A Histochemical Method for Sulfatase Activity in Hemic Cells and Organ Imprints

1. A new histochemical method is described for arylsulfatase activity (ASA)in hemic cells and organ imprints. Some common limitations in histochemicaltechnics have been tested and appear to be minimized in this method.

2. With the present method, a wide series of hemic cells may be identified,and their ASA separately graded from 0-4.

3. A study has been made of normal ASA values in all series of humanhematopoietic cells and of neutrophilic granulocyte ASA in common laboratory animals. Eosinophils, megakaryocytes, and neutrophils have the highestASA. Increases in ASA occur early during cell maturation in neutrophils andeosinophils.

4. Humans have a higher ASA than the laboratory animals tested. Withincertain species, there is some general correlation between neutrophilic granulocyte ASA and ASA of other organs. Under these conditions, leukocyte ASAis a potentially useful general screening method for ASA.

5. Some factors which enhance or inhibit leukocyte ASA have been tested.

Submitted on August 15, 1960 Accepted on November 5, 1960     

FACTOR VIII RELATED ANTIGEN IN CONNECTIVE TISSUE DISEASE PATIENTS AND RELATIVES

This study assayed serum levels of FVIII Rag as a marker ofendothelial injury in patients not only with frank connectivetissue disease but also in those presenting with Raynaud's phenomenonand in families of those with systemic sclerosis. Elevated levelsof FVIII Rag were found in 62% of patients with systemic sclerosis(SS), 38% with systemic lupus erythematosus (SLE), 67% withmixed connective tissue disease (MCTD) and in 17% with primaryRaynaud's phenomenon. Twenty percent of first degree relativesof patients with SS also demonstrated high levels of FVIII Ragand certain antibodies, namely those reacting with U, RNP andthe centromere. The association between elevated FVIII Rag andantibodies linked to Raynaud's and vasculitis lends supportto antibody involvement in pathogenesis. High levels of FVIIIRag in family members may reflect an increased susceptibilityof endothelium to injury particularly since relatives also havea higher frequency of clinical features such as Raynaud's phenomenon. KEY WORDS: Systemic lupus erythematosus, Raynaud's phenomenon, Scleroderma, Mixed connective tissue disease, Vasculitis     

Effects of Procainamide and Lidocaine on Defibrillation Energy Requirements in Patients Receiving Implantable Cardioverter Defibrillator Devices

Effects of Procainamide and Lidocaine on Defibrillation. intntduction: In acute canine studies, lidocaine. but not prucainamidc, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defihrillation energy requirements in 27 patients undergoing intraoperative testing fur implantable cardioverter dcfibrillator device placement.
Methods and Results: Patients were tested off antiarrhythmic drugs and again following either lidocaine (200 to 250 mg loading and 3 mg/min maintenance infusions) or procainamide (1 gm loading and 3 to 4 mg/min maintenance infusions). The defibrillation testing protocol consisted of initial testing at 15 J, followed by higher or lower energies to determine the lowest energy producing three consecutive successful defibrillations. Overall, the mean defibrillation energy increased from 14 ± 5 J to 18 ± 7 J during lidocaine (plasma concentration 5.1 ± 1.6 μ/mL; P < 0.02) but were similar at baseline (12 ± 5 J) and during procainamide infusion (13 ± 6 J) (plasma concentration: procainamide 10.7 ± 7.2 μ/rnl.; N-acetyl procainamide 1.0 ± 0.4 μ/niL). A positive linear correlation was found between lidocaine plasma concentration and percent change in defibrillation energy (lidocaine: r = 0.61; P = 0.01). Procainamide raised the defibrillation energy in three patients, two with supra therapeutic plasma concentrations. The increase in defibrillation energy equaled or exceeded 25 J in four patients after lidocaine and in one patient after procainamide.
Conclusion: The data suggest that at high plasma concentrations, lidocaine and procainamide adversely affect defibrillation energy requirements consistent with an adverse, concentration-dependent effect of sodium channel blockade on defibrillation energy requirements in patients.     

Mechanisms of protective immunity against 5. mansoni infection in mice vaccinated with irradiated cercariae. VI. Influence of the major histocompatibility complex

Summary Inbred mouse strains develop different levels of resistance to challenge infection with Schistosoma mansoni in response to vaccination with irradiated cercariae. The role of the major histocompatibility complex (MHC) in determining this genetic polymorphism in acquired resistance was investigated. Previous studies suggested that inbred mice bearing either the b or d MHC haplotypes develop a higher level of vaccine induced resistance than do mice with other MHC haplotypes. An analysis of an Fi cross between an H-2^b strain (C57BL/6) and an H-2^k strain (C3H/HeJ) indicated that the ability to develop high levels of immunity is inherited in a dominant fashion. In order to confirm that the development of high resistance is an MHC associated trait, B10, C3H, BALB and B6 congenic mice bearing different H-2 haplotypes were compared. On either the BIO, B6, or BALB background, substitution of b or d with k or a MHC alleles resulted in a decreased level of vaccine induced immunity. The observed decreases were more pronounced in BALB and B6 than in B10 congenics suggesting an influence of background (non-MHC linked) genes on protective immunity. Similarly, C3H. SW (H-2^b) mice developed a significantly higher level of acquired resistance than C3H/HeSn (H-2^k) mice. Cross and backcross experiments between H-2^b and H-2^k B6 congenic mice confirmed the dominant inheritance of high resistance as well as the MHC linkage of the trait. These data indicate that the MHC locus exerts a quantitative influence on vaccine induced resistance in certain inbred mouse strains and provide further support for the concept that the protection elicited by irradiated cercariae is the manifestation of a specific host immune response.     

Vitamin E Deficiency in the Monkey. IV. Further Studies of the Anemia with Emphasis on Bone Marrow Morphology

Nuclear abnormalities were observed in all the erythroid precursors in thebone marrow of vitamin E-deficient monkeys. Many of these cells were multinucleated. The remainder of the marrow elements appeared normal. Reasonsfor considering the anemia to be primarily due to inadequate erythropoiesisare given.

Serum iron, glutathione stability of the erythrocytes, hemoglobin electrophoresis, osmotic fragilities and platelet counts were all found to be normalin the vitamin E-deficient monkey.

Submitted on March 23, 1962 Accepted on May 12, 1962