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Biomedical subjects

J D Berman

Publications and source records attributed to J D Berman.

100 records · Page 6Linked to original sources
PubMed1978

Monocyte function in human neonates.

Monocytes of healthy, full-term newborns were isolated from cord blood, and functional and biochemical activities were quantitated. The yield of monocytes per milliliter of cord blood was 60% greater than that from the peripheral blood of healthy adults. Placental monocytes were initially less well spread than cells from adults, but no other morphological differences were noted. During 4 days of in vitro cultivation, placental monocytes secreted lysozyme at a constant rate, lost peroxidase activity, and increased 5'-nucleotidase activity 15- to 25-fold. Similar findings were obtained with monocytes from adults. Placental monocytes also displayed Fc and complement receptor activity. Ingestion and intracellular multiplication of Toxoplasma gondii were identical in normal placental and adult monocytes. Furthermore, toxoplasma multiplication was significantly inhibited by cells from both sources when the monocytes were preincubated with supernatants prepared from sensitized lymphocytes and toxoplasma antigen. Monocytes from newborns were competent cells in terms of the specific functions and activities we examined.

Adult↗
PubMed1971

Rapid and complete purification of acetylcholinesterases of electric eel and erythrocyte by affinity chromatography.

Affinity chromatography has been used to purify acetylcholinesterase both from the electric tissue of Electrophorus electricus and from bovine erythrocyte membranes. For this purpose, several specific enzymic inhibitors of each protein were synthesized and joined covalently to an insoluble support resin. AchE is selectively retained by such inhibitor-resins when highly impure solutions are chromatographed upon them. After removal from the resin, both enzymes are electrophoretically homogeneous and they may be recovered in yields of 75% or more.

Acetylcholinesterase↗
PubMedDate not supplied

Treatment of New World cutaneous and mucosal leishmaniases.

The most extensive investigations of treatment of New World cutaneous leishmaniasis have been performed against L. panamensis disease in Colombia, and the relative value of regimens shown there may be instructive for disease from other areas. In Colombia, a 90-95% cure rate was achieved with three different drug regimens: The standard regimen of pentavalent antimony (20 mg/ kg/day for 20 days parenterally) A short course of pentamidine (3 mg/kg every other day for four injections intramuscularly The marketed combination of topical paromomycin (15%)-MBCl (12%) for 10 days, plus antimony (20 mg/kg/day parenterally) for 7 days. My view is that all these regimens could be chosen as first-line therapy for cutaneous disease in Colombia. The antimony regimen has the advantage of established use; the disadvantages are cost, requirement for injections each day for 20 days, and considerable morbidity in the last two weeks of therapy. The pentamidine regimen has the advantage of a short time course; the disadvantages are lack of experience with this new regimen and frequent, although moderate, morbidity. The combined topical-parenteral regimen has the advantage of requiring few and nontoxic injections; the primary disadvantage is that the regimen is novel and its efficacy has not been confirmed. It would be expected that cases of lesions in other areas caused by L. braziliensis complex would respond in a similar manner to these regimens. To date, however, only the efficacy of the standard antimonial regimen has been confirmed. In certain regions of Central America, other regimens may be effective. Thus, ketoconazole appears to be effective for the more rapidly self-curing forms of disease (cutaneous disease caused by L. mexicana and L. panamensis from Central America), and a short course of antimony may be effective against L. braziliensis in Guatemala.

Administration, Cutaneous↗
PubMedDate not supplied

Causal prophylactic efficacy of atovaquone-proguanil (Malarone) in a human challenge model.

Plasmodia infect the liver for about 7 days before subsequently infecting the blood. Present prophylaxis against Plasmodium falciparum malaria employs agents that primarily kill blood stages and must be continued for 28 days after the last exposure. Atovaquone-proguanil (Malarone) is a new antimalarial agent that is licensed in 35 countries as treatment against blood-stage infection, but its components (atovaquone and proguanil) have separately been shown to be active also against liver stages. To determine whether atovaquone-proguanil is sufficiently active against liver stages to be discontinued 7 days after exposure, we challenged 16 volunteers with P. falciparum via infected mosquitoes. Twelve volunteers received atovaquone-proguanil (1 tablet daily) on the day prior to challenge, on the day of challenge, and for the next 6 days; 4 volunteers received matching placebo. All placebo volunteers demonstrated parasitaemia and malarial symptoms beginning on days 11-12 after challenge. No atovaquone-proguanil volunteer acquired malaria. Atovaquone-proguanil is the first licensed antimalarial agent that kills P. falciparum in the liver and that may be discontinued 7 days after the last exposure.

Adolescent↗
PubMedDate not supplied

Chemotherapy for leishmaniasis: biochemical mechanisms, clinical efficacy, and future strategies.

The 1980s have seen significant advances in the treatment of cutaneous, mucosal, and visceral leishmaniasis. Safe regimens of pentavalent antimony in the form of Pentostam (Wellcome Foundation, London; 20 mg of antimony/[kg.d] for 20-30 days) have produced initial cure rates of greater than 90% in these diseases. Biochemical investigations have demonstrated at least three parasite-specific features relevant to the mechanism of action of chemotherapeutic agents: (1) Organization of glycolytic enzymes and some enzymes of fatty acid catabolism into organelles (glycosomes) occurs in Leishmania but not in mammalian cells. Since antimony inhibits both amastigote catabolism of glucose via glycolytic enzymes and catabolism of fatty acids, the mechanism of action of antimony may relate to alteration of glycosomal structure or function. (2) Purine analogues can be utilized by the salvage pathway of purine biosynthesis in amastigotes to a greater extent than in mammalian cells, and allopurinol and allopurinol ribonucleoside are metabolized into presumably toxic nucleotides by these means. (3) Amastigote sterol biosynthesis is akin to that of such fungi as Candida in that the major demethylated sterol is of the ergostane series and in that ketoconazole inhibits its synthesis. Preliminary clinical studies suggest that the purines and the sterol inhibitors may have clinical utility as oral agents against cutaneous leishmaniasis. Possible treatment strategies for the classic and experimental agents have been proposed.

Animals↗