Intercostal chest drain fixation strength: comparison of techniques and sutures.

OBJECTIVE: The accidental removal of an intercostal chest drain (ICD) is common and may result in serious complications. A number of fixation techniques and suture material are in use, and the selection is often based on personal preferences and equipment availability. This study is designed to determine which of the common techniques provides the strongest ICD fixation. METHODS: This study compared the mechanical strength of eight different ICD fixation techniques (purse string, 'Roman sandal', 'Jo'burg' (JO) technique, a suture through the tube, one and two passes through a locking plastic tie, tape fixation and a commercial disposable drainage tube holder) and two silk suture sizes using porcine cadavers and a digital push-pull dynamometer to simulate accidental removal of an ICD. A total of 14 different experimental set-ups produced 280 measurements. RESULTS: Significant differences in ICD fixation strength were observed. A modified JO technique using a size 1 silk suture was nearly three times stronger than a purse-string fixation using a size 0 silk and 10 times stronger from a commercial, adhesive-based device (180, 70 and 22, respectively). CONCLUSION: In situations where the mechanical strength of ICD fixation is important, using a size 1 silk and a modified JO technique may provide the strongest fixation.

Factors associated with the emotional health of children: high family income as a protective factor.

Anxiety and depressive symptoms have adverse effects on children's development. The present study investigates the associations of socioeconomic factors as well as maternal emotional health with children's emotional health status. The data were collected between 2011 and 2015 in the LIFE Child study, a population-based cohort study in Leipzig, Germany. The emotional health status of 1093 children (2.5-11.9 years old) was investigated using the subscale 'emotional problems' of the Strengths and Difficulties Questionnaire. Associations of maternal emotional health, family status, and socioeconomic status (SES) with the emotional health status of children were estimated via regression analyses. 21.13% of the participating children were assigned to the 'risk' group for emotional problems. The results furthermore revealed that children of mothers reporting more depressive symptoms, children living in single-parent families, and children of families with lower SES scored higher in the emotional problems scale. When considering the different indicators of SES (parental education, occupational status, and monthly net income) separately, only income showed significant associations with children's emotional health status. The prevalence of emotional problems in children in Leipzig, a city in East Germany, appears to be higher than the previously reported German average. Maternal depressive symptoms, single-parent families, lower SES, and especially lower income can be seen as risk factors for children's emotional health.

Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion.

CTF4 and CTF18 are required for high-fidelity chromosome segregation. Both exhibit genetic and physical ties to replication fork constituents. We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint. The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion. We find that Ctf18p, an RFC1-like protein, directly interacts with Rfc2p, Rfc3p, Rfc4p, and Rfc5p. However, Ctf18p is not a component of biochemically purified proliferating cell nuclear antigen loading RF-C, suggesting the presence of a discrete complex containing Ctf18p, Rfc2p, Rfc3p, Rfc4p, and Rfc5p. Recent identification and characterization of the budding yeast polymerase kappa, encoded by TRF4, strongly supports a hypothesis that the DNA replication machinery is required for proper sister chromatid cohesion. Analogous to the polymerase switching role of the bacterial and human RF-C complexes, we propose that budding yeast RF-C(CTF18) may be involved in a polymerase switch event that facilities sister chromatid cohesion. The requirement for CTF4 and CTF18 in robust cohesion identifies novel roles for replication accessory proteins in this process.

[Reference ranges of antioxidant parameters in whole blood (erythrocytes) in a Thüringen region]. / Referenzbereiche antioxidativ wirkender Parameter im Vollblut (Erythrozyten) einer Thüringer Region.

BACKGROUND: The oxidant stress is characterized by measurement of the activities of glutathione peroxidase, superoxiddismutase and also by concentrations of glutathione and selenium in erythrocytes. A standardization of the methods of determination is very important. MATERIAL AND METHODS: In erythrocytes of blood donors (n = 101) the parameters glutathione peroxidase, glutathione, superoxiddismutase and selenium were determined. RESULTS: The following results of the antioxidant parameters in erythrocytes of blood donors were found: Selenium 67.1 +/- 20.1 nmol/mmol Hb, glutathione peroxidase 842 +/- 290 U/mmol Hb, glutathione 108 +/- 48 mumol/mmol Hb, superoxiddismutase 15.8 +/- 6.4 U/mumol Hb. CONCLUSION: Selenium, glutathione peroxidase, glutathione and superoxiddismutase in erythrocytes of blood donors are normally distributed. There are no significant differences between men and women. The use of "own reference values" is necessary because no standardization of the methods of determination exists.

Establishing genetic interactions by a synthetic dosage lethality phenotype.

We have devised a genetic screen, termed synthetic dosage lethality, in which a cloned "reference" gene is inducibly overexpressed in a set of mutant strains carrying potential "target" mutations. To test the specificity of the method, two reference genes, CTF13, encoding a centromere binding protein, and ORC6, encoding a subunit of the origin of replication binding complex, were overexpressed in a large collection of mutants defective in either chromosome segregation or replication. CTF13 overexpression caused synthetic dosage lethality in combination with ctf14-42 (cbf2, ndc10), ctf17-61 (chl4), ctf19-58 and ctf19-26. ORC6 overexpression caused synthetic dosage lethality in combination with cdc2-1, cdc6-1, cdc14-1, cdc16-1 and cdc46-1. These relationships reflect specific interactions, as overexpression of CTF13 caused lethality in kinetochore mutants and overexpression of ORC6 caused lethality in replication mutants. In contrast, only one case of dosage suppression was observed. We suggest that synthetic dosage lethality identifies a broad spectrum of interacting mutations and is of general utility in detecting specific genetic interactions using a cloned wild-type gene as a starting point. Furthermore, synthetic dosage lethality is easily adapted to the study of cloned genes in other organisms.

CHL12, a gene essential for the fidelity of chromosome transmission in the yeast Saccharomyces cerevisiae.

We have analyzed the CHL12 gene, earlier identified in a screen for yeast mutants with increased rates of mitotic loss of chromosome III and circular centromeric plasmids. A genomic clone of CHL12 was isolated and used to map its physical position on the right arm of chromosome XIII near the ADH3 locus. Nucleotide sequence analysis of CHL12 revealed a 2.2-kb open reading frame with a 84-kD predicted protein sequence. Analysis of the sequence upstream of the CHL12 open reading frame revealed the presence of two imperfect copies of MluI motif, ACGCGT, a sequence associated with many DNA metabolism genes in yeast. Analysis of the amino acid sequence revealed that the protein contains a NTP-binding domain and shares a low degree of homology with subunits of replication factor C (RF-C). A strain containing a null allele of CHL12 was viable under standard growth conditions, and as well as original mutants exhibited an increase in the level of spontaneous mitotic recombination, slow growth and cold-sensitive phenotypes. Most of cells carrying the null chl12 mutation arrested as large budded cells with the nucleus in the neck at nonpermissive temperature that typical for cell division cycle (cdc) mutants that arrest in the cell cycle at a point either immediately preceding M phase or during S phase. Cell cycle arrest of the chl12 mutant requires the RAD9 gene. We conclude that the CHL12 gene product has critical role in DNA metabolism.

Identification and cloning of the CHL4 gene controlling chromosome segregation in yeast.

A collection of chl mutants characterized by decreased fidelity of chromosome transmission and by minichromosome nondisjunction in mitosis was examined for the ability to maintain nonessential dicentric plasmids. In one of the seven mutants analyzed, chl4, dicentric plasmids did not depress cell division. Moreover, nonessential dicentric plasmids were maintained stably without any rearrangements during many generations in the chl4 mutant. The rate of mitotic heteroallelic recombination in the chl4 mutant was not increased compared to that in an isogenic wild-type strain. Analysis of the segregation of a marked chromosome indicated that sister chromatid nondisjunction and sister chromatid loss contributed equally to chromosome malsegregation in the chl4 mutant. A genomic clone of CHL4 was isolated by complementation of the chl4-1 mutation and was physically mapped to the right arm of chromosome IV near the SUP2 gene. Nucleotide sequence analysis of CHL4 clone revealed a 1.4-kb open reading frame coding for a 53-kD predicted protein which does not have homology to published proteins. A strain containing a null allele of CHL4 is viable under standard growth conditions but has a temperature-sensitive phenotype (conditional lethality at 36 degrees). We suggest that the CHL4 gene is required for kinetochore function in the yeast Saccharomyces cerevisiae.

CTF4 (CHL15) mutants exhibit defective DNA metabolism in the yeast Saccharomyces cerevisiae.

We have analyzed the CTF4 (CHL15) gene, earlier identified in two screens for yeast mutants with increased rates of mitotic loss of chromosome III and artificial circular and linear chromosomes. Analysis of the segregation properties of circular minichromosomes and chromosome fragments indicated that sister chromatid loss (1:0 segregation) is the predominant mode of chromosome destabilization in ctf4 mutants, though nondisjunction events (2:0 segregation) also occur at an increased rate. Both inter- and intrachromosomal mitotic recombination levels are elevated in ctf4 mutants, whereas spontaneous mutation to canavanine resistance was not elevated. A genomic clone of CTF4 was isolated and used to map its physical and genetic positions on chromosome XVI. Nucleotide sequence analysis of CTF4 revealed a 2.8-kb open reading frame with a 105-kDa predicted protein sequence. The CTF4 DNA sequence is identical to that of POB1, characterized as a gene encoding a protein that associates in vitro with DNA polymerase alpha. At the N-terminal region of the protein sequence, zinc finger motifs which define potential DNA-binding domains were found. The C-terminal region of the predicted protein displayed similarity to sequences of regulatory proteins known as the helix-loop-helix proteins. Data on the effects of a frameshift mutation suggest that the helix-loop-helix domain is essential for CTF4 function. Analysis of sequences upstream of the CTF4 open reading frame revealed the presence of a hexamer element, ACGCGT, a sequence associated with many DNA metabolism genes in budding yeasts. Disruption of the coding sequence of CTF4 did not result in inviability, indicating that the CTF4 gene is nonessential for mitotic cell division. However, ctf4 mutants exhibit an accumulation of large budded cells with the nucleus in the neck. ctf4 rad52 double mutants grew very slowly and produced extremely high levels (50%) of inviable cell division products compared with either single mutant alone, which is consistent with a role for CTF4 in DNA metabolism.