Activación muscular en corredores con el síndrome de la banda iliotibial / Muscle Activation in Runners with Iliotibial Band Syndrome

Esta investigación examinó las diferencias en la activación muscular en los músculos de la cadera y muslo en corredores y corredoras con y sin el síndrome de la banda iliotibial (SFBI). Se registró la actividad neuromuscular en 21 corredores durante la carrera (14 SFBI y 7 sanos). No se han encontrado diferencias significativas en la actividad muscular media entre los corredores y corredoras lesionados. Sin embargo, en el caso de las corredoras lesionadas, se han encontrado diferencias entre el vasto lateral y el tensor fascia lata, y entre el vasto lateral y el bíceps femoral (p<0,05 en ambos casos). En el caso de los corredores hombres lesionados, se han encontrado diferencias entre el glúteo mayor y el tensor fascia lata, y entre el glúteo mayor y el bíceps femoral (p<0,05 en ambos casos). Estos hallazgos proporcionan un mayor entendimiento de la lesión y ayudarían a un tratamiento más específico. (AU)

A study was performed to examine differences in hip and thigh muscle activation in male and female runners with and without iliotibial band syndrome (ITBS). The neuromuscular activity of 21 runners was recorded during run (14 ITBS and 7 healthy). No significant differences were observed in mean muscle activity in injured male and female runners. In contrast, in female runners with ITBS, there were differences between the vastus lateralis and the tensor fasciae latae and between the vastus lateralis and the femoral biceps (p<0.05 in the two cases). With regard to male runners with ITBS, differences in activity were observed between the gluteus maximus and the tensor fasciae latae, and between the gluteus maximus and the femoral biceps (p<0.05 in the two cases). These findings contribute to a better understanding of iliotibial band syndrome and may be useful for the design of targeted treatments. (AU)

Time of Cold Ischemia and Delayed Graft Function in a Cohort of Renal Transplant Patients in a Reference Center.

There are many factors involved in the delayed graft function of a renal graft, with prolonged cold ischemia time being one of the most relevant. The aim of this study is to evaluate the relationship between the time of cold ischemia and the delayed graft function, and acute rejection and graft loss at 1 year of follow-up. A retrospective cohort of 347 renal transplant patients were evaluated during the years 2009-2013. The incidence of delayed graft function was 18.4% (n = 65). The cold ischemia time was an independent risk factor for delayed graft function (odds ratio [OR] 1.10, 95% confidence interval [CI] 1.04-1.16). By grouping the time of cold ischemia by intervals, the risk of delayed graft function was greater in the 12-18 hours group (OR 2.06, 95% CI 1.02-4.15) and in the >18 hours group (OR 3.38, 95% CI 1.57-7.27). The risk of acute rejection did not increase with longer cold ischemia (p = 0.69), and cold ischemia time was not a risk factor for renal graft loss at 1-year follow-up (hazard ratio 0.97, 95% CI 0.88-1.06). In conclusion the time of cold ischemia (>12 hours) in renal transplant recipients of optimal deceased donors increases the risk of delayed graft function; however, this does not negatively impact the results in acute rejection or graft loss in the first year of the transplant.

[p53 expression in the gastric mucosa of patients infected with Helicobacter pylori]. / p53 expresado en la mucosa gástrica de pacientes infectados por Helicobacter pylori.

BACKGROUND: Helicobacter pylori (Hp) is recognized as a type 1 carcinogen for gastric cancer associated with pre-neoplastic lesions (atrophy and intestinal metaplasia [IM]). Its relation with p53, which intervenes in the cell cycle, has had contradictory results. AIMS: To analyze p53 expression in gastric mucosa and its relation with Hp infection. METHODS: A 3-month prospective, observational, cross-sectional study was conducted. Patients that had no evidence of acute or clinically significant gastric pathology had biopsies taken according to the Sydney system at the Hospital Juárez de México and the histopathologic studies were done at the Hospital Español de México. RESULTS: Hp prevalence was 32.7% in 104 patients. There were no cases of atrophy or dysplasia. A total of 91% of the infected patients were positive for p53. Of the non-infected patients, 14% were positive for p53 and 60% of them had IM. Of the IM patients, 75% presented with positive p53. Of the patients without IM, 31 presented with positive p53, and Hp was positive in 85% of them. There was association between Hp and p53 and between p53 and IM (P<.0001 and P<.0006, respectively). CONCLUSIONS: Significant association was shown between Hp and p53 expression, even in patients with pre-neoplastic lesions that no longer presented with Hp. Given that the identification of pre-neoplastic lesions is important for the prevention of cancer, immunohistochemistry could benefit routine biopsy carried out during endoscopy for the detection of Hp, by identifying patients with expression of the important oncogene regulator, p53.

Detection of DNA primary damage by premature chromosome condensation in human peripheral blood lymphocytes treated with methyl methanesulfonate.

Methyl methanesulfonate (MMS) is a direct acting methylating agent which produces apurinic sites that are transformed into DNA single-strand breaks by base excision repair. MMS-induced DNA lesions have to be transformed by DNA synthesis in order to give rise to chromosomal damage. In this study the premature chromosome condensation (PCC) technique was used in G(1) human lymphocytes treated with MMS to investigate whether, with this technique, chromosomal damage could be detected without the cell needing to undergo DNA synthesis. A dose-dependent increase in chromosomal fragmentation was indeed observed in G(1) lymphocytes. MMS treatment at 1.3, 2.5 and 5 mM was characterized by the appearance of highly fragmented chromosomes. This observation induced us to further investigate whether this effect was more connected with triggering of apoptotic cell death than a consequence of the PCC technique. Data obtained by nuclear morphology analysis, by Trypan blue exclusion assay and pulsed field gel electrophoresis seem to suggest that the observed chromosome fragmentation could be due to the onset of apoptosis. Consequently, one should bear in mind that the PCC technique can overestimate chromosomal damage when apoptosis is also induced.

Transcription coupled repair deficiency results in increased chromosomal aberrations and apoptotic death in the UV61 cell line, the Chinese hamster homologue of Cockayne's syndrome B.

Transcription coupled repair (TCR), a special sub-pathway of nucleotide excision repair (NER), removes transcription blocking lesions rapidly from the transcribing strand of active genes. In this study, we have evaluated the importance of the TCR pathway in the induction of chromosomal aberrations and apoptosis in isogenic Chinese hamster cell lines, which differ in TCR efficiency. AA8 is the parental cell line, which is proficient in the genome overall repair of UV-C radiation induced 6-4 photoproducts (6-4 PP) and the repair of cyclobutane pyrimidine dimer (CPD) from the transcribing strand of active genes. UV61 cells (hamster homologue of human Cockayne's syndrome (CS) group B cells) originally isolated from AA8, exhibit proficient repair of 6-4 PP but are deficient in CPD removal by the TCR pathway. Upon UV-C irradiation of cells in G1-phase, UV61 showed a dramatic increase in apoptotic response as compared to AA8 cells. Abolition of TCR by treatment with alpha-amanitin (an inhibitor of RNA polymerase II) in AA8 cells also resulted in an elevated apoptotic response like that observed in UV61 cells treated with UV alone. This suggests that the lack of TCR is largely responsible for increased apoptotic response in UV61 cells. Furthermore, the chromosomal aberrations and sister chromatid exchange (SCE) induced by UV were also found to be higher in UV61 cells than in TCR proficient AA8 cells. This study shows that the increased chromosomal aberrations and apoptotic death in UV61 cells is due to their inability to remove CPD from the transcribing strand of active genes and suggests a protective role for TCR in the prevention of both chromosomal aberrations and apoptosis induced by DNA damage. Furthermore, flow cytometry analysis and time-course appearance of apoptotic cells suggest that the conversion of UV-DNA damage into chromosomal aberrations precedes and determines the apoptotic process.

Turnover of phosphatidylglycerol in Escherichia coli.

In growing cultures of Escherichia coli, the nonacylated glycerol of phosphatidylglycerol (PG) is labeled more rapidly than is the acylated glycerol. This is, in part, due to a rapid exchange reaction of the nonacylated glycerol. Only some of the PG molecules undergo this reaction while others are stable. Using a mutant unable to make glycerophosphate, we have shown that the nonacylated glycerol of PG can exchange with non-phosphorylated glycerol.