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Dendritic spread of dorsal horn neurons in cats.

Observations of neurons in dorsal horn laminae IV-VI of the lumbosacral segments of Golgi-stained spinal cords in kittens and adult cats revealed laminar differences in dendritic architecture. Many neurons in lamina IV had dense, bushy dendritic fields. Lamina V contained, in addition to bushy cells similar in appearance to those of lamina IV, increasing numbers of neurons with radiating dendritic fields. Lamina VI was composed almost exclusively of neurons with radiating dendritic fields. These qualitative differences among laminae were accompanied by systematic variations in mean dendritic spread, which increased more than two-fold in adult cats between laminae IV and VI. A second gradient of dendritic spread was found within individual laminae: dendritic spread, particularly medial to lateral spread, increased for successively more lateral cells within a lamina. These differences in the spread of dendrites for neurons in different regions of the dorsal horn may be related to variations in the areas of peripheral receptive fields of dorsal horn neurons.

Age Factors↗

Carcinoma of the ampulla of Vater: histopathologic analysis of tumor spread in Whipple pancreatoduodenectomy specimens.

Controversies exist regarding the application of the pylorus-preserving pancreatoduodenectomy (PPPD) to malignancies. This study was intended to disclose the pattern of spread of ampullary cancer and to substantiate that tumor spread at resectable stages does not involve the tissues preserved by PPPD. We examined 40 consecutive Whipple pancreatoduodenectomy specimens: mucosal cancer, 4 cases; cancer invading (but not penetrating) the sphincter of Oddi, 1; cancer invading the submucosa of the duodenum, 12; cancer invading the proper muscle of the duodenum, 5; cancer invading the subserosal layer of the duodenum, 7; and cancer invading pancreatic parenchyma, 11. Five cases of mucosal cancer or cancer invading (but not penetrating) the sphincter spread locally without nodal involvement and showed a 5-year survival of 80% without recurrence, being better (p < 0.05) than the 40% survival for patients with more advanced cancers. Sixty-three percent of the remaining 35 cases had metastasis to regional lymph nodes. The 5-year survival of 28% among those with cancer penetrating the proper muscle was worse (p < 0.05) than the 59% survival for those with less advanced cancers. No cases had involved the anatomic structures that would have been preserved by a PPPD. In three cases (7.5%), gastric cancer coexisted. In conclusion, ampullary cancer not penetrating the sphincter spreads locally. Once penetrating the sphincter, it often spreads regionally and causes recurrence. Cancer penetrating the proper muscle of the duodenum bears a worse prognosis. PPPD is an attractive alternative to the Whipple operation for ampullary cancer because no involvement was found in the tissue preserved by the PPPD. However, surgeons should be aware of a concomitant gastric cancer when doing a PPPD.

Adult↗

Faithful in vivo transcription termination of Xenopus laevis rDNA. Correlation of electron microscopic spread preparations with S1 transcript analysis.

DNA sequencing and subsequent functional in vitro analysis of the Xenopus laevis rDNA transcription termination has led to the identification of three transcription termination sequence elements: T1, located at the 3' end of the 28S rDNA; T2, a putative processing site 235 bp downstream of T1; T3, the principal terminator positioned 215 bp upstream of the gene promoter. As demonstrated for nuclear run-off assays, T3 was found to be the main terminator for Xenopus rDNA transcription. These in vitro data are in obvious contradiction to results obtained by electron microscopic (EM) spread preparations from rapidly isolated amplified oocyte nucleoli, i.e., an rDNA chromatin probe thought to represent the in vivo situation, indicative of transcription termination at sites T1-2. However, most interestingly, T3 had--again by the EM method--been identified as the exclusive terminator for NTS spacer transcription units. In order to answer the question of whether read-through transcription of the complete rDNA spacer sequence is obligatory for 40S pre-rRNA in vivo transcription, we analyzed several hundreds of spread rRNA genes from Xenopus oocyte nucleoli in great detail, applying two different spreading procedures, e.g., dispersal of amplified oocyte nucleoli shortly in detergent-free or detergent containing low-salt media prior to the EM spreading technique. Quantitation of EM spreads resulted in the finding that read-through rDNA spacer transcription beyond T1-2 termination sites (i.e., indicative of T3 transcription termination) can be visualized for the in vivo situation at a frequency of less than 3% of rRNA genes analyzed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The spreading of leukocytes released from their liquid environment.

It is known that while leukocytes in conventional blood smears reveal their structures, in smears of erythrocyte-free suspension (EFS) they show a tendency to pyknosis. From the present study it appears that: 1. When any leukocyte suspension is subjected to drying on slides the cells undergo shrinkage (pyknosis in stained state) because their water content is extracted by the suspending fluid that is rendered increasingly hypertonic during drying. 2. When the leukocytes, which while floating within physiological fluids are ball-shaped, are entirely released from their suspending fluid, they suddenly spread into flat cells because the capillary force between the cell membranes and glass overcomes the surface tension of the cells. 3. In contrast to shrunken or even normal (spherical) cells, spread cells are able to display their morphology. Using the smear technique, the cell density of the suspension will determine whether spreading or shrinkage are to occur; with normal blood (high density) the release and consequently the spread are achieved; with EFS (usually of low density) an inadequate release and consequently shrinkage occur. 4. A device (cell spreader) for spreading leukocytes of EFS is presented.

Animals↗

Distal intramural spread in adenocarcinoma of the lower third of the rectum treated with total rectal resection and coloanal anastomosis.

PURPOSE: This study was designed to evaluate the frequency of microscopic distal intramural spread in rectal adenocarcinoma and its correlation to other histopathologic prognostic factors. METHODS: We examined 55 patients with adenocarcinomas of the lower one-third of the rectum and measured the extent of distal intramural spread in the submucosa and/or muscular layer in comparison with Dukes Stage, diameter of tumor, distance of distal margin of resection from tumor, depth of infiltration into perirectal adipose tissue, nodal status, neoplastic infiltration of lymphatic vessels, blood vessels, and nervous branches. RESULTS: Distal intramural spread was found in 40 percent of patients, 77 percent of whom had advanced tumors with nodal metastases. Distal intramural spread appeared to be strictly related to tumor size (superior to 40 mm), infiltration of the perirectal adipose tissue, multiple positive lymph nodes, presence of neoplastic emboli in the intramural lymphatic vessels, and neoplastic invasion of the nervous branches. Local recurrence occurred in one Dukes Stage B patient with a positive distal margin of resection and in four patients with a negative distal margin of resection: three Dukes Stage C and one Dukes Stage B patients with neoplastic involvement of the circumferential margin of resection of the mesorectum. CONCLUSION: These preliminary data suggest that distal intramural spread may carry little importance in determining local recurrence of rectal adenocarcinoma.

Adenocarcinoma↗

Distal intramural spread of rectal carcinomas.

Forty-three consecutive specimens of resected rectal carcinomas, 16 abdominoperineal and 27 anterior resections, were examined for distal intramural spread. Thirty-four of the resections were considered curative and nine palliative. Eighteen carcinomas (42 percent) showed no distal spread, and 14 (33 percent) showed very limited distal spread (0-5 mm). In the remaining cases, 11 (25 percent) had distal spread of more than 5 mm and eight of more than 10 mm. The eight carcinomas with distal spread of greater than 10 mm were advanced Dukes' C tumors. Only three were considered curable. All potentially curable carcinomas would have been resected adequately with a distal margin of only 1.5 cm except one signet-ring carcinoma with extensive lymph node metastases located in the lower rectum.

Aged↗

Effects of fibronectin-related peptides on cell spreading.

Four synthetic peptides related in amino acid sequence to the area of the fibronectin molecule thought to be involved in cell binding were tested for the ability to inhibit cell spreading promoted by several different attachment factors. Effects of the peptides were assayed on a number of cell types. For all cell types tested, peptides effective at inhibiting fibronectin-promoted cell spreading were found also to inhibit cell spreading promoted by human serum spreading factor (SF). These peptides were also capable of inhibiting to a lesser extent cell spreading promoted by other attachment factors, although this phenomenon was dependent on the cell type examined.

Cell Adhesion↗

Collateral damage: spread of repeat-induced point mutation from a duplicated DNA sequence into an adjoining single-copy gene in Neurospora crassa.

Repeat-induced point mutation (RIP) is an unusual genome defense mechanism that was discovered in Neurospora crassa. RIP occurs during a sexual cross and induces numerous G : C to A : T mutations in duplicated DNA sequences and also methylates many of the remaining cytosine residues. We measured the susceptibility of the erg-3 gene, present in single copy, to the spread of RIP from duplications of adjoining sequences. Genomic segments of defined length (1, 1.5 or 2 kb) and located at defined distances (0, 0.5, 1 or 2 kb) upstream or downstream of the erg-3 open reading frame (ORF) were amplified by polymerase chain reaction (PCR), and the duplications were created by transformation of the amplified DNA. Crosses were made with the duplication strains and the frequency of erg-3 mutant progeny provided a measure of the spread of RIP from the duplicated segments into the erg-3 gene. Our results suggest that ordinarily RIP-spread does not occur. However, occasionally the mechanism that confines RIP to the duplicated segment seems to fail (frequency 0.1-0.8%) and then RIP can spread across as much as 1 kb of unduplicated DNA. Additionally, the bacterial hph gene appeared to be very susceptible to the spread of RIP-associated cytosine methylation.

Base Sequence↗

Tyrosine Phosphorylation of a ~30 kD Protein Precedes avb3 Integrin-signaled Endothelial Cell Spreading and Motility on Matrix Proteins.

A microvascular endothelial cell line (CD clone 4) isolated from murine lung adheres to and spreads well on fibronectin, vitronectin, and fibrinogen, but poorly on collagen type IV and laminin. Ligating cell surface av, b3, a4, a5, or b1 integrin receptors with monospecific antibodies promoted a dramatic cell spreading and motility on vitronectin or collagen IV. Antibodies directed to other adhesion molecules, including aIIb, PECAM-1, and P-selectin were ineffective. Ligation with monoclonal anti-av or -b3, but not -a4, -a5, or -b1 antibodies, induced a rapid, and dose-dependent tyrosine phosphorylation of a ~30 kD protein, which preceded CD clone 4 endothelial cell spreading and motility and was partially inhibited by genistein and completely inhibited by BAPTA. All other antibodies tested did not induce the tyrosine phosphorylation of the 30 kD protein as well as cell spreading and motility. The present results suggest that b1 and b3 integrins employ different biochemical mechanisms in signaling endothelial cell spreading and motility and that the tyrosine phosphorylation of the 30 kD protein (and probably other proteins) may play an important role in signaling b3 integrin-mediated endothelial cell interaction with other cells (e.g., tumor cells) and extracellular matrix.

Journal Article↗

Adhesion and spreading of corneal endothelial cells on collagens type I and IV in vitro: a model to study mechanisms of endothelial repair.

In vitro assays using endothelial cells (EC, bovine corneal) were performed to study adhesion and spreading on collagen types I and IV. Adhesion was quantitatively analyzed by counting the EC under a light microscope. Spreading was determined by measuring cell area using a scanning electron microscope (SEM). Collagen types I, IV, and IV-F, a mixture of 70, 120, and 140 KD fragments of type IV, all promoted EC adhesion, Types IV and IV-F showed evidence of giving a more marked adhesion than type I. A study of cell area, carried out under identical conditions, such as those in the adhesion assay, showed that types I and IV-F, but not type IV, promoted cell spreading. This provides evidence that cell adhesion and spreading are indeed separate biological phenomena. Furthermore, the ability of fragments of type IV collagen to promote both cell adhesion and spreading may represent an inherent repair mechanism in damaged endothelium.

Animals↗

[Squamous cell carcinomas of the upper aerodigestive tract. Prognostic significance of the capsular rupture and extracapsular spread of lymph node metastases].

The capsular rupture and subsequent extranodal spread of lymph node metastases is of crucial and well established prognostic value in patients with squamous cell carcinomas of the upper aerodigestive tract. Besides the basic histologic definition of the extranodal spread (i.e. contact of the metastasis with perinodal fatty tissue), there is no agreement on the morphologic extent of transcapsular spread. As a measure of improvement, a histologic evaluation differentiating between seven gradual types of metastatic nodal affection was applied. The histologic scheme considers intranodal growth, infiltration of the capsule, the presence of desmoplasia and especially the rupture of the capsule and the subsequent extranodal spread of the metastasis. As extranodal spread is an easily reproducible and reliably significant prognostic criterion, it should be included in the current TNM classification, e.g., by an addition of the index R+ (lymph node metastasis with capsular rupture) or R- (lymph node metastasis without capsular rupture) to the N category.

Carcinoma, Squamous Cell↗

Primary synovial osteochondromatosis of the hip: extracapsular patterns of spread.

OBJECTIVE: To identify patterns of extracapsular extension of synovial osteochondromatosis of the hip. DESIGN AND PATIENTS: Seven cases of synovial osteochondromatosis of the hip were retrospectively reviewed. Imaging performed included conventional radiography ( n=7), arthrography ( n=1), CT ( n=3) and MR imaging ( n=3). Disease extent on imaging was assessed for each patient and the presence of intra-articular effusion, capsular abnormality and osteochondral bodies recorded. The presence and distribution of extra-articular spread was also assessed and correlated with the surgical findings. In all cases diagnosis was confirmed by biopsy, with all patients undergoing tumor resection with or without synovectomy. RESULTS: In five cases (5/7) disease extended beyond the hip capsule, while the remaining two cases (2/7) were confined to the hip joint. These findings were confirmed at surgery. Two distinct patterns of extracapsular spread were identified. The first pattern, noted in three cases, involved tumor extension along iliopsoas. The second pattern, noted in five cases, involved tumor extension along the obturator externus fat plane. In three cases both patterns were present. CONCLUSIONS: Extra-articular spread of synovial osteochondromatosis is common. Patterns of extra-articular spread may be predictable based on involvement of recognized periarticular bursae of the hip joint. Bursal patterns of extra-articular spread include extension into the iliopsoas bursa as well as communication along the obturator externus bursa of the hip.

Adult↗

Spread rate for a nonlinear stochastic invasion.

Despite the recognized importance of stochastic factors, models for ecological invasions are almost exclusively formulated using deterministic equations [29]. Stochastic factors relevant to invasions can be either extrinsic (quantities such as temperature or habitat quality which vary randomly in time and space and are external to the population itself) or intrinsic (arising from a finite population of individuals each reproducing, dying, and interacting with other individuals in a probabilistic manner). It has been long conjectured [27] that intrinsic stochastic factors associated with interacting individuals can slow the spread of a population or disease, even in a uniform environment. While this conjecture has been borne out by numerical simulations, we are not aware of a thorough analytical investigation. In this paper we analyze the effect of intrinsic stochastic factors when individuals interact locally over small neighborhoods. We formulate a set of equations describing the dynamics of spatial moments of the population. Although the full equations cannot be expressed in closed form, a mixture of a moment closure and comparison methods can be used to derive upper and lower bounds for the expected density of individuals. Analysis of the upper solution gives a bound on the rate of spread of the stochastic invasion process which lies strictly below the rate of spread for the deterministic model. The slow spread is most evident when invaders occur in widely spaced high density foci. In this case spatial correlations between individuals mean that density dependent effects are significant even when expected population densities are low. Finally, we propose a heuristic formula for estimating the true rate of spread for the full nonlinear stochastic process based on a scaling argument for moments.

Animals↗

Spreading speed and linear determinacy for two-species competition models.

One crucial measure of a species' invasiveness is the rate at which it spreads into a competitor's environment. A heuristic spread rate formula for a spatially explicit, two-species competition model relies on 'linear determinacy' which equates spread rate in the full nonlinear model with spread rate in the system linearized about the leading edge of the invasion. However, linear determinacy is not always valid for two-species competition; it has been shown numerically that the formula only works for certain values of model parameters when the model is diffusive Lotka-Volterra competition [2]. This paper derives a set of sufficient conditions for linear determinacy in spatially explicit two-species competition models. These conditions can be interpreted as requiring sufficiently large dispersal of the invader relative to dispersal of the out-competed resident and sufficiently weak interactions between the resident and the invader. When these conditions are not satisfied, spread rate may exceed linearly determined predictions. The mathematical methods rely on the application of results established in a companion paper [11].

Animals↗

Role of ultrasonography in the detection of intraductal spread of breast cancer: correlation with pathologic findings, mammography and MR imaging.

The purpose of this study was to assess the role of US in the detection of intraductal spread of breast cancer in comparison with mammography (MMG) and MRI. In 46 patients with breast cancer, US features of the intraductal component were classified as ductal type or distorted type. Histopathologically, 29 of 46 (63%) cases had intraductal components, and the sensitivity, specificity, and accuracy rates in detection of intraductal spread were 89, 76, and 85%, respectively. Each US pattern demonstrated good correspondence to the histologic components, and the distorted type correlated well with comedo-type carcinoma. Mammography was performed in all cases, and the sensitivity, specificity, and accuracy rates in detection of intraductal spread were 55, 100, and 72%, respectively. In comedo type, MMG could diagnose the extent of intraductal spread more accurately compared with US examination. Magnetic resonance imaging comparison was available in 25 cases. Magnetic resonance imaging depicted intraductal extension as an enhanced area during the early phase of a contrast enhancement study with a sensitivity of 93%. Ultrasound and MRI were closely related in terms of morphologic characteristics: the ductal type of US image correlated well with linear enhancement on MRI, whereas the distorted type correlated with regional or segmental enhancement. Current US examination is useful in depicting the intraductal spread of breast cancer; however, US has a tendency to underestimate intraductal component of comedo type compared with MMG and MRI.

Breast↗

Microscopic spread of low rectal cancer in regions of the mesorectum: detailed pathological assessment with whole-mount sections.

BACKGROUND AND AIMS: The aim was to investigate the regional spread of microscopic tumor nodules in the mesorectum of patients with low rectal cancer, and to provide further pathological evidence for optimal procedure selection of radical resection for rectal cancer. PATIENTS AND METHODS: Sixty-two patients with low rectal cancer underwent low anterior resection and total mesorectal excision (TME). Surgical specimens were sliced transversely on serial embedded blocks at 2.5-mm intervals, and stained with hematoxylin and eosin. On whole-mount sections the mesorectum was divided into three regions: the outer region of the mesorectum (ORM), the middle region of the mesorectum (MRM), and the inner region of the mesorectum (IRM). Microscopic metastatic foci were investigated for metastatic mesorectal region, frequency, types, involvement of the lymphatic system, and correlation with the primary tumor. RESULTS: Microscopic spread of the tumor was observed in 38.7% of patients (24 out of 62) and that in the ORM was observed in 25.8% of the patients (16 out of 62). Microscopic tumor foci spread in the circumferential resection margin (CRM) occurred in 6.5% of the patients (4 out of 62), and distal mesorectum (DMR) involvement was detected in 6.5% (4 out of 62), with the spread extending to within 3 cm from the lower margin of the tumor. CONCLUSIONS: The results of the present study support the theory that complete excision of the mesorectum without destruction of the ORM is essential for surgical management of low rectal cancer, and an optimal DMR clearance resection margin should be no less than 4 cm. Four patients with microscopic tumor nodule spread in the ORM observed in the study suggested that microscopic metastases exist in pelvic lateral areas and in the mesorectum simultaneously, indicating the significance of preoperative and/or postoperative radiochemotherapy.

Adenocarcinoma↗

Absence of correlation between late-replication and spreading of X inactivation in an X;autosome translocation.

We have analysed the spread of X inactivation in an individual with an unbalanced 46,X,der(X)t(X;10)(q26.3;q23.3) karyotype. Despite being trisomic for the region 10q23.3-qter, both the proband and her aunt with the same karyotype presented only with secondary amenorrhoea and lacked any features normally associated with trisomy of distal 10q. Cytogenetic and molecular studies showed that the derivative X;10 chromosome was exclusively inactive. Transcribed polymorphisms were identified in five genes contained within the translocated region of chromosome 10 and were used to perform allele-specific transcription studies. We showed that four of the genes studied are inactive on the derivative chromosome, directly demonstrating the spread of X inactivation over some 30 Mb of autosomal DNA. However, the most distal gene examined remained active, indicating that this spreading was incomplete. In contrast to the gene expression data, replication timing studies showed no spreading of late replication into the translocated portion of 10q. We conclude that silencing of autosomal genes by X inactivation can occur without a delay in the replication timing of the surrounding chromatin. Our findings support the hypothesis that autosomal chromatin lacks certain features present on the X chromosome that are required for the effective spread and/or maintenance of X inactivation.

Adolescent↗

Effects of tilting in the sagittal plane on the cephalad spread of anesthesia.

The effect of tilting in the sagittal plane on the spread of anesthesia was studied in 30 healthy male patients. Two ml of 0.3% hyperbaric dibucaine was used for intrathecal injection in the lateral position. After 3 min of resting on their side, 15 patients were placed in the horizontal supine position. Other 15 patients were turned to the contralateral side at 7-8 degrees in the sagittal plane. Cephalad spread of sensory analgesia by the pin-prick method, degree of motor blockade by Bromage score, mean arterial pressure, and heart rate were assessed. Mean spread of sensory analgesia in the non-dependent side on the dural puncture was significantly higher in the sagittal-tilt group (T7.4 +/- 2.6 at 15 min) compared the horizontal group (T9.5 +/- 1.4 at 15 min). There was no significant difference in the mean cephalad spread of the analgesic level in the dependent side between the two groups. Unilateral motor anesthesia of the dependent side seemed to be canceled by the sagittal tilting maneuver. A 7 to 8 degree tilt in the sagittal plane is recommended to facilitate the cephalad spread of analgesia and to avoid unilateral anesthesia.

Journal Article↗