Retest Reliability of Force-Time Variables of Neck Muscles Under Isometric Conditions

Context:

Proper conditioning of the neck muscles may play a role in reducing the risk of neck injury and, possibly, concussions in contact sports. However, the ability to reliably measure the force-time–based variables that might be relevant for this purpose has not been addressed.

Objective:

To assess the between-days reliability of discrete force-time–based variables of neck muscles during maximal voluntary isometric contractions in 5 directions.

Design:

Cohort study.

Setting:

University research center.

Patients or Other Participants:

Twenty-six highly physically active men (age  =  21.6 ± 2.1 years, height  =  1.85 ± 0.09 m, mass  =  81.6 ± 9.9 kg, head circumference  =  0.58 ± 0.01 m, neck circumference  =  0.39 ± 0.02 m).

Intervention(s):

We used a custom-built testing apparatus to measure maximal voluntary isometric contractions of the neck muscles in 5 directions (extension, flexion, protraction, left lateral bending, and right lateral bending) on 2 separate occasions separated by 7 to 8 days.

Main Outcome Measure(s):

Variables measured were peak force (PF), rate of force development (RFD), and time to 50% of PF (T₅₀PF). Reliability indices calculated for each variable comprised the difference in scores between the testing sessions, with corresponding 95% confidence intervals, the coefficient of variation of the typical error of measurement (CV_TE), and intraclass correlation coefficients (ICC [3,3]).

Results:

No evidence of systematic bias was detected for the dependent measures across any movement direction; retest differences in measurements were between 1.8% and 2.7%, with corresponding 95% confidence interval ranges of less than 10% and overlapping zero. The CV_TE was lowest for PF (range, 2.4%–6.3%) across all testing directions, followed by RFD (range, 4.8%–9.0%) and T₅₀PF (range, 7.1%–9.3%). The ICC score range for all dependent measures was 0.90 to 0.99.

Conclusions:

Discrete variables representative of the force-generating capacity of neck muscles under isometric conditions can be measured with an acceptable degree of reliability. This finding has possible applications for investigating the role of neck muscle strength-training programs in reducing the risk of injuries in sport settings.     

Subjective visual vertical in patients with idiopatic scoliosis

Idiopathic scoliosis (IS) is characterized by a three-dimensional deviation of the vertebral column and its etiopathogenesis is unknown. Various factors are associated with idiopathic scoliosis, among these a prominent role has been attributed to integration of vestibular information with graviception for perception of space. Subjective visual vertical (SVV) is a sensitive sign of verticality perception. The aim of this study was to determine if SVV in adolescents with IS is different from healthy controls. Examination of SVV was performed using the bucket method. Binocular measurements of SVV were made in 23 adolescents with IS (age 14.5 ± 2.5, mean ± SD) and 23 healthy subjects (age 14.0 ± 2.9). The groups differed significantly on SVV deviation (p < 0.01): healthy controls (-0.04° ± 0.64°), IS group (0.86° ± 1.39°). There was also significant difference in SVV uncertainty (p< 0.001): healthy controls (1.50° ± 0.94°), IS group (2.46 ± 0.82°). We conclude that the perception of visual vertical is altered in IS which may play role in development of IS.     

Long-term behavioral and morphological consequences of nonconvulsive status epilepticus in rats

The aims of the present study were to ascertain whether nonconvulsive status epilepticus (NCSE) could give rise to long-term behavioral deficits and permanent brain damage. Two months after NCSE was elicited with pilocarpine (15 mg/kg i.p.) in LiCl-pretreated adult male rats, animals were assigned to either behavioral (spontaneous behavior, social interaction, elevated plus-maze, rotorod, and bar-holding tests) or EEG studies. Another group of animals was sacrificed and their brains were processed for Nissl and Timm staining as well as for parvalbumin and calbindin immunohistochemistry. Behavioral analysis revealed motor deficits (shorter latencies to fall from rotorod as well as from bar) and disturbances in the social behavior of experimental animals (decreased interest in juvenile conspecific). EEGs showed no apparent abnormalities. Quantification of immunohistochemically stained sections revealed decreased amounts of parvalbumin- and calbindin-immunoreactive neurons in the motor cortex and of parvalbumin-positive neurons in the dentate gyrus. Despite relatively inconspicuous manifestations, NCSE may represent a risk for long-term deficits.     

Breastfeeding promotion and support services in local community health centers

This study had a two-fold goal. First, to document services relating to breastfeeding promotion and support in CLSCs and, second, to examine the links between the delivery of such services and certain organizational and environmental factors. The data were collected in 1999 by means of a self-administered questionnaire sent to all CLSCs in Quebec. The responses indicated that breastfeeding is most often systematically addressed at prenatal meetings and through integrated perinatal programs. CLSCs belonging to a multipurpose establishment are more apt to integrate the issue of breastfeeding into perinatal activities; in addition, many of them offer breastfeeding activities considered innovative, although the average for this kind of activities is fairly low (33%). In addition, CLSCs that collaborate more closely with community organizations and those that spend more on perinatal programs are the ones that most often offer "innovative" breastfeeding activities.     

Prevention of neuropathology in the mouse model of Hurler syndrome

A defect of the lysosomal enzyme alpha-L-iduronidase (IDUA) interrupts heparan and dermatan sulfate degradation and causes neuropathology in children with severe forms of mucopolysaccharidosis type I (MPSI, Hurler syndrome). Enzyme substitution therapy is beneficial but ineffective on the central nervous system. We could deliver the missing enzyme to virtually the entire brain of MPSI mice through a single injection of gene transfer vectors derived from adenoassociated virus serotype 2 (AAV2) or 5 (AAV5) coding for human IDUA. This result was reproducibly achieved with both vector types in 46 mice and persisted for at least 26 weeks. Success was more frequent, enzyme activity was higher, and corrected areas were broader with AAV5 than with AAV2 vectors. Treatment presumably reversed and certainly prevented the accumulation of GM2 and GM3 gangliosides, which presumably participates to neuropathology. Lysosomal distension, which already was present at the time of treatment, had disappeared from both brain hemispheres and was minimal in the cerebellum in mice analyzed 26 weeks after injection. This study shows that pathology associated with MPSI can be prevented in the entire mouse brain by a single AAV vector injection, providing a preliminary evaluation of the feasibility of gene therapy to stop neuropathology in Hurler syndrome.     

Increased baclofen-stimulated G protein coupling and deactivation in rat brain cortex during development

The number and affinity of GABA(B) receptors (assayed by the specific antagonist [(3)H]CGP54626A) was unchanged when compared in carefully washed cerebrocortical membranes from young (12-day-old) and adult (90-day-old) rats. In contrast, high-affinity GTPase activity, both basal and baclofen-stimulated was significantly higher (by 45% and 56%, respectively) in adult than in young rats. Similar results were obtained by concomitant determination of agonist (baclofen)-stimulated GTP gamma S binding. Under standard conditions, baclofen-stimulated GTPase activity was further considerably enhanced by exogenously added regulator of G protein function, RGS1, but not by RGS16. RGS16 was able to affect agonist-stimulated GTPase activity only in the presence of markedly increase substrate (GTP) concentrations. RGS1 alone slightly increased GTPase activity in adult rats, but neither RGS1 nor RGS16 influenced GTPase activity in membrane preparations isolated from young animals. These findings indicate increasing functional activity of trimeric G protein(s) involved in GABAergic transmission in the developing rat brain cortex and suggest a high potential of RGS1 in regulation of high-affinity GTPase activity.     

Recurrent familial hypocalcemia due to germline mosaicism for an activating mutation of the calcium-sensing receptor gene

De novo activating mutations in the calcium-sensing receptor (CASR) gene are a common cause of sporadic isolated hypoparathyroidism. Here, we describe a family in which two affected siblings were found to be heterozygous for a novel F788L mutation in the fifth transmembrane domain encoded by exon 7 of the CASR. Both parents and the third sibling were clinically unaffected and genotypically normal by direct sequencing of their leukocyte exon 7 PCR amplicons. However, the mother was revealed to be a mosaic for the mutation by sequence analysis of multiple subclones as well as denaturing HPLC of the CASR exon 7 leukocyte PCR product. A functional analysis of the mutation was performed by transiently transfecting wild-type and mutant CASRs tagged with a c-Myc epitope in human embryonic kidney (HEK293) cells. The mutant CASR was expressed at a similar level as the wild type. The F788L mutant produced a significant shift to the left relative to the wild-type CASR in the MAPK response to increasing extracellular calcium concentrations. This is the first report of mosaicism for an activating CASR mutation and suggests that care should be exercised in counseling for risks of recurrence in a situation where a de novo mutation appears likely.     

Loss of neural cell adhesion molecule induces tumor metastasis by up-regulating lymphangiogenesis

Reduced expression of neural cell adhesion molecule (NCAM) has been implicated in the progression to tumor malignancy in cancer patients. Previously, we have shown that the loss of NCAM function causes the formation of lymph node metastasis in a transgenic mouse model of pancreatic beta cell carcinogenesis (Rip1Tag2). Here we show that tumors of NCAM-deficient Rip1Tag2 transgenic mice exhibit up-regulated expression of the lymphangiogenic factors vascular endothelial growth factor (VEGF)-C and -D (17% in wild-type versus 60% in NCAM-deficient Rip1Tag2 mice) and, with it, increased lymphangiogenesis (0% in wild-type versus 19% in NCAM-deficient Rip1Tag2 mice). Repression of VEGF-C and -D function by adenoviral expression of a soluble form of their cognate receptor, VEGF receptor-3, results in reduced tumor lymphangiogenesis (56% versus 28% in control versus treated mice) and lymph node metastasis (36% versus 8% in control versus treated mice). The results indicate that the loss of NCAM function causes lymph node metastasis via VEGF-C- and VEGF-D-mediated lymphangiogenesis. These results also establish Rip1Tag2;NCAM-deficient mice as a unique model for stochastic, endogenous tumor lymphangiogenesis and lymph node metastasis in immunocompetent mice.