Atom-photon dressed states in a waveguide-QED system with multiple giant atoms.

We study the properties of bound states in waveguide-QED systems consisting of multiple giant atoms coupled to a coupled-resonator waveguide. Based on the general analytical expressions for these states and the corresponding energy spectra, we analyze in detail the threshold conditions for the appearance of bound states and the photon-mediated interactions between dressed atoms for different configurations. In addition, when multiple giant atoms are coupled to the waveguide, different types of interacting atomic chain can be obtained by manipulating the coupling configurations. Accordingly, the energy spectra of the bound states form metaband structures in the photonic band gaps. This makes the system a useful platform for quantum simulation and quantum information processing.

[Growth rate of adult obesity prevalence in China and target population for prevention and control from 2013 to 2018].

Objective: To investigate the annual growth rate of obesity prevalence of residents aged 18 and above in China and prevention keypoints for target populations from 2013 to 2018. Methods: This was a cross-sectional study. Subjects from China Chronic Disease and Risk Factor Surveillance project in 2013 and 2018 were included. The prevalence of obesity and growth rate in 31 provinces (autonomous regions and municipalities) in China were collected through survey questionnaires and on-site measurements. Other demographic data such as the proportion of obesity control measures, diet, exercise and drug use was also analyzed. Obesity among adults was defined as body mass index≥28.0 kg/m². Results: A total of 174 736 residents, aged (51.5±14.2) years, which included 74 704 (42.8%) males were recruited in 2013, and 179 125 residents, aged (55.1±13.8) years, which included 79 337 (44.3%) males were included in 2018. The average annual increase rate of adult obesity prevalence in China from 2013 to 2018 was 3.2% (uncertainty interval (UI) 2.7%-3.6%), and the average increase rate of obesity prevalence among men (5.2% (UI 4.6%-5.9%)) was higher than that of women (0.9% (UI 0.5%-1.3%)). For subgroups analysis, the average increase rate of obesity prevalence among residents aged 18 to 29 (7.4% (UI 6.9%-7.9%)), education level beyond college degree (6.3% (UI 5.5%-7.1%)), and unmarried population (11.2% (UI 10.2%-12.1%)) were higher than that of other subgroups between 2013 and 2018. The residents in Hainan province showed the highest average annual growth rate of obesity. With the exception of Shanxi, Hunan, Gansu and Ningxia province, the annual growth rate of obesity prevalence among adults increased in all other provinces (autonomous regions and municipalities) from 2013 to 2018. For the obese population, the proportion of people who took weight control measures increased from 22.6% in 2013 to 32.7% in 2018. Conclusions: The prevalence of obesity growth characteristics in subpopulations and regions in China are obviously different. Accordingly the focus points of obesity prevention and control in different regions should have their own emphasis.

[Associations between glycated hemoglobin and glucose indicators in adults in areas at different altitude in China].

Objective: To explore the associations of glycated hemoglobin (HbA1c) with FPG and oral glucose tolerance test 2-hour (OGTT-2 h) in areas at different altitude in China. Methods: Subjects who participated in 2018-2019 China Chronic Disease and Risk Factor Surveillance and had no prior type 2 diabetes diagnosis were included. Subsequently, they were categorized into three groups based on altitude of living area (<2 000, 2 000- and ≥3 000 m). With adjustment for intracluster correlation, multivariable linear regression analysis was performed to evaluate the associations of HbA1c with FPG and OGTT-2 h in the context of HbA1c was normal (<5.7%) or abnormal (≥5.7%). Furthermore, the shape of relationships between HbA1c and glucose indicators was examined using restricted cubic spline. Finally, receiver operating characteristic curve was used to evaluate the diagnostic performance of HbA1c for diabetes. Results: A total of 157 277 subjects were included in the analysis. While FPG and OGTT-2 h levels gradually decreased with increase of altitude, HbA1c level was similar among the three groups. When HbA1c was <5.7%, its association with FPG and OGTT-2 h was weak and no obvious difference was observed among the three groups. When HbA1c was ≥5.7%, the FPG and OGTT-2 h increased by 15.45% (95%CI:14.71%- 16.18%) and 24.54% (95%CI:23.18%-25.91%) respectively per one standard deviation increase in HbA1c in group in area at altitude <2 000 m. However, the FPG and OGTT-2 h increased by 13.08% (95%CI:10.46%-15.76%) and 21.72% (95%CI:16.39%-27.31%), respectively, in group in area at altitude 2 000- m, and increased by 11.41% (95%CI:9.32%-13.53%) and 20.03% (95%CI:15.38%- 24.86%), respectively, in group of altitude ≥3 000 m. The restricted cubic spline indicated that the curve showing the association of HbA1c with FPG and OGTT-2 h was flat when HbA1c was <5.7%, but showed a positive linear relationship when HbA1c was ≥5.7%. The area under curve for detecting diabetes was 0.808 (95%CI:0.803-0.812) in group of altitude <2 000 m and 0.728 (95%CI:0.660-0.796, P=0.022) in group of altitude ≥3 000 m. The relevant optimal cutoff value of HbA1c was 5.7%, with a sensitivity of 65.4% and a specificity of 83.0%, and 6.0%, with a sensitivity of 48.3% and a specificity of 93.7%, respectively. Conclusions: When HbA1c was ≥5.7%, the association between HbA1c and glucose indicators became weaker as the increase of altitude. In the area at altitude ≥3 000 m, it may not be appropriate to use HbA1c in the diagnosis of diabetes.

Homogeneously staining region in anthracycline-resistant HL-60/AR cells not associated with MDR1 amplification.

Anthracycline-resistant HL-60/AR cells and their drug-sensitive HL-60/S counterparts were characterized by karyotypic analysis and examined for the overexpression of DNA and mRNA sequences coding for P-glycoprotein (Pgp). The HL-60/S cells were karyotypically stable over a 5-year period of study (1986-1991), except for an additional small Giemsa-positive band noted at 7q22 in cultures harvested in 1987, but not in 1986. This change did not affect drug sensitivity. The drug-resistant HL-60/AR cells examined in 1986, 1987, and 1991 demonstrated a very stable karyotype. The most striking feature was a large homogeneously staining region in the long arm of chromosome 7 (7q11.2), and translocation of the remainder of the long arm to another centromere. Other changes in the HL-60/AR cells included inversion in 9q, partial deletion of the short arm of chromosome 10p, addition of material to the p arm of der(16), loss of chromosome 22, and the appearance of a new marker chromosome. Both HL-60/S and the HL-60/AR cells were found not to amplify DNA or mRNA sequences coding for the Pgp. Thus, although the HL-60/AR cells possess the classical multidrug resistance phenotype and demonstrate a homogeneously staining region near the region of the MDR1 gene, their resistance is due to mechanisms other than those coded for by MDR1.

A shuttle vector system for the investigation of immunoglobulin gene hypermutation: absence of enhanced mutability in intermediate B cell lines.

Somatic hypermutation focused to the rearranged V(D)J segment of the immunoglobulin (Ig) loci contributes substantially to antibody gene diversification. However, neither the precise B cell subset subject to hypermutation nor the molecular mechanism(s) involved is known. One model proposes that Ig segments may be uniquely susceptible to DNA nicking and subsequent error-prone repair during a specific B cell developmental stage. We describe an SV40-based shuttle vector system for testing such a model. Plasmids containing two distinct Ig segments juxtaposed to the supF marker gene have been passaged through cell lines representing intermediate stages of B cell development, rescued and screened for marker gene mutations. To date we have not demonstrated enhanced supF mutation in any cell line examined, irrespective of the adjacent Ig segment. Thus, these cell lines exhibit normal DNA repair mechanisms and no evidence of increased endonuclease activity on the Ig segments tested. The feasibility of this system will allow similar experiments using other Ig target sequences exposed to a broader range of B cells.

Thrombospondin-1 restrains neutrophil granule serine protease function and regulates the innate immune response during Klebsiella pneumoniae infection.

Neutrophil elastase (NE) and cathepsin G (CG) contribute to intracellular microbial killing but, if left unchecked and released extracellularly, promote tissue damage. Conversely, mechanisms that constrain neutrophil serine protease activity protect against tissue damage but may have the untoward effect of disabling the microbial killing arsenal. The host elaborates thrombospondin-1 (TSP-1), a matricellular protein released during inflammation, but its role during neutrophil activation following microbial pathogen challenge remains uncertain. Mice deficient in TSP-1 (thbs1(-/-)) showed enhanced lung bacterial clearance, reduced splenic dissemination, and increased survival compared with wild-type (WT) controls during intrapulmonary Klebsiella pneumoniae infection. More effective pathogen containment was associated with reduced burden of inflammation in thbs1(-/-) mouse lungs compared with WT controls. Lung NE activity was increased in thbs1(-/-) mice following K. pneumoniae challenge, and thbs1(-/-) neutrophils showed enhanced intracellular microbial killing that was abrogated with recombinant TSP-1 administration or WT serum. Thbs1(-/-) neutrophils exhibited enhanced NE and CG enzymatic activity, and a peptide corresponding to amino-acid residues 793-801 within the type-III repeat domain of TSP-1 bridled neutrophil proteolytic function and microbial killing in vitro. Thus, TSP-1 restrains proteolytic action during neutrophilic inflammation elicited by K. pneumoniae, providing a mechanism that may regulate the microbial killing arsenal.

Wolf-Hirschhorn (4p deletion) syndrome: report of one case.

Wolf-Hirschhorn syndrome is an uncommon chromosomal disorder caused by loss of material from the distal aspect of the short arm of chromosome 4. Its characteristic features include profound growth retardation with psychomotor delay, severe mental deficiency, facial dysmorphia, midline defects and skeletal anomalies. We herein report a case of 4p deletion syndrome and review related literature.

Chromosomal DNA homologous to Herpes simplex virus 1 in a mouse L-cell line.

Cytological hybridization in situ was used to identify chromosomes carrying DNA sequences homologous to Herpes simplex I (HSV-I) DNA in a HSV-transformed L-cell line. The L-cell karyotype, frequency of chromosome distribution, and possible homology to the normal chromosome complement are given. The major chromosomal sites for transcription of ribosomal RNA (rRNA) were also determined.

The localization of mouse globin genes: a test of the effectiveness of hybridization in situ.

Hybridization of rabbit reticulocyte mRNA to banded mouse chromosomes in situ labeled several regions, including the globin loci. Whereas the labeling was sufficient to detect unknowns in the globin size class, the chromosome assignments would be doubtful without some means of removing trace contaminants from the probe or of recognizing chromosomal regions to which they hybridize. Mammalian gene mapping by means of hybridization in situ might be feasible with probes cloned in microbial host-vector systems or with kinetic analysis of the hybridization process at every labeled site.

c-myc hypermutation is ongoing in endemic, but not all Burkitt's lymphoma.

Deregulation of c-myc oncogene secondary to chromosomal translocation appears to play an essential role in the genesis of both endemic (African) Burkitt's lymphoma (eBL) and sporadic Burkitt's lymphoma (sBL). In most eBL, mutations in or near exon 1 disrupt normal c-myc regulatory sites. We examined c-myc sequences from a patient with sBL and two patients with eBL to determine (1) whether mutation is ongoing as the tumor clone expands, (2) the nature of mutations in the protein-coding exons 2 and 3, and (3) the extent of c-myc hypermutation in the two clinical forms of BL. Using the polymerase chain reaction (PCR), we amplified segments of c-myc from bulk tumor samples, cloned the products into plasmid vectors, and sequenced multiple subclones of each segment. The mutation frequencies in the control (remission bone marrow) and sBL tumor subclones were 0.65 x 10(-4) and 3.0 x 10(-4) (mutations/base), respectively (P greater than .25). Subclones from the two eBLs exhibited mutation frequencies of 20 x 10(-4) and 16 x 10(-4), respectively (P less than .001 v control). In addition to the consensus mutations seen in one eBL, a random pattern of unshared mutations was observed throughout c-myc in both samples, demonstrating that mutations may be introduced in a stepwise fashion. We noted a clear excess of transitions over transversions (30:9), which is qualitatively similar to the pattern observed in diverse examples of eukaryotic gene mutation. These data demonstrate that c-myc hypermutation is an ongoing process as the eBL tumor clone expands, is qualitatively different from immunoglobulin gene hypermutation, and is not a universal feature of BL, perhaps reflecting the nature of the translocation or the stage of tumor cell maturation.

Location of the genes for 16S and 23S ribosomal RNA in the genetic map of Escherichia coli.

By means of RNA-DNA hybridization with DNA from different merodiploids of Escherichia coli, the genes for 16S and 23S ribosomal RNA were found near minute 74 of the genetic map.

Does the T-locus in the mouse include ribosomal DNA?

The proportion of rDNA in the mouse genome is shown to have no systematic relation to the T-locus genotype, and hybridization in situ with 125I-RNA does not label chromosome 17, which carries the T-locus. Thus rDNA need no longer be taken into account in explaining the unique properties of the alleles at this locus. The number of genes for rRNA precursor averaged 153 per haploid genome, but a large measure of individual variation is suggested.

Variation in ribosomal RNA gene number in mouse chromosomes.

Hybridization of 125-I-ribosomal RNA to mouse chromosomes in situ produced significant differences in grain count at known rDNA sites, depending on the strains from which they were derived. This is interpreted to mean that the number of rRNA genes in a given nucleolar chromosome, and in the entire genome, is polymorphic among strains and among outbred individuals.

Monochromosomal rodent-human hybrids from microcell fusion of human lymphoblastoid cells containing an inserted dominant selectable marker.

An improved system for the production of a series of rodent-human hybrids selectively retaining single human chromosomes marked in known locations is described. Such hybrids have significant applications in gene mapping and other genetic studies. Human lymphoblastoid lines were infected with the retroviral vector SP-1, which contains the bacterial his-D gene allowing mammalian cells to grow in the presence of histidinol. Microcell fusion of the infected lymphoblastoid cells with CHO cells was used to produce hybrids containing single human chromosomes retained by histidinol selection. Hybrids containing a single human chromosome 9 and a single human chromosome 19 are described. These have been characterized cytogenetically by G-banding, in situ hybridization, and Southern blot analysis.

Improved methods of direct and cultured chromosome preparations from chorionic villous samples.

A new method is described for preparing direct mitotic chromosome spreads from chorionic villous samples, which has resulted in sufficiently high yields of well-banded metaphases to permit a complete standard chromosomal diagnosis in 20 of 20 cases. A method of establishing monolayer cultures from this material that can be harvested from 3 to 7 days after initiation is also presented.

The aminoquinazoline group as a replacement for the salicylamide group: the design and synthesis of a novel highly selective beta 1 adrenoceptor partial agonist.

The high potency at beta 1 receptors, excellent selectivity (beta 1/beta 2) and high degree of agonism displayed by compounds such as 1 is believed to be due in part to the salicylamide side chain. Two conformations of salicylamide are known to exist in the crystal state (2 and 3), but ab initio calculations suggest that in the absence of crystal packing forces 2 should be more stable. The aminoquinazoline group was judged to be a good replacement for salicylamide in 1, and consequently the oxypropanolamine derivative 4 was prepared. 4 shows extremely high potency at the beta 1 receptor, and excellent beta 1/beta 2 selectivity. It has comparable in vitro activity to 1, although it displays a lower degree of agonism. These results suggest that in this system aminoquinazoline appears to be an excellent mimic of the salicylamide group.

Differential expression of alternatively spliced forms of MAP4: a repertoire of structurally different microtubule-binding domains.

We previously reported that the microtubule (MT)-binding domain of microtubule-associated protein 4 (MAP4) contains three 18-amino acid imperfect repeats that are homologous to the repeats found in the MT-binding domains of the neuronal MAPs, MAP2 and tau [Chapin, S. J., & Bulinski, J. C. (1991) J. Cell Sci. 98, 27-36]. Here we report the isolation of clones encoding additional isoforms of MAP4, which differ in the number of repeated elements contained within their MT-binding domains. In addition to clones encoding three repeats, we isolated clones encoding a four-repeat isoform, whose MT-binding domain bears a striking similarity to the four-repeat isoform of tau. Other MAP4 clones that we isolated encode five repeats. The additional repeat in the five-repeat isoform of MAP4 is quite unusual in its amino acid sequence; this unusual repeat was also found by Aizawa et al. [Aizawa, H., et al. (1990) J. Biol. Chem. 265, 13849-13855] among the repeats encoded by bovine MAP4 clones possessing four repeats. In humans, MAP4 was recently shown to be encoded by a single-copy gene [West, R. R., et al. (1991) J. Biol. Chem. 266, 21886-21896]; we demonstrated that the human MAP4 gene is located on human chromosome 3p21. Expression of multiple MAP4 isoforms from this gene, which appears to result from alternative RNA splicing, was investigated by RNase protection analysis of mammalian cell lines and rat tissues. The five-repeat isoform was the only form detectable in most cell lines, and it was the most abundant isoform expressed in rat lung, liver, kidney, spleen, and testis. However, in rat brain, heart, and skeletal muscle, although the five-repeat isoform was expressed at all developmental stages examined, the tau-like four-repeat isoform was also expressed, and its expression increased during development. The three-repeat isoform was expressed in heart and, to a lesser extent, in brain, skeletal muscle, and lung. Our results demonstrate that several different MAP4 isoforms are expressed in the rat in different tissues and at various developmental stages. Furthermore, our data suggest that differential expression of MAP4 isoforms possessing distinct MT-binding domains may be involved in the changes in MT dynamics or function that are known to accompany differentiation.

The site of 5S RNA genes in primates. I. The great apes.

A major site of genes for 5S RNA has been localized in representative members of the family Pongidae by means of hybridization in situ. These genes are shown to be concentrated in the most distal bands of the primate chromosome arm homologous to human chromosome 1q.

The site of 5S RNA genes in human chromosome 1.

The major site of genes for human 5S RNA is in the long arm of chromosome 1. We find no evidence of sites in other chromosomes; if such exist, they are much smaller than the site in 1q.