The clinical significance of body composition and anthropometric evaluation in athletes

Body composition and anthropometric assessment provide the sports physician with useful information on the health state of the athlete and with some necessary elements to plan specific training loads in the most appropriate way. In practice, the chemical composition of an athlete’s body (especially those who carry out 1–2 daily workouts) is always in a physiologic condition that we can define as “dynamic” (concentration of electrolytes, hydration state and relationship between intra-and extra-cellular water, stages of growth of muscle mass and/or reduction of fat mass, etc.), with the exception of few times of year, such as the short resting break before resuming training. As a consequence, a real “baseline” (or “stationary”) physiological state, allowing to detect the parameters of body composition under the same conditions several times during the year, is only rarely achieved. In this paper, we wanted to review the most interesting parameters and methods for the evaluation of athletes’ body composition, and underline their potential applications, possible advantages, theoretical and practical limitations.     

Comparative radiographic evaluation of the alveolar bone crest after orthodontic treatment.

This study evaluated and compared the heights of the alveolar bone crests (AC) among orthodontic patients treated with either the simplified standard edgewise technique (group 1, n = 30), the edgewise straight-wire system (group 2, n = 30), or bioefficient therapy (group 3, n = 26). These 3 groups were compared with an untreated control group (group 4, n = 30). A comparison by sex of AC height was also conducted. The first premolars were extracted in every treated patient, and measurements were performed on bitewing radiographs taken after a mean posttreatment period of 2.17 years. The distances from the AC to the cementoenamel junction (CEJ) on the mesial and distal surfaces of the first molars and second premolars and on the distal surface of the canines were measured; the larger the distance, the greater the alveolar bone loss. The data were analyzed by 1-way analysis of variance and the Newman-Keuls test (P <.05) for comparison among the groups. Sex differences of the AC height were evaluated with the t test. All treated groups had larger, statistically significant CEJ-AC distances than the untreated group, primarily at the extraction areas. There were no consistent statistically significant differences in the areas among the treated groups. Mean distances of the CEJ-AC in boys were larger than or similar to those in girls. The patients in the treated groups showed a greater number of proximal surfaces with statistically significant differences between sexes, compared with the control subjects.     

Mutant torsinA, which causes early-onset primary torsion dystonia, is redistributed to membranous structures enriched in vesicular monoamine transporter in cultured human SH-SY5Y cells.

A single GAG deletion in the DYT1 gene causes primary early-onset, generalized torsion dystonia. The DYT1 protein product, torsinA, belongs to the AAA+ family of proteins. When overexpressed, wild-type torsinA localizes mainly to the endoplasmic reticulum, whereas the mutant forms inclusions of unclear biogenetic origin. In this study, overexpressed wild-type torsinA in human neuroblastoma (SH-SY5Y) cell lines was distributed throughout the cell body and colocalized with a marker for the endoplasmic reticulum, confirming it is an endoplasmic reticulum protein. However, mutant torsinA showed perinuclear staining and formed distinct globular inclusions, which did not colocalize with endoplasmic reticulum markers. Immunoelectron microscopy of the mutant torsinA inclusions revealed membrane whorls staining for torsinA, as well as labeling of lamellae, isolated bilayers, and perinuclear membranes. This finding shows that mutant torsinA redistributes to specific membranous structures, which may represent different stages of maturation of the intracellular inclusions. The mutant torsinA-containing bodies were immunoreactive for vesicular monoamine transporter 2 (VMAT2). VMAT2 expression is important for the exocytosis of bioactive monoamines in neurons. Abnormal processing, transport, or entrapment of VMAT2 within the mutant torsinA membranous inclusions, therefore, may affect cellular dopamine release, providing a potential pathogenic mechanism for the DYT1-dependent dystonia.     

Relation of glucose tolerance to complications of pregnancy in nondiabetic women

An increase in fetal and maternal complications has been documented in cases of gestational diabetes, but the glucose levels that predict an increased risk have not been clearly defined. We evaluated the frequency of several neonatal complications (macrosomia, congenital anomalies, perinatal mortality, and prematurity) and maternal complications (toxemia, cesarean section, or both) in relation to glucose tolerance in 249 women in the third trimester of pregnancy. None of the women had previous evidence of diabetes, and all had normal results on an oral glucose-tolerance test, according to accepted criteria. On the basis of their two-hour plasma glucose levels, women were divided into three groups: A (glucose less than 100 mg per deciliter), B (glucose 100 to 119 mg per deciliter), and C (glucose 120 to 164 mg per deciliter). The higher two-hour plasma glucose levels were associated with a significant increase in the incidence of macrosomia (9.9, 15.5, and 27.5 percent in Groups A, B, and C, respectively), congenital abnormalities (0.7, 3.5, and 5.0 percent), and toxemia, cesarean section, or both (19.9, 25.9, and 40.0 percent). A significant correlation between the infant's weight and the mother's two-hour plasma glucose level was also observed. These data indicate that even limited degrees of maternal hyperglycemia, which are currently considered to be within the normal range, may affect the outcome of pregnancy.     

Integrin-mediated cell adhesion and spreading engage different sources of reactive oxygen species

The tightly regulated production of intracellular reactive oxygen species (ROS) participates in several biologic processes such as cellular growth, programmed cell death, senescence, and adhesion. It is increasingly evident that the same enzymatic processes that were originally linked to ROS generation during host defence or apoptosis execution are also involved in redox-mediated signal transduction. We investigated in murine NIH3T3 fibroblasts the contribution of a variety of redox-dependent events during signal transduction initiated by integrin engagement due to fibronectin stimulation and report that a mitochondrial ROS release occurs, strictly confined to the early phase of extracellular matrix (ECM) contact (10 min). Besides, 5-lipoxygenase (5-LOX) is engaged by integrin receptor ligation as another ROS source, contributing to the more-intense, second ROS burst (45 min), possibly orchestrating the spreading of cells in response to ECM contact. To define a potential mechanism for ROS signaling, we demonstrate that on integrin recruitment, the Src homology-2 domain-containing phosphatase 2 (SHP-2) undergoes a reversible oxidization/inactivation to which mitochondrial and 5-lipoxygenase ROS contribute differentially. In keeping with a key role of oxidants during integrin signaling, the inactivation of SHP-2 prevents the dephosphorylation and inactivation of SHP-2 substrates (p125FAK and SHPS-1), thus enabling the continued propagation of the signal arising by integrin engagement.     

Glutamate-rich protein (GLURP) induces antibodies that inhibit in vitro growth of Plasmodium falciparum in a phase 1 malaria vaccine trial

The glutamate-rich protein (GLURP) of P. falciparum is the target of cytophilic antibodies which are significantly associated with protection against clinical malaria. A phase 1 clinical trial was conducted in healthy adult volunteers with the long synthetic peptide (LSP) GLURP(85-213) combined with either Aluminum Hydroxide (Alum, 18 volunteers) or Montanide ISA 720 (ISA, 18 volunteers) as adjuvants. Immunizations with 10, 30 or 100 microg GLURP(85-213) were administered subcutaneously at days 0, 30, and 120. Adverse events occurred more frequently with increasing dosage of GLURP(85-213) LSP and were more prevalent in the ISA group. Serious vaccine-related adverse events were not observed. The vaccine induced dose-dependent cellular and humoral immune responses, with high levels of (mainly cytophilic IgG1) antibodies that recognize parasites by immunofluorescence (IFA). Plasma samples collected 30 days after the last immunization induced a dose-dependent inhibition of parasite growth in vitro in the presence of monocytes. In conclusion, immunizations with GLURP(85-213) LSP formulations induce adverse events but can be administered safely, generating antibodies with capacity to mediate growth-inhibitory activity against P. falciparum in vitro.     

Antigen degradation by macrophages as an obligatory step in the presentation of antigen to T lymphocytes

Summary Evidence is presented which supports the hypothesis of protein degradation taking place in macrophages as a part of the presentation of antigen to T lymphocytes. It is postulated that the ability of T cells to recognize both native and denatured forms of the same protein is dependent upon degradation of both forms of the protein to yield the same peptides and thus results in the stimulation of identical subsets of T cells. The occasional observation of a lack of cross-reactivity could result if the native antigen is particularly resistant to the denaturing conditions found within macrophages.     

Transmembrane electron transfer in diabetic nephropathy

OBJECTIVE: Erythrocytes (red blood cells [RBCs]) reduce extracellular ferricyanide by transmembrane transfer of reducing equivalents involving ascorbate recycling. RESEARCH DESIGN AND METHODS: Because ascorbate regeneration is glutathione (GSH) dependent and cells may be depleted of GSH in diabetes, we measured RBC GSH, plasma sulfhydryl (SH) groups, and RBC-mediated ferricyanide reduction in 30 type 1 diabetic patients (age 34 +/- 10 years, disease duration 20 +/- 8 years; no complications, n = 10; retinopathy, n = 10; nephropathy, n = 10), their 36 siblings (age 39 +/- 13 years), and matched healthy volunteers. RESULTS: Fasting plasma glucose was 15 +/- 7 mmol/l (vs. 5 +/- 1 in control subjects, P < 0.001), HbA1c 8.4 +/- 1.5% (vs. 5.4 +/- 0.3, P < 0.001), GSH 0.76 +/- 0.12 mg/ml packed RBCs (vs. 0.88 +/- 0.18, P < 0.01), SH groups 401 +/- 72 micromol/l (vs. 444 +/- 56, P < 0.05), and ferrocyanide generation 15 +/- 5 micromol/ml RBC per h (vs. 13 +/- 5, NS). In comparison with 10 normoalbuminuric diabetic subjects with retinopathy, 10 patients with diabetic nephropathy had similar fasting plasma glucose, HbA1c, and SH groups; lower RBC GSH (0.73 +/- 0.08 vs. 0.85 +/- 0.11, P < 0.05); and higher ferrocyanide generation (18 +/- 4 vs. 14 +/- 5, P < 0.05). The 10 patients without complications differed from the 10 healthy volunteers in glycemic control and RBC GSH. RBC electron transfer correlated with plasma lactate (r = 0.8, P = 0.01) only in the uncomplicated group. No difference was detected between siblings and healthy control subjects or between siblings of subjects in the nephropathy and retinopathy groups. Among diabetic patients, the rate of ferrocyanide generation was associated with urinary albumin excretion, plasma creatinine, and SH groups (multiple r = 0.6, P < 0.01). CONCLUSIONS: Transmembrane electron transfer is selectively increased in diabetic nephropathy, where RBC GSH is also depleted. The abnormality is peculiar to the nephropathy group and not contributed by familial or hereditary components because the electron flow was normal in siblings. The close relationship between cytosolic NADH and RBC electron transfer observed in diabetic patients without complications seems to be lost in the microangiopathic patients. Whereas patients with retinopathy alone still had normal activity of the RBC-reducing system, patients with nephropathy showed significantly increased activity, unrelated to metabolic parameters or plasma lactate concentration and correlated with renal function parameters and plasma thiols.