Acute Appendicitis

Acute appendicitis still is a cause of considerable morbidity and now and then of death. The diagnostic accuracy in 316 patients operated on for acute appendicitis at Holy Cross Hospital was 76 per cent. In 24 of 239 cases of proved acute appendicitis, perforation had occurred, and the morbidity in those cases was three times that in the cases without perforation. Review of the cases did not reveal any clear-cut diagnostic criteria that might be used to predict perforation.A study of 30 patients with mesenteric lymphadenitis who were inadvertently operated on in the belief they had appendicitis, revealed that this condition is most likely to occur in young females with only a slight increase in the number of leukocytes. Although positive diagnosis of acute appendicitis is a difficult problem, the morbidity associated with needless operation is so much less than that which occurs in acute perforated appendicitis, that prompt exploration in any questionable case seems warranted.     

Localization of Arbutin in Pyrvs by Means of Alkaline P-Phenylenediamine

A reagent composed of 0.2% p-phenylenediamine in 2 N NH₄OH was used for the cytochemical demonstration of arbutin in plant tissue. Sections of fresh tissue were cut at 25-50 μ, mounted in a drop of the reagent, and allowed to stand uncovered 15-20 min before applying a coverslip. Arbutin stained dark blue to dark purple and was easily distinguished from other constituents of the cell, such as chlorogenic acid, isochlorogenic acid, caffeic acid, and quinic acid, which stained yellow, yellow-green, red or brown in color. The limit of sensitivity of the p-phenylenediamine-arbutin reaction was 1:100,000, as determined by spot-plate tests.     

Suppression of programmed neuronal death by a thapsigargin-induced Ca2+ influx

Rat sympathetic neurons undergo programmed cell death (PCD) in vitro and in vivo when they are deprived of nerve growth factor (NGF). Chronic depolarization of these neurons in cell culture with elevated concentrations of extracellular potassium ([K⁺]_o) prevents this death. The effect of prolonged depolarization on neuronal survival is thought to be mediated by a rise of intracellular calcium concentration ([Ca²⁺]_i) caused by Ca²⁺ influx through voltage-gated channels. In this report we investigate the effects of chronic treatment of rat sympathetic neurons with thapsigargin, an inhibitor of intracellular Ca²⁺ sequestration. In medium containing a normal concentration of extracellular Ca²⁺ ([Ca²⁺]_o), thapsigargin caused a sustained rise of intracellular Ca²⁺ concentration and partially blocked death of NGF-deprived cells. Elevating [Ca²⁺]_o in the presence of thapsigargin further increased [Ca²⁺]_i, suggesting that the sustained rise of [Ca²⁺]_i was caused by a thapsigargin-induced Ca²⁺ influx. This treatment potentiated the effect of thapsigargin on survival. The dihydropyridine Ca²⁺ channel antagonist, nifedipine, blocked both a sustained elevation of [Ca²⁺]_i and enhanced survival caused by depolarization with elevated [K⁺]_o, suggesting that these effects are mediated by Ca²⁺ influx through L-type channels. Nifedipine did not block the sustained rise of [Ca²⁺]_i or enhanced survival caused by thapsigargin treatment, indicating that these effects were not mediated by influx of Ca²⁺ through L-type channels. These results provide additional evidence that increased [Ca²⁺]_i can suppress neuronal PCD and identify a novel method for chronically raising neuronal [Ca²⁺]_i for investigation of this and other Ca²⁺-dependent phenomena. © 1995 John Wiley & Sons, Inc.     

The Structure and Origin of the Plasmodium of Rhopalura ophiocomae(Phylum Orthonectida)

Abstract Adult orthonectids develop from germinal cells within a cytoplasmic matrix called a plasmodium. This is generally assumed to be formed by the parasite. In the case of Rhopalura ophiocomae, which lives in the brittle star Amphipholis squamata, the plasmodia occupying the perivisceral coelom are closely associated with the walls of the genital bursae or the gut, and they are covered by peritoneum. They have been reported to contain scattered small nuclei distinct from those within germinal cells, embryos, and adults, but the results of the present study indicate that such nuclei probably do not exist. Furthermore, electron micrographs show that some plasmodia are in continuity with the cytoplasm of contractile cells that lie beneath the peritoneum of a genital bursa or the gut of the host. The matrix of a plasmodium of R. ophiocomaeappears, therefore, to consist of cytoplasm of a contractile cell. It is proposed that after a contractile cell has been entered by an infective cell of the parasite, it hypertrophies, bulging progressively farther into the perivisceral coelom and lifting up the peritoneum, which remains in intimate contact with it.     

Molecular Genetics of the Brown (B)-Locus Region of Mouse Chromosome 4. II. Complementation Analyses of Lethal Brown Deletions

Numerous new mutations at the brown (b) locus in mouse chromosome 4 have been recovered over the years in germ-cell mutagenesis experiments performed at the Oak Ridge National Laboratory. A large series of radiation- and chemical-induced b mutations known to be chromosomal deletions, and also known to be prenatally lethal when homozygous, were analyzed by pairwise complementation crosses as well as by pseudodominance tests involving flanking loci defined by externally visible phenotypes. These crosses were designed to determine the extent of each deletion on the genetic and phenotype map of the chromosomal region surrounding the b locus; the crosses also provided basic data that assigned deletions to complementation groups and defined four new loci associated with aberrancies in normal development. Specifically, the pseudodominance tests identified deletions that include the proximally mapping whirler (wi) and the distally mapping depilated (dep) genes, thereby bracketing these loci defined by visible developmental abnormalities with landmarks (deletion breakpoints) that are easily identified on the physical map. Furthermore, the complementation crosses, which were supplemented with additional crosses that allowed determination of the gross time of lethality of selected deletions, defined four new loci required for normal development. Homozygous deletion of one of these loci (b-associated fitness, baf) results in a runting syndrome evident during postnatal development; deletion of one locus [l(4)2Rn] causes death in the late gestation/neonatal period; and deletion of either of two loci [l(4)1Rn or l(4)3Rn] results in embryonic death, most likely in pre-, peri- or postimplantation stages. The placement of these new functionally defined loci on the evolving molecular map of the b region should be useful for continuing the analysis of the roles played in development by genes in this segment of chromosome 4.     

The potential energy surface of methyl 2-O-(α-D-mannopyranosyl)-α-D-mannopyranoside in aqueous solution: Conclusions derived from optical rotation

The optical rotation of methyl 2-O -(α-D -mannopyranosyl)-α-D -mannopyranoside is calculated semiempirically as a function of the linkage dihedral angles ? (H1-C1-O1-C2′) and ψ (C1-O1-C2′-H2′). Although the rotation calculated for the global energy minimum conformation found in several rigid-residue modeling calculations (?,ψ = ?40°,?20°) is in good agreement with the observed solution rotation, the observed rotation is also compatible with the limited flexibility inferred from more recent relaxed residue modeling calculations on a structurally related rhamnose disaccharide © 1994 John Wiley & Sons, Inc.