Determination of orthophosphoric and orthophosphorous acids in the workplace air using ion chromatography

The authors elaborated a method measuring air level of orthophosphorous and orthophosphoric acids by means of ion chromatography within the range of 0.1-25 mg/cu m. The samples are extracted through concentration on a filter. The analysis regime includes depression of the background levels. The separating column (4 x 200 mm) is filled with anion exchanger BT IAN, the suppressing column (6 x 150 mm) is filled with cation exchanger Dowex 50 x 8, the elutriating agent is 1.5 mM of sodium carbonate, the detector is conductometric. Minimal amounts of ions that could be detected in the analyzed solution are 7-10 ng (HPO32-), 10-15 ng (HPO 42-). The method is designed to analyze the air of workplace.     

Identification of glycoprotein 330 as an endocytic receptor for apolipoprotein J/clusterin

Glycoprotein 330 (gp330) is a member of a family of endocytic receptors related to the low density lipoprotein receptor. gp330 has previously been shown to bind a number of ligands in common with its family member, the low density lipoprotein receptor-related protein (LRP). To identify ligands specific for gp330 and relevant to its localization on epithelia such as in the mammary gland, gp330-Sepharose affinity chromatography was performed. As a result, a 70-kDa protein was selected from human milk and identified by protein sequencing to be apolipoprotein J/clusterin (apoJ). Solid-phase binding assays confirmed that gp330 bound to apoJ with high affinity (Kd = 14.2 nM). Similarly, gp330 bound to apoJ transferred to nitrocellulose after SDS-polyacrylamide gel electrophoresis. LRP, however, showed no binding to apoJ in either type of assay. The binding of gp330 to apoJ could be competitively inhibited with excess apoJ as well as with the gp330 ligands apolipoprotein E, lipoprotein lipase, and the receptor-associated protein, a 39-kDa protein that acts to antagonize binding of all known ligands for gp330 and LRP. Several cultured cell lines that express gp330 and ones that do not express the receptor were examined for their ability to bind and internalize 125I-apoJ. Only cells that expressed gp330 endocytosed and degraded radiolabeled apoJ. Furthermore, F9 cells treated with retinoic acid and dibutyryl cyclic AMP to increase expression levels of gp330 displayed an increased capacity to internalize and degrade apoJ. Cellular internalization and degradation of radiolabeled apoJ could be inhibited with unlabeled apoJ, receptor-associated protein, and gp330 antibodies. The results indicate that gp330 but not LRP can bind to apoJ in vitro and that gp330 expressed by cells can mediate apoJ endocytosis leading to lysosomal degradation.     

Chemistry of the pyrrolo[1,2-alpha]benzimidazole antitumor agents: influence of the 7-substituent on the ability to alkylate DNA and inhibit topoisomerase II

This study addresses the influence the 7-substituent on the cytotoxicity of pyrrolo[1,2-alpha]-benzimidazole quinones possessing a 6-aziridinyl group (PBIs) and a 6-acetamido group (APBIs). Reduction of a PBI to the aziridinyl hydroquinone results in both nucleophile trapping (alkylation) and 1,5-sigmatropic shift reactions. The latter process is essentially an internal redox reaction wherein the hydroquinone causes reductive opening of the aziridinyl ring. The 7-substituent controls the fate of the aziridinyl ring by means of steric and electronic effects. An electron-rich 7-substituent favors the 1,5-sigmatropic shift reaction. If the 7-substituent distorts the 6-aziridinyl group from the conformation required for the 1,5-sigmatropic shift, then nucleophile trapping occurs. The 7-methyl substituent results in significant nucleophilic trapping, and the 7-unsubstituted and 7-methoxy substituents favor the 1,5-sigmatropic reaction. Thus, the 7-methyl PBIs show the most cytotoxicity of the analogues studied. The APBIs are cytotoxic only as quinones, and reduction to the hydroquinone results in loss of activity. Consistent with this observation, the change from 7-methyl to the more electron-rich 7-methoxy results in a substantial loss of APBI cytotoxicity as well as decreased topoisomerase II inhibition. The mechanism of inhibition is thought to involve the interacalation of only electron deficient APBIs into DNA.     

Myocardial protection for reoperative cardiac surgery in acquired heart disease

This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2 (N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.     

An approach for treating the hepatobiliary disease of cystic fibrosis by somatic gene transfer

Cystic fibrosis (CF) is an inherited disease of epithelial cell ion transport that is associated with pathology in multiple organ systems, including lung, pancreas, and liver. As treatment of the pulmonary manifestations of CF has improved, management of CF liver disease has become increasingly important in adult patients. This report describes an approach for treating CF liver disease by somatic gene transfer. In situ hybridization and immunocytochemistry analysis of rat liver sections indicated that the endogenous CFTR (cystic fibrosis transmembrane conductance regulator) gene is primarily expressed in the intrahepatic biliary epithelial cells. To specifically target recombinant genes to the biliary epithelium in vivo, recombinant adenoviruses expressing lacZ or human CFTR were infused retrograde into the biliary tract through the common bile duct. Conditions were established for achieving recombinant gene expression in virtually all cells of the intrahepatic bile ducts in vivo. Expression persisted in the smaller bile ducts for the duration of the experiment, which was 21 days. These studies suggest that it may be feasible to prevent CF liver disease by genetically reconstituting CFTR expression in the biliary tract, using an approach that is clinically feasible.     

The effects of lead exposure on learning in a multiple repeated acquisition and performance schedule

This study sought to determine the selectivity of Pb-induced changes in learning, as distinct from non-specific or performance effects, and to explore the nature of the underlying error patterns contributing to any learning deficits. To accomplish this, rats were chronically exposed to 0, 50, or 250 ppm Pb acetate in drinking water from weaning and trained on a multiple repeated acquisition (RA) and performance (P) schedule beginning at 55 days of age. The RA component required the rat to learn a new 3-member sequence of responses during each experimental session (Center Right Left, RLC, CLR, RCL, and LRC), while the correct sequence of responses for the P component was constant across sessions (LCR). Significant decrements in accuracy on the RA component but not on the P component were found in Pb-exposed groups compared to control, effects that could not be attributed to differential rates of responding. Analyses of error patterns revealed that the effects of Pb exposure on RA accuracy levels derived from two sources. The first consisted of a perseveration of P-like sequence responding (LCR) even during the RA component. Secondly, Pb exposure increased perseverative responding on a single lever, even though the schedule itself never directly reinforced such repetitive responding. The increase in frequency of these two types of perseverative behavior was incompatible with acquisition of non P-like sequences during the RA component. Adding a 5 sec tone to the light stimuli signalling the transition between RA and P components of the multiple schedule failed to attenuate these effects of Pb, suggesting that deficits in stimulus control were not the sole behavioral mechanism of these impairments. Examination of individual data revealed the presence of both 'learners' and 'non-learners' in each group, with the prevalence of the latter being suggestively higher in Pb-exposed groups than in controls. These findings may be relevant to the classroom setting, where periods requiring learning may frequently be interspersed with periods of performance of learned skills.     

The cost of treating heart valve related complications

This paper presents 5 patients with repeated recurrence of osteosarcoma (RROS). The primary focus of 3 patients were in the distal portion of femur, and 2 patients were in the proximal portion of tibia. Three patients, whose chest X ray film were negative, were treated by amputation and chemotherapy. Two patients had isolated metastatic focus 1.5 cm in diameter in lung, were treated by amputation after 1 week of chemotherapy and then treated by lobectomy after 2 weeks of chemotherapy. After operation, the chemotherapy was carried out for 3 courses of treatment. The roentgenogram of chest and affected limb were taken once every two months. There were metastatic focuses found in the lung of 1 patient and in the distal portion of femur of 2 patients. One patient was operated on for 4 times. Up to now, 3 patients have been living for 5 years and 2 patients for 6 years after operation.     

Autonomic paroxysms: their pathogenesis, diagnosis and treatment

In the article the rules about etiology and pathogenesis of vegetative paroxysms are stated based on careful analysis of the publications of researches as Russian, so foreign authors, and also own experimental and clinical supervision. During experimental and clinical researches the modern methods were used, enabling to estimate from positions of the system analysis different parts of pathogenesis of vegetative paroxysms, and also to offer ways of differential diagnostics of the various forms of disease. The application of some new preparations and direction of therapy of vegetative paroxysms are substantiated, and also the various circuits of treatment of the patients with distinguishing forms of given pathology are motivated.     

Genomic imprinting in the brain

Biopsies of cervix uteri from 166 patients with benign and malignant lesions (12 normal, 48 inflammatory lesion, 6 adenocarcinoma, 2 adenosquamous carcinoma and 98 from squamous cell carcinomas) were studied histochemically. The stains used were PAS with/without diastase, AB/PAS (pH 2.5) and OR/AB. In inflammatory lesions neutral mucin was predominent which was replaced by sialomucin and sulphomucin in endocervical polyps. In malignant lesions sulphomucin was predominent. Seventeen percent cases of squamous cell carcinomas needed reclassification after mucin staining. Of the fourteen large cell non-keratinizing squamous cell carcinomas, 12 were reclassified as squamous cell carcinoma with mucin secretion and 2 as adenosquamous carcinoma. One case of small cell non-keratinizing squamous cell carcinoma was reclassified as moderately differentiated adenocarcinoma. None of the keratinizing carcinomas had evidence of mucin secretion. Mucin histochemistry should be done routinely on non-keratinizing squamous cell carcinomas to pick up more cases of carcinoma with evidence of mucin secretion which can be missed on routine haematoxylin and eosin stains. Such carcinomas are known to pursue a more aggressive clinical course and have a poorer prognosis than non-mucin secreting type of squamous cell carcinoma.