Wall Deficiency Research Articles

Effects of cell wall deficiency on the synthesis of polysaccharide-degrading exoenzymes: a study on mycelial and wall-less phenotypes of the fz; sg; os-1 ('slime') triple mutant of Neurospora crassa

The production of exoenzymes which degrade cellulose, polygalacturonic acid and xylan was studied in mycelial and wall-less phenotypic derivatives of Neurospora crassa obtained by vegetative selection applied to a single fz;sg;os-1 ('slime'-like) segregant (strain RCP-3) of a cross 'slime' x wild type. The unrelated stable 'slime' strain FGSC 1118 was also studied. The synthesis of polysaccharide-degrading enzymes was normally induced by polysaccharidic substrates and was sensitive to carbon-catabolite repression for both mycelium-forming phenotypes (mycelial intermediate and spheroplast-hyphal intermediate) of strain RCP-3. The stable 'slime' from RCP-3 produced cellulose-degrading activity and xylan-degrading activity constitutively but was fully sensitive to glucose repression. The stable 'slime' RCP-3 did not synthesize polygalacturonic-acid-degrading activity, even in the presence of inducers. For the stable 'slime' FGSC 1118, all of the polysaccharide-degrading activities were produced constitutively and were markedly resistant to glucose repression. The possible epigenetic origin of the different properties of stable 'slimes' RCP-3 and FGSC 1118 is considered. These results may relate to the role of the cell surface in the processing of regulatory signals which control the adaptation of the fungal cell to the nutritional environment.

Effects of cell wall deficiency in 'slime'strains of Neurospora crassa: a study on mycelial and wall-less phenotypic derivatives of a single fz; sg; os-1 ('slime'-like) segregant

Some morphological, physiological, enzymic and genetic characteristics of mycelial and plasmodioid phenotypes of Neurospora crassa, obtained by vegetative selection of a single fz; sg; os-1 (‘slime’-like) segregant of a cross ‘slime’ × wild-type, were studied. The mycelial phenotype of the segregant, albeit altered in morphology, was otherwise fully normal for export and regulation of invertase and β-glucosidase. In contrast, both enzymes were oversecreted and were resistant to catabolic regulation in the stable ‘slime’ phenotype, derived from the same isolate. These results suggested that the enzymic defects of ‘slime’ appeared gradually, concomitantly with the loss of ability to construct a cell wall, as a consequence of the process of vegetative selection required to produce stable ‘slime’ from mycelium-forming ‘slime’-like segregants. This idea was reinforced by the isolation of an intermediate phenotype, which exhibited mycelial/spheroplast dimorphism conditioned by the osmolarity of the culture medium. Crosses of the two extreme phenotypes of the fz; sg; os-1 segregant (the mycelial and the stable ‘slime’) failed to demonstrate any significant genetic difference between them.

Acetabular Preparation in Cementless Revision TotaI Hip Arthroplasty

The rationale for and experience with the use of a hemispherical, cementless, microporous socket (Harris-Galante prosthesis) are presented as an approach to acetabular revision arthroplasty. Advantages are noted in preservation of existing bone, ease of rigid fixation, and bone grafting with either lyophylized particle allograft or autograft. The early results of a series of 75 sockets show no loss of fixation, mild to major resorption of non-contained bone graft, and favorable roentgenographic appearance of contained bone graft. In bone-grafted regions, a high percentage of lucencies at the graft-porous interface implies a lack of bone ingrowth. The authors were unable to characterize any roentgenographic behavioral differences between allograft or autograft. The approach is successful in severely deficient acetabulae, especially of the Type III combined cavitary and segmental medial wall deficiency.

The etiology of venous ulceration.

AbstractVenous ulceration is caused by the disorganization of the microcirculation that is induced by prolonged venous hypertension. The most common cause of calf pump inefficiency that permits superficial venous hypertension during exercise is deep vein thrombosis. Venous hypertension causes venular dilatation and an increased capillary permeability. Fibrin is deposited around the capillaries and not removed because of a vein wall deficiency of the fibrinolytic activator. The fibrin acts as a diffusion barrier and the overlying dermis becomes anoxic. Any minor trauma then causes an ulcer. Ulcers can be cured by restoring calf pump function to normal. Postthrombotic skin changes caused by irreparable calf pump damage can be reversed by the regular use of elastic compression and the pharmacological long‐term enhancement of fibrinolysis.

Coagulase-negative staphylococci

It is becoming clear that modern medical practices leading to the compromise of patients (e.g., by the ntroduction of prostheses or • -atheters and immunosuppressive therapy) have greatly enhanced the risk of infection by resident coagulase-negative Staphylococcus species. Table 1 lists the various species according to species group and pathogenic potential. Although Staphylococcus epidermidis and S. saprophyticus are now well documented as opportunistic pathogens, additional research will be required to assess the pathogenicity of the other species, especially with regard to possible site or tissue specificity, severity of infection, and problems with antibiotic treatment. Coagulase-negative staphylococci Ihave been frequently implicated in infections of prosthetic heart valves (7), vascular and joint prostheses (19, 27), and cerebral spinal fluid dshunts (10), subacute bacterial endocarditis (12), peritonitis in patients receiving continuous peritoneal dialysis (21), and in urinary tract (11), eye (25), ear (6), and ~vound (20) infections. They have ,also been isolated frequently from he blood, urine, and tumors of ancer patients, and from these sources often exhibit altered strut~tural and biochemical features (e.g., las L-forms with cell wall deficiencies Table 1 Coagulase-Negative Staphylococcus Species

Compression-Related Defects from Early Amnion Rupture

The features of 27 cases of limb/body wall deficiency (formerly termed cyllosomus and pleurosomus) were evaluated and the anomalies were interpreted as being band-related defects and/or compression-related defects. The latter included limb deficiency, body wall deficiency, neural tube defects, scolliosis, postural deformations, growth deficiency, and short umbilical cord. It is hypothesized that the single event of early amnion rupture can explain both the band-related defects and the compression-related defects. Experimental animal studies are in accord with this hypothesis: amnion puncture of rat fetuses during early gestation produces a comparabable array of defects. The term amnion rupture sequence is suggested to describe the overall pattern of malformation that results from amnion rupture whether these defects are band related, compression related, or a combination of the two. There is considerable variation in the phenotype of amnion, rupture sequence, with limb/body wall deficiency representing the more severe end of the spectrum. Sit is important to recognize and correctly diagnose amiion rupture sequence because it is usually a sporadic event.

Preaxial polydactyly of the foot associated with early amnion rupture: Evidence for mechanical teratogenesis?

THE SPECTRUM of resultant defects for early amnion rupture has been expanded to include defects other than those caused by amniotic band disruption per se. These include craniofacial defects, limb reduction defects, cutaneous syndactyly, body wall deficiency, a short umbilical cord, scoliosis, and growth deficiency. 1-~ The nature of these additional defects is thought to relate to early intrauterine compression of the embryo resulting from at least a temporary loss of amniotic fluid. Support for this hypothesis derives from experimental studies in rats, in which the same duster of anomalies is induced by early amnion puncture at a time equivalent to four to six weeks in the human. 6 The purpose of this communication is to report yet another potential consequence of early amnion rupture, namely, a rare form of preaxial polydactyly of the foot, observed in two unrelated patients who had evidence of early amnion rupture.

Compression-related defects from early amnion rupture: Evidence for mechanical teratogenesis

The features of 27 cases of limb/body wall deficiency (formerly termed cyllosomus and pleurosomus) were evaluated and the anomalies were interpreted as being band-related defects and/or compression-related defects. The latter included limb deficiency, body wall deficiency, neural tube defects, scoliosis, postural deformations, growth deficiency, and short umbilical cord. It is hypothesized that the single event of early amnion rupture can explain both the band-related defects and the compression-related defects. Experimental animal studies are in accord with this hypothesis; amnion puncture of rat fetuses during early gestation produces a comparable array of defects. The term amnion rupture sequence is suggested to describe the overall pattern of malformation that results from amnion rupture whether these defects are band related, compression related, or a combination of the two. There is considerable variation in the phenotype of amnion rupture sequence, with limb/body wall deficiency representing the more severe end of the spectrum. It is important to recognize and correctly diagnose amnion rupture sequence because it is usually a sporadic event.

Further observations on the pathology of the atrioventricular canal malformation.

THIRTY-TWO human hearts having atrioventricular (AV) canal malformation were recently studied. The attention was drawn to the anatomical and geometric aspects of the diseased hearts. It was noted that the defect included a significant portion of the muscular septum as far as its junction with the diaphragmatic wall and significant deficiency in the posterior base of the heart. Also, there were major anomalies of the right ventricle, mainly hypoplasia of the septal portion of the right ventricular sinus, and hyperdevelopment of the conal portion of the right ventricle. To the best of our knowledge, the anomalies involving the base of the heart and the ventricles were not described before and they may have some implication as to the surgical approach as well as to the developmental anomaly. The purpose of this communication is to give an anatomic description of the AV canal heart and to define the involved structures, morphologically.