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Biomedical subjects

D Parent

Publications and source records attributed to D Parent.

At least 55 records · Page 3Linked to original sources
PubMed1995

Downregulation of neutrophil CD43 by opsonized zymosan.

CD43, a prevalent white blood cell molecule distinguished by its mucin-like surface region, has been proposed as a "functional barrier" that prevents or negatively regulates a variety of cell surface interactions. Implicit in this hypothesis is the expectation that CD43 will be altered or removed when white blood cells are activated. To investigate alterations of CD43 in a dramatic example of functional cell activation, suspension neutrophils were challenged with opsonized zymosan, a characterized stimulator of phagocytosis and respiratory burst oxidase. Flow cytometry showed decreased surface density of CD43 in opsonized zymosan-treated neutrophils, and immune precipitation showed decreased cellular CD43 content, indicating that opsonized zymosan downregulates CD43 by a proteolytic mechanism. Based on densitometry of immune precipitates, CD43 levels were decreased 42% +/- 6% in neutrophils treated for 10 minutes with opsonized zymosan and decreased 70% +/- 3% in neutrophils treated with phorbol 12-myristate 13-acetate (PMA). CD43 downregulation in response to opsonized zymosan, like PMA-induced CD43 downregulation, was insensitive to the serine protease inhibitor diisopropylfluorophosphate (DFP). In contrast, CD43 downregulation in response to opsonized zymosan or PMA was prevented by 4-(2-aminoethyl)-benzenesulfonylfluoride (AEBSF) and 3'4'-dichloroisocoumarin (3,4-DCI), both of which are characterized serine protease inhibitors. Activation of the neutrophil respiratory burst oxidase by opsonized zymosan or PMA was also insensitive to DFP and prevented by AEBSF and 3,4-DCI. These findings indicate a requirement for a proteolytic step in activation of the respiratory burst of intact suspension neutrophils by opsonized zymosan and PMA and suggest that CD43 cleavage may be a required proteolytic event.

Antigens, CD↗
PubMed1994

Two proteolytic pathways for down-regulation of the barrier molecule CD43 of human neutrophils.

CD43, an anionic rod-like mucin molecule on white blood cells, is thought to provide a barrier that prevents interactions of other surface molecules and acts as negative regulator of cell function. As a correlate, CD43 is expected to be altered or down-regulated when blood cells are functionally activated. This study examines CD43 of blood neutrophils before and after treatment with known activating agents. Flow cytometry indicated that PMA and A23187, and to a much lesser extent, FMLP and IL-8, decrease neutrophil expression of CD43. Two separate mechanisms were identified for CD43 down-regulation. Both are proteolytic processes. PMA-induced down-regulation is a rapid process involving proteolysis at a minimum of two sites, one within the N-terminal distal region recognized by mAbs and the other at a membrane-proximal site. The PMA-induced protease, cd43' ase, is characterized by insensitivity to DFP, TLCK, leupeptin, pepstatin, and 1,10 phenanthroline (< 5 mM). PMA-induced CD43 down-regulation is extensive but never complete, terminating at approximately 10 min after down-regulating 65 to 85% of molecules, and thereby converting neutrophils from dense to sparse CD43 expression. The second CD43 down-regulation mechanism, although likely a regulated event in vivo, occurred slowly in this study in neutrophils incubated without additives; the process is not affected by PMA, involves the action of a DFP-sensitive protease, releases N-terminal mAb-reactive fragments of 52 kDa or 40 kDa and can be mimicked by exogenous neutrophil elastase. The complexity and apparent tight regulation described here for the two down-regulatory mechanisms are consistent with an important role for CD43 in preventing or dampening cell surface interactions of blood neutrophils.

Antigens, CD↗
PubMed1994

FB1, a monoclonal antibody reacting with a keratin 14 epitope, stains only a small subset of psoriatic basal keratinocytes.

A murine monoclonal antibody, FB1, reacted with the basal keratinocytes of human stratified epithelia. One-dimensional and two-dimensional immunoblotting assays, performed on keratins extracted from HaCat cells and normal human keratinocytes, showed that FB1 recognizes K14. When LL002, another K14 monoclonal antibody is added, the FB1 stained area in the 2D-immunoblot seems to cover a fraction of the LL002 spot. Immunohistochemical data obtained from studies on normal human tissues supported the K14 specificity of FB1, but when compared with two other monoclonal antibodies, LL002 and RCK107 reacting with K14, some differences appeared. These differences were mainly seen in sweat glands, hair follicles, psoriatic epidermis and salivary glands. In psoriatic epidermis, FB1 showed a heterogeneous pattern of staining of the basal cell compartment. Intense reactivity was only observed at the bottom of the rete ridges. Staining diminished and finally disappeared in the basal cells above the dermal papillae. This observation supports the view that an increased germinative cell population in psoriasis involves a partially differentiated amplifying compartment in which the number of cell divisions is increased.

Animals↗
PubMed1994

Clinical experience with short schedules of itraconazole in the treatment of tinea corporis and/or tinea cruris.

BACKGROUND: Superficial fungal infections have usually been considered to be caused only by dermatophytes. In recent years their epidemiology has been changing with other fungi being isolated and, thus, antifungal agents with a broad spectrum of activity, such as itraconazole, may be particularly useful. The risk/benefit ratio for any such treatment is determined by its tolerability profile and the duration of therapy. OBJECTIVE: The aim was to compare the efficacy and tolerance of a shorter treatment regimen, using a higher dose of itraconazole, with a standard itraconazole regimen in the treatment of tinea corporis/cruris. METHODS: An open study compared oral itraconazole 200 mg daily for 7 days with oral itraconazole 100 mg for 15 days in 153 patients with tinea corporis/cruris. RESULTS: At follow-up all patients in both groups were clinically cured or markedly improved. However, mycological cures were greater in the 7-day treatment group (90%), and the onset of clinical and mycological cure was faster in this group. CONCLUSIONS: Itraconazole, 200 mg daily for 7 days, offers a short convenient and effective treatment option for tinea corporis and tinea cruris.

Administration, Oral↗
PubMed1994

Herpes simplex virus tracheitis in a patient with the acquired immunodeficiency syndrome.

Herpetic tracheobronchitis and pneumonia occur basically in immunodepressed patients, but have rarely been reported in patients with the acquired immunodeficiency syndrome (AIDS). Some large reviews on pulmonary manifestations in AIDS report a small number of herpetic pulmonary infections, without determining any prevalence of this particular viral involvement. Predisposing factors are alteration of cell-mediated immunity and invasive procedures (such as endotracheal tube use) in debilitated patients. The case we report illustrates the occurrence of a herpetic tracheitis in an HIV-infected patient with severe P. carinii pneumonia, needing systemic corticotherapy and mechanical ventilation. It illustrates the risk of dissemination of herpes simplex virus (HSV) from a herpetic stomatitis to the lower respiratory tract, even after the endotracheal cannula has been removed.

AIDS-Related Opportunistic Infections↗
PubMed1993

Fatal varicella in an immunocompromised adult.

A fatal case of disseminated varicella in a 28-year-old immunocompromised woman is reported. Abdominal pain was the first manifestation of the disease, generalized vesicular eruption developed later. The cutaneous lesions became purpuric, and spontaneous hematomas appeared as a result of disseminated intravascular coagulation. Primary varicella infection remains a serious problem in immunocompromised patients.

Adult↗
PubMed1993

[Streptococcus beta hemolytic necrotizing fasciitis. 5 cases in the Brussels area].

In the Brussels area five cases of necrotizing fasciitis occurred during the past two years in patients devoid of any pathology likely to lower the immune defence mechanisms. Alcoholism and the use of non-steroidal anti-inflammatory drugs seem to act as contributory factors. Necrotizing fasciitis develops alone or as complication of a pre-existent dermo-hypodermic infection. A massive use of antibiotics and a wide surgical slitting up failed to prevent a fatal issue in all five patients. Extremely early massive surgery remains vital in this disease.

Adult↗
PubMed1992

In vitro infection of normal human keratinocytes by human papillomavirus type 1 followed by amplification of the viral genome in reconstructed epidermis.

Primary cultures of normal human keratinocytes were inoculated in vitro with human papillomavirus type 1 (HPV-1), the agent responsible for deep plantar warts. Upon transfer to dead de-epidermized dermis and growth at the air-liquid interface, keratinocytes reconstituted a pseudoepidermis. Under these highly differentiating conditions, HPV-1 DNA amplification was found to take place in the reconstructed epidermis, being detectable from 7 days after the transfer and persisting for at least 10 days thereafter. The extent of keratinocyte differentiation may be insufficient to allow a complete HPV infectious cycle.

Cell Differentiation↗
PubMed1992

Renewal and differentiation of keratinocytes cultured on dead de-epidermalized dermis.

Human keratinocytes grown at an air-liquid interface on dead de-epidermalized dermis exhibit a pattern of organization similar to that seen in vivo. Cell renewal is limited to the basal layer. The cell cycle time determined after 7 days of culture, using a percentage labelled mitoses (PLM) technique, was about 15 h. This result is comparable with published data for cultivated keratinocytes but is shorter than the parameter proposed for epidermis in vivo. Appearance of labelled cells in the granular layer was observed 4 days after pulse labelling. Despite this high cell renewal, a normal cell differentiation with expression of various keratinization markers was maintained.

Adult↗
PubMed1990

Spreading of psoriatic plaques: alteration of epidermal differentiation precedes capillary leakiness and anomalies in vascular morphology.

To approach the temporal relationship between alterations in keratinization and capillary leakiness in psoriasis, we studied the topography of these anomalies in spreading psoriatic lesions. Histological and immunohistochemical studies were performed on skin biopsies obtained from normal individuals and from psoriatic patients. In the latter case, biopsies were taken in uninvolved skin, in the center of lesions, and at the edge of evolving plaques (spanning uninvolved and involved skin). Alterations in epidermal differentiation were assessed by the distribution of filagrin, involucrin, and epidermal membrane-bound transglutaminase. Capillary leakiness was evaluated by the abundance of plasma proteins such as albumin, fibrinogen, and immunoglobulin G within the epidermis. Typical alterations of epidermal differentiation were already obvious at the edge of the lesions, in areas devoid of vessel abnormalities and leakiness, or significant cellular infiltration. These results strongly suggest that, during the formation of a psoriatic plaque, defects in keratinocyte differentiation precede the development of vascular anomalies.

Adult↗
PubMed1989

Characteristics of megakaryocyte colony formation in normal individuals and in primary thrombocythemia: studies using an optimal cloning system.

Colony formation by megakaryocyte (MK) progenitors was studied in 36 normal individuals and in 26 patients with primary thrombocythemia (PT) using an improved plasma clot cloning system. MK colonies were identified by immunoperoxidase staining using a monoclonal antibody against human platelet glycoprotein IIb/IIIa complex. In normal individuals, a frequency of 194 +/- 23 MK colony-forming units (CFU-MK) per 5 X 10(5) bone marrow nonadherent mononuclear cells and 11 +/- 4 CFU-MK per 5 X 10(5) blood mononuclear cells was found. These CFU-MK grew as large (greater than 20 cells), mean (11-20 cells), small (3-10 cells), or mix-MK colonies (at least two MK) that comprised 15%, 23%, 62%, or 5% of all MK colonies in bone marrow and 0%, 8%, 92%, or 1% in peripheral blood, respectively. In PT, several abnormalities of MK colony formation were observed: 1) increased circulating CFU-MK numbers, 2) increased mix-MK colony formation, 3) spontaneous MK colony formation without phytohemagglutinin-stimulated leukocyte-conditioned medium and normal serum, 4) decreased proportion of larger MK colonies (greater than 11 cells) in PT bone marrow, and 5) failure of PT plasma or serum to stimulate MK colony formation by normal marrow cells in a normal fashion. These results indicate some of the characteristics of quantitative and qualitative abnormalities of in vitro megakaryocytopoiesis in PT.

Cells, Cultured↗
PubMed1988

Characteristics of circulating megakaryocyte progenitors (CFU-MK) in patients with primary myelofibrosis.

Characteristics of circulating CFU-MK and the effect of serum and plasma on CFU-MK growth were studied in 14 patients with primary myelofibrosis (MF) using short- and long-term culture methods. The number of CFU-MK in short-term cultures was significantly increased in the non-splenectomized patient group (p less than 0.01). Without added PHA-LCM and normal serum, spontaneous colony formation was found in 9 out of 10 patients. In long-term blood cultures from 6 MF patients, 3 untreated patients formed confluent adherent layers and produced in suspension an equal number or an even greater number of nucleated cells, megakaryocytes and CFU-MK than those obtained in long-term bone marrow culture from normal individuals. 2 splenectomized patients showed neither an increased numbers of CFU-MK nor the capacity to develop an adherent layer. The serum and plasma of MF patients failed to stimulate megakaryocyte colony formation by normal bone marrow in a normal fashion. These findings indicate a megakaryocytopoietic abnormality, and a central role of the spleen in extramedullary haematopoiesis in MF.

Blood Cell Count↗
PubMed1987

Spontaneous formation of megakaryocyte progenitors (CFU-MK) in primary thrombocythaemia.

An improved plasma clot culture method for CFU megakaryocytes (MK) has been developed with a higher plating efficiency and easier identification and enumeration of MK colonies by an indirect immunoperoxidase staining using a monoclonal antibody specific to the platelet glycoprotein IIb/IIIa complex. This technique has been used to study megakaryocytopoiesis in 20 normal individuals, 4 recently diagnosed patients with untreated primary thrombocythaemia (PT) and 2 patients with secondary thrombocytosis (ST). An increased number of MK colonies was evident in peripheral blood (mean 115 +/- 31 CFU-MK/5 X 10(5) seeded cells or 206 +/- 91/ml) and to a lesser extent in bone marrow (mean 188 +/- 26 CFU-MK/5 X 10(5) seeded cells or 696 +/- 103/ml) of PT patients as compared to controls (mean 11 +/- 4/5 X 10(5) seeded cells or 13 +/- 3/ml of peripheral blood and 153 +/- 15/5 X 10(5) seeded cells or 319 +/- 43/ml of bone marrow). There was a very obvious difference between PT patients and the others (controls plus ST patients) because CFU-MK growth with no added stimulus (PHA-LCM or PHA-LCM and normal serum) could be seen in PT patients only.

Blood Cells↗