in levels of inherited thrombophilic factors and in particular APCR between IBD patients and controls. In conclusion, the presence of inherited thrombophilic defects, in particular APCR, is uncommon in patients with IBD and does not merit routine screening.