Home About us Contact
|
Home About us Contact | ||
|
|
||
Morphological Signs (morphological + sign)
Selected AbstractsGene expression and digit homology in the chicken embryo wingEVOLUTION AND DEVELOPMENT, Issue 1 2005Monique C. M. Welten Summary The bird wing is of special interest to students of homology and avian evolution. Fossil and developmental data give conflicting indications of digit homology if a pentadactyl "archetype" is assumed. Morphological signs of a vestigial digit I are seen in bird embryos, but no digit-like structure develops in wild-type embryos. To examine the developmental mechanisms of digit loss, we studied the expression of the high-mobility group box containing Sox9 gene, and bone morphogenetic protein receptor 1b (bmpR-1b),markers for precondensation and prechondrogenic cells, respectively. We find an elongated domain of Sox9 expression, but no bmpR-1b expression, anterior to digit II. We interpret this as a digit I domain that reaches precondensation, but not condensation or precartilage stages. It develops late, when the tissue in which it is lodged is being remodeled. We consider these findings in the light of previous Hoxd-11 misexpression studies. Together, they suggest that there is a digit I vestige in the wing that can be rescued and undergo development if posterior patterning cues are enhanced. We observed Sox9 expression in the elusive "element X" that is sometimes stated to represent a sixth digit. Indeed, incongruity between digit domains and identities in theropods disappears if birds and other archosaurs are considered primitively polydactyl. Our study provides the first gene expression evidence for at least five digital domains in the chick wing. The failure of the first to develop may be plausibly linked to attenuation of posterior signals. [source] Treatment of choroidal neovascularization using intravitreal bevacizumabACTA OPHTHALMOLOGICA, Issue 5 2007Robert Pedersen Abstract. Purpose:, This study aimed to assess the pharmacodynamic profile of intravitreal bevacizumab in relation to best corrected visual acuity (BCVA), foveal thickness, and other aspects of macular morphology after intravitreal injection of bevacizumab in eyes with subretinal choroidal neovascularization (CNV). Methods:, A retrospective observational, uncontrolled case series including 26 eyes in 25 patients followed for up to 6 months after intravitreal injection of bevacizumab 1 mg repeated as deemed necessary after monthly assessments by biomicroscopy, optical coherence tomography, colour fundus photography, fluorescein angiography and BCVA determination. At follow-up, cases were classified by morphological treatment response (reduction or elimination of pathological neovascular leakage, retinal thickening or serous retinal detachment) or absence of response (deterioration or lack of improvement). Primary disease entities included age-related macular degeneration (22 eyes, four of which had evidence of retinal angiomatous proliferation), idiopathic peripapillary neovascularization (one eye), and angioid streaks (three eyes in two patients). Results:, One month after the first injection, apparent morphological improvement was observed in 24/26 eyes and mean BCVA had improved by 3.1 ± 7.8 letters (p = 0.05). Of these 24 responders, which included all primary diagnoses, 11 (46%) demonstrated BCVA improvement of ,,5 letters. The two non-responders (7.7%) had lost >,3 lines of vision at 2 months follow-up. Overall, 18 eyes completed 6 months follow-up, with a mean BCVA improvement of 0.5 ± 12.7 letters, and 22 eyes completed 3 months follow-up, with a mean BCVA improvement of 2.0 ± 11.0 letters. Two months after the first injection, 11 (46%) of the 24 responders demonstrated signs of recurrent CNV activity, defined as decreased BCVA and/or increased retinal thickness and/or fluorescein angiographic CNV leakage. No serious drug-related adverse events were observed during the course of the study. Conclusions:, Overall mean BCVA remained stable throughout the study. Morphological signs of reduced CNV activity were seen in the majority of eyes at 2,4 weeks after intravitreal bevacizumab injection. Half the responders showed signs of renewed CNV activity at 2 months after their first injection. All first-injection responders were also second-injection responders. [source] Development of heterodont dentition in house shrew (Suncus murinus)EUROPEAN JOURNAL OF ORAL SCIENCES, Issue 6 2007Atsushi Yamanaka Mammalian heterodont dentition comprises incisors, canines, premolars, and molars. Although there has been intensive research, the patterning of these specific tooth types has not yet been elucidated. In order for the gene expression data to be linked with tooth type determination, it is first necessary to determine precisely the incisor-, canine-, premolar-, and molar-forming regions in the jaw primordia. To accomplish this, we studied dentition development in the house shrew (Suncus murinus), which has retained all the tooth types, using three-dimensional reconstructions from serial histological sections and the Sonic hedgehog (Shh) expression patterns. Before the appearance of morphological signs of odontogenesis, Shh expression localized to the presumptive tooth-forming regions, in which the mesial and distal expression domains corresponded to the incisor- and premolar-forming regions, respectively. The upper incisor region was found to extend across the boundary between the frontonasal and the maxillary processes. The canine-forming regions later appeared in the intermediate portions of the maxillary and the mandibular processes. The molar-forming regions later appeared distal to the initially demarcated tooth-forming regions by secondary extension of the distal ends. The demarcation visualized by the Shh expression pattern in the jaw primordia of the house shrew probably represents the basic developmental pattern of mammalian heterodont dentition. [source] Segmented filamentous bacteria in a defined bacterial cocktail induce intestinal inflammation in SCID mice reconstituted with CD45RBhigh CD4+ T cellsINFLAMMATORY BOWEL DISEASES, Issue 10 2007Renata Stepankova PhD Abstract Background: The aim was to analyze the influence of intestinal microbiota on the development of intestinal inflammation. We used the model of chronic inflammation that develops spontaneously in the colon of conventional severe combined immunodeficiency (SCID) mice restored with the CD45 RBhigh subset of CD4+T cells isolated from the spleen of normal BALB/c mice. Methods: A CD4+CD45RBhigh subpopulation of T cells was purified from the spleen of conventional BALB/c mice by magnetic separation (MACS) and transferred into immunodeficient SCID mice. Germ-free (GF) SCID mice or SCID mice monoassociated with Enterococcus faecalis, SFB (segmented filamentous bacteria), Fusobacterium mortiferum, Bacteroides distasonis, and in combination Fusobacterium mortiferum + SFB or Bacteroides distasonis + SFB were used as recipients. SCID mice were colonized by a defined cocktail of specific pathogen-free (SPF) bacteria. Mice were evaluated 8,12 weeks after the cell transfer for clinical and morphological signs of inflammatory bowel disease (IBD). Results: After the transfer of the CD4+CD45RBhigh T-cell subpopulation to SCID mice severe colitis was present in conventional animals and in mice colonized with a cocktail of SPF microflora plus SFB. Altered intestinal barrier in the terminal ileum of mice with severe colitis was documented by immunohistology using antibodies to ZO-1 (zona occludens). Conclusions: Only SFB bacteria together with a defined SPF mixture were effective in triggering intestinal inflammation in the model of IBD in reconstituted SCID mice, while no colitis was detected in GF mice or in mice colonized either with SPF microflora or monoassociated only with SFB or colonized by Bacteroides distasonis + SFB or Fusobacterium mortiferum + SFB. (Inflamm Bowel Dis 2007) [source] Psoriasis under the microscopeJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 2006BJ Cribier Abstract Histopathology is a major diagnostic tool in dermatology, particularly in psoriasiform diseases. Morphological studies showed that the initial event in psoriatic lesions is perivascular infiltrate, followed by dilatation of superficial papillary vessels. Proliferation of keratinocytes and neutrophil exocytosis are secondary events. Fully developed psoriasis has a very characteristic pattern, which includes elongation of rete ridges leading to regular acanthosis, oedema of the papillary dermis associated with tortuous dilated vessels, thinning of suprapapillar area, decreased thickness of granular layer, and exocytosis of neutrophils in the spinous layer (Kogoj's pustule) or in the cornified parakeratotic layer (Munro microabscesses). Pustular psoriasis is characterized by large or confluent intra-epidermal multilocular pustules. Whatever the clinical variant of psoriasis, common morphological signs suggest that it is basically a unique pathological process, with many possible presentations according to various factors such as age, size and localization of lesions, or therapy. Similar microscopic elementary lesions indicate that Hallopeau's acrodermatitis continua, Reiter's disease and geographical tongue are variants of psoriasis. Because of the many faces of the disease, psoriasis can resemble many other squamous or pustular disorders. Differential diagnosis by microscopic analysis is based on pattern analysis, PAS (Periodic Acid Schiff) staining to rule out fungal infection, and immunohistochemistry to characterize lymphocytic infiltrate. Psoriasis is one of the most common inflammatory skin diseases. In its characteristic presentation, psoriasis comprises well-circumscribed red scaly papules and plaques. In this form, the disease is generally easy to identify, especially when the elbows, knees and scalp are affected. Nevertheless, the term ,psoriasis' includes more clinical variants than any other inflammatory dermatosis: psoriasis vulgaris vs. pustular, localized vs. generalized, topographic variants, mucous membranes involvement, hair and nail lesions. Although some of these conditions might be extremely different from psoriasis vulgaris, common pathological findings can be identified in all of them. Microscopic analysis of psoriatic lesions may therefore help clinicians to make the diagnosis and to understand that, whatever the clinical presentation, signs and symptoms are mainly due to a unique pathological process. [source] Protein phosphatase 1, activity prevents oncogenic transformationMOLECULAR CARCINOGENESIS, Issue 9 2006Cathy W.Y. Liu Abstract Cyclin-dependent kinase 2 (Cdk2) phosphorylates Thr320 of protein phosphatase 1, (PP1,) in late G1, thereby inhibiting its activity. Phosphorylation-resistant PP1,T320A, acting as a constitutively active (CA) mutant, causes a late G1 arrest by preventing the phosphorylation and inactivation of the retinoblastoma protein (pRb). Both PP1,-mediated G1 arrest and PP1, phosphorylation in late G1 require the presence of pRb, indicating that PP1, is a crucial regulator of the pRb pathway, which is almost invariably mutated in human cancer. These findings prompted us to investigate whether PP1, interferes with oncogenic transformation. The ability of NIH 3T3 cells to form foci after transformation with ras/cyclin D1 was significantly inhibited by co-transfection with PP1,T320A, but not PP1,. Likewise, cells expressing PP1,T320A or PP1,T320A fused to green fluorescent protein (GFP) were unable to form colonies in soft agar, regardless of whether PP1, constructs were co-transfected with ras/cyclin D1 or transfected into stably transformed cells. Overexpressed wild-type (Wt) PP1, and GFP-PP1, were phosphorylated in Thr320, most likely explaining its lack of effect. Expression of GFP-PP1,T320A was associated with caspase-cleaved pRb in Western blots (WB) and morphological signs of cell death. These findings demonstrate that PP1, activity can override oncogenic signaling by causing cell-cycle arrest and/or apoptosis rather than restoring contact inhibition or anchorage dependence. © 2006 Wiley-Liss, Inc. [source] Ultrastructural and MRI study of the substantia nigra evolving exofocal post-ischemic neuronal death in the ratNEUROPATHOLOGY, Issue 3 2002Fengyu Zhao To clarify the morphological characteristics of exofocal post-ischemic neuronal death (EPND) in the substantia nigra (SN), we investigated the course of light- and electron-microscopic changes of the SN of rats subjected to occlusion of the left middle cerebral artery (MCA) for 1, 2, 4, 7 and 12 days. To assess cellular edema, sequential magnetic resonance (MR) mapping of the apparent diffusion coefficient (ADC) and the T2 value test was performed. Histological and electron-microscopic examination on day 1 showed dotted chromatin clumps in the nuclei of some neurons and mild swelling of the perivascular endfeet of astrocytes in the ipsilateral SN. On day 2, a few cells of the ipsilateral SN pars reticulata (SNr) revealed key morphological signs of apoptosis , apoptotic body-like condensation and segregation of the chromatin and DNA fragmentation-like nuclear remnants. On day 4, 38% of neurons became swollen (pale neurons) with cytoplasmic microvacuoles, which appeared to originate from rough endoplasmic reticulum (rER), mitochondria and Golgi apparatus. Twenty percent of neurons showed massive proliferation of the cisternae of the rER, some of which were fragmented or had lost their normal parallel arrangement. In addition, MR mapping revealed a transient ADC decrease with a T2 increase (signifying a phase of cellular edema), which coordinated with the phase of ultrastructural cellular swelling. Further, the total number of neurons started to decrease gradually, the perivascular endfeet of astrocytes were markedly swollen, and the neuropil became loose on day 4. On day 7, reactive astrocytes and dark neurons occurred most frequently. These results suggest that the EPND in the SN after occlusion of the MCA in adult rats is due to both apoptosis and necrosis, although necrosis seems to be the dominant mechanism of the EPND. However, the morphologic resemblances of EPND to delayed neuronal death suggest these processes have a common pathomechanism. [source] Rat Cytomegalovirus Infection Interferes with Anti-CD4 mAb-(RIB 5/2) Mediated Tolerance and Induces Chronic Allograft DamageAMERICAN JOURNAL OF TRANSPLANTATION, Issue 9 2006A. Pascher In order to assess the role of heterologous immunity on tolerance induction (TI) by signal 1 modification, the influence of rat cytomegalovirus infection (RCMVI) on TI by a non-depleting monoclonal anti-CD4 mAb (monoclonal antibody) (RIB 5/2) in a rat kidney transplant (KTx) model was investigated. Orthotopic rat KTx (Dark Agouty (DA) , Lewis (LEW)) was performed after TI with RIB 5/2 [10 mg/kg body weight (BW); day ,1, 0, 1, 2, 3; i.p. (intraperitoneal route)]. RCMVI (5 × 10E5 Plaque forming units [PFU] i.p.) was simultaneously conducted to KTx, 50 days after KTx, and 14 days before and after KTx. RIB 5/2 induced robust allograft tolerance even across the high-responder strain barrier. RCMVI broke RIB 5/2-induced tolerance regardless of the time of RCMVI but did not induce acute graft failure during the 120 days follow-up. RCMVI induced a significant chronic deterioration of allograft function (p < 0.01) and enhanced morphological signs of chronic allograft damage (p < 0.05). Cellular infiltrates and major histo-compatibility complex (MHC)-expression were more pronounced (p < 0.05) in the infected groups. RCMVI induced not only RCMV-specific T-cell response but also enhanced the frequency of alloreactive T cells. RCMV interferes with anti-CD4 mAb-induced tolerance and leads to chronic allograft damage. The data we presented suggest a potentially important role of viral infections and their prophylaxis in clinical TI protocols. [source] Expression of Cell Death-Associated Proteins in Neuronal Apoptosis Associated with Pontosubicular Neuron NecrosisBRAIN PATHOLOGY, Issue 3 2001Christine Stadelmann Expression of apoptosis-associated proteins p53, bcl-2, bax, and caspase-3/CPP32, activation of caspase-3, and modification of proteins via poly(ADP-ribosyl)ation was studied in pontosubicular neuron necrosis (PSN), a form of perinatal brain damage revealing the morphological hallmarks of neuronal apoptosis. Immunoreactivity for p53 was completely absent. The majority of cells stained with the bax and procaspase-3 antibodies did not show morphological signs of apoptosis. In contrast, an antibody against activated caspase-3 almost exclusively stained cells with apoptotic morphology. Poly(ADP-ribosyl)ated proteins were only rarely detected in cells with apoptotic morphology. The expression patterns of bax, procaspase-3, bcl-2, and p53 in PSN were similar to that found in age-matched control brains. However, activated caspase-3 and poly-ADP-ribosylated proteins were exclusively found in apoptotic cells. These data indicate that detection of active caspase-3 is a reliable marker for apoptosis in formalin-fixed human tissue, and that neuronal apoptosis in pontosubicular neuron necrosis is accompanied by a pronounced activation of caspase-3. [source] 2436: A critical look at meibometry as a means to monitor Meibomian gland functionACTA OPHTHALMOLOGICA, Issue 2010P VERSURA Purpose To evaluate the diagnostic performance of meibometry in classifying and quantifying Meibomian gland dysfunction(MGD) Methods Ninety-six patients with MGD (138 eyes, 62 women, 34 men) and 30 normal control subjects(55 eyes)were enrolled. Eighty six eyes were classified as high delivery (HD)-MGD (meibomian seborrhea/hypersecretory MGD), 52 as low delivery (LD)-MGD on the basis of expression quality scores and morphological signs. Direct Meibometry (DM) measurements were made with an MB550 Meibometer (Courage-Khazaka GmbH). Standard curves were constructed relating arbitrary Meibometer optical density units (AU). Integrated Meibometry (IM) was performed on scanned images of the lipid blots. Symptoms were scored by OSDI,Schirmer test I, Break Up Time (BUT), tear osmolarity (Tearlab, Ocusense), conjunctival scraping cytology were performed. Statistical analysis used SPSS 14.0 and MedCalc 5.0 Results AU values plotted on a log scale correlated highly with the lipid equivalent values (R2= 0.913). Significant differences were found between control subjects vs all MGD patients and between HD vs LD-MGD patients for all the parameters evaluated. In particular: controls: 300+/-121 AU (0.04+/-0.015 microliter), LD-MGD: 218+/-122 AU (0.03+/-0.015) and HD-MGD: 564+/-115 AU (0.07+0.015) (median+/-SD). Significant correlation was found DM vs IM (r=0.691,p<0.0001) and DM was shown to be correlated with BUT, OSDI score, scraping score and tear osmolarity, especially in LD-MGD patients. The selected DM diagnostic cut off for LD-MGD was <275 AU (sens 73, spec 60, PPV 63) and for HD-MGD was >450 AU; (sens 86, spec 87, PPV 91) Conclusion Meibometry is confirmed to be a reliable method to distinguish normal subjects from MGD subgroups with a good degree of accuracy [source] | ||||||||||