Membranes defects

Ronk R, White MK. 1985. Hydrogen sulfide and the probabilities of inhalation through a tympanic membrane defect. J Occup Med 27 337-340. 

The dead-end setup is by far the easiest apparatus both in construction and use. Reactor and separation unit can be combined and only one pump is needed to pump in the feed. A cross-flow setup, on the other hand, needs a separation unit next to the actual reactor and an additional pump to provide a rapid circulation across the membrane. The major disadvantage of the dead-end filtration is the possibility of concentration polarization, which is defined as an accumulation of retained material on the feed side of the membrane. This effect causes non-optimal membrane performance since losses through membrane defects, which are of course always present, will be amplified by a high surface concentration. In extreme cases concentration polarization can also lead to precipitation of material and membrane fouling. A membrane installed in a cross-flow setup, preferably applied with a turbulent flow, will suffer much less from this... 

Hemolytic anemia results from decreased RBC survival time due to destruction in the spleen or circulation. The most common etiologies are RBC membrane defects (e.g., hereditary spherocytosis), altered Hb solubility or stability (e.g., sickle cell anemia [see Chap. 34] and thalassemias), and changes in intracellular metabolism (e.g., glucose-6-phosphate dehydrogenase deficiency). Some drugs cause direct oxidative damage to RBCs (see Appendix 3). 

We emphasize that these theories are not mutually exclusive. Thus, a genetically determined membrane defect could produce a dysregulation in the neurotransmitter-receptor interaction. This, in turn, may impact second messenger systems within specific neural circuits, resulting in a disturbance of biological rhythms such as neuroendocrine function. 

Meltzer HL. Is there a specific membrane defect in bipolar disorders Biol Psychiatry 1991 30 1071-1074. 

Later Henis and Tripodi [73] showed that membrane defects in anisotropic Loeb-Sourirajan membranes could be overcome in a similar way by coating the membrane with a thin layer of a relatively permeable material such as silicone rubber. A sufficiently thin coating does not change the properties of the underlying selective layer but does plug defects, through which simple convective gas flow can occur. Henis and Tripodi s membrane is illustrated in Figure 3.29. The silicone rubber layer is many times more permeable than the selective layer and... 

Figure 3.28 Method developed by Ward. Browall and others membrane defects in composite membranes made by the wa e...

Microfiltration membranes are often used in applications for which penetration of even one particle or bacterium through the membrane can be critical. Therefore, membrane integrity, that is, the absence of membrane defects or oversized pores,... 

From 1978 to 1980, Henis and Tripodi [6,23], then at Monsanto, devised an ingenious solution to the membrane defect problem their approach is illustrated in Figure 8.8. The Monsanto group made Loeb-Sourirajan hollow fiber membranes... 

Part of the increase in antibacterial effect on mutants with membrane defects may also be due to increased permeability. These mutants not only have shorter saccharide chains but at the same time are not able to incorporate proteins in the outer membrane, which leads to domains of glycerophospholipids in the bilayer of the outer membrane [103]. 

Although ABO incompatibility and Rh-anti-body formation are the most common causes of hemolysis, other causes need to be considered, such as cephalohematoma formation during delivery with resultant increase in bilirubin production as the hematoma is resorbed hereditary spherocytosis, which is a red cell membrane defect that results in premature breakdown of the red cells and glucose 6-phosphate dehydrogenase deficiency, which is involved in maintaining adequate reduced glutathione levels in the red cell. Infection in the neonatal period is uncommon but still must be considered as a cause of jaundice. In particular, infections of the urinary tract lead frequently to jaundice as a preliminary symptom. The increase in infection associated with instrumentation in the premature infant is always a concern. 

Using the principle of ion pair formation between ammonium cations and the phosphate anions of lipids, Matile et al.33 prepared 8, an amphiphilic polyamine dendrimer. Rather than acting as a membrane channel, 8 was expected to form reversible membrane defects in the lipid bilayer. The steroid moiety was expected to act as the hydrophobic anchor for bilayer orientation and steric bulk was expected to prevent the polyamine penetrating the bilayer. Proton transport was assessed in unilamellar vesicles using the pH-fluorescence technique in which the external pH was increased to 7.8 relative to the internal pH at 7.4. The results demonstrated that 8 was almost as active as gramicidin, and maximal flux was achieved in ca. 20 s. 

Nitsh R., Blusztajns J. K. Pittas A. G. et al. Evidence for a membrane defect in Alzheimer disease brain. Proc. Natl. Acad. Sci USA 1992, 89 1671-1675. 

Ultrastructural changes include abnormalities in the epithelial basement membrane, defective or absent hemidesmosomes, and decreased anchoring fibrils. The condition may occur after superficial corneal trauma, in conjunction with ABMD, or may be idiopathic. 

Phillips DR, Agin PP Platelet membrane defects in Glatuanann s thrombasthenia. Evidence for decreased amounts of two major glycoproteins. J Clin Invest 60 535-545,1977. 

The insulin resistance and hyperglycemia of severe bums has been observed to persist for 1-2 weeks and has been described as pseudodiabetes. Apart from insulin antagonism of endocrine origin some cell membrane defect may be present and increased levels of the antagonist syn-albumin has been found in a significant number of patients recovering from myocardial infarction (VI). 

Sodium-lithium countertransport, anion exchange, and the leak mechanism are the most important transport routes for lithium in vivo. Lithium appears to substitute for sodium in all of these pathways in the erythrocytes (131) and also in the squid axon membrane (132). Sodium-lithium countertransport has been claimed to be abnormal in patients suffering from essential hypertension and in their close relatives (133). However, despite a decade of experimental study by many different laboratories, there is no consensus with regard to the true basis of the membrane defect, if indeed it is really present. Nor is it clear under what precise conditions the abnormality is manifest (134). 

There may be abnormalities in eiythrocyte membrane transport properties in patients with bipolar affective disorders, though the interpretation is confounded by the uncertainty with regard to the contribution of hypertension in patients who are coincidentally hypertensive and manic depressive. The administration of lithium also may cause adaptive change (93,117,135-137). This results in an increase in erythrocyte lithium concentrations after prolonged lithium therapy, which could be mediated either by increased flux into the cell or via reduction in efflux rate. An increased content of ankyrins, red cell membrane proteins affecting cytoskeletal structure and functions, has been found in some patients with bipolar affective disorder (138) and this raises further the role of erythrocyte membrane defects in the etiology of the disease. 

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