Human T-Lymphotropic Virus Type 2 (HTLV-2) Provirus in Circulating Cells of the Monocyte/Macrophage Lineage in Patients Dually Infected with Human Immunodeficiency Virus Type 1 and HTLV-2 and Having Predominantly Sensory Polyneuropathy

We investigated the presence of human T-lymphotropic virus type 2 (HTLV-2) DNA in the peripheral blood mononuclear cell subsets obtained from 18 patients coinfected with human immunodeficiency virus type 1 and HTLV-2, 6 of whom also had predominantly sensory polyneuropathy (PSP). HTLV-2 DNA and RNA were found in CD8- and CD19-positive cells, and, for patients with PSP, in CD14-positive cells as well. Furthermore, the patients with PSP had higher proviral loads than those without PSP.     

In vitro and in vivo evaluation of insulin-producing beta TC6-F7 cells in microcapsules

In the present study, the insulin secretory capacity ofTC6-F7 cells in microcapsules was evaluated. The cell mass within capsules was found to expand in a three-dimensional fashion, in contrast to cells seeded on plates that grew as a monolayer. In invitro studies, both free and encapsulated cells were found to secreteinsulin in the absence of glucose, at 13.6 ± 1.1 and 14.5 ± 0.9 ng · 10⁶cells¹ · 60 min¹, respectively, withthe response rising to a maximum of 26.0 ± 0.8 and 31 ± 2.3 ng · 10⁶cells¹ · 60 min¹ in the presence of16.8 mM glucose. Encapsulated cells were able to produceCa²⁺ responses in the presence ofKCl (50 mM) and BAY K 8644 (100 µM). In in vivo studies,intraperitoneal transplantation of 3.0 ×10⁶ microencapsulated cellsinto mice (n = 5) withstreptozotocin-induced diabetes resulted in the restoration ofnormoglycemia up to 57 days. Insulin concentrations rose from 0.4 ± 0.1 ng/ml before the graft administration to 2.2 ± 0.8 ng/ml afterthe transplantation in the normoglycemic recipients. An oral glucosechallenge in transplant recipients demonstrated a flat glucoseresponse, suggesting extremely high glucose clearance rates. These datademonstrate the potential use of the immunoisolated -cell lines forthe treatment of diabetes.

     

THE ULTRASTRUCTURE OF DERBESIA TENUISSIMA (DE NOTARIS) CROUAN. I. ORGANIZATION OF THE GAMETOPHYTE PROTOPLAST,GAMETANGIUM, AND GAMETANGIAL PORE1,2,3

The fine structure of vegetative and reproductive gametophytes of Derbesia tenuissima is described. Development of the gametangium and release of the gametes progress as follows: (1) In initial stages of gametangium formation, prior to 24 hr before gamete release, there is an accumulation and proliferation of nuclei, chloroplasts, and other organelles. (2) This is followed by separation of the gametangium from the rest of the plant by a gametangial membrane; segregation of organelles into gametes has begun by 12 hr before release and the process is completed by 2.5 hr before release. (3) Enzymatic wall dissolution of the pore area occurs between 2.5 and, 12 hr before normal lights-on time. (4) The release mechanism appears to be an instantaneous light-induced increase in lurgor pressure rupturing the weakened pore area, of the wall and causing a forcible expulsion of the gametes. (5) Following release, the pore is sealed by organellar debris and the gametangial membrane. Additional wall layers are presumed to be laid down internal to the plugged pore by the vegetative protoplasm which migrates into the area.     

The pancreatic -cell recognition of insulin secretagogues. VII. Binding and permeation of chloromercuribenzene-p-sulphonic acid in the plasma membrane of pancreatic -cells

The uptake of chloromercuribenzene-p-sulphonic acid (CMBS) was studied in microdissected pancreatic islets of ob/ob-mice. After rapid initial binding, the uptake increased linearly with time, suggesting that CMBS diffused into the plasma membrane. The binding of CMBS was rapidly reversed on exposure to l-cysteine. Whereas glibenclamide had no effect, glucose and 4-acetamido-4′-isothiocyanostilbene-2,2′-disulphonic acid (SITS) inhibited diffusion without affecting the initial binding. SITS, but not glucose, also inhibited CMBS-induced insulin release. The results support the hypothesis that CMBS stimulates insulin release by reacting with thiol groups in the β-cell plasma membrane. These thiol groups may be located in an anion diffusion channel, entrance to which is blocked by SITS and exit from which is inhibited by glucose. In comparison with erythrocytes, the β-cells contain a large number of superficial thiol groups, which may explain why these cells accumulate alloxan.     

ULTRASTRUCTURAL BASIS OF BIOCHEMICAL EFFECTS IN A SERIES OF LETHAL ALLELES IN THE MOUSE : Neonatal and Developmental Studies

The fine structure of newborn and fetal mouse liver and of newborn kidney cells homozygous for any of three albino alleles known to have multiple biochemical effects was investigated. Electron microscope studies of mutant cells revealed dilation and vesiculation of the rough endoplasmic reticulum in parenchymal liver cells, as well as dilation and other anomalies of the Golgi apparatus. These abnormalities were observed in all newborn mutants but never in littermate controls. Although they were most pronounced in liver parenchymal cells, they were found also to a lesser degree in kidney cells, but they were absent altogether in other cell types of the mutant newborn. Homozygous fetuses showed similar anomalies in the liver at 19 days of gestational age. In one of the alleles studied, mutant liver parenchymal cells were found to be abnormal as early as the 18th day of gestation. There appears to be a striking parallelism between the biochemical defects and those of the cellular membranes in homozygous mutant newborn and fetuses. Although the specific nature of the mutational effect on membrane structure remains unknown, the results are compatible with the assumption that a mutationally caused defect in a membrane component interferes with a mechanism vital in the integration of morphological and biochemical differentiation.