[Association between ambient air pollution and biological aging among the middle-aged and older adults: a systematic review].

Objective: To summarize and elucidate the impact of ambient air pollution on biological aging among middle-aged and older adults. Methods: "Air pollution""Biological age""Epigenetic age""Biological aging"and"Epigenetic aging", as well as specific names of air pollutants and biological age were used as search keywords. This study searched the databases of PubMed and Web of Science for eligible English articles and CNKI, CQVIP, Wanfang, CBM, CSTP and other Chinese databases for eligible Chinese articles from inception until June 30, 2023. The language was limited to Chinese and English. Results: Among the 14 included articles, five studies investigated the impact of air pollution on DNA methylation age using different algorithms, while six studies explored the relationship between air pollutants and telomere length. Six studies focused on frailty as an outcome, and an additional study revealed the relationship between fine particulate matter (PM2.5) and its components with composite indicator age (KDM age). The results indicated that, although different forms of biological ages were susceptible to different ambient air pollutants at different degrees, previous studies had consistently found that the increased levels of PM2.5 and one of its major components, black carbon (BC), could significantly accelerate the biological aging of middle-aged and older adults. Similar trends were observed with nitrogen oxides (NOx) and ozone (O3) but with relatively limited evidence. Conclusion: Major air pollutants could accelerate the biological aging of middle-aged and older adults.

[The correlations between serum vitamin D, parathyroid hormone, and bone mineral density with benign paroxysmal positional vertigo].

Objective:To detect serum 25-hydroxyvitamin D[25-（OH）2-VitD3], parathyroid hormone (PTH), and bone mineral density in patients with benign paroxysmal positional vertigo (BPPV), and to analyze their correlations with BPPV. Method:Fifty cases of BPPV were selected as the study group, 50 healthy persons were selected as control group. Chemiluminescence assay was used to detect serum VD level, chemiluminescence immunoassay was used to detect serum PTH level, dual energy X-ray absorptiometry was used to detect bone mineral density (BMD) and T value of lumbar vertebrae 1 to lumbar vertebrae 4 in two groups. Result:The serum 25-（OH）2-VitD3 level in the study group was significantly lower than that in the control group (P<0.05); the serum PTH level of the study group was significantly higher than that of the control group (P<0.05); there was no significant difference in T value between male BPPV patients and female BPPV patients younger than 48 years old with the control group (P>0.05), T value of female BPPV patients older than 48 years old was significantly lower than that of the control group (P<0.05). Logistic regression analysis showed that the decrease of serum 25-（OH）2-VitD3 level, the increase of PTH level, and the decrease of bone mineral density were risk factors for BPPV. Conclusion:The level of serum 25-（OH）2-VitD3 is decreased in BPPV patients, PTH level is increased and bone mineral density is decreased, they are risk factors for BPPV.

[Clinical characteristics in patients with hypervirulent Klebsiella pneumoniae infection and its capsular serotypes and multilocus sequence typing].

Objective: To describe the clinical characteristics of hypervirulent Klebsiella pneumoniae (hvKP) infection. To analyze the antibiotic susceptibility of hvKP to provide the empiric antibiotic options. To investigate capsule serotype and sequence type (ST) of hvKP and their correlation with clinical profiles. Methods: hvKP was defined as bacteria isolated from patients with community-acquired pyogenic liver abscess (CA-PLA) with co-infection sites outside liver or a bloodstream infection in a host without underlying biliary tract diseases. Patients with CA-PLA hospitalized in the First Hospital of China Medical University were retrospectively analyzed from January 2011 to December 2017. Antibiotic susceptibility was detected by automatic bacterial identification and antibiotic susceptibility analysis system in vitro. Polymerase chain reaction method and gene sequencing were used to detect the main capsule serotype and ST. Results: A total of 140 cases with hvKP infection were enrolled. The co-infections outside liver abscess included 98 bloodstream infections, 53 pneumonia, 11 perianal abscess, 10 urinary system infections, 3 subphrenic abscess, 3 endophthalmitis, 2 spleen abscess, and other miscellaneous infections including 1 peritonitis, 1 skin and soft tissue infection, 1 myelitis, 1 colitis, 1 psoas major abscess and 1 myocardial abscess. Among the 140 cases, 106 presented with single co-infection site, 32 with 2 sites, and 2 with 3 sites. HvKP manifested high antibiotic susceptibility up to 80% for most commonly used antibiotics. Capsule serotyping of 43 revived isolates indicated that K1 serotype accounted for 53.49% (23/43), K2 34.88 (15/43), K54 2.33% (1/43), K57 2.33% (1/43), and other serotypes 6.98%(3/43). There was no significant distribution among K1, K2, K54 and K57 of hvKP capsule serotypes in patients with or without diabetes mellitus (P>0.05). Multilocus sequence typing (MLST) suggested that ST23 and ST65 were predominant accounting for 39.53% (17/43) and 25.58% (11/43) respectively. No serotype or ST predominance was seen in any of the clinical infections. Conclusion: HvKP is related to a wide spectrum of infectious diseases, including multiple extrahepatic sites and bloodstream infections besides CA-PLA with high antibiotic susceptibility. K1 and K2 are the predominant capsule serotypes, and ST 23 and ST65 are the predominant sequence types.

[Value of R2(*) in evaluating the biological behavior of primary hepatocellular carcinoma].

OBJECTIVE: To investigate the correlation between R2(*) value of enhanced T2 star-weighted angiography (ESWAN) sequence and primary hepatocellular carcinoma infiltration and tumor thrombus, and investigate the biological behavior of HCC. METHODS: A total of 221 cases of patients' imaging data with MRI examination(including ESWAN sequence) diagnosed as primary HCC were retrospectively analyzed.All the patients were collected from January 2014 to September 2015 in the First Affiliated Hospital of Dalian Medical University.The differences of R2(*) values in different MR types of HCC were analyzed.All patients were divided into infiltration group and non-infiltration group, tumor thrombus group and non-tumor thrombus group, the R2(*) values of the paired groups were compared.The diagnostic efficiency of R2(*) in HCC infiltration and tumor thrombus were evaluated by ROC curve, and to find out the threshold values. RESULTS: The MR types of 221 patients included 90 cases of nodular type, 62 cases of massive type, 69 cases of diffuse type.70 patients had tumor thrombus.The R2(*) values of different MR types were (21.82±8.52), (24.17±8.84)and (34.45±11.73) Hz, respectively.There was no statistically significant difference between the nodular and the massive types (P=0.144), while the difference between the nodular and diffuse type, the massive and diffuse types were statistically significant(P=0.000). The R2(*) values of infiltration group and non-infiltration group were (34.45±11.73) and (22.78±8.70) Hz , the R2(*) values of tumor thrombus group and non-tumor thrombus group were (31.20±12.17) and (24.21±9.90) Hz, the difference also had statistically significant(t=7.397 and 4.534, P=0.000 and 0.000). The AUC of R2(*) values for infiltration and tumor thrombus were 0.804, 0.681. R2(*) ≥24.68 Hz was the threshold value to diagnose the infiltration and tumor thrombus. CONCLUSION: R2(*) value can be used as a MR non-enhancement quantitative index to evaluate the biological behavior of HCC.

Resistance trends among clinical isolates in China reported from CHINET surveillance of bacterial resistance, 2005-2014.

With the aim of gathering temporal trends on bacterial epidemiology and resistance from multiple laboratories in China, the CHINET surveillance system was organized in 2005. Antimicrobial susceptibility testing was carried out according to a unified protocol using the Kirby-Bauer method or automated systems. Results were analyzed according to Clinical and Laboratory Standards Institute (CLSI) 2014 definitions. Between 2005 and 2014, the number of bacterial isolates ranged between 22,774 and 84,572 annually. Rates of extended-spectrum ß-lactamase production among Escherichia coli isolates were stable, between 51.7 and 55.8%. Resistance of E. coli and Klebsiella pneumoniae to amikacin, ciprofloxacin, piperacillin/tazobactam and cefoperazone/sulbactam decreased with time. Carbapenem resistance among K. pneumoniae isolates increased from 2.4 to 13.4%. Resistance of Pseudomonas aeruginosa strains against all of antimicrobial agents tested including imipenem and meropenem decreased with time. On the contrary, resistance of Acinetobacter baumannii strains to carbapenems increased from 31 to 66.7%. A marked decrease of methicillin resistance from 69% in 2005 to 44.6% in 2014 was observed for Staphylococcus aureus. Carbapenem resistance rates in K. pneumoniae and A. baumannii in China are high. Our results indicate the importance of bacterial surveillance studies.

[The understanding of Epstein-Barr virus associated lymphoproliferative disorder].

In recent years, there are increasing articles concerning Epstein-Barr virus associated lymphoproliferative disorder (EBV+ LPD), and the name of EBV+ LPD is used widely. However, the meaning of EBV+ LPD used is not the same, which triggered confusion of the understanding and obstacles of the communication. In order to solve this problem. Literature was reviewed with combination of our cases to clarify the concept of EBV+ LPD and to expound our understanding about it. In general, it is currently accepted that EBV+ LPD refers to a spectrum of lymphoid tissue diseases with EBV infection, including hyperplasia, borderline lesions, and neoplastic diseases. According to this concept, EBV+ LPD should not include infectious mononucleosis (IM) and severe acute EBV infection (EBV+ hemophagocytic lymphohistiocytosis, fatal IM, fulminant IM, fulminant T-cell LPD), and should not include the explicitly named EBV+ lymphomas (such as extranodal NK/T cell lymphoma, aggressive NK cell leukemia, Burkitt lymphoma, and Hodgkin lymphoma, etc.) either. EBV+ LPD should currently include: (1) EBV+ B cell-LPD: lymphomatoid granulomatosis, EBV + immunodeficiency related LPD, chronic active EBV infection-B cell type, senile EBV+ LPD, etc. (2) EBV+ T/NK cell-LPD: CAEBV-T/NK cell type, hydroa vacciniforme, hypersensitivity of mosquito bite, etc. In addition, EBV+ LPD is classified, based on the disease process, pathological and molecular data, as 3 grades: grade1, hyperplasia (polymorphic lesions with polyclonal cells); grade 2, borderline (polymorphic lesions with clonality); grade 3, neoplasm (monomorphic lesions with clonality). There are overlaps between EBV+ LPD and typical hyperplasia, as well as EBV+ LPD and typical lymphomas. However, the most important tasks are clinical vigilance, early identification of potential severe complications, and treating the patients in a timely manner to avoid serious complications, as well as the active treatment to save lives when the complications happened.

[Codon usage of Chinese hamster ovary cells.].

BACKGROUND: To investigate the optimal codons of dihydrofolate reductase (dhfr) minus Chinese hamster ovary cells (CHO dhfr-). METHODS: A cDNA library of CHO dhfr- containing high abundence mRNA was constructed and protein-coding sequences were obtained after identification and analysis. Codon frequence of CHO dhf- was compared with that of Chinese hamster in CUTG database. Then codon usage variation among cDNA was investigated using correspondence analysis (COA). RESULTS: Fifty qualified cDNAs from CHO dhfr- were selected, which encodes proteins of high abundence. Comparing with the codon frequence of Chinese hamster, the highest frequence of synonymous codons for amino acids in CHO dhfr- cells were the same as Chinese hamster except that of Arg and Pro. This method of COA identifies the first main factor which can account for the largest fractions (14.7%) of variation among cDNAs. Twenty-two synonymous codons were identified as the optimal codons of CHO cell. CONCLUSION: CHO dhfr- cell has its own optimal codons, it is suggested that codon bias is one of reasons for functional diversity of different mammal cells and it is an effective stratagy to modification of the codon usage of the foreign gene according to the optimal codons of CHO dhfr- to increase the production of foreign gene.

[Chromosome aberration and carcinogenicity of CHO dhfr- cells transformed by plasmid containing S+ and Pre S1 of fusion gene of hepatitis B virus].

OBJECTIVE: To investigate the chromosome aberrations and carcinogenicity of CHO-dhfr- cell induced by integration of plasmid containing S+ and Pre S1 fusion gene of hepatitis B surface antigen (HBsAg). METHODS: The plasmid pCHBSS1G was constructed with S+ Pre S1 of HBsAg. CHO-dhfr- cells were transformed with this recombinant plasmid DNA and CHO cells lines with integrated DNA were cloned and named GdSS118. The GdSS1 18 cell lines secreting the S+ Pre S1 fusion protein of HBsAg at high level were developed by screening in increased concentration of MTX and MSX in cultured media. To make sample of cells chromosome, the cells integrated DNA were subcutaneously injected into nude mouse. RESULTS: The CHO-dhfr- cell lines integrated with S and Pre S1 fusion protein of HBsAg were developed and named GdSS1-18 cell lines. The frequencies and type of chromosome aberrations of the GdSS1-18 cell lines with different passage generations were 11%, 56% and 29%, respectively, while that of the control CHO-dhfr- cell lines was 6%. There was no change in the mode of chromosomes, both cell lines having 20 chromosome s. Both cell lines were non-oncogenic in nude mouse. CONCLUSIONS: The chromosome aberration of CHO-dhfr- cells with integrated DNA were obviously higher than that of the original CHO-dhfr- cells without integrated DNA. Both cell lines were non oncogenic in nude mouse.

Glycation decreases the stability of the triple-helical strands of fibrous collagen against proteolytic degradation by pepsin in a specific temperature range.

When fibrous collagen of rat tail tendons was glycated by incubation with ribose, it became highly insoluble in dilute acetic acid and resistant to pepsin digestion at 5 degrees C, since it was cross-linked by advanced glycation end products. Extensively glycated fibrous collagen was found to be much less stable than non-glycated control fibrous collagen against pepsin digestion at 30 degrees C. Under conditions where nearly all of the glycated fibrous collagen was degraded into small peptides by pepsin, approximately 45% of the control collagen was left as large polypeptides having nearly the whole length of its triple-helical region. A soluble collagen, which consisted primarily of the triple-helical region of monomeric collagen, was found to be glycated as efficiently as the fibrous collagen on incubation with ribose at 30 degrees C, while the rate of cross-linking of the soluble collagen was very low, suggesting that the triple-helical strands do not undergo intramolecular cross-linking and that most of the cross-links produced in the glycated fibrous collagen are intermolecular ones. The glycated soluble collagen was as stable as the control collagen against pepsin digestion at 30 degrees C. These results indicate that the triple-helical strands of glycated fibrous collagen are much less stable than those of the non-glycated form against proteolytic digestion by pepsin at a temperature close to but below their melting point. Sugar-derived intermolecular cross-links are supposed to underly the decreased stability of the triple-helical strands.

The mechanism of interaction of sodium dodecyl sulfate with elastic fibers.

Sodium dodecyl sulfate (SDS), an anionic hydrophobic ligand, is known to alter the mechanical properties of elastic fibers. In order to analyze the mechanism of the alteration, two forms of fibrous elastins, "solid" and "powder" elastins, which consisted of fascicular elastic fibers and single or oligomeric elastic fibers, respectively, were prepared from bovine aorta, and the interactions of SDS with these elastins in the presence and absence of 0.15 M NaCl were studied. The solid elastin was able to retain 1.2- to 1.4-fold larger amounts of SDS than the powder elastin under both conditions, and both elastins retained 1.2-fold or larger amounts of SDS in the presence of NaCl than in its absence. Whereas both elastins released the retained SDS gradually on repeated washing with an SDS-free buffer, the release rates from the solid elastin, especially the rate in the presence of NaCl, were much smaller than those from the powder elastin, and the solid elastin retained approximately 40% of the bound SDS under conditions where the powder elastin lost most of its SDS. The SDS-binding capacities of both elastins were significantly lower than those of soluble kappa-elastin and serum albumin, which bound SDS homogeneously on the polypeptide chains. When the washed SDS-bound solid elastin was incubated with methylene blue and examined under a microscope, most of the methylene blue-SDS complex was located at the interfiber spaces of the elastic fibers. These results suggest that SDS alters the mechanical properties of elastic fibers by binding to the interfiber spaces and surfaces of the fibers rather than by binding to the internal polypeptide chains.

Biochemical characterization of the fibres of collagen and elastin in the aortic wall of SHRSP.

1. Vessel wall fragments consisting of collagen, elastin and other insoluble proteins were prepared from the aortas of 6 month old WKY and SHRSP and dead, elderly humans. 2. Prolonged incubations of these fragments with pepsin below or at 30 degrees C resulted in different amounts of insoluble materials containing similar or larger proportions of collagen and other insoluble proteins than the respective vessel fragments. The amounts of the pepsin-insoluble materials obtained from SHRSP were larger than those from WKY but were much smaller than those from elderly humans. 3. The elastins isolated from the vessel fragments were solubilized by pepsin much more effectively than the respective vessel fragments. 4. The pepsin-insoluble materials from WKY were composed of thin mesh-shaped materials, while these materials from both rats did not contain a significant number of distinctive fibrils of collagen, the materials from elderly humans did contain numerous distinctive fibrils of collagen. 5. Large fractions of both the collagen and other proteins in the pepsin-insoluble materials were solubilized by incubation with a crude bacterial collagenase below 30 degrees C or by incubation with pepsin above 40 degrees C where the triple-helical regions of the collagens were unfolded. 6. These results appear to indicate that the aortic wall of SHRSP contains larger amounts of some insoluble components that immobilize the collagen fibrils than that of WKY, but the aortic walls of elderly humans contain much larger amounts of these components than that of SHRSP.

Host dependence of naturally occurring temperature-sensitive influenza A viruses and location of their genetic lesions.

Naturally occurring temperature-sensitive (ts) strains have been found in large number in human influenza A viruses of all subtypes (J. Virol. 41 (1982) 353). Further studies have demonstrated that the ts phenotype of these viruses is host-dependent in that they are highly ts in chick embryos and chick embryonic cells, but are ts+ in MDCK cells. Previous studies have located by complementation tests the ts lesion of two H3N2 viruses (HK/8/68 and Ningxia/01/72, also known as Xia-ts) on the NP gene and that of two H1N1 viruses (Tianjin/78/77 and Beijing/1/79) on the M protein gene. By recombination and polyacrylamide electrophoresis migration of the RNA segments of its ts+ recombinant with PR8, the ts lesion of a later H3N2 virus A/Qi/39/79 has now been located on the M protein gene. The possibility for Qi/39/79 of acquiring the M gene lesion by reassortment with concurrently circulating Tianjin/78/77-like (H1N1) virus which also has ts lesion on the M gene was investigated. In contrast to Tianjin/78/77 (H1N1), however, Qi/39/79 complemented well with ts 51, a WSN ts strain with a single M gene lesion. Qi/39/79 and Tianjin/78/77 also complemented each other. Thus, there are two intra-segmental complementation groups of the M gene: Qi/39/79 belongs to one complementation group, while WSN ts 51 and Tianjin/78/77 belong to another. At present, there is no evidence of reassortment involving the genes concerned in the ts lesions of H3N2 and H1N1 viruses under natural conditions.

Nucleoprotein and membrane protein genes are associated with restriction of replication of influenza A/Mallard/NY/78 virus and its reassortants in squirrel monkey respiratory tract.

An avian influenza A virus, A/Mallard/NY/6750/78(H2N2), was restricted in in replication in the respiratory tract of squirrel monkeys. Avian-human influenza A reassortant viruses possessing the six RNA segments coding for nonsurface proteins (i.e., internal genes) of this avian virus were as restricted in replication in squirrel monkeys as their avian influenza parent. These findings indicated that restriction of replication of the avian influenza virus is a function of one or more of its internal genes. For an investigation of which of the avian influenza genes was responsible for restricted replication in the respiratory tract of primates, reassortant viruses were produced that contained human influenza virus surface antigens from the A/Udorn/72(H3N2) virus and one or more of the internal genes derived from the avian influenza virus parent. Avian-human reassortant influenza A viruses containing only the nucleoprotein or matrix protein RNA segment from the avian influenza virus parent were as restricted in their growth as an avian-human influenza reassortant virus containing each of the six avian influenza internal genes. In addition, an avian-human influenza reassortant virus possessing only the avian RNA 1 and nonstructural genes (which by themselves do not specify restricted replication) manifested a significant reduction of virus replication in squirrel monkey tracheas. Thus, the avian nucleoprotein and matrix genes appear to play a major role in the host range restriction exhibited by the A/Mallard/78 virus and its reassortants, but the combination of RNA 1 and nonstructural genes also contributes to restriction of replication.

Characterization of the genotype and level of attenuation of an influenza A reassortant virus produced by mating the Xia-ts donor virus with A/Beijing/70 (H1N1) wild type virus.

Two H1N1 progeny viruses derived by mating the attenuated donor virus, the A/Ningxia/72-ts (H3N2), and the A/Beijing/70 (H1N1) wild type virus were characterized for their genotype and their level of attenuation in susceptible adult volunteers. One progeny virus, clone PX62, was not a reassortant since it received each of its eight RNA segments from the H1N1 wild type virus. THis virus caused febrile influenza illness. Another progeny virus, clone PXH107, was a reassortant which received the genes coding for the surface antigens from the H1N1 parent virus but each of the other six RNA segments from the H3N2 parent virus. This clone was satisfactorily attenuated in susceptible adults and induced an immune response in at least 60% of the vaccinees. These results indicate that the genetic determinants of attenuation of the A/Ningxia/72-ts virus reside on one or more of the RNA segments that do not code for the surface antigens.

Identification of naturally occurring temperature-sensitive strains of influenza A virus and location of their genetic lesions.

Influenza A viruses of different subtypes isolated in different years and from different parts of China were examined for temperature-sensitiveness (ts) in their early egg passages. The validity of ts character has been confirmed by the results of parallel tests in chick embryos and in cell cultures. From 12 strains of the old H1N1 subtype isolated between 1949 and 1957, no ts strain was detected. Two out of 6 strains of new H1N1 isolated after February 1979 were found to be ts. For the H3N2 subtype, only 8 out of 23 strains isolated between 1968 and 1978 were ts, but the proportion increased abruptly of 13 out of 15 strains isolated in 1979-1980. We also found 6 out of 16 strains of the H2N2 subtype to be ts. Two H2N2 and one H3N2 strains examined were found to be composed of mixed ts and ts+ particles. By recombination-complementation test against 7 standard ts strains of WSN virus with known genetic lesions, the ts lesions of the H3N2 strain Hong Kong/8/68 was located on the nucleoprotein gene, whereas that of the H1N1 strain Tianjin/78/77 was located on the matrix protein gene.

Occurrence of temperature-sensitive influenza A viruses in nature.

The origin and characteristics of the first naturally occurring temperature-sensitive (ts) strain of influenza A virus identified in 1973, Xia-ts, are described. Natural ts strains were found to occur in the early egg passage material of all influenza A subtypes examined, but the proportion of ts virus varied from 8.3% for old H1N1 virus (1949 to 1957) to 82.4% for recent H3N2 virus (1979 to 1980). A number of strains were found to be composed of a mixture of ts and wild-type (ts+) particles. Six natural ts strains with different shutoff temperatures and one ts+ strain of the H1N1 subtype were tested in antibody-free volunteers. Strains with a shutoff temperature of 38 degrees C or lower caused very mild symptoms, whereas those with a shutoff temperature of 39 degrees C and the ts+ strain were much more reactogenic. By complementation tests against a set of prototype WSN ts mutants with a defined genetic lesion, the ts lesion of two H3N2 viruses (HK/8/68 and Xia-ts) was located on the NP gene and that of two H1N1 viruses (Tianjin/78/77 and Beijing/1/79) was located on the M protein gene. The present study demonstrates the widespread occurrence in nature of influenza viruses of different degrees of temperature sensitivity and presumably of different degrees of virulence.