Arterial Stiffness,Carotid Intima-Media Thickness,Endocan, and A Disintegrin and Metalloproteinase With Thrombospondin Type I Motif 9 Levels and Their Relationship With Disease Activity in Patients With Acromegaly With and Without Cardiovascular Risk Factors

ObjectiveCardiovascular complications such as cardiomyopathy and endothelial dysfunction, which are frequently seen in patients with acromegaly, are among the most important causes of morbidity and mortality. In this study, we aimed to investigate arterial stiffness, carotid intima-media thickness, endocan level, and A disintegrin and metalloproteinase with thrombospondin type I motif 9 level and their relationship with disease activity in patients with acromegaly with and without cardiovascular risk factors.MethodsA total of 60 patients with acromegaly—25 with active disease, 26 with well-controlled disease, and 9 with newly diagnosed disease—and 60 age-, sex-, and body mass index (BMI)-matched healthy control subjects were enrolled in this study. All the subjects’ height, weight, BMI, systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting plasma glucose (FPG) level, insulin, hemoglobin A1C (HbA1C), C-reactive protein , lipid, endocan, A disintegrin and metalloproteinase with thrombospondin type I motif 9 levels, pulse wave velocity (PWV), and carotid intima-media thickness were measured.ResultsThe SBP, DBP, FPG level, HbA1C level, and PWV of the acromegaly group were higher than those of the control group. In patients with acromegaly with cardiovascular disease (CVD) risk factors, the PWV was higher than that in the control group, and in patients with acromegaly without CVD risk factors, the PWV was similar to that in the control group. In a correlation analysis, a positive correlation was found between PWV and age, BMI, SBP, DBP, FPG level, and HbA1C level in the acromegaly group.ConclusionIn our study, we found that arterial stiffness increased in patients with acromegaly with CVD risk factors and that increased arterial stiffness was associated with hemodynamic (SBP and DBP) and metabolic (BMI, FPG level, and HbA1C level) parameters.     

Does resistive loading decrease diaphragmatic contractility before task failure?

While sustaining a load that leads to taskfailure, it is unclear whether diaphragmatic fatigue developsprogressively or occurs only at task failure. We hypothesized thatincremental loading produces a progressive decrease in diaphragmaticcontractility ever before task failure. Ten subjectsgenerated 60% of maximal transdiaphragmatic pressure(Pdi_max) for 2 min, 4 min, anduntil task failure. Before loading, 20 min after each period ofloading, and ~20 h after the last period of loading,Pdi_max, nonpotentiated andpotentiated Pdi twitch pressure(Pdi_tw), and the pattern of respiratory muscle recruitment during aCO₂ challenge were recorded. Sensation of inspiratory effort at the 4th min of the task-failure protocol was greater than at the same time in the preceding 4-min protocol. Surprisingly, potentiatedPdi_tw andPdi_max were reduced after 2 min ofloading and decreased further after 4 min of loading and after taskfailure; nonpotentiated Pdi_tw wasreduced after 4 min of loading and after task failure. The gastricpressure contribution to tidal breathing during aCO₂ challenge decreased progressively in relation to duration of the preceding loading period,whereas expiratory muscle recruitment progressively increased. A restperiod of ~20 h after task failure was not sufficient to normalizethese alterations in respiratory muscle recruitment or fatigue-inducedchanges in diaphragmatic contractility. In conclusion, while sustaininga mechanical load, the diaphragm progressively fatigued, ever beforetask failure, and when challenged the rib cage-to-diaphragmaticcontribution to tidal breathing and recruitment of the expiratorymuscles increased pari passu with duration of the preceding loading.

     

Differential enumeration of silage inoculants based on utilization of enzymatic activity and antibiotic sensitivity of bacteria

The differences in the composition of culture media inoculated with strains of Leuconostoc oenos were more quantitative than qualitative. Both temperature of incubation and pH significantly affected bacterial growth, the rates of substrate consumption and consequently the amount of metabolites produced. All strains degraded 5 g 1^-1 malate, except one at pH 3.5 and 25°C. Malate was metabolized before glucose except at higher pH (4.0 and 4.5) and temperature (32°C). Citrate was completely metabolized and its consumption rate was pH- and temperature-dependent. Neither acids contributed energy for growth as the Y_glu remained constant in the presence or absence of acids. There was a significant increase in fructose consumed at higher temperature. Also, the final concentration of mannitol was higher but not significantly different. The addition of acids, particularly citrate, significantly repressed mannitol formation.