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PubMed1976

Sugar binding to purified fractions from bovine taste buds and epithelial tissue. Relationships to bioactivity.

Binding of various sugars was compared in purified subfractions of taste buds isolated from bovine circumvallate papillae and of non-taste bud-bearing epithelium isolated from tissue surrounding these papillae. Binding of 14C-labeled sugars was greater in purified subfractions obtained from taste bud than from non-taste bud-bearing tissue and was, in general, greater in those taste bud subfractions in which a greater membrane purification was achieved. Binding specificity of the 14C-labeled sugars sucrose, fructose, glucose and of 14C-labeled cyclamate and saccharine was measured by competition of each 14C-labeled sugar or synthetic sweetener with its unlabeled homologous sugar in P4(B) taste bud subfractions; this binding, as shown for sucrose, was reversible and temperature dependent. Essentially no competition of the 14C-lageled sugars sucrose, fructose, glucose or 14C-labeled cyclamate and saccharine by their respective unlabeled homologues occurred in epithelial tissue P4(B) subfractions; this binding was not reversible. Binding specificity was further observed by the competition of 14C-labeled sucrose, fructose and glucose with each unlabeled sugar for binding sites on P4(B) taste bud subfractions; unlabeled sucrose was more effective in competing with each 14C-labeled surgar than was unlabeled fructose or glucose. The relatively non-sweet sugar lactose did not compete with 14C-labeled lactose in P4(B) subfractions from either taste bud or non-taste bud-bearing epithelial tissue. Binding of 14C-labeled sucrose in purified P4(B) bud subfractions was inhibited by increased concentrations of unlabeled sucrose, phospholipase C, neuraminidase, EDTA, NaCl and urea. Dissociation constants for sugar or synthetic sweetener binding were low (approx. 10(-3) M) but in a rank order (sucrose greater than fructose greater than glucose greater than saccharine) consistent with preference and electrophysiological responses in cow. The cow is behaviorally indifferent to saccharine and lactose consistent with the data obtained in the present study.

Animals↗

PubMed1997

Mice with a targeted disruption of the neurotrophin receptor trkB lose their gustatory ganglion cells early but do develop taste buds.

The alleged ability of taste afferents to induce taste buds in developing animals is investigated using a mouse model with a targeted deletion of the tyrosine kinase receptor trkB for the neurotrophin BDNF. This neurotrophin was recently shown to be expressed in developing taste buds and the receptor trkB has been shown to be expressed in the developing ganglion cells that innervate the taste buds. Our data show a reduction of geniculate ganglion cells to about 5% of control animals in neonates. Degeneration of ganglion cells starts when processes reach the central target (solitary tract) but before they reach the peripheral target (taste buds). Degeneration of ganglion cells is almost completed in trkB knockout mice before taste afferents reach in control animals the developing fungiform papillae. Four days later the first taste buds can be identified in fungiform papillae of both control and trkB knockout mice in about equal number and density. Many taste buds undergo a normal maturation compared to control animals. However, the more lateral and caudal fungiform papillae grow less in size and become less conspicuous in older trkB knockout mice. No intragemmal innervation can be found in trkB knockout taste buds but a few extragemmal fibers enter the apex and end between taste had cells without forming specialized synapses. Taste buds of trkB knockout mice appear less well organized than those of control mice, but some cells show similar vesicle accumulations as control taste bud cells in their base but no synaptic contact to an afferent. These data strongly suggest that the initial-development of many fungiform papillae and taste buds is independent of the specific taste innervation. It remains to be shown why others appear to be more dependent on proper innervation.

Animals↗

PubMed1996

The chick limbless mutation causes abnormalities in limb bud dorsal-ventral patterning: implications for the mechanism of apical ridge formation.

In chick embryos homozygous for the limbless mutation, limb bud outgrowth is initiated, but a morphologically distinct apical ridge does not develop and limbs do not form. Here we report the results of an analysis of gene expression in limbless mutant limb buds. Fgf4, Fgf8, Bmp2 and Msx2, genes that are expressed in the apical ridge of normal limb buds, are not expressed in the mutant limb bud ectoderm, providing molecular support for the hypothesis that limb development fails in the limbless embryo because of the inability of the ectoderm to form a functional ridge. Moreover, Fgf8 expression is not detected in the ectoderm of the prospective limb territory or the early limb bud of limbless embryos. Since the early stages of limb bud outgrowth occur normally in the mutant embryos, this indicates that FGF8 is not required to promote initial limb bud outgrowth. In the absence of FGF8, Shh is also not expressed in the mutant limb buds, although its expression can be induced by application of FGF8-soaked beads. These observations support the hypothesis that Fgf8 is required for the induction of Shh expression during normal limb development. Bmp2 expression was also not detected in mutant limb mesoderm, consistent with the hypothesis that SHH induces its expression. In contrast, SHH is not required for the induction of Hoxd11 or Hoxd13 expression, since expression of both these genes was detected in the mutant limb buds. Thus, some aspects of mesoderm A-P patterning can occur in the absence of SHH and factors normally expressed in the apical ridge. Intriguingly, mutant limbs rescued by local application of FGF displayed a dorsalized feather pattern. Furthermore, the expression of Wnt7a, Lmx1 and En1, genes involved in limb D-V patterning, was found to be abnormal in mutant limb buds. These data suggest that D-V patterning and apical ridge formation are linked, since they show that the limbless mutation affects both processes. We present a model that explains the potential link between D-V positional information and apical ridge formation, and discuss the possible function of the limbless gene in terms of this model.

Animals↗

PubMed1988

Intermediate filaments in mouse taste bud cells.

The intermediate filaments in mouse taste bud cells were studied by immunocytochemistry using antikeratin antibodies, and by conventional electron microscopy. Taste bud cells (types I, II, and III) possessed less densely aggregated bundles of intermediate filaments than the surrounding epithelial cells. Type III cells, however, contained more densely aggregated bundles than type I or II cells. Basal cells in the taste buds showed aggregations of filaments as dense as those seen in the epithelial cells, although their bundles were more slender than those of the epithelial cells. The antibodies to keratins from the bovine muzzle and human stratum corneum stained all types of the taste bud cells as well as the surrounding epithelial cells. PKK2 antibody reacted with the surrounding epithelial cells, but did not react with the taste bud cells. These results show that keratins are present in both taste bud and surrounding epithelial cells, although the keratin subtype differs between those cells. This finding has led us to the supposition that all cell types comprising the taste buds--including type III (receptor) cells--originate from the epithelial cells surrounding the taste buds. It is also suggested that both keratin subtypes and aggregation patterns of intermediate filament bundles change during differentiation from surrounding epithelial cells to taste bud cells, and from basal cells in the taste buds to types I, II, or III cells.

Animals↗

PubMed2004

Taste buds and nerve fibers in the rat larynx: an ultrastructural and immunohistochemical study.

We investigated the rat laryngeal taste buds and their innervation by electron microscopy and immunohistochemical methods. Taste buds were densely arranged in the surface facing the laryngeal cavity of the epiglottis, the aryepiglottic fold, and the cuneiform process of the arytenoid cartilages. The cells of the buds were classified into types I, II, III, and basal cells, the ultrastucture of which was almost the same as that previously reported in lingual taste buds. The type III cells that had synaptic contacts with nerve fibers were considered to be sensory cells. Immunohistochemical analysis revealed thick calbindin D28k-immunoreactive fibers and thin varicose fibers immunoreactive for calcitonin gene-related peptide or substance P in and around the taste bud. Serotonin-immunoreactive cells were also observed here. The results revealed the innervation pattern of laryngeal taste buds to be the same as that in lingual taste buds. Carbonic anhydrase (CA) is known to catalyze the hydration of CO2 and dehydration of H2CO3, and seems to be essential in CO2 reception. Immunoreactivity for CAI was detected in slender cells and that for CAIII was observed in barrel-like cells in the laryngeal taste buds. The pH-sensitive inward rectifier K+ (Kir) channel in the cell membrane may be involved in CO2 reception as well. CAII-reactive cells were also reactive to Kir4.1, PGP 9.5 and serotonin. Our results indicated that CAII and Kir4.1 are located in type III cells of the laryngeal taste buds, and supported the idea that the buds may be involved in the recognition of CO2.

Animals↗

PubMed2002

Analysis of cell lineage relationships in taste buds.

Taste buds are a heterogeneous population of cells exhibiting diverse morphological and biochemical characteristics. Because taste buds arise from multiple progenitors, the different types of taste cells may represent distinct lineages. The present study was undertaken to determine the following: (1) how many progenitors contribute to a taste bud, and (2) whether the specific subpopulation of serotonin-immunoreactive (IR) taste cells are related by lineage to a restricted set of progenitor cells. These questions were addressed using cell lineage analysis of taste buds from H253 X-inactivation mosaic mice. After random X-inactivation of the lacZ transgene, the tongue of hemizygous female mice displays discrete patches of epithelial cells, which are either beta-galactosidase (beta-gal) positive or beta-gal negative. By analyzing the proportion of the two differently stained cell populations in taste buds located at the boundary between positive and negative epithelial patches, we can determine the minimum number of progenitors that may contribute to the formation of a taste bud. The presence of taste buds containing only 6-12% labeled cells indicates that at least eight progenitors contribute to an average taste bud of 55 cells, assuming progenitors contribute equally to the cell population. Cell lineage analysis of serotonin-IR taste cells in such mixed taste buds suggests that this subpopulation likely arises from only one to two progenitors and often is related by lineage. Thus, at least some of the cell types in a taste bud represent distinct lineages of cells and are not merely phenotypic stages as a cell progresses from a young to a mature state.

Animals↗

PubMed1992

Talpid2 limb bud mesoderm does not express GHox-8 and has an altered expression pattern of GHox-7.

We have studied the expression patterns of the chick homeobox-containing genes, GHox-7 and GHox-8, in the talpid2 (ta2) chick mutant whose limbs have abnormal pattern. These studies provide new insight into how homeobox gene expression and limb patterning may be related. This is the first study demonstrating a natural change in GHox-7 and GHox-8 along the anteroposterior axis. While GHox-7 is expressed asymmetrically in normal limb buds, it is expressed at a uniform level across the anteroposterior axis of ta2 limb buds. GHox-8 is expressed in anterior mesoderm of normal limb buds, but is undetectable in ta2 limb bud mesoderm. These data are consistent with the subtle anteroposterior polarity in ta2 limbs, and allow us to propose that ta2 limb buds lack anterior positional information, but have a narrow range of posterior positional values. We suggest that in normal limb buds GHox-8 may establish the anterior limb bud boundary. Furthermore, we point out that coexpression of GHox-7 and GHox-8 in normal anterior limb bud mesoderm can be correlated with the reduced apical ridge maintenance activity of this tissue, while the lack of coexpression in ta2 limb buds is correlated with the strong ridge maintenance activity in the mutant's anterior limb bud mesoderm. Last, ta2 limbs contain no dying cells in their anterior and posterior border mesoderm; nevertheless, they express GHox-7 in these regions. These data challenge the proposal that this gene determines cell death.

Animals↗

PubMed2003

Budding as a useful prognostic marker in pT3 well- or moderately-differentiated rectal adenocarcinoma.

BACKGROUND: Budding along the invasive margin is reported to be associated with greater malignant potential in colorectal adenocarcinoma. We examined the prognostic significance of budding in patients with pT3 rectal carcinoma, particularly in comparison to other routine pathological findings. METHODS: Surgically resected specimens from 83 well- or moderately-differentiated pT3 rectal adenocarcinomas were studied. All resections were curative (R0), and the median postoperative follow-up was 47 months. We examined the presence of budding according to Morodomi's criteria, using hematoxylin-eosin stained sections. RESULTS: Budding was found in 48 patients (57.9%). The incidence of budding was significantly higher in lesions displaying lymphatic invasion and lymph-node metastasis than in those without (P < 0.0001). Both local recurrence and liver metastasis were more frequent in patients with budding-positive lesions (P < 0.002 and 0.02, respectively). Moreover, postoperative survival was significantly decreased in patients with budding-positive lesions than in those with budding-negative lesions (cumulative 5-year survival rate were 51.8 and 85.0%, respectively: P < 0.002). Multivariate proportional hazard model revealed that the presence of budding was the only significant co-factor of postoperative survival. CONCLUSIONS: Budding is a pathological marker suggesting high malignant potential and decreased postoperative survival in patients with well- or moderately-differentiated pT3 rectal adenocarcinoma.

Adenocarcinoma↗

PubMed1991

Changes in mesenchymal cell-shape, matrix collagen and tenascin accompany bud formation in the early chick lung.

In the chick, lung branches arise as buds from the center of the pre-existing mesobronchial tube. Budding is known to be controlled by the mesenchyme. We have investigated mesenchymal properties in budding vs non-budding regions of the early chick lung, including sources of mesenchyme, cell shapes and densities, morphology and composition of the basement membrane, and distribution of the ECM components collagen, fibronectin and tenascin. We found that at points of outgrowth--the buds and the distal tip of the mesobronchus-mesenchymal cells adjacent to the lung epithelium are flattened, and the basement membrane is markedly thinned. In these basement membranes collagen is largely absent and tenascin redistributed into amorphous clumps. Of these characteristics only the cell-shape change, which results in the flattened mesenchymal cells at the bud tips, is correlated with initiation of the bud. We suggest that the cell-shape change leads to localized loss of collagen, which promotes emergence of buds, and that tenascin, which is found in the mesenchyme only in the budding region, promotes outgrowth and elongation of the bud.

Animals↗

PubMed1986

End buds: non-ampullary electroreceptors in adult lampreys.

Shared anatomical and physiological characters indicate that the low-frequency sensitive electrosensory system of lampreys is homologous with those of non-teleost fishes and amphibians. However, the ampullary electroreceptor organs which characterize all of these gnathostomes are not found in lampreys. Experimental anatomical and physiological studies reported here demonstrate that the epidermal end buds are the electroreceptors of adult lampreys. End buds, consisting of both sensory and supporting cells, are goblet-shaped with the top (25-60 microns diameter) at the epidermal surface and the stem directed toward the dermis (Fig. 1A). Short lines or clusters of 2-8 end buds (Fig. 1B) are distributed over both trunk and head. Injections of horseradish peroxidase (HRP) into vitally-stained end buds labeled anterior lateral line afferents terminating in the ipsilateral dorsal nucleus (Fig. 2A) - the primary electrosensory nucleus of the lamprey medulla. Conversely, after HRP injection into the dorsal nucleus HRP-filled fibers and terminals were present on ipsilateral end buds (Fig. 2B). End buds are usually not visible without staining. However, in adult sea lampreys the presence of end buds was histologically confirmed in skin patches containing the receptive fields of electroreceptor fibers recorded in the anterior lateral line nerve. Additionally, in the rare instance of two silver lampreys in which end buds were visible without staining, electrosensory activity indistinguishable from that of the primary electroreceptor afferents was recorded from the end bud surface (Figs. 3, 4). End buds were initially characterized as chemoreceptors (Johnston 1902) but were later correctly advanced as lateralis receptors based on the presence of presynaptic dense bodies in the receptor cells (Whitear and Lane 1981).(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

PubMed1998

Dormancy-associated gene expression in pea axillary buds. Cloning and expression of PsDRM1 and PsDRM2.

Pea (Pisum sativum L. cv. Alaska) axillary buds can be stimulated to cycle between dormant and growing states. Dormant buds synthesize unique proteins and are as metabolically active as growing buds. Two cDNAs, PsDRM1 and PsDRM2, were isolated from a dormant bud library. The deduced amino acid sequence of PsDRM1 (111 residues) is 75% identical to that of an auxin-repressed strawberry clone. PsDRM2 encodes a putative protein containing 129 residues, which includes 11 repeats of the sequence [G]-GGGY[H][N] (the bracketed residues may be absent). PsDRM2 is related to cold- and ABA-stimulated clones from alfalfa. Decapitating the terminal bud rapidly stimulates dormant axillary buds to begin growing. The abundance of PsDRM1 mRNA in axillary buds declines 20-fold within 6 h of decapitation; it quickly reaccumulates when buds become dormant again. The level of PsDRM2 mRNA is about three fold lower in growing buds than in dormant buds. Expression of PsDRM1 is enhanced in other non-growing organs (roots >> root apices; fully-elongated stems > elongating stems), and thus is an excellent "dormancy" marker. In contrast, PsDRM2 expression is not dormancy-associated in other organs.

Amino Acid Sequence↗

PubMed1992

Regulation of mammary morphogenesis: evidence for extracellular matrix-mediated inhibition of ductal budding by transforming growth factor-beta 1.

Branching morphogenesis in the mammary gland involves focal regions of cell proliferation, the terminal and lateral ductal buds, that exist simultaneously with extensive regions of differentiated ducts in which budding and growth are actively suppressed. Exogenous transforming growth factor-beta 1 (TGF-beta 1) has previously been shown to locally inhibit the formation and growth of mammary ductal buds. Here we report that endogenous TGF-beta 1, produced by epithelial and stromal mammary cells, forms complexes with extracellular matrix (ECM) molecules surrounding those ductal structures in which budding is inhibited. The largest amounts of immunostainable TGF-beta 1 are found in mature periductal ECM, and the least in newly synthesized ECM. In all areas of active ductal growth, where DNA-synthetic buds were forming new ductal branches, we found a highly focal loss of TGF-beta 1 from the periductal ECM at the bud-forming region of the duct. When growth of the new buds terminated, the structures again became associated with TGF-beta-rich ECM. These findings indicate that ECM must reach a certain state of maturity before it becomes associated with TGF-beta 1 and that TGF-beta 1 can be depleted selectively from the periductal ECM at focal growth points. A different type of growth point, the alveolar (secretory) buds, was also investigated. These buds are known not to be inhibited by exogenous TGF-beta 1, and we found them not to be associated with changes in ECM-bound TGF-beta 1. Our results support the concept that the periductal ECM acts as a reservoir for TGF-beta 1 that functions to maintain an open pattern of mammary branching by inhibiting ductal, but not alveolar, bud formation.

Animals↗

PubMed2000

Dynamics of non-structural carbohydrates in developing leaves, bracts and floral buds of cotton.

Development of cotton (Gossypium hirsutum L.) squares (i.e. floral buds with bracts) is fundamental for yield formation. A 2-year field study was conducted to determine dry weight (DW) accumulations of cotton leaves, floral bracts and floral buds, and the changes in concentrations of non-structural carbohydrates (hexoses, sucrose and starch) in these tissues during square ontogeny as affected by fruiting positions within the plant canopy. During square development, DW accumulation of a subtending sympodial leaf and floral bracts followed a sigmoid growth curve with increasing square age, whereas the DW increase of a floral bud followed an exponential curve. Main-stem node (Node 8, 10 or 12) and branch position (proximal vs. distal) within a plant canopy significantly affected DW accumulations of the leaf, bracts and floral bud. Starch was the dominant non-structural carbohydrate in the three tissues, accounting for more than 65% of total non-structural carbohydrates (TNC). Subtending leaf TNC increased as square age increased. The bracts exhibited a smaller change in TNC than leaves. Non-structural carbohydrate concentration was the lowest in 10-day-old floral buds, and had little change during the first 15 days of square development. Within 5 days prior to anthesis, the floral-bud TNC increased dramatically, tripling at the time of floral anthesis compared with 15-day-old floral buds. Square age and fruiting position significantly affected non-structural carbohydrate concentrations of subtending leaves, bracts, and floral buds. The correlation did not exist between final boll retention and non-structural carbohydrate concentrations of floral buds at different fruiting positions under normal growth conditions. The pattern of floral-bud non-structural carbohydrates during square ontogeny suggests that major events in carbohydrate metabolism occur just prior to anthesis.

Journal Article↗

PubMed1996

Retinoic acid is required for the initiation of outgrowth in the chick limb bud.

BACKGROUND: Retinoic acid (RA) is present in the chick limb bud, and excess RA induces limb duplications. Here, we have investigated the role of endogenous RA during chick limb development by preventing the synthesis of RA and testing the effect on various genes expressed during limb initiation and outgrowth. RESULTS: We demonstrate that the stage 20/21 limb bud synthesizes didehydroretinoic acid (ddRA), and that the posterior half of the limb bud synthesizes ddRA at a higher rate than the anterior half. Disulphiram inhibits this synthesis at micromolar concentrations. Administering disulphiram to embryos prior to limb bud outgrowth (stages 12-18) abolishes outgrowth, and no limb develops in the majority of cases. Disulphiram treatment also prevents the expression of Sonic hedgehog (Shh), but the expression of the fibroblast growth factor-8 gene (Fgf-8) appears as normal in the ectoderm over the prospective limb bud. The application of a bead soaked in RA can rescue Shh expression. Disulphiram treatment of later limb buds (stages 20-23) similarly down-regulates Shh, and also Fgf-4, expression, whereas the expression of Fgf-8, as at earlier stages, is initially unaffected. Again, RA can rescue the expression of Shh in these limb buds. CONCLUSIONS: RA, in conjunction with Fgf-8, may be needed for the induction of the chick limb bud and the induction of Shh and Fgf-4 expression. The expression of Shh and Fgf-4 remains dependent upon the continued synthesis of RA within the limb bud. Didehydroretinoic acid is the major active retinoid in the stage 20 chick limb bud.

Animals↗

PubMed2003

Conservation of mechanisms controlling entry into mitosis: budding yeast wee1 delays entry into mitosis and is required for cell size control.

BACKGROUND: In fission yeast, the Wee1 kinase delays entry into mitosis until a critical cell size has been reached; however, a similar role for Wee1-related kinases has not been reported in other organisms. SWE1, the budding yeast homolog of wee1, is thought to function in a morphogenesis checkpoint that delays entry into mitosis in response to defects in bud morphogenesis. RESULTS: In contrast to previous studies, we found that budding yeast swe1 Delta cells undergo premature entry into mitosis, leading to birth of abnormally small cells. Additional experiments suggest that conditions that activate the morphogenesis checkpoint may actually be activating a G2/M cell size checkpoint. For example, actin depolymerization is thought to activate the morphogenesis checkpoint by inhibiting bud morphogenesis. However, actin depolymerization also inhibits bud growth, suggesting that it could activate a cell size checkpoint. Consistent with this possibility, we found that actin depolymerization fails to induce a G2/M delay once daughter buds pass a critical size. Other conditions that activate the morphogenesis checkpoint block bud formation, which could also activate a size checkpoint if cell size at G2/M is monitored in the daughter bud. Previous work reported that Swe1 is degraded during G2, which was proposed to account for failure of large-budded cells to arrest in response to actin depolymerization. However, we found that Swe1 is present throughout G2 and undergoes hyperphosphorylation as cells enter mitosis, as found in other organisms. CONCLUSIONS: Our results suggest that the mechanisms known to coordinate entry into mitosis in other organisms have been conserved in budding yeast.

Blotting, Western↗

PubMed2000

Chemical genetic analysis of the budding-yeast p21-activated kinase Cla4p.

The p21-activated kinases (PAKs) are effectors for the Rho-family GTPase Cdc42p. Here we define the in vivo function of the kinase activity of the budding yeast PAK Cla4p, using cla4 alleles that are specifically inhibited by a cell-permeable compound that does not inhibit the wild-type kinase. CLA4 kinase inhibition in cells lacking the partially redundant PAK Ste20p causes reversible SWE1-dependent cell-cycle arrest and gives rise to narrow, highly elongated buds in which both actin and septin are tightly polarized to bud tips. Inhibition of Cla4p does not prevent polarization of F-actin, and cytokinesis is blocked only in cells that have not formed a bud before inhibitor treatment; cell polarization and bud emergence are not affected by Cla4p inhibition. Although localization of septin to bud necks is restored in swe1Delta cells, cytokinesis remains defective. Inhibition of Cla4p activity in swe1Delta cells causes a delay of bud emergence after cell polarization, indicating that this checkpoint may mediate an adaptive response that is capable of promoting budding when Cla4p function is reduced. Our data indicate that CLA4 PAK activity is required at an early stage of budding, after actin polarization and coincident with formation of the septin ring, for early bud morphogenesis and assembly of a cytokinesis site.

Alleles↗

PubMed2006

Tumour budding at the deepest invasive margin correlates with lymph node metastasis in submucosal colorectal cancer detected by anticytokeratin antibody CAM5.2.

In the past few years, tumour budding at the invasive margin has been reported as a new risk factor for lymph node metastasis in advanced colorectal cancers, but it is sometimes difficult to detect tumour budding in submucosal colorectal cancer by haematoxylin and eosin staining. We immunohistochemically examined tumour budding at the deepest invasive margin of 56 surgically resected submucosal colorectal carcinomas using anticytokeratin antibody CAM5.2, furthermore checked by AE1/AE3, and determined the relation between tumour budding and clinicopathological factors. Moreover, we used the monoclonal antibody D2-40 for immunohistochemistry to detect lymphatic involvement. Tumour budding was detected in 42 cases (75.0%), and the budding-positive group showed a significantly higher rate of lymph node metastasis (including isolated tumour cells) (16/42 vs 0/14; P=0.004) than the budding-negative group. The sensitivity and negative predictive value of tumour budding alone for lymph node metastasis were superior to those of lymphatic invasion alone. Furthermore, the specificity and positive predictive value of the combination of either lymphatic invasion or tumour budding were superior to those of lymphatic invasion alone. Tumour budding detected immunohistochemically by using CAM5.2 is a newly found risk factor for lymph node metastasis and may help to avoid oversurgery in the future.

Adenocarcinoma↗

PubMed2000

Basement membrane chondroitin sulfate proteoglycan and vascularization of the developing mammalian limb bud.

We used immunocytochemistry to study the basement membrane-chondroitin sulfate proteoglycan (BM-CSPG) distribution in mammalian limb bud and its relationship to and possible role in limb development. Anti-BM-CSPG immunostaining was examined in the developing limb buds of 24 Sprague-Dawley rats at embryonic days 12 to 14 and 19. BM-CSPG immunostaining was present in 3 regions. The first region was located peripherally in the limb bud ectodermal basement membrane (BM) that separates ectoderm from mesoderm and was present at all embryonic stages examined. The second region was in the mesenchymal extracellular matrix independent of the vascular system. This staining pattern was diffuse, granular, and often homogeneous, except for clustering adjacent to developing vessels, and was observed distally in the limb bud. In the mesenchymal extracellular matrix adjacent to the distal BM this staining pattern formed fibrils that were perpendicular and connected to the limb bud BM and extended into the underlying mesenchyme. The third region was localized to the BM of developing blood vessels of the limb bud. Blood vessel staining allowed analysis of limb bud vessel formation. The early developing blood vessels at the proximal limb bud were organized differently from those located distally. Large central vessels were present proximally, whereas a rich plexus of smaller vascular channels was present at the distal margin. A subectodermal avascular zone was observed at the margin of the limb bud, except beneath the apical ectodermal ridge where immunostained blood vessels extended from the distal vascular plexus toward the apical ectodermal ridge. The formation of central larger vessels occurs proximally, whereas formation of peripheral smaller vessels seems to take place locally and distally under the influence of the apical ectodermal ridge. BM-CSPG plays an important role in blood vessel formation and mammalian limb bud development. (J Hand Surg 2000; 25A:150-158.

Animals↗