Case report: transverse colon volvulus: unusual appearance on barium enema and review of the literature.
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Adult↗
Biomedical subjects
C S Chan
Publications and source records attributed to C S Chan.
Bronchial rupture caused by blunt chest injury.
We have surgically treated six patients with bronchial rupture caused by blunt chest injury in the past 5 years. All injuries resulted from traffic accidents, except in one patient who was hit by a crane. Clinical manifestations included chest pain (n = 6), subcutaneous emphysema (n = 4), and dyspnea (n = 6). Roentgenographic findings were tension (n = 3) or nontension (n = 3) pneumothorax, subcutaneous emphysema (n = 4), pneumomediastinum (n = 3), deep cervical emphysema (n = 5), and delayed collapse of the affected lung (n = 3). Three patients had associated injuries: right clavicle and rib fractures in the first; right humeral, scapular, and multiple rib fractures and left sternoclavicular joint dislocation in the second; and left clavicle fracture in the third. These six patients all underwent immediate tube thoracostomy and then bronchoplasty. Bronchoplasty was performed within 3 days in four patients and on days 16 and 30, respectively, in the other two patients. The affected lung demonstrated full expansion in all patients immediately after bronchoplasty. Follow-up bronchoscopy showed good patency of all bronchi.
Accidents, Traffic↗
Distinct parasegmental and imaginal enhancers and the establishment of the expression pattern of the Ubx gene.
The expression domain of the Ubx gene in Drosophila embryos is bounded by the product of the hb gene, acting as a repressor. We show that all Ubx fragments that bind Hb protein in vitro contain parasegmental enhancers active in the embryo in specific parasegmental patterns. We have found three new embryonic enhancer elements in the upstream region, in addition to the two previously identified. Each produces a pattern initially bounded at PS6 by Hb but sooner or later breaks down this boundary and begins to express in the anterior region. These enhancers do not respond to the long-term maintenance mediated by the Polycomb group of genes. They also cease functioning after germ band extension. Expression in imaginal tissues is due to a set of entirely separate and independent imaginal disc enhancers. These do not contain Hb binding sites and by themselves have no anterior/posterior positional information, although some distinguish between ventral and dorsal discs. A third kind of element, the Polycomb Response Element (PRE), has no enhancer activity but causes long-term maintenance of the expression domain of other enhancers present in the vicinity. The interaction of these elements results in the correct expression of Ubx in imaginal tissues.
Animals↗
MRI of intraspinal nerve sheath tumours presenting with sciatica.
The magnetic resonance imaging (MRI) characteristics of 14 intraspinal nerve sheath tumours (NST) presenting with sciatica were reviewed. The group comprised seven schwannomas, six neurofibromas and one perineuroma. The tumours were either iso- or hypointense with respect to spinal cord on T1-weighted (T1W) images; almost all tumours were hyperintense compared with spinal cord on T2-weighted (T2W) images. The tumours were all detectable on unenhanced T1W images. Nine NST were scanned following Gadolinium-Diethylenetriamine penta acetic acid (DTPA) injection and all showed intense enhancement. This aids differentiation from sequestrated disc fragments. Tumours were more likely to show homogeneous enhancement unless they were recurrent tumours. Rim enhancement occurs more commonly in schwannomas and this can be used to differentiate these from neurofibromas. However, on unenhanced images, schwannomas cannot be distinguished from neurofibromas. Four tumours occurred at T11-T12. There was poor correlation of the site of the lesion with the clinical findings. MRI studies in patients with sciatica should include the lower thoracic region especially if no protruded disc was found in the lumbar region.
Adolescent↗
Regulation of chromosome segregation by Glc8p, a structural homolog of mammalian inhibitor 2 that functions as both an activator and an inhibitor of yeast protein phosphatase 1.
The Ipl1 protein kinase is essential for proper chromosome segregation and cell viability in the budding yeast Saccharomyces cerevisiae. We have previously shown that the temperature-sensitive growth phenotype of conditional ipl1-1ts mutants can be suppressed by a partial loss-of-function mutation in the GLC7 gene, which encodes the catalytic subunit (PP1C) of protein phosphatase 1, thus suggesting that this enzyme acts in opposition to the Ipl1 protein kinase in regulating yeast chromosome segregation. We report here that the Glc8 protein, which is related in primary sequence to mammalian inhibitor 2, also participates in this regulation. Like inhibitor 2, the Glc8 protein is heat stable, exhibits anomalous electrophoretic mobility, and functions in vitro as an inhibitor of yeast as well as rabbit skeletal muscle PP1C. Interestingly, overexpression as well as deletion of the GLC8 gene results in a partial suppression of the temperature-sensitive growth phenotype of ipl1ts mutants and also moderately reduces the amount of protein phosphatase 1 activity which is assayable in crude yeast lysates. In addition, the chromosome missegregation phenotype caused by an increase in the dosage of GLC7 is totally suppressed by the glc8-delta 101::LEU2 deletion mutation. These findings together suggest that the Glc8 protein is involved in vivo in the activation of PP1C and that when the Glc8 protein is overproduced, it may also inhibit PP1C function. Furthermore, site-directed mutagenesis studies of GLC8 suggest that Thr-118 of the Glc8 protein, which is equivalent to Thr-72 of inhibitor 2, may play a central role in the ability of this protein to activate and/or inhibit PP1C in vivo.
Amino Acid Sequence↗
p53 and behaviour of colorectal cancer.
The tumour suppressor gene p53 is altered in most colorectal tumours. We found that lymphatic dissemination was driven by the presence of mutated p53 whether or not the cell contained wild-type p53. In a total sample of 187 specimens, point mutation of the p53 gene occurred in 70% and 43% of cases with and without lymph-node involvement, respectively. By contrast, haematogenous dissemination was apparently the result of absent functional wild-type p53 (whether or not the cell contained mutated p53). These results are of potential importance in the prediction of the clinical behaviour of a tumour.
Colorectal Neoplasms↗
A Polycomb response element in the Ubx gene that determines an epigenetically inherited state of repression.
Segmentation genes provide the signals for the activation and regulation of homeotic genes in Drosophila but cannot maintain the resulting pattern of expression because their activity ceases halfway through embryogenesis. Maintenance of the pattern is due to the Polycomb group of genes (Pc-G) and the trithorax group of genes (trx-G), responsible for the persistence of the active or repressed state of homeotic genes. We have identified a regulatory element in the Ubx gene that responds to Pc-G and trx-G genes. Transposons carrying this element create new binding sites for Pc-G products in the polytene chromosomes. This Pc-G maintenance element (PRE), establishes a repressive complex that keeps enhancers repressed in cells in which they were originally repressed and maintains this state through many cell divisions. The trx-G products stimulate the expression of enhancers in cells in which they were originally active. This mechanism is responsible for the correct regulation of imaginal disc enhancers, which lack themselves antero-posterior positional information. The PRE also causes severe variegation of the mini-white gene present in the transposon, a phenomenon very similar to heterochromatic position-effect variegation. The significance of this mechanism for homeotic gene regulation is discussed.
Animals↗
Case report: inflammatory pseudotumour of liver--review of clinical and radiological features.
We report a 2-year-old girl with a rare benign tumour: an inflammatory pseudotumour of the liver. The clinical, investigative and radiological features are described. The role of percutaneous fine needle aspiration and core biopsy are discussed.
Biopsy, Needle↗
Control of cellular morphogenesis by the Ip12/Bem2 GTPase-activating protein: possible role of protein phosphorylation.
The IPL2 gene is known to be required for normal polarized cell growth in the budding yeast Saccharomyces cerevisiae. We now show that IPL2 is identical to the previously identified BEM2 gene. bem2 mutants are defective in bud site selection at 26 degrees C and localized cell surface growth and organization of the actin cytoskeleton at 37 degrees C. BEM2 encodes a protein with a COOH-terminal domain homologous to sequences found in several GTPase-activating proteins, including human Bcr. The GTPase-activating protein-domain from the Bem2 protein (Bem2p) or human Bcr can functionally substitute for Bem2p. The Rho1 and Rho2 GTPases are the likely in vivo targets of Bem2p because bem2 mutant phenotypes can be partially suppressed by increasing the gene dosage of RHO1 or RHO2. CDC55 encodes the putative regulatory B subunit of protein phosphatase 2A, and mutations in BEM2 have previously been identified as suppressors of the cdc55-1 mutation. We show here that mutations in the previously identified GRR1 gene can suppress bem2 mutations. grr1 and cdc55 mutants are both elongated in shape and cold-sensitive for growth, and cells lacking both GRR1 and CDC55 exhibit a synthetic lethal phenotype. bem2 mutant phenotypes also can be suppressed by the SSD1-vl (also known as SRK1) mutation, which was shown previously to suppress mutations in the protein phosphatase-encoding SIT4 gene. Cells lacking both BEM2 and SIT4 exhibit a synthetic lethal phenotype even in the presence of the SSD1-v1 suppressor. These genetic interactions together suggest that protein phosphorylation and dephosphorylation play an important role in the BEM2-mediated process of polarized cell growth.
Amino Acid Sequence↗
Type 1 protein phosphatase acts in opposition to IpL1 protein kinase in regulating yeast chromosome segregation.
The IPL1 gene is required for high-fidelity chromosome segregation in the budding yeast Saccharomyces cerevisiae. Conditional ipl1ts mutants missegregate chromosomes severely at 37 degrees C. Here, we report that IPL1 encodes an essential putative protein kinase whose function is required during the later part of each cell cycle. At 26 degrees C, the permissive growth temperature, ipl1 mutant cells are defective in the recovery from a transient G2/M-phase arrest caused by the antimicrotubule drug nocodazole. In an effort to identify additional gene products that participate with the Ipl1 protein kinase in regulating chromosome segregation in yeast, a truncated version of the previously identified DIS2S1/GLC7 gene was isolated as a dosage-dependent suppressor of ipl1ts mutations. DIS2S1/GLC7 is predicted to encode a catalytic subunit (PP1C) of type 1 protein phosphatase. Overexpression of the full-length DIS2S1/GLC7 gene results in chromosome missegregation in wild-type cells and exacerbates the mutant phenotype in ipl1 cells. In addition, the glc7-1 mutation can partially suppress the ipl1-1 mutation. These results suggest that type 1 protein phosphatase acts in opposition to the Ipl1 protein kinase in vivo to ensure the high fidelity of chromosome segregation.
Amino Acid Sequence↗
A detailed study of p53 mutations in colorectal cancer in Singapore.
The p53 tumour suppressor gene plays a pivotal role in colorectal cancer formation. Understanding the mechanisms by which p53 is altered in tumour cells could lead to a better understanding of this common cancer. Unfortunately, there is no published information on Chinese patients. We have therefore conducted a series of studies on the p53 tumour suppressor gene in Singaporean colorectal cancer patients and have since demonstrated that 69% of patients have lost one copy of the p53 gene by allelic deletion of chromosome 17p, 55% of patients have a point mutation in one copy of the p53 gene, and that these changes are associated with tumour site, DNA aneuploidy and the pattern of disease dissemination. We present here a further study conducted on the specific nature and frequency of p53 mutations. DNA sequence analysis of 38 tumours from Chinese colorectal cancer patients with p53 mutations showed that 97% (37/38) of the mutations consisted of base substitutions, leading to the incorporation of alternate amino-acids in the p53 protein. The remaining mutation consisted of a single base insertion leading to the generation of a stop-codon, leading to the truncation of the protein some 14 amino-acids downstream from the site of the mutation. Sixty-eight percent of the mutants consisted of guanine to adenine (G-->A) transitions and 58% occurred at CpG dinucleotides. Eighty-seven percent of all mutations occurred at evolutionarily highly conserved regions, with 50% of mutations occurring in codons 175, 248 and 282.(ABSTRACT TRUNCATED AT 250 WORDS)
Aneuploidy↗
Regulation of yeast chromosome segregation by Ipl1 protein kinase and type 1 protein phosphatase.
Chromosome segregation is a complicated process that involves the coordinated functioning of a large number of cellular components. In this process, many proteins are activated and inactivated in a strict temporal order. While much progress has been made recently in the identification of structural components that are involved in chromosome segregation, relatively little is known about their regulation. We have investigated the chromosome segregation process in the budding yeast Saccharomyces cerevisiae. Our results indicate that this process absolutely requires a functional Ipl1 protein kinase. Upon inactivation of this protein kinase, yeast cells missegregate chromosomes severely and die within a single cell cycle. Furthermore, the inviability caused by a partial reduction in Ipl1 function can be rescued by perturbations that reduce type 1 protein phosphatase activity, thus suggesting that type 1 protein phosphatase acts in opposition to the Ipl1 protein kinase to insure the high fidelity of chromosome segregation in yeast cells. The purpose of this article is to describe some of our ongoing efforts to characterize Ipl1 and PP1 functions.
Aurora Kinases↗
Hypercalcemia in tuberculous peritonitis without active pulmonary tuberculosis.
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Humans↗
Levels of hepatitis C virus RNA and liver histology in chronic type C hepatitis.
BACKGROUND: The clinical and pathologic significance of quantitative serum hepatitis C virus (HCV) RNA levels in patients with chronic type C hepatitis is unknown. The aim of this study was to determine whether serum levels of HCV RNA were associated with mode of viral transmission or with histological severity of liver disease. METHODS: A branched DNA signal amplification assay for HCV RNA was done on the sera of 127 patients with well-defined risk factors for viral hepatitis. Seventy persons acquired HCV infection by blood transfusion and 57 via tattoo application or former intravenous drug use. Group I included 42 patients with chronic persistent hepatitis, group II consisted of 39 patients with chronic active hepatitis, and group III included 40 individuals whose liver biopsies showed both chronic active hepatitis and cirrhosis, as well as six patients with clinically decompensated cirrhosis. RESULTS: The median HCV RNA level [equivalents/ml (eq/ml) x 10(5)] for patients who acquired infection from transfusion [73.5 x 10(5) (eq/ml)] was not significantly different from that of patients who reported prior intravenous drug use [50 x 10(5) eq/ml] (p = 0.283). The median HCV RNA level for groups I, II, and III was 29.5, 76, and 71, respectively. Group I differed significantly from groups II and III combined (median = 73) (p = 0.02). No difference was noted between group II and group III (p = 0.947). Age did not correlate with level of viremia (r2 = 0.01). No relationship was found between serum alanine aminotransferase and the level of viremia (p = 0.52). Multivariate analysis showed that only the histological severity of the disease proved to be predictive of HCV RNA level (p = 0.04). CONCLUSION: The lowest levels of hepatitis C viremia are, in general, associated with minimal liver disease. Overall, histological severity of chronic hepatitis C infection best predicts HCV RNA levels.
Biopsy↗
Significance of serum hepatitis C virus RNA levels in chronic hepatitis C.
Hepatitis C virus (HCV) is the main cause of parenteral non-A, non-B hepatitis and serum can be tested for the virus itself by reverse-transcription polymerase chain amplification. What of the level of this viraemia? To find out if quantitative study of HCV RNA might be useful clinically we took advantage of participation in trials of interferon-alpha in patients with chronic HCV infection and applied a new assay, branched DNA (bDNA) signal amplification. Paired serum and liver biopsy specimens from 47 patients with confirmed chronic HCV infection and evidence of HCV RNA in their serum were studied. The quantitative bDNA assay (detection limit 350,000 equivalents/mL [eq/mL]) was positive in 34 sera (sensitivity 72%). Patients who acquired HCV infection by blood transfusion had a higher viraemia (median 2,701,000 eq/mL, n = 29) than health workers and intravenous drug users (635,000 eq/mL, n = 13; p < 0.01). Patients with a sustained complete response to interferon-alpha therapy had lower pre-treatment viraemia levels (median at bDNA cut-off, n = 11) than complete responders who relapsed after the drug was stopped (1,613,000 eq/mL, n = 15; p < 0.01) and non-responders (3,066,000 eq/mL, n = 20; p < 0.01). High viraemia levels were not related to the histological diagnosis but were associated with lobular inflammation, lymphoid aggregates, and bile-duct lesions. These findings indicate that mode of acquisition is an important determinant of HCV viraemia and that patients with low HCV viraemia levels are more likely to respond to interferon in a sustained fashion.
Adult↗
Related chromosome binding sites for zeste, suppressors of zeste and Polycomb group proteins in Drosophila and their dependence on Enhancer of zeste function.
Polycomb group genes are necessary for maintaining homeotic genes repressed in appropriate parts of the body plan. Some of these genes, e.g. Psc, Su(z)2 and E(z), are also modifiers of the zeste-white interaction. The products of Psc and Su(z)2 were immunohistochemically detected at 80-90 sites on polytene chromosomes. The chromosomal binding sites of these two proteins were compared with those of zeste protein and two other Polycomb group proteins, Polycomb and polyhomeotic. The five proteins co-localize at a large number of sites, suggesting that they frequently act together on target genes. In larvae carrying a temperature sensitive mutation in another Polycomb group gene, E(z), the Su(z)2 and Psc products become dissociated from chromatin at non-permissive temperatures from most but not all sites, while the binding of the zeste protein is unaffected. The polytene chromosomes in these mutant larvae acquire a decondensed appearance, frequently losing characteristic constrictions. These results suggest that the binding of at least some Polycomb group proteins requires interactions with other members of the group and, although zeste can bind independently, its repressive effect on white involves the presence of at least some of the Polycomb group proteins.
Animals↗
Isolation and characterization of chromosome-gain and increase-in-ploidy mutants in yeast.
We have developed a colony papillation assay for monitoring the copy number of genetically marked chromosomes II and III in Saccharomyces cerevisiae. The unique feature of this assay is that it allows detection of a gain of the marked chromosomes even if there is a gain of the entire set of chromosomes (increase-in-ploidy). This assay was used to screen for chromosome-gain or increase-in-ploidy mutants. Five complementation groups have been defined for recessive mutations that confer an increase-in-ploidy (ipl) phenotype, which, in each case, cosegregates with a temperature-sensitive growth phenotype. Four new alleles of CDC31, which is required for spindle pole body duplication, were also recovered from this screen. Temperature-shift experiments with ipl1 cells show that they suffer severe nondisjunction at 37 degrees. Similar experiments with ipl2 cells show that they gain entire sets of chromosomes and become arrested as unbudded cells at 37 degrees. Molecular cloning and genetic mapping show that IPL1 is a newly identified gene, whereas IPL2 is allelic to BEM2, which is required for normal bud growth.
Alleles↗
Reciprocal expression of pleiotrophin and midkine in normal versus malignant lung tissues.
Abundant evidence suggests that growth factors are important mediators of non-small cell lung cancer (NSCLC) growth. Although multiple growth factors have been found to be produced by NSCLC tissues, little is known about possible differences in growth factor expression between malignant and adjacent normal lung tissues. Variation in growth factor expression between normal and malignant lung tissues could be potentially useful diagnostically and therapeutically. In studies reported here, the expression of the angiogenic growth factor pleiotrophin (PTN) and homolog midkine (MK) was assessed in resected normal and malignant lung tissues. Primers specific for the two growth factors were used to amplify reverse transcriptase-produced DNA copies of RNA transcripts harvested from the tissues. This analysis revealed that all normal lung tissues examined (n = 17) expressed PTN but only two expressed MK. Conversely, all of the resected lung cancers (n = 20) expressed MK but only one expressed PTN. These results demonstrated a striking reciprocal expression pattern of MK and PTN in normal versus malignant lung tissue.
Base Sequence↗