[The factor analysis results of the relationship of socio-demographic, clinical and functional indicators with the likelihood of identifying age-related disorders in the population in North-Western Russia].

By using the method of factor analysis (principal component method) the determinants of disease in elderly and senile patients were searched with an estimate of their influence degree in the population of the North-West Russia. The data from medical records of 712 patients of both sexes aged 59 to 98 years were analyzed. The factor 1 proved to be associated with: marital status, living conditions, family relationships, bad habits, appearance, cough, diet, hearing and vision, laxatives, joint health, ability to move and sleep disturbances. Factor 2 combined diseases of older: cerebral stroke, myocardial infarction, cardiac arrhythmia, diabetes, kidney disease, obesity, thyroid disease, Parkinson's disease, lung disease, anemia, arthritis, osteoporosis, the number of surgeries and joint diseases. The factor 3 was found to self-association ability before and after admission to the assessment of the patients' mental state for MMSE test after admission. It is concluded that the development of age-related (especially the musculoskeletal system pathology) is associated with social characteristics and living conditions of patients, and treatment of the most age-related diseases requires consideration of comorbidity.

[Diagnostics of ataxia-telangiectasia by the express-test found on the method of indirect immunofluorescence].

Ataxia-telangiectasia (AT) is a hereditary severe neurodegenerative disease developing, when mutations take place in both alleles of the atm gene, which encodes the key protein of the cellular response to DNA damage (DDR)--ATM proteinkinase. In response to the occurrence of double-strand DNA breaks, the ATM proteinkinase pass the autophosphorylation, and its active form--the phospho-ATM (P-ATM) appears in cells. In the nuclei of cells having the atm gene, P-ATM is revealed, being absent in cells with mutated forms of this gene, by means of the application of the modified method of indirect immunofluorescence. This peculiarity may be applied in the clinic, in order to confirm the diagnosis of AT.

[An atypical case of Werner syndrome: epigenetic control and DNA damage response alterations].

A case of adult progeria has been described. It has been suggested that this case is an atypical form of Werner syndrome with laminopathy--not WRN helicase-nuclease defect. During detailed studies of the patient's cells, epigenetic control and DNA damage response alterations were detected.

[Simple photometric and fluorometric assays are insufficient for assessing UV-induced mutagenesis in genes controlling tryptophan synthesis in Escherichia coli]. / Nedostatochnost' prostykh fotometricheskikh i fluorimetricheskikh protsedur dlia otsenki UF-indutsirovannogo mutageneza v genakh, otvechaiushchikh za sintez triptofana v kletkakh Escherichia coli.

A new approach to detecting induced mutations was tested based on the assay of cell extracts and special growth media following cultivation of UV irradiated Escherichia coli cells. No correlation was found between the UV dose and the optical densities of cultural media or cell extracts prepared by Triton X-100 treatment. Blue fluorescence of concentrated cultural media varied with cell dose, according to a rather complex law, which differed substantially from the known dose-effect curves for induced mutations. Nevertheless, a certain extent of the brown staining of tryptophan containing medium could, presumably, serve as a quite sensitive indicator of the integral metabolic activity of bacteria grown in the medium. Besides, we observed that overnight lag phase cultures became gradually more transparent, when analysed in the spectrophotometer cuvette just after their dilution with fresh medium.

Some routine and novel approaches to chemical dosimetry of far-ultraviolet light emitted by bactericidal tubes.

Detailed protocols are presented of two improved chemical procedures, based upon a photochemical decomposition of uranyl oxalate or potassium ferrioxalate, enabling a reliable measurement of the far-ultraviolet light emitted by a low-pressure mercury-vapour lamp. Besides, an original semi-quantitative method of UV dosimetry is presented and discussed, employing optical detection of a chromophore formed in the photo-oxidized glutathione. In addition to exemplary computations of UV light dose rate, a simple formula is proposed for recalculating its value while varying the distance from the lamp.

[Effect of thermal shock on resistance of filamentous Bacillus subtilis strain to some hazardous substances]. / Vliianie teplovogo shoka na rezistentnost filamentoobrazuiushchego shtamma Basillus subtilis k nekotorym povrezhdaiushchim agentam.

When grown at 30 degrees C and heat shocked in a liquid medium at 45 degrees C, the filamentous cells of Bacillus subtilis 168 became more sensitive to subsequent killing with N-methyl-N'-nitro-N-nitrosoguanidine and UV light but not with gamma-rays. Certain characteristics (for instance, the increased tolerance to damaging agents at 30 degrees C and the time-dependent changes in the sensitivity to MNNG induced by thermal shock) evidence against direct involvement of repair systems in this phenomenon.

[Stress-induced breakdown of chained cells in Bacillus subtilis filaments]. / Indutsirovannyi stressovymi vozdeistviiami raspad tsepochechnykh kletochnykh filamentov Bacillus subtilis.

Triple auxotroph of Bacillus subtilis 168 grew as chains of unseparated cells of normal morphology at 30 degrees C. The strain displayed reduced competence for DNA-mediated transformation and showed strong interbacterial aggregation in liquid media. On the solid media the colonies had a typical rough appearance. Environmental stresses (heat shock, UV light, gamma-rays, and methylating agent) resulted in gradual dechaining during extended incubation of the bacteria in the static liquid medium with or without required amino acids at room temperature. Simultaneously with this process, the suspensions of cells acquired homogeneity and a new pattern of electrophoretic mobility. These phenomena may be interpreted in terms of stress-inducible RS-dissociation. Alternative explanations are also discussed.

[Absence of various manifestations of adaptive response in Bacillus subtilis transformants]. / Otsutstvie nekotorykh proiavlenii adaptivnogo otveta v transformantakh Bacillus subtilis.

Competent cells of Bacillus subtilis are more sensitive to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) than total population, exhibit higher level of spontaneous mutations to kanamycin resistance. However, the absolute number of mutated transformants doesn't rise with MNNG treatment in the range of 5 to 50 micrograms per ml. The adaptation to low concentrations of MNNG affects neither spontaneous nor MNNG-induced mutagenesis in the competent (transformed) cells, in contrast to their resistance which is stronger for the adapted transformants. The transformation by MNNG-treated plasmid pUB 110 doesn't reveal any difference between adapted and non-adapted cultures in transformation efficiency decline.

[Survival and repair of single-stranded DNA breaks after gamma-irradiation of Escherichia coli cells depending on the presence of plasmids pKN101 and COIIB-P9]. / Vyzhivaemost' i reparatsiia odnonitevykh razryvov DNK posle gamma-oblucheniia v kletkakh Escherichia coli v zavisimosti ot prisutstviia plazmid pKM101 i COIIB-P9.

Plasmids, pKM101 and ColIb-P9, present in an autonomous state in E. coli AB 1157, JC5519, and P3478 cells at the stationary and logarithmic phases of growth, somewhat sensitize the cells to the lethal effect of gamma-radiation and do not influence the radiosensitivity of B/r, Bs-1 gamma R, Bs-1, and W3110 cells. The efficiency of repair of gamma-ray-induced DNA single-strand breaks in AB1157 and P3478 cells containing plasmids is somewhat lower than that in the same non-plasmid strains.

[Postreplication DNA repair in Escherichia coli cells. III. Repair independent of the presence of pKM101 and COLIb-P9 plasmids]. / Postreplikativnaia reparatsiia DNK v kletkakh Escherichia coli. III. Nezavisimost' reparatsii ot prisutstvii plazmid pKM101 i COLIb-P9.

The presence of pKM101 or ColIb-P9 plasmids in E. coli leads to the increase in the survival of UV-irradiated cells of wild type and of polAI, recB21 recC22 and dnaGts mutants; it does not change the survival of recA13 and lex3 mutants and does not influence kinetics and efficiency of postreplication repair (PRR) of DNA in cells of all the strains examined (with the exception of PG3 dnaGts mutant whose PRR of DNA in the presence of pKM101 plasmid is somewhat lower). The survival of both plasmid-containing and plasmid-free bacteria treated with chloramphenicol decreases in the same degree, but the survival of chloramphenicol-treated recA13, lex3 recB21 rec C22 mutants does not change. The pKM101 plasmid does not lend the dnaGts mutant a new capacity of repairing postreplication gaps with the participation of inducible component of PRR; the chloramphenicol-sensitive component of PRR is absent in this mutant. Plasmid and plasmid-free E. coli strains of wild type and of the polA1 mutant do not differ by the kinetics and level of inducible chloramphenicol-sensitive component of PRR of DNA.

The roles of different repair mechanisms in the ultraviolet resistance of Micrococcus luteus.

In ultraviolet-irradiated Micrococcus luteus wild type the replication of DNA was not interrupted at every pyrimidine dimer, in contrast to that in ultraviolet-sensitive G7 and some other mutants. The contribution of uninterrupted replication to the ultraviolet resistance of M. luteus proved to be equal to the contributions of excision repair and inducible postreplication repair. It was found that some postreplication gaps could be filled by constitutive pathways of postreplication repair when inducible pathways were suppressed by chloramphenicol. Prolonged treatment with chloramphenicol was shown to block not only inducible repair but also other processes essential for ultraviolet irradiation survival.

An analysis of the repair processes in ultraviolet-irradiated Micrococcus luteus using purified ultraviolet-endonuclease.

The measurement of the frequency of endonucleolytic incisions in ultraviolet-irradiated DNA serves as the test for the presence of pyrimidine dimers. In accordance with this approach, the lysates of three Micrococcus luteus strains containing radioactively labeled chromosomes were treated with purified M. luteus ultraviolet-endonuclease to trace segregation of dimers amongst parental and newly synthesized DNA and their removal during postreplication and excision DNA repair. A considerable proportion of the dimers in all strains tested proved to be insensitive to the action of exogenous incising enzyme. The use of chloramphenicol as an inhibitor of postirradiation protein synthesis in combination which ultraviolet-endonuclease treatment of DNA allowed to reveal at least two alternative pathways of postreplication repair: constitutively active recombinational pathway and inducible nonrecombinational one.

Effects of chloramphenicol on the postreplication repair and sister recombinational DNA exchanges in ultraviolet-irradiated Micrococcus luteus.

The filling of about one third of postreplication DNA gaps in u.v.-irradiated Micrococcus luteus ATCC 4698 is blocked by chloramphenicol (CA) added just before irradiation. Addition of CA 15 min after u.v.-irradiation does not prevent the complete repair of the gaps. U.v.-sensitive M. luteus mutants (ML 6 and ML 15) are identified as defective in different steps of inducible postreplication DNA repair (PRR). PRR in unexcising M. luteus strain G7 is accompanied by the transfer of about 20% of pyrimidine dimers from parental to daughter DNA strands, which indicates the existance of recombinational pathway of PRR. Recombinational PRR in M. luteus is not inhibited by CA.

Postreplication DNA repair in ultraviolet-irradiated Micrococcus luteus.

Postreplication DNA repair was studies in three strains of Micrococcus luteus having different sensitivity to ultraviolet light: a wild type ATCC 5698, a ultraviolet-sensitive mutant G7, deficient in the incision step of repair and in ultraviolet-resistant transformant obtained from G7 by treatment with DNA of wild type cells, Trf(G7). It is shown that the G7 mutant has a low capacity for repair of postreplication DNA gaps compared with the wild type or Trf(G7). It seems to be that postreplication repari capacity contributes significantly to the ultraviolet resistance of M. luteus in addition to the excision repair. In contrast with G7 the size of the DNA fragments synthesized immediately after ultraviolet irradiation in the wild type (and Trf(G7)) seems to be much higher than that expected if each dimer produces one DNA gap in the daughter strand. Since this cannot only be explained by the excision of dimers from parental DNA we have suggested that a rapid repair of postreplication DNA gap occurs in M. luteus.