Biomedical subjects

N Hu

Publications and source records attributed to N Hu.

At least 19 recordsLinked to original sources

PubMed2002

Complete genomes of two Human hepatitis A virus isolates from China: analysis and comparison with other isolates.

Complete sequences of the genomes of two wild type (wt) Human hepatitis A virus (HHAV) isolates, LU38 and LY6 from China were determined and compared with those of wt HHAV isolates AH1, AH2, AH3, FH1, FH2, FH3, GBM, HM175, LA and MBB. The genomes of both LU38 and LY6 consisting of 7477 nucleotides (nts) contained a 5'-non-translated region (5'-NTR, 733 nts), an open reading frame (ORF, 6681 nts), and a 3'-NTR (63 nts) followed by a poly(A)-tail. It encoded a polyprotein of 2227 amino acids (aa) Sequence comparison showed that LU38 shared the highest identities of 98.1% for nt (140 differences) and 99.2% for as (17 differences) with AH1, and the lowest identities of 91.4% for nt (741 differences) with HM175 and 98.1% for aa (43 differences) with GBM. LY6 shared the highest identities of 97.4% for nt (196 differences) and 98.7% for aa (28 differences) with H1 and the lowest identities of 91.2% for nt (642 differences) with HM175 and 97.7% for as (51 differences) with GBM. The subgenotyping revealed that the LU38 and LY6 isolates are of IA subgenotype. The phylogenetic analysis showed that LU38 is closest to AH1 and the LY6 to FH3, suggesting that the epidemiological link of hepatitis A (HA) had developed in China and Japan.

Amino Acid Sequence↗

PubMed2001

Identification of the first invertebrate interleukin JAK/STAT receptor, the Drosophila gene domeless.

The JAK/STAT signaling pathway plays important roles in vertebrate development and the regulation of complex cellular processes. Components of the pathway are conserved in Dictyostelium, Caenorhabditis, and Drosophila, yet the complete sequencing and annotation of the D. melanogaster and C. elegans genomes has failed to identify a receptor, raising the possibility that an alternative type of receptor exists for the invertebrate JAK/STAT pathway. Here we show that domeless (dome) codes for a transmembrane protein required for all JAK/STAT functions in the Drosophila embryo. This includes its known requirement for embryonic segmentation and a newly discovered function in trachea specification. The DOME protein has a similar extracellular structure to the vertebrate cytokine class I receptors, although its sequence has greatly diverged. Like many interleukin receptors, DOME has a cytokine binding homology module (CBM) and three extracellular fibronectin-type-III domains (FnIII). Despite its low degree of overall similarity, key amino acids required for signaling in the vertebrate cytokine class I receptors [3] are conserved in the CBM region. DOME is a signal-transducing receptor with most similarities to the IL-6 receptor family, but it also has characteristics found in the IL-3 receptor family. This suggests that the vertebrate families evolved from a single ancestral receptor that also gave rise to dome.

Amino Acid Motifs↗

PubMed2001

Persistent expression of cyclin D1 disrupts normal photoreceptor differentiation and retina development.

The differentiation of neuronal cells in the developing mammalian retina is closely coupled to cell cycle arrest and proceeds in a highly organized manner. Cyclin D1, which regulates cell proliferation in many cells, also drives the proliferation of photoreceptor progenitors. In the mouse retina, cyclin D1 protein normally decreases as photoreceptors mature. To study the importance of the down-regulation of cyclin D1 during photoreceptor development, we generated a transgenic mouse in which cyclin D1 was persistently expressed in developing photoreceptor cells. We observed numerous abnormalities in both photoreceptors and other nonphotoreceptor cells in the retina of these transgenic mice. In particular, we observed delayed opsin expression in developing photoreceptors and alterations in their number and morphology in the mature retina. These alterations were accompanied by disorganization of the inner nuclear and plexiform layers. The expression of cyclin D1 caused excess photoreceptor cell proliferation and apoptosis. Loss of the p53 tumor suppressor gene decreased cyclin D1-induced apoptosis and led to microscopic hyperplasia in the retina. These findings are distinct from other mouse models in which the retinoblastoma gene pathway is disrupted and suggest that the IRBP-cyclin D1 mouse model may recapitulate an early step in the development of retinoblastoma.

Animals↗

PubMed2001

Mitochondrial DNA decrease in subcutaneous adipose tissue of HIV-infected individuals with peripheral lipoatrophy.

OBJECTIVE: To determine whether the peripheral fat wasting (lipodystrophy), which is seen in association with highly active antiretroviral therapy (HAART) that includes a nucleoside reverse transcriptase inhibitor (NRTI), is associated with a decrease in subcutaneous adipose tissue mitochondrial DNA (mtDNA) content or with large mtDNA deletions or insertions. DESIGN: A four cohort cross-sectional study. METHODS: The mtDNA content of subcutaneous fat tissue from the neck, abdomen and thigh was determined by polymerase chain reaction utilizing the amplification of three different mtDNA fragments. The results from HIV-infected patients with peripheral fat wasting following more than 6 months of NRTI-containing HAART were compared with the results from three different control cohorts: HIV-infected patients with a similar treatment history without lipodystrophy; HIV-infected patients naive to antiretroviral therapy and HIV sero-negative participants. RESULTS: A decrease in mtDNA content was found in HAART-treated HIV-infected patients with peripheral fat wasting in comparison with subjects in the control cohorts. No large mitochondrial deletions or insertions were found. CONCLUSIONS: Lipodystrophy with peripheral fat wasting following treatment with NRTI-containing HAART is associated with a decrease in subcutaneous adipose tissue mtDNA content.

Adipose Tissue↗

PubMed2001

Cardiac morphology and blood pressure in the adult zebrafish.

Zebrafish has become a popular model for the study of cardiovascular development. We performed morphologic analysis on 3 months postfertilization zebrafish hearts (n > or = 20) with scanning electron microscopy, hematoxylin and eosin staining and Masson's trichrome staining, and morphometric analysis on cell organelles with transmission electron photomicrographs. We measured atrial, ventricular, ventral, and dorsal aortic blood pressures (n > or = 5) with a servonull system. The atrioventricular orifice was positioned on the dorsomedial side of the anterior ventricle, surmounted by the single-chambered atrium. The atrioventricular valve was free of tension apparati but supported by papillary bands to prevent retrograde flow. The ventricle was spanned with fine trabeculae perpendicular to the compact layer and perforated with a subepicardial network of coronary arteries, which originated from the efferent branchial arteries by means of the main coronary vessel. Ventricular myocytes were larger than those in the atrium (P < 0.05) with abundant mitochondria close to the sarcolemmal. Sarcoplasmic reticulum was sparse in zebrafish ventricle. Bulbus arteriosus was located anterior to the ventricle, and functioned as an elastic reservoir to absorb the rapid rise of pressure during ventricular contraction. The dense matrix of collagen interspersed across the entire bulbus arteriosus exemplified the characteristics of vasculature smooth muscle. There were pressure gradients from atrium to ventricle, and from ventral to dorsal aorta, indicating that the valves and the branchial arteries, respectively, were points of resistance to blood flow. These data serve as a framework for structure-function investigations of the zebrafish cardiovascular system.

Animals↗

PubMed2001

Genetic progression and heterogeneity associated with the development of esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma is a common fatal cancer, and Shanxi province, a region in north-central China, has some of the highest esophageal cancer rates in the world. Chromosomal regions with frequent allelic loss may point to major susceptibility genes that will assist us in understanding the molecular events involved in esophageal carcinogenesis and may serve as the basis for the development of markers for genetic susceptibility and screening for early detection of this cancer. This study was designed to identify events in the molecular progression of precursor and invasive lesions of squamous esophageal cancer. Twelve marker loci identified during our previous studies as having some of the highest rates of loss of heterozygosity (LOH) in invasive esophageal cancer were evaluated in laser-microdissected DNA obtained from low- and high-grade dysplastic lesions and invasive tumor foci from 10 fully embedded esophageal resection specimens. Each resection specimen contained a spectrum of disease, from epithelium that appeared histologically normal to invasive cancer, including a single dominant tumor surrounded by a region of precursor lesions (low- and high-grade dysplasia) and occasional "remote," nonadjacent precancerous foci. Using the 12 polymorphic markers, LOH was found in all of the three stages of disease. The frequency of LOH for all of the markers together increased with increasing disease severity. Among the informative low-grade dysplasia samples, LOH was detected with markers D3S1766 (3p), D4S2632 (4p), D9S910 (9q), and D13S1493 (13q), suggesting that LOH at these loci may be associated with early stages of tumor initiation and/or progression. LOH was detected among the informative high-grade (but not low-grade) dysplasia samples for the other eight markers tested, suggesting that LOH at these loci may occur later in the neoplastic process. In addition to the association between disease progression and these genetic changes, considerable genetic heterogeneity was found in each fully embedded resection specimen both between and within geographically separate neoplastic lesions.

Adult↗

PubMed2001

Allelic loss on chromosome bands 13q11-q13 in esophageal squamous cell carcinoma.

Allelic loss on chromosome 13 occurs frequently in esophageal squamous cell carcinoma. However, studies of the two known tumor suppressor genes located on 13q, RB1 and BRCA2, have shown few mutations, suggesting that other genes are likely to be involved in the development of this tumor type. To identify a minimal deletion interval, we first analyzed 42 microsatellite markers spanning chromosome bands 13q11-q13 in 56 esophageal squamous cell carcinoma patients, including 34 with a family history of upper gastrointestinal cancer and 22 without a family history of cancer. Lifestyle risk factors and clinical/pathologic characteristics were also collected. Two commonly deleted regions were identified: one was located on band 13q12.11, between markers D13S787 and D13S221; the other was located on bands 13q12.3-q13.1 from markers D13S267 to D13S219. We observed higher allelic loss frequencies for eight of the microsatellite markers in those patients with a family history of upper gastrointestinal cancer compared to patients without such a history. This study suggests that one or more unidentified tumor suppressor genes are located on chromosome arm 13q that play a role in the development of esophageal squamous cell carcinoma.

Carcinoma, Squamous Cell↗

PubMed2001

Rapid acquisition of entire DNA polymerase gene of a novel herpesvirus from green turtle fibropapilloma by a genomic walking technique.

A 4837-bp sequence of a newfound green turtle herpesvirus (GTHV), implicated in the etiology of green turtle fibropapilloma, was obtained from tumor tissues of a green turtle with fibropapilloma using a genomic walking method based on restriction enzyme digestion, self-ligation and inverse polymerase chain reaction (IPCR). The 4837-bp sequence was 56.23% G/C rich and contained three nonoverlapping open reading frames (ORF). The largest ORF (3507-bp) encoded the DNA polymerase gene (pol gene), which exhibited a high degree of homology at both amino acid and nucleotide levels with the DNA pol genes of human and animal herpesviruses, with a predicted protein of 1169 amino acids and molecular weight of 132.6 kilodaltons. The ATG at 518 to 520 was the first initiation codon in the ORF and was presumed to be the first methionine codon of the pol gene. Phylogenetic analysis, based on the amino acid sequence of the GTHV DNA pol gene and the corresponding regions of other known human and animal herpesviruses, indicated that GTHV belonged to the Alphaherpesvirinae subfamily. The upstream ORF of the pol gene encoded the N-terminal region of the GTHV homologue of the DNA-binding protein gene, whereas the downstream ORF was the C-terminal region of a gene which was homologous to ORFs conserved in human and animal herpesviruses, i.e., herpes simplex virus 1 (HSV1) gene UL31, Epstein-Barr virus (EBV) gene BFLF2, equine herpesvirus 1 (EHV1) gene 29, and alcelaphine herpesvirus 1 (AHV1) hypothetical protein 69 gene. The arrangement of these three genes in GTHV genome was identical to that seen in other alphaherpesviruses. The sequence and location of the DNA pol gene in the GTHV genome should greatly facilitate future studies of the viral life cycle.

Alphaherpesvirinae↗

PubMed2001

Direct electrochemistry of hemoglobin in layer-by-layer films with poly(vinyl sulfonate) grown on pyrolytic graphite electrodes.

Stable layer-by-layer electroactive films were grown on pyrolytic graphite (PG) electrodes by alternate adsorption of layers of polyanionic poly(vinyl sulfonate) (PVS) and positively charged hemoglobin (Hb) from their aqueous solutions. Cyclic voltammetry (CV) of [PVS/Hb]n films showed a pair of well-defined and nearly reversible peaks at about - 0.28 V vs. SCE at pH 5.5, characteristic of Hb heme Fe(III)/Fe(II) redox couple. The process of (PVS/Hb) bilayer growth was monitored and confirmed by CV, X-ray photoelectron spectroscopy (XPS) and UV-Vis spectroscopy. While the amount of Hb adsorbed in each bilayer was the same, the amount of electroactive Hb in each bilayer decreased dramatically with increase of the number of bilayer, and electroactivity was just extended to 8 [PVS/Hb] bilayers. CVs of [PVS/Hb]8 films maintained stable in buffers containing no Hb. Positions of Soret band of Hb in [PVS/Hb]n films grown on transparent glass slides suggest that Hb in the films keeps its secondary structure similar to its native state in a wide pH range. Trichloroacetic acid and nitrite were catalytically reduced by [PVS/Hb]8 films with significant lowering of the electrode potential required.

Catalysis↗

PubMed2001

Direct electrochemistry and electrocatalysis with horseradish peroxidase in Eastman AQ films.

Stable films made from ionomer poly(ester sulfonic acid) or Eastman AQ29 on pyrolytic graphite (PG) electrodes gave direct electrochemistry for incorporated enzyme horseradish peroxidase (HRP). Cyclic voltammetry of HRP-AQ films showed a pair of well-defined, nearly reversible peaks at about -0.33 V vs. SCE at pH 7.0 in blank buffers, characteristic of HRP heme Fe(III)/Fe(II) redox couple. The electron transfer between HRP and PG electrode was greatly facilitated in AQ films. The electrochemical parameters such as apparent heterogeneous electron transfer rate constant (k(s)) and formal potential (E(o')) were estimated by fitting the data of square-wave voltammetry (SWV) with nonlinear regression analysis. Reflectance absorption infrared (RAIR) and UV-Vis absorption spectra demonstrated that HRP retained a near native conformation in AQ films. The embedded HRP in AQ films retained the electrocatalytic activity for oxygen, nitrite and hydrogen peroxide. Possible mechanism of catalytic reduction of H(2)O(2) with HRP-AQ films was proposed.

Catalysis↗

PubMed2001

Frequent inactivation of the TP53 gene in esophageal squamous cell carcinoma from a high-risk population in China.

Esophageal squamous cell carcinoma (ESCC) is one of the most common fatal cancers worldwide, and north central China has some of the highest rates in the world. Previous studies from tumors in this area of China have shown high frequencies of allelic loss on chromosome 17p13-11, which includes the region where the TP53 gene is found. We examined 56 ESCC patients using single-strand conformation polymorphism and DNA sequencing to assess the frequency and spectrum of TP53 mutation and the association between allelic loss at microsatellite marker TP53 and TP53 mutations. Ninety-six % of cases were found to have at least one genetic alteration, including TP53 mutation (77%), allelic loss within the TP53 gene (73%), and/or loss of heterozygosity at the TP53 microsatellite marker (80%); 75% had two or more such alterations, including 59% with both a point mutation and an intragenic allelic loss ("two hits"). The majority of mutations observed were in exon 5, where the most common type of nucleotide substitution was a G:C-->A:T or C:G-->T:A transition, including half that occurred at CpG sites. Allelic loss was most commonly found in exon 4 but was very common in exon 5 as well. Taken together, the multiple genetic alterations of TP53 in this population at high risk for ESCC indicate that there is a very high degree of genetic instability in these tumors, that TP53 is a primary target for inactivation, and that this tumor suppressor gene plays a critical role in the carcinogenesis process for ESCC.

Adult↗

PubMed2000

Loss of annexin 1 correlates with early onset of tumorigenesis in esophageal and prostate carcinoma.

Annexin I protein expression was evaluated in patient-matched longitudinal study sets of laser capture microdissected normal, premalignant, and invasive epithelium from human esophageal squamous cell cancer and prostatic adenocarcinoma. In 25 esophageal cases (20 by Western blot and 5 by immunohistochemistry) and 17 prostate cases (3 by Western blot and 14 by immunohistochemistry), both tumor types showed either complete loss or a dramatic reduction in the level of annexin I protein expression compared with patient-matched normal epithelium (P < or = 0.05). Moreover, by using Western blot analysis of laser capture microdissected, patient-matched longitudinal study sets of both tumor types, the loss of protein expression occurred in premalignant lesions. Concordance of this result with immunohistochemical analysis suggests that annexin I may be an essential component for maintenance of the normal epithelial phenotype. Additional studies investigating the mechanism(s) and functional consequences of annexin I protein loss in tumor cells are warranted.

Adenocarcinoma↗

PubMed2000

Structure and function of the developing zebrafish heart.

The combination of optical clarity and large scale of mutants makes the zebrafish vital for developmental biologists. However, there is no comprehensive reference of morphology and function for this animal. Since study of gene expression must be integrated with structure and function, we undertook a longitudinal study to define the cardiac morphology and physiology of the developing zebrafish. Our studies included 48-hr, 5-day, 2-week, 4-week, and 3-month post-fertilization zebrafish. We measured ventricular and body wet weights, and performed morphologic analysis on the heart with H&E and MF-20 antibody sections. Ventricular and dorsal aortic pressures were measured with a servonull system. Ventricular and body weight increased geometrically with development, but at different rates. Ventricle-to-body ratio decreased from 0.11 at 48-hr to 0.02 in adult. The heart is partitioned into sinus venosus, atrium, ventricle, and bulbus arteriosus as identified by the constriction between the segments at 48-hr. Valves were formed at 5-day post-fertilization. Until maturity, the atrium showed extensive pectinate muscles, and the atrial wall increased to two to three cell layers. The ventricular wall and the compact layer increased to three to four cell layers, while the extent and complexity in trabeculation continued. Further thickening of the heart wall was mainly by increase in cell size. The bulbus arteriosus had similar characteristics to the myocardium in early stages, but lost the MF-20 positive staining, and transitioned to smooth muscle layer. All pressures increased geometrically with development, and were linearly related to stage-specific values for body weight (P < 0.05). These data define the parameters of normal cardiac morphology and ventricular function in the developing zebrafish.

Animals↗

PubMed2000

Activation of protein kinase A modulates trafficking of the human cardiac sodium channel in Xenopus oocytes.

Voltage-gated Na(+) channels are critical determinants of electrophysiological properties in the heart. Stimulation of beta-adrenergic receptors, which activate cAMP-dependent protein kinase (protein kinase A [PKA]), can alter impulse conduction in normal tissue and promote development of cardiac arrhythmias in pathological states. Recent studies demonstrate that PKA activation increases cardiac Na(+) currents, although the mechanism of this effect is unknown. To explore the molecular basis of Na(+) channel modulation by beta-adrenergic receptors, we have examined the effects of PKA activation on the recombinant human cardiac Na(+) channel, hH1. Both in the absence and the presence of hbeta(1) subunit coexpression, activation of PKA caused a slow increase in Na(+) current that did not saturate despite kinase stimulation for 1 hour. In addition, there was a small shift in the voltage dependence of channel activation and inactivation to more negative voltages. Chloroquine and monensin, compounds that disrupt plasma membrane recycling, reduced hH1 current, suggesting rapid turnover of channels at the cell surface. Preincubation with these agents also prevented the PKA-mediated rise in Na(+) current, indicating that this effect likely resulted from an increased number of Na(+) channels in the plasma membrane. Experiments using chimeric constructs of hH1 and the skeletal muscle Na(+) channel, hSKM1, identified the I-II interdomain loop of hH1 as the region responsible for the PKA effect. These results demonstrate that activation of PKA modulates both trafficking and function of the hH1 channel, with changes in Na(+) current that could either speed or slow conduction, depending on the physiological circumstances.

Animals↗

PubMed2000

Identification of novel regions of allelic loss from a genomewide scan of esophageal squamous-cell carcinoma in a high-risk Chinese population.

Esophageal cancer is one of the most common fatal cancers worldwide. Deletions of genomic regions are thought to be important in esophageal carcinogenesis. We conducted a genomewide scan for regions of allelic loss using microdissected DNA from 11 esophageal squamous-cell carcinoma patients with a family history of upper gastrointestinal tract cancer from a high-risk region in north central China. Allelic patterns of 366 fluorescently labeled microsatellite markers distributed at 10-cM intervals over the 22 autosomal chromosomes were examined. We identified 14 regions with very high frequency (>/= 75%) loss of heterozygosity (LOH), including broad regions encompassing whole chromosome arms (on 3p, 5q, 9p, 9q, and 13q), regions of intermediate size (on 2q, 4p, 11p, and 15q), and more discrete regions identified by very high frequency LOH for a single marker (on 4q, 6q, 8p, 14q, and 17p). Among these 14 regions were 7 not previously described in esophageal squamous-cell carcinoma as having very high frequency LOH (on 2q, 4p, 4q, 6q, 8p, 14q, and 15q). The very high frequency LOH regions identified here may point to major susceptibility genes, including potential tumor suppressor genes and inherited gene loci, which will assist in understanding the molecular events involved in esophageal carcinogenesis and may help in the development of markers for genetic susceptibility testing and screening for the early detection of this cancer. Genes Chromosomes Cancer 27:217-228, 2000. Published 2000 Wiley-Liss, Inc.

Adult↗

PubMed2000

High frequency allelic loss on chromosome 17p13.3-p11.1 in esophageal squamous cell carcinomas from a high incidence area in northern China.

Allelic loss on chromosome 17p has been reported frequently in esophageal squamous cell carcinoma (ESCC) and generally encompasses the p53 locus at 17p13.1. However, a good correlation between allelic loss on 17p and mutation of p53 has not been found. This suggests the possibility that unknown tumor suppressor genes near p53 may be involved in the development of ESCC. To evaluate this possibility, we analyzed 30 microsatellite markers covering the entire short arm of chromosome 17 in 56 ESCC patients from a high risk population in northern China, including 34 with a family history of upper gastrointestinal (UGI) cancer and 22 without a family history of any cancer. Cancer lifestyle risk factors and clinical/pathological characteristics were also collected. We found frequent allelic loss (>/=65%) at 28 of the 30 markers evaluated in these ESCC patients. The highest frequencies of allelic loss (> or =80%) were found in three smaller regions: deletion region I located at 17p13.3-p13.2 (between D17S849 and D17S1828); deletion region II located at 17p13.2-p13.1 (between D13S938 and TP53); deletion region III located at 17p13.1-p12 (between D17S804 and D17S799). A number of genes have already been identified in these deleted regions, including: OVCA1, OVCA2 and HIC-1 in deletion region I; p53 in deletion region II; ZNF18, ZNF29, ALDH3 and ALDH10 in deletion region III. These results will help us direct future testing of candidate genes and narrow the search region for major new tumor suppressor genes that may play a role in the pathogenesis of ESCC.

Adult↗

PubMed2000

An approach to proteomic analysis of human tumors.

A strategy for proteomic analysis of microdissected cells derived from human tumor specimens is described and demonstrated by using esophageal cancer as an example. Normal squamous epithelium and corresponding tumor cells from two patients were procured by laser-capture microdissection and studied by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE). Fifty thousand cells resolved approximately 675 distinct proteins (or isoforms) with molecular weights ranging between 10 and 200 kDa and isoelectric points of pH 3-10. Comparison of the microdissected protein profiles showed a high degree of similarity between the matched normal-tumor samples (98% identical). However, 17 proteins showed tumor-specific alterations, including 10 that were uniquely present in the tumors and seven that were observed only in the normal epithelium. Two of the altered proteins were characterized by mass spectrometry and immunoblot analysis and were identified as cytokeratin 1 and annexin I. Acquisition of 2D-PAGE protein profiles, visualization of disregulated proteins, and subsequent determination of the identity of selected proteins through high-sensitivity MS-MS microsequencing are possible from microdissected cell populations. These separation and analytical techniques are uniquely capable of detecting tumor-specific alterations. Continued refinement of techniques and methodologies to determine the abundance and status of proteins in vivo holds great promise for future study of normal cells and associated neoplasms. Mol.

Electrophoresis, Gel, Two-Dimensional↗

PubMed2000

[Hyperconjugation, characteristic infrared absorption of methylsulfones and crystal structures of selected aromaticsulfones].

A branched absorption peak with medium intensity at (970 +/- 20) cm-1 appears only in the infrared spectra of methylsulfones. The below mentioned aromaticsulfones are chosen to reveal the specificity. Crystal and molecular parameters of CH3CONH-C6H4-SO2R(R = -CH3, -CH2CH2OH)-CH2CONH2, are determined by application of single crystal diffraction of X-ray through Nicolet R3M/E diffracometer. The existence of hyperconjugation and its natures in group -SO2CH3, confirmed by further analyses on the parameters, result in the specificity of IR absorption of the group, which is proved characteristic and can be used to identify methylsulfones. The first part describes the detection results, ascertains their crystal and molecular structures, and shows that the aromaticsulfone exists as cross linking multi-molecules when R = -CH2CONH2 or as double molecules when R = -CH2CH2OH because of H bonds. The second part covers analyses on their molecular structures. The analyses demonstrate the hyperconjugation between sigma S-C and pi S-C in group -SO2CH3. The sigma C-H hyperconjugate with pi S-O. The strength of hyperconjugated bond C-H decreases and its length tends longer. Due to the effect, the bond S-C is not a pure single bond sigma, but one which possesses a certain degree of a double bond. Its IR wave number, between those of sigma S-C and pi S-C, attributes to the medium branched peak at (970 +/- 20) cm-1. The peak branch reflects two groups of the most stable hyperconjugating conformational isomers. The hyperconjugation is weakened by the substitution of one non H group for one H atom in -SO2CH3 and if the non H group does not conjugate with pi S-O, the absorption at (970 +/- 20) cm-1 disappears as a characteristic peak. The intensity of absorption at (970 +/- 20) cm-1 conforms to the intensity of hyperconjugation between pi S-O and its adjacent sigma C-H. The third part introduces syntheses of the products, crystal preparations and their detections through X-ray diffraction.

English Abstract↗