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Biomedical subjects

V Goffin

Publications and source records attributed to V Goffin.

At least 37 records · Page 2Linked to original sources
PubMed2001

Beneficial effects of softened fabrics on atopic skin.

There is general concern about the possible cutaneous adverse effects of wearing garments treated with household laundry products, particularly on atopic skin. Our objective was to compare softened and non- softened fabrics in a forearm wet and dry test, under conditions simulating real-life conditions. Twenty atopic volunteers entered a single-blind 12-day (3 sessions per day) forearm wetting and drying test. Cotton fabrics were machine washed and liquid fabric conditioner was added or not to the final rinse. To simulate conditions of skin damage, a dilute solution of sodium lauryl sulphate was applied under occlusion to the forearm of each volunteer before the start of the study. Skin effects were evaluated by visual grading (redness, dryness and smoothness), squamometry and in vivo instrumental measurements (capacitance, transepidermal water loss and colorimetry). Rubbing of atopic skin with fabrics generally resulted in discrete to moderate alterations of the structure of the stratum corneum. Both for control and pre-irritated skin, all measured parameters indicated that softened fabric was less aggressive to the skin than unsoftened fabric. In the case of pre-irritated skin, the recovery of the skin was significantly faster when rubbed with softened than with unsoftened fabrics. In conclusion, softened fabrics help mitigate the skin condition in atopic patients.

Adult↗
PubMed2001

S179D-human PRL, a pseudophosphorylated human PRL analog, is an agonist and not an antagonist.

For many years, our group has been involved in the development of human PRL antagonists. In two recent publications, S179D-human PRL, a human PRL analog designed to mimic a putative S179-phosphorylated human PRL, was reported to be a highly potent antagonist of human PRL-induced proliferation and signaling in rat Nb2 cells. We prepared this analog with the aim of testing it in various bioassays involving the homologous, human PRL receptor. In our hands, S179D- human PRL was able to stimulate 1) the proliferation of rat Nb2 cells and of human mammary tumor epithelial cells (T-47D), 2) transcriptional activation of the lactogenic hormone response element-luciferase reporter gene, and 3) activation of the Janus kinase/signal transducer and activator of transcription and MAPK pathways. Using the previously characterized antagonist G129R-human PRL as a control, we failed to observe any evidence for antagonism of S179D-human PRL toward any of the human PRL-induced effects analyzed, including cell proliferation, transcriptional activation, and signaling. In conclusion, our data argue that S179D-human PRL is an agonist displaying slightly reduced affinity and activity due to local alteration of receptor binding site 1, and that the antagonistic properties previously attributed to S179D-human PRL cannot be confirmed in any of the assays analyzed in this study.

Animals↗
PubMed2001

[Dirty nails and mycotoxins].

Some mycotoxins are among the most toxic natural products. They are metabolites produced by food-borne and feed-borne moulds. Dirty and soiled nails, and contaminated or infected onyxis by these specific moulds can be the origin of oral contamination and mycotoxicosis. Hence, nail cleaning, correct hygiene and treatment of mould onychomycosis have a potentially great impact on health.

Hand Disinfection↗
PubMed2001

[Latex allergy -- when uncertainty remains the only certainty].

Latex devices release allergenic proteins which are responsible for immune IgE mediated reactions. Casual surgical gloves are most often responsible for contact urticaria. Other allergic manifestations include conjunctivitis, rhinitis, asthmatiform dyspnoea and diverse gastro-intestinal troubles. Cardiovascular collapse and anaphylactic shock are possible. Physicians and the paramedical staff are particularly affected by the allergy to latex proteins. Multi-operated patients and those under prolonged health care using latex-made medical probes also present a high-risk group for this type of allergy.

Anaphylaxis↗
PubMed2001

[Cutaneous infections contracted during sports and recreational activities].

Going in for sports is at increased risk for cutaneous infections that can be viral, bacterial, mycotic and parasitic in nature. The specific conditions of sports practice have a major influence on their occurrence. Other factors such as age, gender and genetic predisposition can also play a role. The cutaneous infections should be the target of preventive measures. To assume the worse, they should be recognized and treated without delay in order to avoid the more or less prolonged arrest of the sports activity and the disease transmission to partners.

Adolescent↗
PubMed2001

[Research on the wisdom between defensins and antiseptics at the skin surface].

The density in the natural bacterial flora is quite controlled at the skin surface. The barrier to their penetration inside the body is a major function of the stratum corneum. Its more or less anfractuous structure, its hydration and acidic pH are important to maintain the microbiological equilibrium. The non-immune innate or inducible natural defenses rely on the production of epithelial peptide antibiotics (defensins, calprotectin) by keratinocytes. The phagocytic and immune defenses are superimposed to such mechanisms. This whole conundrum may be helped by, but it may also suffer from some skin care products and antiseptics.

Anti-Infective Agents, Local↗
PubMed2000

Human prolactin (hPRL) antagonists inhibit hPRL-activated signaling pathways involved in breast cancer cell proliferation.

The involvement of human prolactin (hPRL) in breast cancer has been recently reconsidered based on its autocrine/paracrine proliferative effect described in human mammary tumor epithelial cells. Therefore, there is growing interest in the development of potent hPRL antagonists that may inhibit this effect. We previously designed hPRL analogs displaying antagonistic properties in a human transcriptional bioassay. We now report that the most potent of those analogs, G129R-hPRL, antagonizes all hPRL-induced effects analysed in various breast cancer cell lines, including cell proliferation. The analog per se lacks intrinsic agonistic activity on PRL receptor-activated signaling cascades, cell proliferation and apoptosis, indicating that its mode of action only occurs through competitive inhibition of hPRL. We provide some molecular basis of this antagonistic effect by demonstrating that G129R-hPRL competitively inhibits hPRL-activation of the JAK-STAT and MAPK pathways, two signaling cascades involved in the mitogenic effect of hPRL in mammary epithelial cells. This competitive inhibition persists for at least 48 h, as evidenced by long term analysis of STAT5b activation or of progression through cell cycle. These results are the first demonstration at the molecular level that hPRL antagonists interfering with receptor dimerization disrupt signaling events in breast cancer cells, which prevents hPRL-induced cell proliferation.

Autocrine Communication↗
PubMed2000

High-level expression of biologically active human prolactin from recombinant baculovirus in insect cells.

We examined the feasibility of high-level production of recombinant human prolactin, a multifunctional protein hormone, in insect cells using a baculovirus expression system. The human prolactin cDNA with and without the secretory signal sequence was cloned into pFastBac1 baculovirus vector under the control of polyhedrin promoter. Prolactin was produced upon infection of either Sf9 or High-Five cells with the recombinant baculovirus containing the human prolactin cDNA. The production of recombinant prolactin varied from 20 to 40 mg/L of monolayer culture, depending on the cell types. The prolactin polypeptide with its own secretory signal was secreted into the medium. N-terminal amino acid sequence analysis of the recombinant polypeptide purified from the culture medium indicated that the protein was processed similar to human pituitary prolactin. Carbohydrate analysis of the purified protein indicated that a fraction of the recombinant prolactin made in insect cells appeared to be glycosylated. Also, both secreted and nonsecreted forms of the recombinant prolactin in insect cells were biologically equivalent to the native human prolactin (pituitary derived) in the Nb2 lymphoma cell proliferation assay.

Animals↗
PubMed2000

Involvement of prolactin in breast cancer: redefining the molecular targets.

The mammary gland is the major target tissue of prolactin (PRL) in mammals. Although this pituitary hormone has been long suspected to be involved in the progression of human breast cancer, the failure of clinical improvement by treatment with dopamine agonists (which lower circulating levels of PRL) rapidly reduced the interest of oncologists concerning a potential role of PRL in the development of breast cancer. Within the last few years, however, several studies reported first, that PRL is also synthesized by mammary epithelial cells, and second that it may exert a proliferative action in an autocrine/paracrine manner. In agreement with a recent epidemiological study, these observations have led to a reconsideration of the role of PRL as an active participant in breast cancer, and are an impetus to redefine the molecular targets of anti-prolactin strategies since dopamine analogs are assumed to be inefficient on extrapituitary PRL synthesis. In this review, we briefly summarize the current knowledge of PRL effects on both normal and tumor mammary cells, and we discuss the most relevant articles supporting the autocrine-paracrine action of PRL in the breast. With the aim of defining putative new molecular targets, we propose an overview of the main PRL receptor signaling cascades known to be triggered by PRL in mammary epithelial cells or, when not available, in other cell types. Finally, because proteolytic fragments of rat PRL have been shown to inhibit the angiogenic process, which may be relevant for preventing the progression of solid tumors such as breast tumors, we discuss the hypothesis that the enzymatic cleavage of human PRL could also represent a new molecular target in the search for alternative strategies in the treatment of breast cancer.

Animals↗
PubMed2000

Responsiveness of irradiated rat anterior pituitary cells to hypothalamic releasing hormones is restored by treatment with growth hormone.

Hypopituitarism is a common sequela of irradiation in cancer patients. Here we report that recombinant human growth hormone (r-hGH) prevents cell death and restores secretory capacity of irradiated rat pituitary cells in vitro. Dispersed rat pituitary cells from male Sprague-Dawley rats, irradiated with a 9-Gy sublethal dose, were incubated with r-hGH before, after, or before and after irradiation. Treatment with GH resulted in increased cell survival, which reached its maximum at the concentration of 5 nM, with an EC(50) of 3.5 nM. Protective effects of GH on pituitary cells were more pronounced in cultures treated before and after irradiation. Similarly, beneficial effects of GH were observed on the secretory capacity of surviving cells. In fact, irradiated pituitary cells treated with GH secreted substantial amounts of GH, luteinizing hormone, follicle-stimulating hormone, prolactin, thyroid-stimulating hormone and adrenocorticotropic hormone in response to specific releasing hormones. Such effects of GH were prevented in the presence of the specific GH receptor antagonists B2036 and G120K. Our results show that r-hGH exerts a specific protective effect on irradiated rat pituitary cells and suggest possible use of GH as an adjuvant agent for prevention of postirradiation hypopituitarism.

Adrenocorticotropic Hormone↗
PubMed2000

Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5.

Growth hormone (GH) regulates both bone growth and remodeling, but it is unclear whether these actions are mediated directly by the GH receptor (GHR) and/or IGF-I signaling. The actions of GH are transduced by the Jak/Stat signaling pathway via Stat5, which is thought to regulate IGF-I expression. To determine the respective roles of GHR and IGF-I in bone growth and remodeling, we examined bones of wild-type, GHR knockout (GHR(-/-)), Stat5ab(-/-), and GHR(-/-) mice treated with IGF-I. Reduced bone growth in GHR(-/-) mice, due to a premature reduction in chondrocyte proliferation and cortical bone growth, was detected after 2 weeks of age. Additionally, although trabecular bone volume was unchanged, bone turnover was significantly reduced in GHR(-/-) mice, indicating GH involvement in the high bone-turnover level during growth. IGF-I treatment almost completely rescued all effects of the GHR(-/-) on both bone growth and remodeling, supporting a direct effect of IGF-I on both osteoblasts and chondrocytes. Whereas bone length was reduced in Stat5ab(-/-) mice, there was no reduction in trabecular bone remodeling or growth-plate width as observed in GHR(-/-) mice, indicating that the effects of GH in bone may not involve Stat5 activation.

Animals↗
PubMed2000

Corneocyte desquamation.

Corneocyte desquamation at the skin surface is a complex biologic event which is normally regulated for providing an inconspicuous shedding of single corneocytes. When altered, the process gives rise to xerotic and ichthyotic conditions. The present review focusses on important biologic and molecular aspects responsible for normal and altered corneocyte desquamation. There is a complex relationship between epidermal cell production, maturation and desquamative loss. Corneocyte hydration, stratum corneum barrier function and enzymatic corneodesmolysis are involved in a dynamic interrelationship. Many physiological and environmental factors acting in a different time frame influence desquamation.

Cell Adhesion↗
PubMed2000

[Tropical bacterial dermatoses].

There is a number of bacterial dermatoses confined to or aggravated by the tropical environment. They are prone to develop due to the lack of hygiene, the difficult access to water, the hostile geoclimatic conditions and malnutrition. Several clinical categories are distinguished according to the nature of the pathogens and the type of disease spread.

Climate↗
PubMed2000

[Leprosy and its cutaneous and neurologic manifestations].

Leprosy is one of the most ancient diseases recognized in the history of man. It has been progressively eradicated from many countries. However, the disease remains a major problem of public health in a dozen of countries where it still represents an archetype of the tropical infectious pathology.

Humans↗
PubMed1999

Biological properties of human prolactin analogs depend not only on global hormone affinity, but also on the relative affinities of both receptor binding sites.

Zinc increases the affinity of human growth hormone (hGH) for the human prolactin receptor (hPRLR) due to the coordination of one zinc ion involving Glu-174(hGH) and His-18(hGH). In contrast, binding of hPRL to the hPRLR is zinc-independent. We engineered in binding site 1 of hPRL a hGH-like zinc coordination site, by mutating Asp-183(hPRL) (homologous to Glu-174(hGH)) into Glu (D183E mutation). This mutation was also introduced into G129R hPRL, a binding site 2 mutant (Goffin, V., Kinet, S., Ferrag, F., Binart, N., Martial, J. A. , and Kelly, P. A. (1996) J. Biol. Chem. 271, 16573-16579). These analogs were characterized using a stable clone expressing both the hPRLR and a PRLR-responsive reporter gene. The D183E mutation per se decreases the binding affinity and transcriptional activity of hPRL. However, this loss is partially rescued by the addition of zinc and the effect is much more marked on bioactivity than on binding affinity. These data indicate that the D183E mutation confers zinc sensitivity to hPRL biological properties. Due to an impaired site 2, the agonistic activity of G129R analog is almost nil. Although the double mutant D183E/G129R displays lower affinity ( approximately 1 log) compared with G129R hPRL, it unexpectedly recovers partial agonistic activity in the absence of zinc. Moreover, whereas zinc increases the affinity of D183E/G129R, it paradoxically abolishes its agonistic activity. Our results demonstrate that the biological properties of hPRL analogs do not necessarily parallel their overall affinity. Rather, the relative affinities of the individual binding sites 1 and 2 may play an even more important role.

Base Sequence↗