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Using a special selection technique, normal guinea-pig melanocytes were maintained in highly purified but sparse cultures (∼104 cells/25 cm2 culture vessel) which showed little proliferative activity. The applicability of the Pomerantz tyrosinase assay was tested in this in vitro model system using three different approaches, namely crude cell extracts and viable cell cultures either in situ or in suspension. The latter modifications both proved too insensitive, whereas crude cell extracts allowed accurate measurements of the basal tyrosinase activity and its stimulation by various agents. In unstimulated cultures basal tyrosinase activities ranged from 30% to 700% (mean 260%) above the blank values; intra-assay and inter-assay variability were 4.2% and 77.5%, respectively. Stimulation with α-MSH (10-5 M, 10-6 M), β-MSH (10-5 M), choleratoxin(10-11 M)and cAMP(10-4 M) plus theophylline (10-4 M) resulted in an increase of tyrosinase activity 30-65%, above basal values. Melanotropin potentiating factor (10-8 M) enhanced the effects of α-MSH (10-6 M) by 20%. This assay modification provides a sensitive tool for comparative studies of melanogenesis in normal melanocytes, malignant melanocytes and otherwise altered melanocytes. [ABSTRACT FROM AUTHOR]

Biopsy specimens from 185 patients with 52 different skin disorders were investigated by indirect immunofluorescence staining for the presence of HLA-DR bearing keratinocytes and their association with an underlying inflammatory infiltrate mid in particular with activated (HLA-DR-positive, Leu-4-positive) T lymphocytes. HLA-DR expression on keratinocytes was demonstrated in 38 dermatoses, including lymphocytic vasculitis, lupus erythematosus, morphea, viriligo, Iichen planus, cutaneous T-cell lymphoma, various infectious dermatoses, allergic contact dermatitis, granulomatous dermatoses, Sweet's syndrome, lichen sclerosus and erythema nodosum. In 27 of these this had not previously been reported. Occurrence of HLA- DR on keratinocytes was invariably linked to the presence of a lymphocytic infiltrate containing numerous activated T-cells (Leu-4 +, HLA-DR+) whereas such infiltrates were not accompa- nied by HLA-DR expression on keratinocytes in all the dermatoses investigated, as in pseudolymphoma and erythema anulare centrifugum. However, HLA-DR positive keratinocytes were consistently absent m skin disorders lacking any significant lymphocytic infiltration (e.g. leukocytoclastic vasculitis, bullous autoimmune dermatoses, genodermatoses and mastocytosis). Although it has been suggested that HLA-DR-positive keratinocytes are involved in various immune responses of the skin, their exact functional significance is, as yet, unknown. [ABSTRACT FROM AUTHOR]

Cytotoxic T-cell lines (TCL) were raised m vitro using stimulator cells with a defined major histocompatibility complex (MHC) mismatch and tested in a cytotoxic chromium-release assay against haemopoietic and non-haemopoietic target cells from the original stimulator. Monoclonal antibody (mAb)-blocking experiments and simultaneous determination of MHC class I, class II, lymphocyte function-associated antigen-1 (LFA-1) and intracellular adhesion molecule-1 (ICAM-1) density by quantitative radioimmunometric methods and flow cytometry on target cells demonstrated that lysis was restricted by MHC class I and dependent upon the constitutive MHC class I antigen expression. Measurements showed a high constitutive expression of class I MHC antigens on peripheral blood mononuclear cells (PBMC), but a low one on keratinocytes (K). Also. PBMC were more susceptible to lysis by TCL than K, interferon-γ (IFN-γ) treatment of K resulted in increased MHC class I antigen expression and enhanced lyric susceptibility to TCL. IFN-α and tumour necrosis factor-α (TNF-α) treatment, which did not modulate MHC class I antigen expression on K, did not influence the amount of K lysis either. None of the cytokines tested in this analysis, however, increased the expression of MHC class I, class II, ICAM-1 and LFA-1 on PBMC. Only IFN-γ pretreatment showed a minimal, statistically significant increase in MHC class I antigen expression. In spite of the minimal effect of IFN-γ and no effect of IFN-α on class I MHC expression, pretreatment of target cells with both cytokines considerably increased their lyric susceptibility. The mechanism of cytokine-induced enhanced lyric susceptibility to TCL was not explained by increased MHC class I, LFA-1 or ICAM-1 expression, since no correlation was found between surface expression of these molecules and lytic susceptibility to TCL. These data demonstrate that: (I) the constitutive density of MHC class I antigens determines the extent of TCL lysis; (2) IFN-γ, and not IFN-α or TNF-α, controls the amount of K target cell lysis by increasing their MHC class I antigen expression; and (3) IFN-γ and IFN-α control the amount of PBMC target cell lysis by a mechanism independent of MHC class I, 1CAM-I or LFA-1 expression. [ABSTRACT FROM AUTHOR]

Background: The literature reports an increased incidence of thyroid disorders in human immunodeficiency virus (HIV)-positive persons. We therefore retrospectively analyzed the strategy of collecting thyroid parameters on a routine basis., Methods: Overall 410 patients (147 women, 263 men; age, 10-74 years; median age, 45 years) were included. For screening purposes, three parameters were determined; basal thyroid-stimulating hormone (TSH), free thyroxine (fT4), and free triiodothyronine (fT3). Descriptive and statistical analyses were performed in the patient groups with increased bTSH (> 4.0 µU/ml) and with decreased fT4 (< 8.9 pg/ml) to evaluate possible correlation with age, gender, duration of antiretroviral therapy (ART), substance classes of ART (nucleosidal reverse transcriptase inhibitors (NRTIs), nonnucleosidal reverse transcriptase inhibitors, and protease inhibitors (PIs)), Centers for Disease Control and Prevention (CDC) disease stage, lowest number of CD4 cells during course of disease, and coexistent hepatitis C., Results: Elevated bTSH was found in 27 patients (median, 5.26 µU/ml), who also showed a correlation with ART duration and NRTI use. Decreased fT4 was seen in 53 persons, and a correlation with PI intake was observed. Of these patients, 31 exhibited normalization in follow-up. Decreased fT3 was observed in eight cases related to nonthyroid illness, and fT3 was elevated in ten patients. No overt hyperthyroidism was noticed; three cases of subclinical hyperthyroidism were transient., Conclusions: In the examined group of patients, the prevalence of abnormal thyroidal parameters was 23 %. Decreased fT4, which does not require therapy, was observed most frequently (12 %) and correlated with PI use. On the other hand, elevated bTSH (6 %) correlated with ART duration and NRTI use. In mild subclinical hypothyroidism as observed in this patient population, thyroxine medication is not indicated in principle. Annual TSH screening is probably sufficient in HIV-infected patients with no clinical symptoms suggestive for thyroid disease.

Porcine ear skin is frequently used as a substitute for human skin in dermatological research and is especially useful for tape stripping experiments where the penetration of active substances into the uppermost skin layers is investigated. However, certain differences between the surface properties of these skin types exist, and reports on the comparability of tape stripping data obtained in vitro using porcine ear skin and data obtained in vivo on human forearm skin are scarce. Thus, we performed comparative tape stripping experiments in which the skin penetration of curcumin and fluorescein sodium from conventional microemulsions and hydrogels was investigated. In this context, the skin penetration potential of novel semi-solid macroemulsions and fluid nanoemulsions based on sucrose stearate was evaluated as well. The removed corneocytes were quantified by NIR-densitometry using recent correlation data for human and porcine proteins. The trends observed for the skin penetration into porcine ear skin were highly representative for the in vivo situation on human skin, confirming that the porcine ear is an excellent in vitro model for tape stripping experiments. Moreover, the validity of the NIR-densitometric approach for the quantification of both human and porcine stratum corneum proteins was confirmed in this study for the first time., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Vitiligo is a disorder of pigmentation associated with an autoimmune-mediated loss of melanocytes from the epidermis. Humoral immunity and the involvement of cellular immunity have been investigated in the pathogenesis of vitiligo. We evaluated the role of pro-inflammatory cytokines and lymphocyte fractions in peripheral blood in a cohort of Austrian patients with vitiligo. Morning blood samples from 40 patients with vitiligo were collected. Twenty-one patients had active and 19 had stable vitiligo disease. All patients were suffering from non-segmental vitiligo at different stages of the disease. Sixteen persons presented with an additional autoimmune thyroid disease. To evaluate a possible involvement of proinflammatory cytokines in vitiligo we measured sTNF-RI (soluble tumour necrosis factor receptor I), IL-6 and additionally CIC (circulating immune complexes). We compared these findings to the data from matched normal persons. To investigate the mechanisms of cellular immunity, peripheral blood cell count and lymphocyte subtype analysis by flow cytometry were done. sTNF-RI, IL-6 and CIC serum levels were in the normal range. In the patient group median sTNF-RI level was 1.5 ng/ml and median CIC level was 35.2 microg/ml, and no statistically significant differences to the control group were observed. Median IL-6 level in vitiligo patients was 2.7 pg/ml and in the normal range-but higher than the median level of 0.5 pg/ml observed in normal persons (p < 0.001). Absolute and relative counts of lymphocyte subtypes were normal. The ratio of CD4+/CD8+ T-cells had an elevated median value of 2.6 [quartiles 2.0; 3.1]. 61% of the vitiligo patients had a ratio higher than 2.4, which was the normal cut-off point. In most vitiligo patients the balance of cytotoxic/suppressor and helper/inducer T-cells in peripheral blood is disturbed which might lead to a predominance of T-cell subtypes in the intracutaneous site of autoimmune melanocyte loss.

Vitiligo is a depigmenting disorder characterized by the development of white patches with evidence in favour of an autoimmune mechanism. We investigated the role of melanotropins and the plasma levels of alpha-melanotropin and ACTH-like immunoreactivities in 40 vitiligo patients with the aim of detecting a possible influence of neuropeptide regulation of immunity. Twenty-one patients had active and 19 had stable vitiligo disease, 16 persons presented with an additional autoimmune thyroid disease. Median alpha-MSH levels in vitiligo patients were 6.4p mol/l [5.2;11.3] and significantly lower than in control persons with 11.4 pmol/l [8.6;13.4]. Median ACTH levels of the affected patient group were 17 pg/ml [10.5;28] and appeared statistically higher than 12 pg/ml [7;17] measured in the control group. Measured morning cortisol levels in both groups were not significantly different. Reduced cutaneous alpha-MSH immunoreactivities have been related to the development of autoimmune-induced depigmenting disorders. Our data present lower alpha-MSH plasma levels in vitiligo patients which may be associated with the development of vitiligo depigmentation and may indicate a condition of impaired peripheral tolerance in this autoimmune disorder.

A 56 year old man presented with ichthyosis vulgaris since early childhood, clinically characterised by fine scaling of the trunk and hyperkeratotic scales on the exterior surfaces of the upper and lower extremities. The patient also showed hypothyroidism due to hypoplastic thyroid, cataract, hypercholesterinemia with concommitant arcus cornealis and biliary concrements. Renal lithiasis caused by calcio-oxalate was additionally present. Endocrinological screening revealed growth hormone deficiency in the 1.55 m tall man-(secondary) osteoporosis was observed. The clinical symptomatology indicates that this case cannot be considered as a subtype of the inherited ichthyosis group, but suggests a new syndrome as a separate nosologic entity.

Melanotropins (MSH) are involved in tanning by stimulating melanocytes via the activation of the melanocortin-1 receptor to melanin production. Its main site of production is the pituitary gland, but alpha-MSH and related ACTH peptides are produced at other sites, including the skin. It has been hypothesized that systemic levels of alpha-MSH are controlled by a varying UV radiation (UVR) exposure. A seasonal rhythm of plasma levels has been proposed by some authors. We investigated healthy females in southern Spain and central Austria in summer and winter. The alpha-MSH and ACTH-like immunoreactivity plasma levels did not present marked differences between the groups of Malaga and Linz, dark and light skin and between seasons. An association of alpha-MSH to ACTH or cortisol levels could not be observed. Individual values of alpha-MSH were shown to be relatively constant at both times of measurement (p<0.05 by rank correlation) indicating an independent personal disposition for individual systemic alpha-MSH immunoreactivity levels. Our data do not support the concept of a marked involvement of melanotropins of pituitary origin in tanning, and no seasonal rhythm was observed.

The primary step of local ulcer therapy consists in debridement. Cleaning the ulcers from necrotic tissue can be achieved by surgical, mechanical, osmotic, autolytic and enzymatic means. The introduction of (semi-)occlusive wound dressings for moist wound healing has significantly improved ulcer treatment, since critical steps of wound healing, such as fibroblast proliferation, angiogenesis and epithelialisation are markedly accelerated. In contrast, topical antimicrobial therapy and traditional local treatment with "wound ointments" are of diminishing value because of frequent side effects such as inhibition of granulation tissue or allergic sensitization.

Peripheral blood mononuclear cells (PBMC) from 17 patients receiving HLA-identical sibling bone marrow grafts were stimulated with host pretransplant PBMC. Cytotoxic T-cell lines (TCL) with specificity for host pretransplant PBMC were obtained from 9 of these patients, all presenting with severe graft-versus-host disease (GVHD), but from none of the remaining cases lacking evidence of disease. Cytotoxic TCL were specific for host targets and failed to lyse donor cells. Monoclonal antibodies (MoAbs) blocking experiments and donor population screening analyses demonstrated that minor histocompatibility antigen (MiHA)-specific lysis of host targets was restricted by class I major histocompatibility complex (MHC) determinants. Whereas hematopoietic cells such as phytohemagglutinin (PHA) blasts or lymphoblastoid cell lines were susceptible to lysis by MiHA-specific TCL, keratinocytes (K) representing the natural targets of GVHD were quite resistant. Quantitative radioimmunometric measurements indicated very low constitutive expression of class I MHC antigens on K targets, which was readily increased by treatment with interferon-gamma (IFN-gamma). IFN-gamma treatment at the same time rendered these cells susceptible to lysis by MiHA-specific TCL. Host leukemic cells of 3 patients were recognized by MiHA-specific TCL in a chromium release assay and in one experiment host leukemic cells were effectively killed and their growth specifically inhibited in a leukemia colony assay by a clone. These data demonstrate that (1) host-specific cytotoxic TCL are detected exclusively in the PB of patients with acute GVHD grades II through IV after allogeneic matched bone marrow transplantation, and (2) their target antigens are simultaneously expressed on several host cell lines, including lymphoblastoid cell lines, PHA blasts, leukemic cells, and K. We also extend previous findings by showing that, besides the expression of the nominal MiHA, the density of the restricting class I MHC elements also crucially determines the extent of TCL lysis. Because of its capacity to enhance class I MHC antigen expression, IFN-gamma represents a key cytokine for determining the susceptibility of MiHA targets for lysis by TCL and clones, and in one patient an MiHA-specific clone recognized host leukemic cells and also inhibited host leukemic cell growth in a colony inhibition assay.

A patient had acquired perforating dermatosis and suffered from renal disease, diabetes mellitus, and lupus vulgaris. Histologic and immunohistochemical studies revealed that the bulk of the coarse granular basophilic material being extruded by transepidermal elimination was of nuclear origin obviously derived from polymorphonuclear leukocytes that were particularly abundant in an early, nonperforated lesion. At the lower boundary of the material being eliminated transepidermally, leukocytes were seen to accumulate, to undergo pyknosis and karyorrhexis, and to transform into nuclear debris. As a minor component, the material contained collagen fibers with altered staining qualities and, in an early lesion, elastic fibers. We speculate that accumulation, disintegration, and enzyme release from polymorphonuclear leukocytes may represent an important, hitherto disregarded driving force in transepidermal elimination. Lysosomal enzymes may later be responsible for the alteration of staining properties in collagen fibers, the degradation of elastic fibers, and for opening up the transepidermal route by impairing intercellular keratinocyte cohesion.

Dermal keratin bodies, consisting mainly of keratin intermediate filament aggregates (KIFA) coated with IgM anti-KIF autoantibodies, are present in normal human skin and occur in increased quantities in certain skin diseases. Keratin bodies are normally rapidly removed, but in primary localized cutaneous amyloidosis (PLCA) they are converted by an unknown mechanism to amyloid. Amyloid P component (AP), a glycoprotein identical to, and derived from, the normal plasma protein serum amyloid P component (SAP), is present in all forms of amyloid including PLCA. We investigated the interaction between SAP, keratin bodies, and KIFA. Immunofluorescence staining of normal skin using fluoresceinated anti-SAP and rhodamine-conjugated anti-IgM, or AE-1/AE-3 anti-keratin antibodies followed by Texas Red-conjugated anti-mouse immunoglobulin, showed that 52% +/- 4 (mean +/- sem, n = 6) of keratin bodies bound anti-SAP. Similar findings were present in a biopsy from a patient with lichen planus. Isolated KIFA, prepared by 8M urea extraction of normal human epidermis or cultured keratinocytes, were preincubated with normal human serum as a source of SAP and then stained with fluoresceinated anti-SAP. Bright fluorescence seen when the incubation medium contained Ca++ was absent in the presence of ethylenediamine tetraacetic acid. Specific Ca++-dependent binding of SAP to KIFA was confirmed using immunoblotting. Binding of SAP to KIFA did not prevent their degradation following exposure to trypsin or alpha-chymotrypsin. Similarly, partial enzymatic digestion of KIFA did not abrogate their ability to bind SAP. Our findings, that SAP is associated with keratin bodies in skin and exhibits Ca++-dependent binding to KIFA in vitro, identify keratin filaments as a newly recognized ligand for SAP.

Autologous cultured epidermis (CE) grown from small skin biopsies in vitro has been successfully applied for wound grafting in humans. Since it has been reported recently that allogeneic CE might be tolerated as permanent wound cover, we investigated the properties of CE and its use as autologous and allogeneic grafts. Except for some differences, such as the absence of Langerhans cells and the lack of a stratum corneum, CE resembled its natural analogue. Autologous CE applied for grafting of leg ulcers and various surgical skin defects adhered firmly and permanently to the wound bed within 2 weeks, became regularly stratified, and formed a stratum corneum. Langerhans cells gradually entered the grafts; the dermis contained no inflammatory infiltrate. Allogeneic CE unmatched for MHC and blood group antigens used to partially cover tangentially excised third-degree burns, donor sites of split-thickness skin, and a defect after tumor excision initially survived well like the autografts. However, they were completely rejected after 10-22 (mean, 14.5) days, which is 4-5 days later than reported for split-thickness skin allografts. Clinically, rejection presented as "melting" of the graft. (Immuno)histologically, we found a dense mononuclear dermal infiltrate consisting predominantly of activated T cells, vacuolization, and single-cell necrosis of keratinocytes, as well as HLA-DR expression on keratinocytes, and finally separation and lysis of the epidermis. Limiting dilution analysis in 2 out of 4 allograft recipients revealed a considerable increase of circulating donor-specific cytotoxic T cell precursors during graft rejection. We conclude that grafting of allogeneic CE does not lead to permanent but to slightly prolonged graft survival.

Parallel fluctuations of potential difference (P.D.) across oral and rectal mucosa are probably related to the activity of autonomic nerves rather than adrenal steroids. Unlike rectal mucosa, oral mucosa does not respond to exogenous or endogenous aldosterone. Therefore subtraction of oral P.D. from rectal P.D. gives a closer indication of mineralocorticoid activity than does rectal P.D. alone. In normal subjects plasma-aldosterone correlated well with subtraction P.D. (r = 0.74; P is less than 0.001). A subtraction P.D. higher than 26 mV in subjects on a normal sodium intake indicated primary or secondary hyperaldosteronism; if the level was lower than 11 mV four hours after intramuscular injection of 0.25 mg tetracosactrin this suggested mineralocorticoid deficiency. Measurement of oral and rectal P.D. permits rapid and inexpensive diagnosis of aldosterone excess and deficiency. The method may also be used in study of the mineralocorticoid effect of other adrenal steroids: as assessed with this bioassay, the plasma 18-OH-deoxycorticosterone, which is raised in some patients with essential hypertension, lacked any in vivo mineralocorticoid activity.

We describe the progression of bleomycin-induced inflammatory lesions to linear hyperpigmentations in 2 patients. Striking, hitherto unreported observations were the development of streaking after a single dose of 5 mg bleomycin (patient 1) and vacuolar degeneration of melanocytes in the inflammatory stage (patient 2).

A case of mycetoma of the lower leg (Madura foot) with bone involvement caused by Petriellidium boydii is presented. After an initially favourable therapeutic response to ketoconazole (2 X 200 mg/die) the process recurred despite proven sensitivity of the fungus in vitro. It could not be controlled with conservative treatment and ultimately necessitated amputation of the lower leg. A striking, hitherto unreported feature of mycetoma was the episodic occurrence of circulating immune complexes with febrile monoarthritis of the adjacent ankle.

The cover of cutaneous wounds with cultured epidermis can be significantly improved by prior backing of the epithelium with meshed silastic sheets, whereas other materials, such as vaseline gauze, foam rubber etc., are not as satisfactory. Meshed silastic is affixed to the epithelium surface just before the enzymatic detachment from the culture flask is completed. Thus it protects the delicate epithelial membrane from injury during transplantation and helps to control its polar orientation. In addition, the silastic mesh prevents the graft, which initially does not possess any horny layer, from drying up and allows adequate drainage of wound secretions. Cultured epidermal grafts prepared by this method take very well (more than 90%) attaching to the wound bed quite firmly within a week.

Plasma renin, adrenaline and noradrenaline were measured by the respective radioenzymic and radioimmunological methods in 69 patients with essential hypertension, 40 patients with secondary hypertension from chronic parenchymatous renal disease and in 18 normotensive controls. Plasma levels of adrenaline and noradrenaline were not statistically different in primary secondary hypertension and were comparable with normotensive controls. Compared with secondary hypertension, only 4% of patients with primary hypertension had a marginally raised plasma noradrenaline, compared with normotensive subjects, only 6% had a definitely raised plasma noradrenaline level. Though absolutely normal, noradrenaline in high renin essential hypertension was significantly higher than in low renin essential hypertension; it correlated neither with age nor blood pressure. Plasma adrenaline was reduced in about 30% of patients with primary and secondary hypertension, leading to a positively skewed frequency distribution; plasma adrenaline correlated positively with heart rate (p less than 0.001), pulse pressure (p less than 0.01) and plasma noradrenaline (p less than 0.01) and negatively with diastolic blood pressure (p less than 0.05). Supine plasma catecholamine levels do not demonstrate differences in adrenergic tone in primary and secondary hypertension and do not add any new evidence for an increased sympathetic tone in primary hypertension. In fact, plasma adrenaline is suppressed in about 30% of patients with primary and secondary hypertension.

20 normotensive subjects (10 with a family history of hypertension) were investigated as to whether moderate salt restriction and/or a high potassium intake had a beneficial effect on blood pressure regulation and prevention of hypertension. In all subjects a moderate reduction of salt intake from 200 to 50 mmol/day over 2 weeks reduced the rise in blood pressure induced by various doses of noradrenaline (0.1, 0.2, and 0.4 microgram/kg/min). Furthermore, of 20 subjects 12 (8 with a family history of hypertension) responded to salt restriction with a fall in systolic or diastolic blood pressure of at least 5 mm Hg. There were no significant differences in plasma renin, aldosterone, vasopressin, and catecholamine levels between responders (salt-sensitive subjects) and non-responders, but salt-sensitive subjects had a mean baseline diastolic blood pressure which was higher than that of salt-insensitive subjects by 13 mm Hg (77.3+/-3.26 vs. 64.6+/-2.06, p less than 0.001). A high potassium intake reduced diastolic blood pressure by at least 5 mm Hg in 10 out of 20 subjects, of the 10 7 had a family history of hypertension and 9 responded to salt restriction. A high potassium intake also improved compliance with a low salt regimen, promoted sodium loss, prevented the rise in plasma catecholamines induced by a low salt diet, and increased the sensitivity of the baroreceptor reflex. These four effects occurred in the group as a whole and were probably the means by which a high potassium intake reduced blood pressure. In all subjects 2 weeks of a combined low sodium/high potassium intake reduced blood pressure rises induced by mental stress or noradrenaline infusion by 10 mm Hg. The results of this study suggest that moderate salt restriction combined with a high potassium intake helps to prevent hypertension, that salt-sensitive subjects exist, and that these individuals would profit most.

1. Twenty-one normotensive subjects were studied to assess any possible benefits of moderate salt restriction and of high potassium intake in the prevention of hypertension in man. 2. The effects of salt reduction from 200 to 50 mmol/day and/or of an increase of potassium intake from 80 to 200 mmol/day over a 2 week period, on blood pressure, plasma noradrenaline, adrenaline, vasopressin, renin and aldosterone, were measured both at rest and after mental stress. The effects of graded infusion of noradrenaline on blood pressure and heart rate were also studied. 3. Salt restriction lessened the increase of blood pressure during noradrenaline infusion; the combination with high potassium intake also reduced the pressure rise after mental stress. There were no major changes in plasma levels of vasopressin and adrenaline. Plasma noradrenaline increased during the low sodium diet. 4. High potassium intake improved baroreceptor function as revealed by the greater decrease in heart rate for a given rise in pressure after noradrenaline infusion. 5. The results of this study are compatible with a protective effect of a practicable low sodium/high potassium diet on the development of human hypertension.

Epidermal skin of only a few cm2 in size can be expanded several thousand times in cell cultures within 3 or 4 weeks and then be used to cover wounds. There have been reports on some patients with severe burns, whose skin was successfully replaced by autologous cultured epidermis in up to 50% of their body surface. The major drawbacks of this technique of skin replacement are the long culture period as well as the inferior mechanical stability and increased rate of wound contractures due to the lack of the dermal component. Since allogenic epidermal cell cultures are immunologically rejected, they are not suitable for the permanent coverage of wounds.