Determination of residual Kryptofix 2.2.2 levels in [F]-labeled radiopharmaceuticals for human use

4,7,13,16,21,24-Hexaoxa-1,10-diazabicyclo[8.8.8]hexacosane (Kryptofix^® 2.2.2) is used in the routine preparation of [¹⁸F]-labeled tracers employed in positron emission tomography (PET) imaging. Confirming the absence of Kryptofix^® in radiopharmaceuticals is a quality control criterion required before they can be released for human use. Analysis of Kryptofix^® levels using the iodoplatinate spot-test can be complicated by false-positive results due to nitrogen containing tracers and/or false-negative results caused by added stabilizers. To overcome this issue, we have developed a universal TLC method for the rapid and reliable determination of Kryptofix^® levels in the wide range of fluorine-18 radiopharmaceuticals we prepare, including complex multi-component formulations.     

What proteins are present in polyethylene glycol precipitates from rheumatic sera?

The proteins present in 4% polyethylene glycol (PEG) precipitates of 10 normal sera and 60 samples from patients with rheumatic diseases were studied. A variety of immunochemical methods were used, including estimation of the percentages of total serum proteins precipitated by PEG, gel filtration analyses of the precipitates, and affinity chromatography with protein A and anti-immunoglobulin columns. Substantial amounts of protein were precipitated from normal sera. Many non-immunoglobulin proteins were precipitated from patients' sera, including fibronectin, haptoglobin, albumin, transferrin, and alpha 1-antitrypsin. Affinity chromatography with anti-immunoglobulin columns bound non-immunoglobulin proteins from PEG precipitates, but the protein A affinity column did not do so. The view that circulating antibody-antigen complexes alone are precipitated by 4% PEG is too simplistic; many non-immunoglobulin proteins are involved. They may either bind to immune complexes or be coprecipitated owing to non-specific protein aggregation.     

Studies of Whole Blood Associated Acetaldehyde as a Marker for Alcohol Intake in Mice

Thirty C57BI mice were randomized into two groups. Group 1 served as controls while Group 2 was given 10% V/V ethanol with the drinking water. Whole blood- associated acetaldehyde (WBAA) was measured on capillary blood samples using a fluorigenic high performance chromatographic assay. WBAA peaked at Day 2. A stable mean plateau of 263 +/- 71 SD with a range of 160-400 nmoles/g hemoglobin WBAA was found in the group consuming ethanol compared with 122 +/- 17 SD and a range of 88-150 nmoles/g hemoglobin for controls (p less than 0.001). When ethanol was discontinued, levels of WBAA declined and became similar to those of controls by 9 days following cessation of ethanol. The quantitative difference between ethanol-consuming and control animals and also the rapid rise of whole blood-associated acetaldehyde and the relatively slow decline following cessation of ethanol intake indicate that such a test might be a useful monitor of drinking behavior.     

Improvement in depressive illness is not associated with altered release of neurophysins over a course of ECT

The hypothesis that the release of vasopressin-associated neurophysin (hNpI) or oxytocin-associated neurophysin (hNpII) is modified by a course of electroconvulsive therapy (ECT) was tested by the measurement of serum neurophysins before and after the first and last ECTs given to 17 unipolar depressed patients. Neither basal nor ECT-induced neurophysin release changed between the first and last ECTs. Data from the present study were combined with data from a previous published study to provide a sample of 29 unipolar depressed patients. In this extended sample, the release of hNpII after the first ECT was significantly correlated with improvement in symptoms of depression over a course of ECT as measured by the Hamilton Rating Scale for Depression and the Montgomery-Asberg Depression Rating Scale.     

The use of blood components in patients with malignancy

Many recent improvements in the management of patients with malignancy would have been impossible without parallel improvements in our ability to support patients through periods of severe bone marrow aplasia produced by the disease or aggressive therapy of the disease. The purpose of this article is to review the use of transfusion of platelets, erythrocytes, and granulocytes in the treatment of these patients.

---

Resumen Muchos de los recientes adelantos en el manejo de pacientes con neoplasias malignas habrían sido imposibles sin un desarrollo paralelo en la capacidad de proveer soporte en el curso de severa aplasia de la medula ósea producida por la enfermedad misma o por terapia antineoplásica agresiva. El propósito de este artículo es revisar el uso de las transfusiones de plaquetas, eritrocitos, y granulocitos en el manejo de estos pacientes.

---

Résumé De nombreuses améliorations récentes du traitement des malades atteints d'une affection maligne auraient été impossibles sans des améliorations parallèles du traitement des épisodes d'aplasie médullaire grave produits par l'affection elle-même ou par les agents thérapeutiques agressifs employés pour les traiter. Le but de l'article est de passer en revue l'emploi respectif des plaquettes, des érythrocytes et des granulocytes pour traiter ces malades.

     

S-Adenosylhomocysteine, but not homocysteine, is toxic to yeast lacking cystathionine β-synthase

Elevated plasma homocysteine is associated with a variety of diseases in humans including coronary heart disease, stroke, peripheral vascular disease, and birth defects. However, the mechanism by which plasma homocysteine affects cells is unknown. We have examined the growth of isogenic wild-type and cystathionine beta-synthase (CBS) deficient yeast in response to homocysteine and its immediate metabolic precursor, S-adenosylhomocysteine (SAH). CBS deficient yeast export significantly more homocysteine into the media than wild-type yeast and have elevated internal pools of homocysteine and SAH. We found that 5 mM homocysteine added to the media had very little effect on the growth of wild-type or CBS deficient yeast, although intracellular homocysteine concentrations increased five- to tenfold. In contrast, as little as 25 microM S-adenosylhomocysteine inhibited the growth of CBS deficient yeast, but had no effect on wild-type yeast. Measurements of the intracellular S-adenosylmethionine (SAM) and SAH indicate that CBS deficient yeast contain reduced SAM/SAH ratios relative to wild-type, and this ratio is further reduced by adding SAH to the media. Growth inhibition by SAH in CBS deficient yeast can be totally reversed by addition of SAM to the media, indicating that the ratio and not absolute level is critical for cell growth. These results suggest that CBS plays a key role in the regulation of the SAM/SAH ratio inside cells and that excessive perturbations of this ratio can inhibit growth. We hypothesize that elevated extracellular homocysteine present in humans may reflect an altered intracellular SAM/SAH ratio and that this may be related to disease pathogenesis.