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PubMed1995

Cutaneous barrier function after cold exposure in hairless mice: a model to demonstrate how cold interferes with barrier homeostasis among workers in the fish-processing industry.

Dry skin and eczema only seldomly occur in workers in the Danish fish-processing industry (FPI) during work, when their fingers and palms have a low skin surface temperature, low transepidermal water loss (TEWL), and a high capacitance. However, shortly after work, when the skin temperature has become normal, TEWL levels increase to above normal, and capacitance decreases to below normal, followed by the development of dry skin or chapping, which subsequently revert to normal over a period of hours. These observations suggest that workers in the FPI may have a defect in skin barrier function, which is, however, masked by a low skin temperature, resulting in misleadingly low TEWL levels during work. To test this hypothesis, we disrupted the permeability barrier in hairless mice with topical acetone, and exposed the treated skin to ice for 3.5 h. Although TEWL rates immediately after cold exposure were low, suggesting normal barrier recovery, TEWL increased to levels slightly above pre-cold exposure levels (i.e. levels just after the barrier was disrupted with acetone) when the skin temperature reverted to normal (> or = 15 min). The changes in TEWL were paralleled by equivalent changes in percutaneous penetration of the electron-dense tracer lanthanum nitrate. This indicates that cold masks a defective barrier, and inhibits barrier repair. After a few hours at ambient temperatures, normal barrier recovery was observed. Electron microscopy revealed empty or partially empty lamellar bodies during the first 30 min post-cold exposure. After 1 h the majority of nascent LBs displayed normal morphology. Moreover, histochemical studies showed a delayed reappearance of stratum corneum intercellular lipids following cold exposure. These results demonstrate that cold exposure prevents barrier recovery after acetone disruption, and provide an explanation for the occupational dermatosis observed in the fish-processing industry and related occupations.

Acetone↗

PubMed1991

Sphingolipids are required for mammalian epidermal barrier function. Inhibition of sphingolipid synthesis delays barrier recovery after acute perturbation.

Stratum corneum lipids comprise an approximately equimolar mixture of sphingolipids, cholesterol, and free fatty acids, arranged as intercellular membrane bilayers that are presumed to mediate the epidermal permeability barrier. Prior studies have shown that alterations in epidermal barrier function lead to a rapid increase in cholesterol and fatty acid synthesis which parallels the early stages of the repair process. Despite an abundance of indirect evidence for their role in the barrier, the importance of sphingolipids has yet to be demonstrated directly. Whereas sphingolipid synthesis also increases during barrier repair, this response is delayed in comparison to cholesterol and fatty acid synthesis (Holleran, W.M., et al. 1991. J. Lipid Res. 32:1151-1158). To further delineate the role of sphingolipids in barrier homeostasis, we assessed the impact of inhibition of sphingolipid synthesis on epidermal barrier recovery. A single topical application of beta-chloro-L-alanine (beta-CA), an irreversible inhibitor of serine-palmitoyl transferase (SPT), applied to acetone-treated skin of hairless mice resulted in: (a) greater than 75% inhibition of SPT activity at 30 min (P less than 0.001); (b) a global decrease in sphingolipid synthesis between 1 and 3 h (P less than 0.02); (c) reduction of epidermal sphingolipid content at 18 h (P less than 0.01); (d) delayed reaccumulation of histochemical staining for sphingolipids in the stratum corneum; and (e) reduced numbers and contents of lamellar bodies in the stratum granulosum. Finally, despite its immediate, marked diminution of sphingolipid synthesis, beta-CA slowed barrier recovery only at late time points (greater than 6 h) after acetone treatment. This inhibition was overridden by coapplications of ceramides (the distal SPT product), indicating that the delay in repair was not due to non-specific toxicity. These studies demonstrate a distinctive role for epidermal sphingolipids in permeability barrier homeostasis.

Acyltransferases↗

PubMed2007

Effects of butyrate on intestinal barrier function in a Caco-2 cell monolayer model of intestinal barrier.

Production of short-chain fatty acids (SCFA) in the intestinal lumen may play an important role in the maintenance of the intestinal barrier. However, overproduction/accumulation of SCFA in the bowel may be toxic to the intestinal mucosa and has been hypothesized to play a role in the pathogenesis of neonatal necrotizing enterocolitis (NEC). By using a Caco-2 cell monolayer model of intestinal barrier, we report here that the effect of butyrate on the intestinal barrier is paradoxical. Butyrate at a low concentration (2 mM) promotes intestinal barrier function as measured by a significant increase in transepithelial electrical resistance (TER) and a significant decrease in inulin permeability. Butyrate at a high concentration (8 mM) reduces TER and increases inulin permeability significantly. Butyrate induces apoptosis and reduces the number of viable Caco-2 cells in a dose-dependent manner. Intestinal barrier function impairment induced by high concentrations of butyrate is most likely related to butyrate-induced cytotoxicity due to apoptosis. We conclude that the effect of butyrate on the intestinal barrier is paradoxical; i.e. whereas low concentrations of butyrate may be beneficial in promoting intestinal barrier function, excessive butyrate may induce severe intestinal epithelial cell apoptosis and disrupt intestinal barrier.

Apoptosis↗

PubMed1993

Microsurgery alone or with INTERCEED Absorbable Adhesion Barrier for pelvic sidewall adhesion re-formation. The INTERCEED (TC7) Adhesion Barrier Study Group II.

Adhesion re-formation after a reproductive operation, particularly involving the pelvic sidewall, is a prominent cause of failure in the surgical treatment of infertility. This study was done to evaluate the impact of standard microsurgery through laparotomy and the additional benefit of an oxidized regenerated cellulose adhesion barrier (INTERCEED [TC7] Absorbable Adhesion Barrier [Ethicon Inc.]), in reducing pelvic sidewall adhesion re-formation. One hundred and thirty-four patients with bilateral pelvic sidewall adhesions undergoing adhesiolysis by standard microsurgical techniques through laparotomy were treated during a prospective randomized trial involving 13 centers. After adhesiolysis, the deperitonealized surface of one pelvic sidewall was randomly assigned to be covered with INTERCEED Barrier, the contralateral sidewall serving as control. A second-look laparoscopy was performed ten days to 14 weeks postoperatively. Microsurgical adhesiolysis alone resulted in 24 percent of the sidewalls becoming free of adhesions and a 55.6 percent reduction in the area of adherent peritoneum. With microsurgery alone, 60 and 39 percent of adhesions initially characterized as filmy or severe, respectively, were not seen at second-look laparoscopy. The use of INTERCEED Barrier increased the incidence of adhesion-free sidewalls twofold. The treatment was also associated with a statistically significant reduction in the area of peritoneum affected by adhesion re-formation, compared with the control wall. Of the adhesions originally graded as severe, 61 percent of those treated with INTERCEED Barrier did not re-form at all. When evaluated on filmy adhesions, the use of the barrier was associated with a 72 percent reduction in adhesion re-formation. A measurable reduction in adhesion re-formation was found, depending on the initial adhesion type, with microsurgery alone. The addition of INTERCEED Barrier further reduced the incidence, extent and severity of postoperative adhesion re-formation. In this study, 90 percent of the patients benefited from the use of INTERCEED Barrier.

Cellulose, Oxidized↗

PubMed1993

A new approach to the integrity of dual blood-brain barrier functions of global ischemic rats. Barrier and carrier functions.

BACKGROUND AND PURPOSE: We studied the influence of reperfusion on carrier and barrier functions of the blood-brain barrier after transient global ischemia in rats. METHODS: We used iodine-125-labeled 3-iodo-alpha-methyl-L-tyrosine and carbon-14-labeled sucrose as tracers for studying carrier and barrier functions of the blood-brain barrier, respectively. Brain uptakes of these two tracers were measured in Wistar rats subjected to either 15- or 30-minute four-vessel occlusion developed by Pulsinelli and Brierly before recirculation for 3, 6, 24, 48, and 72 hours. Tracer (5 microCi) was injected intravenously in each rat 30 minutes before killing the animal. RESULTS: Following 15- or 30-minute ischemia, [14C]sucrose uptakes were significantly higher at 3 and 6 hours of reperfusion before recovery to control values after reperfusing for 24 to 48 hours in almost all brain regions. However, a rebound in radioligand uptake was significantly manifested in some sites at 72 hours after reperfusion (p < 0.05 to p < 0.01). Uptakes of 125I-3-iodo-alpha-methyl-L-tyrosine were brain site-dependent: significantly (p < 0.05) higher in cortex (3 and 48 hours after reperfusion) and thalamus (3, 6, and 48 hours after reperfusion) but significantly (p < 0.05 to p < 0.01) lower in striatum, cortex (72 hours after reperfusion), and midbrain (6, 24, and 72 hours after reperfusion). Because the [14C]sucrose uptake in brain was 10% lower than that of 125I-3-iodo-alpha-methyl-L-tyrosine, the change in absolute transport of the latter tracer was approximated to its brain uptake. CONCLUSIONS: The carrier and barrier functions of the blood-brain barrier should be evaluated separately. The radioligand 125I-3-iodo-alpha-methyl-L-tyrosine may serve as a useful tool to evaluate the carrier function of the blood-brain barrier after transient cerebral ischemia in rats.

Animals↗

PubMed1995

Barriers to condom use and barrier method preferences among low-income African-American women.

Low-income African-American women (N = 178) entering health clinics completed surveys assessing perceived barriers to condom use for themselves personally and for African-American women generally. Following the survey, each woman received a demonstration of five barrier contraceptive methods and then rated her preference among those methods. The women perceived relatively few personal barriers to use of the male condom but perceived significantly greater barriers for other African-American women (all p < .0001). The male condom was first choice of the largest percentage of women (45%) and last choice of the smallest percentage of women (11%). The male condom was preferred for its convenience, availability, and safety, although the necessity for active cooperation by the male partner was considered a hindrance to using the method. Only 23% of women ranked the female condom as first choice and 35% ranked the female condom as last choice. Reasons for selecting the female condom included preference for a female-controlled method, safety, and protection. However, the female condom was perceived to be uncomfortable, to require the partner's acquiescence, and to interfere with sexual experience. Differences in the women's perceptions of barriers to condom use for themselves and for other African-American women are consistent with Weinstein's theory of optimistic bias. Preferences among barrier methods indicate that further research and product development are needed to develop barrier methods that are female-controlled, do not require the awareness of the male partner, and are safe, comfortable, and convenient.

Adolescent↗

PubMed2006

Drug permeability across a phospholipid vesicle based barrier: 3. Characterization of drug-membrane interactions and the effect of agitation on the barrier integrity and on the permeability.

Recently, we reported on the development and structural characterization of a phospholipid vesicle based barrier useful for medium throughput screening of passive drug permeability. Here, we investigate the physical and functional integrity of the phospholipid vesicle based barriers to agitation by stirring or shaking, and whether agitation affects drug permeability of sulpiride, metoprolol and testosterone. In addition, three drugs (caffeine, naproxen and sulphasalazine) which were shown in a previous study to affect the electrical resistance of the barriers, were investigated for their influence on the permeability of a simultaneously applied hydrophilic marker (calcein), and on the thermotropic phase transition of the phospholipid bilayers using differential scanning calorimetry (DSC). Electrical resistance measurements indicated that the barriers should withstand shaking speeds up to 150rpm without losing their integrity, but significant release of phospholipids from the membrane barriers to the donor and acceptor chambers was observed under agitation >or=150rpm. When using agitation up to 100rpm no increase in permeability was observed for sulpiride, metoprolol and testosterone. The phospholipid vesicle-based barrier thus differ from other permeability models in that agitation does not lead to an increase in permeability, not even for highly lipophilic drugs such as testosterone. This is explained by the different morphology of the vesicle-based barrier which is containing a 100microm thick layer of mostly aqueous compartments immobilised within a matrix of phospholipids vesicles. Sulphasalazine and naproxen were shown to decrease the electrical resistance and increase the permeability of the hydrophilic marker calcein. The DSC experiments showed that these two drugs probably interact with the head groups of the phospholipids. In contrast, caffeine gave an increase in electrical resistance and a decrease in permeability of calcein. From the DSC experiments no signs of interaction of caffeine with the phospholipid bilayer could be observed.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2002

Negative electric potential induces alteration of ion gradient and lamellar body secretion in the epidermis, and accelerates skin barrier recovery after barrier disruption.

Previous reports suggested that ion gradients of ions such as calcium and magnesium in the epidermis play a crucial part in skin barrier homeostasis. We hypothesized that external electric potential affects the ionic gradient and skin barrier homeostasis. We demonstrated here that application of a negative electric potential (0.50 V) on hairless mice skin accelerated the barrier recovery approximately 60.7% of the original level within 1 h compared with control (37.5%) after barrier disruption by acetone treatment. Even after the application of a negative potential, the skin showed accelerated repair for 6 h. On the contrary, the skin that was applied a positive potential for 1 h showed a significant delay in barrier recovery (25.3%) than the control. Ultrastructural studies by electron microscopy suggested that the extent of lamellar body exocytosis into the stratum corneum/stratum granulosum interface increased under a negative potential. Magnesium and calcium ion concentrations in the upper epidermis were relatively higher in the negative portion than in the portion where the positive potential was applied. Topical application of these ions on mice skin also accelerated the barrier recovery. These results suggest that the external electric potential affects the ionic gradients in the epidermis and also influences the skin barrier homeostasis.

Acetone↗

PubMed2002

P2X purinergic receptor antagonist accelerates skin barrier repair and prevents epidermal hyperplasia induced by skin barrier disruption.

The effects of ATP receptor agonists/antagonists on skin barrier recovery rate were evaluated in hairless mice. Topical application of ATP and alpha,beta-methylene ATP (agonist of P2X receptor) delayed barrier recovery. Topical application of suramin (nonspecific ATP receptor antagonist), pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) (P2X receptor antagonist), and 2',3'-O-(2,4,6-trinitrophenyl)adenosine 5'-triphosphate (TNP-ATP) (P2X1, P2X3, P2X2/3 antagonist) after barrier disruption accelerated the barrier repair. The P2Y type receptor antagonist Reactive Blue 2 did not affect the barrier repair process. Moreover, topical application of TNP-ATP prevented epidermal hyperplasia induced by barrier insult under low environmental humidity. ATP was secreted immediately after tape stripping on skin in organ culture. alpha,beta-Methylene ATP increased intercellular calcium in cultured keratinocytes and the increase was blocked by TNP-ATP. Both reverse transcription polymerase chain reaction assay and immunohistochemical study showed the existence of protein that had a structure similar to P2X3 on hairless mouse epidermis. These results suggest that cutaneous barrier homeostasis can be regulated by cation flux through a P2X3-like ATP receptor.

Adenosine Triphosphate↗

PubMed1980

The permeability barrier in essential fatty acid deficiency: evidence for a direct role for linoleic acid in barrier function.

Essential fatty acid (EFA) deficient rodents demonstrate abnormal epidermal permeability barrier function and differentiation, defects which can be corrected by either topical or systemic administration of linoleic acid. Since linoleic acid is a precursor of prostaglandins, correction of the defect in barrier function may either reflect a prostaglandin-mediated return toward normal epidermal differentiation, or, instead, a direct effect of linoleic acid. To test these possibilities severely EFA-deficient mice were pretreated daily with indomethacin and/or 5,8,11,14-eicosatetrayeonic acid, and then placed on normal (lineolic acid-supplemented) diets. Endogenous formation of prostaglandin E2 was determined by thin-layer chromatography after transformation into prostaglandin B2 with ethanolic-hydrochloric acid. Animals treated with both indomethacin and TYA DEMONSTRATED SUBSTANTIAL REDUCTIONS IN PROSTAGLANDIN E2 levels in liver and skin. Animals replenished with linoleic acid invariably demonstrated a rapid return of barrier function toward normal whether or not they were blockaded, while nonreplenished animals, with or without inhibition of prostaglandin biosynthesis, demonstrated continued deterioration in barrier function. In other experiments, topically applied linoleic acid rapidly reversed the defect in barrier function at the sites of application prior to systemic correction of the EFA deficient state. These results suggest that: (1) defective cutaneous barrier function in EFA deficiency can be corrected locally without prior systemic reversal of the deficiency state; and (2) that linoleic acid may play a direct role in the epidermal permeability barrier independent of its role in prostaglandin metabolism.

Animals↗

PubMed2005

Dopamine D2-like receptor agonists accelerate barrier repair and inhibit the epidermal hyperplasia induced by barrier disruption.

Two families of G protein-coupled receptors of the neurotransmitter dopamine, i.e., dopamine 1-like family (D1-like receptor) and dopamine 2-like family (D2-like receptor), show dopaminergic activity in nerve cells. The D2-like receptor family, composed of D2, D3, and D4 receptors, downregulates the intracellular cAMP signaling pathway, and dopamine receptor agonists reduce the cAMP level in neurons. We previously demonstrated that the cAMP level in epidermal keratinocytes is related to epidermal barrier homeostasis. Since keratinocytes are known to carry various neurotransmitter receptors, we hypothesized that D2-like receptors on keratinocytes might be related to skin barrier homeostasis. In this study, we examined the effect of topical application of receptor agonists and antagonists on skin barrier recovery after barrier disruption. Application of D2-like receptor agonists accelerated barrier recovery, whereas D2-like receptor antagonists delayed it. D2-like receptor agonists also reduced the epidermal hyperplasia induced by barrier disruption under low environmental humidity. Immunohistochemical study and RT-PCR analysis revealed the expression of the D2 receptor in the basal epidermis and the D4 receptor in the uppermost layer of the epidermis. These results suggest that dopaminergic receptors are involved in epidermal barrier homeostasis.

Animals↗

PubMed2002

Postnatal ecdysis establishes the permeability barrier in snake skin: new insights into barrier lipid structures.

A competent barrier to transepidermal water loss (TEWL) is essential for terrestrial life. In various vertebrates, epidermal water barriers composed of lipids prevent excessive TEWL, which varies inversely with habitat aridity. Little is known, however, about the mechanisms and regulation of permeability relative to natal transition from the 'aqueous' environments of gestation to the 'aerial' environments of terrestrial neonates. We investigated newly hatched California king snakes Lampropeltis getula to test the hypothesis that the first ecdysis is important for establishing the barrier to TEWL. We found that skin resistance to TEWL increases twofold following the first postnatal ecdysis, corresponding with a roughly twofold increase in thickness and deposition of lamellar lipids in the mesos layer, the site of the skin permeability barrier in snakes. In addition, novel observations on lipid inclusions within the alpha layer of epidermis suggest that this layer has functional similarities with avian epidermis. It appears that emergence of the integument from embryonic fluids, and its subsequent pan-body replacement following contact with air, are essential for completion of barrier competence in the newborn. These conditions provide a potentially useful model for investigations on the mechanism of barrier formation. We also found that hatchling snakes are transiently endothermic, with skin temperatures elevated by approximately 0.6 degrees C above ambient air temperature during the period of barrier formation. Behaviourally, hatchlings showed a higher tendency to seek humid microenvironments before the first ecdysis than after. The degree of water movement across the integument might explain the switch from reclusive to dispersive behaviours associated with postnatal ecdysis in snakes.

Aging↗

PubMed2005

Cultured podocytes establish a size-selective barrier regulated by specific signaling pathways and demonstrate synchronized barrier assembly in a calcium switch model of junction formation.

Podocytes form unique cell-cell junctions (slit diaphragms) that are central to glomerular selectivity, although regulation and mechanisms of slit diaphragm assembly are poorly understood. With the use of cultured podocytes, a paracellular permeability flux assay was established to characterize properties of the size-selective barrier. Paracellular flux of differentiated podocytes was measured using anionic fluorescent dextrans of 3, 10, 40, and 70 kD. Podocytes form a highly selective barrier with a 160-fold difference in flux from the 3-kD dextran (11 pmol/min) to the 70-kD dextran (0.06 pmol/min). Barrier development was dependent on podocyte differentiation and not affected by dextran charge. Puromycin, a known podocyte toxin, increased flux 250% in a dose-dependent manner without affecting cell viability. Screening with modulators of specific signaling pathways identified reversible increases in flux with Src tyrosine and Rho kinase inhibition. The calcium switch model of epithelial junction assembly was modified to determine whether podocytes regulate barrier assembly. When cultured in low calcium for 90 min, flux increased by 300% and consistently returned to baseline 24 to 48 h after switching to normal calcium. Similar to classical epithelial junctions, barrier recovery occurred in the presence of cyclohexamide, an inhibitor of protein synthesis. During the calcium switch, there were reversible changes in localization and detergent solubility of the slit diaphragm protein ZO-1 and alpha-actinin-4, whereas nephrin and podocin solubility were unchanged. Taken together, these findings demonstrate that cultured podocytes develop a selective size barrier that is regulated by specific signaling pathways, and similar to classical epithelial junctions, podocytes demonstrate synchronized assembly of the barrier.

Animals↗

PubMed1998

Clinical comparison of bioabsorbable barriers with non-resorbable barriers in guided tissue regeneration in the treatment of human intrabony defects.

The purpose of the study was to compare the effects of guided tissue regeneration (GTR) with expanded polytetrafluoroethylene (ePTFE) non-resorbable barriers and polylactic acid bioabsorbable barriers in humans with intrabony defects due to periodontitis. Ten patients presented with 2 intrabony defects each. Mucoperiosteal flaps were performed. One of the defects was randomly assigned for placement of the ePTFE barrier over the roots and alveolar bone and the other defect with placement of the polylactic acid barrier. A minimum of 9 months after barrier placement, surgical reentry was performed. The data were evaluated by the Wilcoxon matched-pairs signed-ranks test and the Fisher exact test. Treatment with both types of barriers produced significant changes from baseline for all parameters, except in the ePTFE group for the amount of bony crest resorption (P = 0.055) and in the polylactic acid group for increased recession (P = 0.109). The results showed no significant differences between the barriers for any parameters: probing depth reduction (polylactic acid 2.60 +/- 1.90, ePTFE 2.80 +/- 1.40; P = 1.000); attachment gain (polylactic acid 1.40 +/- 1.43, ePTFE 1.90 +/- 1.29; P = 0.336); increased recession (polylactic acid 0.80 +/- 1.40, ePTFE 1.10 +/- 0.99; P = 0.531); amount of vertical bone fill (polylactic acid 1.60 +/- 1.84, ePTFE 2.00 +/- 2.49; P = 0.984); bony crest resorption (polylactic acid -1.30 +/- 1.06, ePTFE -1.30 +/- 1.63; P = 1.000); depth of bony defect reduction (polylactic acid 2.90 +/- 1.20, ePTFE 3.30 +/- 1.70; P = 0.750); width of bony defect reduction (polylactic acid 2.20 +/- 1.23, ePTFE 2.20 +/- 1.23; P = 0.875); or volumetric changes (polylactic acid 33.50 +/- 19.70 microl, ePTFE 34.00 +/- 18.40 microl; P = 0.750).

Absorption↗

PubMed2006

Pertussis toxin transiently affects barrier integrity, organelle organization and transmigration of monocytes in a human brain microvascular endothelial cell barrier model.

Encephalopathies and neurological disorders are sometimes associated with respiratory tract infections caused by Bordetella pertussis. For these complications to occur cerebral barriers have to be compromised. Therefore, the influence of pertussis toxin (PT), a decisive virulence determinant of B. pertussis, on endothelial barrier integrity was investigated. Human brain microvascular endothelial cells cultured on Transwell filter devices were used as model for the blood brain barrier. PT, but not its B-oligomer, induced a reduction of the transendothelial resistance and enhanced the permeability for the protein marker horseradish peroxidase. Moreover, transmigration of human monocytes was also elevated suggesting a PT-associated enhancement of the diapedesis of blood leucocytes. Uptake and trafficking of PT was followed by electron microscopy via clathrin-coated pits and accumulation in lysosomes and microvesicular bodies. The breach in barrier integrity was accompanied by a transient disintegration of Golgi structures. Interestingly, PT-induced effects were only transient and restoration of barrier function was observed after 24 h. In summary, intoxication by PT causes a transient destruction of the cellular organization in human brain-derived endothelial cells resulting in a transient disruption of barrier functions. We suggest that these findings reflect early steps in the development of neurological disorders associated with pertussis disease.

Blood-Brain Barrier↗

PubMedDate not supplied

[Brain barriers. Part I. Blood-brain tissue barrier].

Brain barriers are morphological and functional structures responsible for selective transport of different biological substances between blood and brain. There are three kinds of brain barriers: blood/brain tissue barrier, blood/brain fluid barrier and brain fluid/brain tissue barrier. The blood/brain tissue barrier which consists of brain vascular epithelial cells is thought to play the main role in intracranial homeostasis.

Blood-Brain Barrier↗

PubMed1984

Ultrastructural and histophysiological studies on the blood-nerve barrier and perineurial barrier in leprosy neuropathy.

Onset and nature of ultrastructural changes in endoneurial vasa nervorum during the pathogenesis of leprosy neuropathy and possibly associated alterations in the "blood-nerve barrier" were investigated, together with perineurial barrier functioning, in mice infected 20-28 months previously with Mycobacterium leprae and in (ageing) non-infected mice. Barriers were tested by i.v. administration of markers (Trypan blue and ferritin) 1-4 days before killing the mice. Twenty-eight months after infection, histopathology of sciatic nerves was comparable to that seen in sensory nerves in clinically early human (borderline-) lepromatous leprosy. Schwann cells and endoneurial macrophages were bacillated, endothelia of endoneurial vessels not, and the perineurium rarely. Many infected mice and all (ageing) controls possessed ultrastructurally and functionally normal endoneurial vessels. Their continuous endothelium with close junctions had prevented marker passage, even when surrounding endoneurial tissue cells were quite heavily bacillated. The perineurium was also normal. By contrast, in infected mice showing hind limb paralysis serious histopathologic involvement and large globi of bacilli intrafascicularly in sciatic nerves, endoneurial blood vessels were abnormal. Open endothelial junctions, extreme attenuation, fenestrations, and luminal protrusions were all features comparable to neural microangiopathy encountered in leprosy patients (Boddingius 1977a, b). The "blood-nerve barrier" clearly had become defective allowing excessive exudation of Trypan blue and ferritin, via four pathways from the vessel lumen, deep into surrounding endoneurial tissues but halted by a normal perineurial barrier. Markers in such "blue" nerves were not found in bacillated or non-bacillated Schwann cells, thus denying significant phagocytotic and lysosomal activities of Schwann cells at this stage of neuropathy. Possible implications of barrier performances for anti-leprosy drug treatment of patients are discussed.

Age Factors↗

PubMed2001

Barriers to rotation in methyl formate by dynamic NMR spectroscopy and barriers to 1,3 oxygen-to-oxygen migration in methyl formate and trifluoromethyl formate by ab initio calculations.

Free-energy barriers of 9.85 and 11.91 +/- 0.15 kcal/mol at -70.8 degrees C were found by dynamic NMR spectroscopy for the E-to-Z and Z-to-E conversions, respectively, of methyl formate (1) enriched in 13C to 99% for the carbonyl carbon [methyl formate 13C (2)]. These barriers are higher than the literature values reported for -53 degrees C. The free-energy barrier to 1,3 oxygen-to-oxygen migration of the methyl group in methyl formate was determined by ab initio calculations at several levels. The value of 58.7 kcal/mol obtained at the MP2/6-311+G (df,pd) level was compared to a literature barrier for this process (MINDO/3) and to barriers for related compounds. A free-energy barrier of 63.0 kcal/mol for the oxygen - to - oxygen migration of the CF3 group in trifluoromethyl formate (3) was calculated at the MP2/6-31+G level.

Carbon Isotopes↗