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D Matt

Publications and source records attributed to D Matt.

8 recordsLinked to original sources

Phosphorus-phosphorus coupling in a diphosphine with a ten bond P...P separation.

The large, unsymmetrical diphosphine 5,11,17,23-tetra-tert-butyl-25,26-bis(diphenylphosphinomethoxy)-27(or 28)-benzoyloxy-28(or 27)-hydroxycalix[4]arene, in which the phosphorus atoms are separated by ten bonds, was prepared by monobenzoylation of 5,11,17,23-tetra-tert-butyl-25,26-bis(diphenylphosphinoylmethoxy)-27,28-bis(hydroxy)calix[4]arene, followed by reduction with phenyl silane. Its molecular structure has been determined by X-ray crystallography. In the solid state, the phosphorus atoms are separated by 5.333(1) A. NMR investigations reveal an unexpected "through-space"J(PP') coupling constant of 8.0 Hz and also show that, in solution, the calixarene is conformationally mobile, the phenoxy ring flipping rapidly through the calixarene annulus. The spatial proximity of the two phosphorus atoms was further demonstrated by the ease of obtaining the cis-chelate complex [Pd(eta3-C3H4Me)(THF)2]BF4 (THF = tetrahydrofuran).

Journal Article↗

Metal-capped alpha-cyclodextrins: squaring the circle.

This report describes the four-step synthesis of 6A,6D-diamino-6A,6D-dideoxy-2(A),2(B),2(C),2(D),2(E),2(F),3(A),3(B),3(C),3(D),3(E),3(F), 6(B),6(C),6(E),6(F)-hexadeca-O-methylcyclomaltohexaose (5), a methylated alpha-CD that bears two -CH(2)NH(2) ligands located on diametrically opposed glucopyranose rings. Reaction of 5 with K(2)PtCl(4) afforded the water-soluble chelate complex [PtCl(2)(5)] where the metal center is bonded to cis-arranged nitrogen atoms. A single-crystal X-ray structure of the latter reveals the high distortion imposed on the CD structure by the short metallo-organic cap. The cyclodextrin core adopts an unprecedented elongated, almost rectangular shape, the shortest and longest O(4)(n). O(4)(n+3) distances being respectively 5.44 and 9.98 A. Two opposing glucose rings are no longer in the usual (4)C(1) chair conformation, but adopt an elongated (O)S(2) skew-boat structure. The observed CD-flattening produces a highly preorganized hydrophilic pocket that complexes through multiple hydrogen bonding a single water molecule. Complex [PtCl(2)(5)] and the corresponding synthetic intermediates were characterized by elemental analysis, MS, and IR and NMR spectroscopy.

Journal Article↗

Sporadic trichoepithelioma demonstrates deletions at 9q22.3.

BACKGROUND: Trichoepithelioma (TE) is a benign cutaneous tumor that originates from hair follicles and occurs either in multiple or solitary lesions. Multiple TE is transmitted as an autosomal dominant trait, and a region at 9p21 is thought to be involved in the tumorigenesis. Solitary TE occurs more commonly than multiple TE and is not inherited. Histologically, TE tumors contain horn cysts and abortive hair papillae. A basal cell carcinoma appearance in some or all regions of a TE tumor can happen. In sporadic basal cell carcinoma, frequent deletions at 9q22.3 (Drosophila patched gene) have occurred. The objective of this study is to test whether loss of heterozygosity (LOH) on either 9p21 or on chromosome 9q22.3 could be detected in archival sporadic TE. OBSERVATIONS: We studied 29 randomly selected cases of sporadic TE by microdissection and polymerase chain reaction using paraffin-embedded, formalin-fixed tissue specimens on glass slides. Analysis was performed with the polymorphic markers IFNA and D9S171 (9p21) as well as D9S15, D9S303, D9S287, and D9S252 (9q22.3). RESULTS: The LOH at 9q22.3 was identified in 14 (48%) of 29 cases with at least 1 marker, while LOH could not be demonstrated using the markers IFNA and D9S171 (9p21). CONCLUSIONS: The results show that the Drosophila patched gene LOH can be frequently identified in paraffin-embedded sporadic TE after routine processing and indicates a common gatekeeper mechanism for both TE and basal cell carcinoma.

Chromosomes, Human, Pair 9↗

The sebaceous nevus: a nevus with deletions of the PTCH gene.

Sebaceous nevi (SN) are congenital malformations of the skin with the potential to develop into basal cell carcinoma (BCC). To date, the molecular basis for their carcinogenic potential remains unknown. The genetic defect in BCC is known and involves the human homologue of Drosophila patched (PTCH) on chromosome 9q22.3. The objective of this study was to test whether allelic deletion of the PTCH gene could already be detected in SN. Twenty-one paraffin-embedded SN were investigated in this study. Basaloid cells in conjunction with mature sebaceous glands as well as epidermal layer apart from SN were microdissected and subjected to single-step DNA extraction. We performed the analysis with polymorphic markers at 9q22.3 (D9S15, D9S252, D9S287, and D9S303). Of the 20 informative SN, 8 (40%) exhibited loss of heterozygosity at least at one locus. Here, we provide the first evidence of the involvement of the tumor suppressor gene PTCH in SN. Whether PTCH deletion in SN is associated with progression to BCC and/or other appendageal tumors should be addressed in future studies.

Basal Cell Carcinoma↗

Ultraviolet-induced acute histological changes in irradiated nevi are not associated with allelic loss.

BACKGROUND: Transformed melanocytes in atypical nevi, which are thought to be precursors of melanoma, are frequently deleted on chromosomes 1p, 9q, and 9p21 (p16 locus). Single UV irradiation induces histological changes that are similar to those of atypical nevi and, in part, of melanoma in situ. OBJECTIVE: To determine the effects of UV irradiation on benign melanocytic nevi in vivo. DESIGN: We investigated one half of a symmetric nevus 1 week after a single UV exposure with 4 times the patient's minimal erythema dose and compared it with the nonirradiated, shielded half of the same nevus. Two to 3 areas containing 5 to 30 melanocytes in 7 nevi were microdissected (a total of 18 areas in each nonirradiated and irradiated part), followed by a single-step DNA extraction. Extracted genomic DNA was amplified using a polymerase chain reaction with polymorphic markers D1S450 (1p), D9S12 (9q), IFNA, and D9S171 (9p21) and subjected to autoradiography. OBSERVATIONS: Two, 3, 2, and 2 of 18 areas were homozygous for D1S450, D9S12, IFNA, and D9S171, respectively. No allelic loss could be demonstrated in either nonirradiated or irradiated nevi. CONCLUSIONS: Acute histological changes demonstrated in melanocytic nevi after UV irradiation are not followed by allelic loss on identical chromosomal areas found in dysplastic melanocytes of atypical nevi. This finding supports the hypothesis that initial nonspecific genetic events may occur after UV irradiation, followed by an increase in various repair mechanisms potentially leading to specific genetic damage and loss of heterozygosity; however, loss of heterozygosity is not detectable at an early stage.

Cell Nucleus↗

Chromosomal allele loss in primary cutaneous melanoma is heterogeneous and correlates with proliferation.

Loss of heterozygosity at specific loci in neoplastic cells suggests the presence of a tumor suppressor gene within the deleted region. Using the microdissection technique, loss of heterozygosity has been identified in paraffin-embedded primary melanomas on chromosomes 1p and 9q. Our purpose was to determine loss of heterozygosity in primary cutaneous melanomas and to relate chromosomal alterations with cell morphology and proliferation of the tumor. Two to seven morphologic different areas in 12 primary cutaneous high risk melanomas (Breslow > 1.5 mm), as well as adjacent normal tissue, were microdissected and subjected to single step DNA extraction. Extracted genomic DNA was amplified by polymerase chain reaction using two polymorphic markers on chromosomes 1p (D1S450, between D1S548 and D1S228) and 9q (D9S12). Proliferation was evaluated by MIB-1 (Ki67) immunoreactivity and cell morphology, pigmentation and inflammation surrounding microdissected areas were investigated by microscopic inspection of hematoxylin and eosin stained sections. Twelve of 34 different areas (35%) showed loss of heterozygosity with at least one marker. Two of 32 areas showed loss of heterozygosity with D1S450 (two areas noninformative), seven of 30 with D9S12 (four areas noninformative), and three areas showed loss of heterozygosity at both loci. In three of these cases, analysis of different tumor foci revealed areas with/without loss of heterozygosity. In these cases, the percentage of MIB-I-positive cells was at least four times higher in areas with loss of heterozygosity compared with areas without loss of heterozygosity. Most areas with loss of heterozygosity consisted of small cuboidal to epitheloid cells. Spindle shaped and large anaplastic cells showed loss of heterozygosity less frequently. Neither melanization of tumor cells nor the presence of inflammation had an influence on the frequency of loss of heterozygosity. Primary cutaneous melanomas show intratumoral morphologic and chromosomal heterogeneity. Loss of heterozygosity on chromosomes 1p and 9q correlated with cell proliferation, suggesting that selected cell clones are responsible for tumor progression.

Alleles↗

Interleukin-1 beta, human leukocyte antigen HLA-DR alpha, and transforming growth factor-beta expression in endometrium, placenta, and placental membranes.

Maternal immune recognition of the fetal semiallograft appears to be necessary and beneficial for fetal survival and growth. Interleukin-1 beta and human leukocyte antigen HLA-DR are important for foreign antigen recognition by the immune system, whereas transforming growth factor-beta inhibits many of the immunostimulatory properties of interleukin-1 beta. In this study we found that first-trimester decidua and term placental membranes expressed significantly higher levels of interleukin-1 beta, interleukin-1 beta messenger ribonucleic acid, and human leukocyte antigen HLA-DR alpha messenger ribonucleic acid expression. All tissues found at the maternal-fetal interface, including first-trimester decidua, placenta, and placental membranes, contained transforming growth factor-beta and expressed transforming growth factor-beta 1 messenger ribonucleic acid. On the basis of these findings, we suggest that the increase in decidual interleukin-1 beta and human leukocyte antigen HLA-DR alpha during pregnancy may be involved in maternal recognition of the fetal semiallograft and that transforming growth factor-beta production may regulate the local maternal immune response and prevent rejection of the fetus.

Blotting, Northern↗

Anxiety and postoperative recovery in ambulatory surgery patients.

There has been a growing trend toward one-day ambulatory surgery. Unfortunately, there has been little research evaluating how patients recover at home after one-day surgery. This study examined the relationship between preoperative anxiety and postoperative recovery in ambulatory surgery patients. Fifty women who were scheduled for a laparascopy completed a series of questionnaires on the day before surgery and on each of three days after surgery. One month after surgery, the patients were telephoned and reported on their recovery. The surgeon rated each patient on their estimated degree of anxiety and length of recovery. The results showed that preoperative anxiety partially predicted the patients' psychological and physiological reaction to surgery. Identification of those patients who show high anxiety and distress may help to prevent postoperative complications. These patients may benefit from patient education and psychological interventions to decrease their fears and anxiety and they may benefit from more intensive observation periods following their surgery.

Ambulatory Care↗