Redistribution of glucose from skeletal muscle to adipose tissue during catch-up fat. A link between catch-up growth and later metabolic syndrome.

Catch-up growth, a risk factor for later obesity, type 2 diabetes, and cardiovascular diseases, is characterized by hyperinsulinemia and an accelerated rate for recovering fat mass, i.e., catch-up fat. To identify potential mechanisms in the link between hyperinsulinemia and catch-up fat during catch-up growth, we studied the in vivo action of insulin on glucose utilization in skeletal muscle and adipose tissue in a previously described rat model of weight recovery exhibiting catch-up fat caused by suppressed thermogenesis per se. To do this, we used euglycemic-hyperinsulinemic clamps associated with the labeled 2-deoxy-glucose technique. After 1 week of isocaloric refeeding, when body fat, circulating free fatty acids, or intramyocellular lipids in refed animals had not yet exceeded those of controls, insulin-stimulated glucose utilization in refed animals was lower in skeletal muscles (by 20–43%) but higher in white adipose tissues (by two- to threefold). Furthermore, fatty acid synthase activity was higher in adipose tissues from refed animals than from fed controls. These results suggest that suppressed thermogenesis for the purpose of sparing glucose for catch-up fat, via the coordinated induction of skeletal muscle insulin resistance and adipose tissue insulin hyperresponsiveness, might be a central event in the link between catch-up growth, hyperinsulinemia and risks for later metabolic syndrome.

IUGR in the absence of postnatal 'catch-up' growth leads to improved whole body insulin sensitivity in rat offspring

A suboptimal in utero environment leads to fetal adaptations to ensure short-term survival but in the long-term may lead to disease when the postnatal growth does not reflect that in utero. This study examined the effect of IUGR on whole body insulin sensitivity and metabolic activity in adult rats. Female Wistar-Kyoto rats were fed either a normal protein diet (NPD 20% casein) or a low protein diet (LPD; 8.7% casein) during pregnancy and 2 wk of lactation. In offspring at 32 wk of age, indirect calorimetry and dual energy x-ray absorptiometry (DEXA) were performed to assess metabolic activity and body composition. Insulin sensitivity was assessed using a euglycemic-hyperinsulinemic clamp. At 3 d of age, male and female LPD offspring were 23 and 27% smaller than controls, respectively. They remained significantly smaller throughout the experimental period (~10% smaller at 32 wk). Importantly, there was increased insulin sensitivity in LPD offspring (47% increase in males and 38% increase in females); pancreatic insulin content was normal. Body composition, O2 consumption, respiratory exchange ratio (RER), and locomotor activity were not different to controls. These findings suggest that in the absence of “catch-up” growth IUGR programs for improved insulin sensitivity.

Do dot coms add value : a preliminary study of the market capitalisation of Australian and Indian telecoms and banking sectors

E-Business is increasingly reshaping the way businesses operate across the globe. Globally, businesses in the banking and telecoms sectors have been re-engineering their value chains by adopting e-Business presence by means of dot com launches. The second half of the 1990s, however, saw both the rise and subsequent collapse of dot com entities as a major focus of investment interest, with consequent speculation over the viability of this corporate vehicle. The perceived increase in market capitalisation by means of these ventures during the boom period is now not so certain. In this paper, we report the results of a preliminary study which investigated the impact of dot com launches on market capitalisation within the banking and telecoms sectors of Australia and India.

Speed up health research through topic modeling of coded clinical data

Although random control trial is the gold standard in medical research, researchers are increasingly looking to alternative data sources for hypothesis generation and early-stage evidence collection. Coded clinical data are collected routinely in most hospitals. While they contain rich information directly related to the real clinical setting, they are both noisy and semantically diverse, making them difficult to analyze with conventional statistical tools. This paper presents a novel application of Bayesian nonparametric modeling to uncover latent information in coded clinical data. For a patient cohort, a Bayesian nonparametric model is used to reveal the common comorbidity groups shared by the patients and the proportion that each comorbidity group is reflected individual patient. To demonstrate the method, we present a case study based on hospitalization coding from an Australian hospital. The model recovered 15 comorbidity groups among 1012 patients hospitalized during a month. When patients from two areas of unequal socio-economic status were compared, it reveals higher prevalence of diverticular disease in the region of lower socio-economic status. The study builds a convincing case for routine coded data to speed up hypothesis generation.

Does training affect growth? - answers to common questions

Adolescent athletes may be at risk of restricted growth and delayed maturation when intense training is combined with insufficient energy intake. Because catch-up growth commonly occurs when training is reduced or ceases, final adult stature is unlikely to be compromised. However, in athletes who have long-term, clinically delayed maturation, catch-up growth may be incomplete. By charting individual growth patterns, physicians, coaches, and athletic trainers can detect vulnerable periods when the training intensity should be reduced and energy intake may need to be increased.

Does gymnastics training inhibit growth of females?

OBJECTIVE: The increasingly dominant performance of smaller-sized female gymnasts and increased magnitude of training beginning at an early age have prompted public and medical concerns, especially from an auxological perspective. The objective of this review is to determine if gymnastics training inhibits growth of females. DATA SOURCES: An extensive research of MedLine (PubMed interface) along with cross-referencing was conducted using the Text and MeSH words "gymnastics" in combination with "growth," "maturation," "body height," "body weight," and "growth plate." Our analysis is limited to English articles only.
STUDY SELECTION: All published studies that included data related to the research questions were included. MAIN RESULTS: Although data from three historical cohort studies indicate that female gymnasts are short even before they begin training, clinical reports and cohort studies do suggest that some female gymnasts experience attenuated growth during training followed by catch-up growth during periods of reduced training or retirement. There is conflicting evidence whether the "catch-up" is complete. There were no studies reporting prevalence or incidence of inadequate growth. Three cohort studies provide evidence of reduced growth but training was not partitioned from other confounding factors in the gymnastics environment. Although there is a paucity of studies examining the link of dietary practices with diminished growth in female gymnasts, a review of related dietary literature indicates the potential for insufficient energy and nutrient intake among female gymnasts.
CONCLUSIONS: Elite level or heavily involved female gymnasts may experience attenuated growth during their years of training and competition followed by catch-up growth during reduced training schedules or the months following retirement. However, a cause-effect relation between gymnastics training and inadequate growth of females has not been demonstrated.

A role for skeletal muscle stearoyl-CoA desaturase 1 in control of thermogenesis

An enhanced metabolic efficiency for accelerating the recovery of fat mass (or catch-up fat) is a characteristic feature of body weight regulation after weight loss or growth retardation and is the outcome of an "adipose-specific" suppression of thermogenesis, i.e., a feedback control system in which signals from the depleted adipose tissue fat stores exert a suppressive effect on thermogenesis. Using a previously described rat model of semistarvation-refeeding in which catch-up fat results from suppressed thermogenesis per se, we report here that the gene expression of stearoyl-coenzyme A desaturase 1 (SCD1) is elevated in skeletal muscle after 2 wk of semistarvation and remains elevated in parallel to the phase of suppressed thermogenesis favoring catch-up fat during refeeding. These elevations in the SCD1 transcript are skeletal muscle specific and are associated with elevations in microsomal ^9 desaturase enzyme activity, in the ^9 desaturation index, and in the relative content of SCD1-derived monounsaturates in several lipid fractions extracted from skeletal muscle. An elevated skeletal muscle SCD1, by desaturating the products of de novo lipogenesis and diverting them away from mitochondrial oxidation, would inhibit substrate cycling between de novo lipogenesis and lipid oxidation, thereby leading to a state of suppressed thermogenesis that regulates the body’s fat stores.—Mainieri, D., Summermatter, S., Seydoux, J., Montani, J. P., Rusconi, S., Russell, A. P., Boss, O., Buchala, A. J., Dulloo, A. G. A role for skeletal muscle stearoyl-CoA desaturase 1 in control of thermogenesis.

EBanking adaptation and dot.com viability : a comparison of Australian and Indian experiences in the banking sector

With the advent of widely-accepted eBusiness activities, many banks have floated dot.com entities to create a presence on the Internet and take advantage of its power and reach. Like many other businesses, banks expected an increase in market capitalisation as a result of their dot.com floats, perceived broadly as a measure of growing profitability. Despite the negative publicity that the recent spate of dot.com crashes has generated, banks seem to continue floating online spin-offs. Our exploratory study investigates this phenomenon, studying the drivers for change in the evolution of the banking sector, and the move towards electronic banking. We focussed on two economies – Australia and India – to aggregate the major factors in this evolution from the perspective of two disparate economies.

The paper describes our qualitative, document-based investigation of the Australian and Indian banking sectors, and subsequent quantitative analysis of the impact of dot.com floats on market capitalisation within this market sector. We then describe the effect of applying both Transaction Cost Economics to our findings, which indicates that the cost of transacting business has been reduced overall by the creation of dot.com entities; and “catch-up, fall-behind, forge ahead” theory to gain an economic perspective. The paper provides both practical assistance for banks in making decisions regarding e-portfolios, as well as for policy makers in the economies reviewed; and has the potential to contribute to academic research into eBanking more generally.

Is growth inhibited in non-elite competitive female gymnasts?

PURPOSE
We asked: 1) is statural growth inhibited in non-elite competitive female gymnasts?; and 2) if growth is reduced, is the effect similar for legs and spine?

METHODS
Height(Ht), sitting height(StHt) and leg length(LL) were measured in gymnasts and controls at baseline and every 12 mths for 2 yrs. Pubertal status was assessed by Tanner stage. Gymnasts were from USGF levels 4–10 and trained 7.5 to 22.5 hrs/wk. Age-adjusted Z-scores were determined for gymnasts on the anthropometric measures and based on linear regression analyses of data for 45 controls.

RESULTS
At baseline, pre-(N=40), peri-(N=16) and post-pubertal(N=11) gymnasts were shorter than controls(-0.9 to -1.3 SD, p < 0.01). In pre- and peri-pubertal gymnasts, this was due to a reduction in StHt (-0.8 to -1.3 SD) and LL (-0.8 to -1.1 SD)(p < 0.01). In post-pubertal gymnasts, StHt (-0.8 SD) was reduced (p < 0.05). No differences were observed in z-score deficits between pubertal groups, nor were there any differences in StHt and LL deficits. During 12 mths follow-up in 39 gymnasts, deficits in Ht z-scores were reduced further in pre-pubertal gymnasts (-0.2 SD, p < 0.001) due to a greater increase in the deficit in LL (-0.3 SD, p < 0.001). While the magnitude of z-score deficits for peri-pubertal gymnasts remained unchanged, Ht z-scores improved in post-pubertal gymnasts(+0.2SD, p < 0.05) due primarily to an increase in StHt (+0.4 SD, p < 0.01). Similar results were found in 16 gymnasts followed for 2 yrs.

CONCLUSION
Although small size may relate to self-selection for gymnastics, some non-elite female gymnasts may experience attenuated growth during early puberty due mainly to reduced leg growth. The increased growth observed in post-pubertal gymnasts is consistent with catch-up growth associated with delayed maturation.

Thrifty metabolism that favors fat storage after caloric restriction: a role for skeletal muscle phosphatidylinositol-3-kinase activity and AMP-activated protein kinase

Energy conservation directed at accelerating body fat recovery (or catch-up fat) contributes to obesity relapse after slimming and to excess fat gain during catch-up growth after malnutrition. To investigate the mechanisms underlying such thrifty metabolism for catch-up fat, we tested whether during refeeding after caloric restriction rats exhibiting catch-up fat driven by suppressed thermogenesis have diminished skeletal muscle phosphatidylinositol-3-kinase (PI3K) activity or AMP-activated protein kinase (AMPK) signaling—two pathways required for hormone-induced thermogenesis in ex vivo muscle preparations. The results show that during isocaloric refeeding with a low-fat diet, at time points when body fat, circulating free fatty acids, and intramyocellular lipids in refed animals do not exceed those of controls, muscle insulin receptor substrate 1-associated PI3K activity (basal and in vivo insulin-stimulated) is lower than that in controls. Isocaloric refeeding with a high-fat diet, which exacerbates the suppression of thermogenesis, results in further reductions in muscle PI3K activity and in impaired AMPK phosphorylation (basal and in vivo leptin-stimulated). It is proposed that reduced skeletal muscle PI3K/AMPK signaling and suppressed thermogenesis are interdependent. Defective PI3K or AMPK signaling will reduce the rate of substrate cycling between de novo lipogenesis and lipid oxidation, leading to suppressed thermogenesis, which accelerates body fat recovery and furthermore sensitizes skeletal muscle to dietary fat-induced impairments in PI3K/AMPK signaling.—Summermatter, S., Mainieri, D., Russell, A. P., Seydoux, J., Montani, J. P., Buchala, A., Solinas, G., Dulloo, A. G. Thrifty metabolism that favors fat storage after caloric restriction: a role for skeletal muscle phosphatidylinositol-3-kinase activity and AMP-activated protein kinase.

Money and VELS

An evidence-based formative assessment or a diagnostic profile of a student can be constructed to meet the objectively assessed needs of each student. This will help identify at the outset what individual students already know and can do and the lessons can begin building directly on that. A few other students whose level of knowledge may not be the same can be provided with extra different help so that they can catch up.

Profiles of language development in pre-school children : a longitudinal latent class analysis of data from the early language in Victoria study

Background Pre-school language impairment is common and greatly reduces educational performance. Population attempts to identify children who would benefit from appropriately timed intervention might be improved by greater knowledge about the typical profiles of language development. Specifically, this could be used to help with the early identification of children who will be impaired on school entry.

Methods This study applied longitudinal latent class analysis to assessments at 8, 12, 24, 36 and 48 months on 1113 children from a population-based study, in order to identify classes exhibiting distinct communicative developmental profiles.

Results Five substantive classes were identified: Typical, i.e. development in the typical range at each age; Precocious (late), i.e. typical development in infancy followed by high probabilities of precocity from 24 months onwards; Impaired (early), i.e. high probabilities of impairment up to 12 months followed by typical language development thereafter; Impaired (late), i.e. typical development in infancy but impairment from 24 months onwards; Precocious (early), i.e. high probabilities of precocity in early life followed by typical language by 48 months. The entropy statistic (0.84) suggested classes were fairly well defined, although there was a non-trivial degree of uncertainty in classification of children. That half of the Impaired (late) class was expected to have typical language at 4 years and 6% of the numerically large Typical class was expected to be impaired at 4 years illustrates this. Characteristics indicative of social advantage were more commonly found in the classes with improving profiles.

Conclusions Developmental profiles show that some pre-schoolers' language is characterized by periods of accelerated development, slow development and catch-up growth. Given the uncertainty in classifying children into these profiles, use of this knowledge for identifying children who will be impaired on school entry is not straightforward. The findings do, however, indicate greater need for language enrichment programmes among disadvantaged children.

Media gets its mojo on

People everywhere have the means to create and publish mobile content, but as mainstream media begins its catch up the possibilities of a mobile led communications revolutions has never been greater. This articel discusse a new form of creating user genereted stories (UGS) using mobiles. Whether it's in remote communities or being used by frontline journalists, mojo is an accessible technology and skill set that closes the  gap between the three major spheres of communication: community, education and professional media.

Recombinant human growth hormone for the treatment of growth disorders in children: a systematic review and economic evaluation

Recombinant human growth hormone (rhGH) is licensed for short stature associated with growth hormone deficiency (GHD), Turner syndrome (TS), Prader-Willi syndrome (PWS), chronic renal insufficiency (CRI), short stature homeobox-containing gene deficiency (SHOX-D) and being born small for gestational age (SGA). To assess the clinical effectiveness and cost-effectiveness of rhGH compared with treatment strategies without rhGH for children with GHD, TS, PWS, CRI, SHOX-D and those born SGA. The systematic review used a priori methods. Key databases were searched (e.g. MEDLINE, EMBASE, NHS Economic Evaluation Database and eight others) for relevant studies from their inception to June 2009. A decision-analytical model was developed to determine cost-effectiveness in the UK. Two reviewers assessed titles and abstracts of studies identified by the search strategy, obtained the full text of relevant papers, and screened them against inclusion criteria. Data from included studies were extracted by one reviewer and checked by a second. Quality of included studies was assessed using standard criteria, applied by one reviewer and checked by a second. Clinical effectiveness studies were synthesised through a narrative review. Twenty-eight randomised controlled trials (RCTs) in 34 publications were included in the systematic review. GHD: Children in the rhGH group grew 2.7 cm/year faster than untreated children and had a statistically significantly higher height standard deviation score (HtSDS) after 1 year: -2.3 ± 0.45 versus -2.8 ± 0.45. TS: In one study, treated girls grew 9.3 cm more than untreated girls. In a study of younger children, the difference was 7.6 cm after 2 years. HtSDS values were statistically significantly higher in treated girls. PWS: Infants receiving rhGH for 1 year grew significantly taller (6.2 cm more) than those untreated. Two studies reported a statistically significant difference in HtSDS in favour of rhGH. CRI: rhGH-treated children in a 1-year study grew an average of 3.6 cm more than untreated children. HtSDS was statistically significantly higher in treated children in two studies. SGA: Criteria were amended to include children of 3+ years with no catch-up growth, with no reference to mid-parental height. Only one of the RCTs used the licensed dose; the others used higher doses. Adult height (AH) was approximately 4 cm higher in rhGH-treated patients in the one study to report this outcome, and AH-gain SDS was also statistically significantly higher in this group. Mean HtSDS was higher in treated than untreated patients in four other studies (significant in two). SHOX-D: After 2 years' treatment, children were approximately 6 cm taller than the control group and HtSDS was statistically significantly higher in treated children. The incremental cost per quality adjusted life-year (QALY) estimates of rhGH compared with no treatment were: 23,196 pounds for GHD, 39,460 pounds for TS, 135,311 pounds for PWS, 39,273 pounds for CRI, 33,079 pounds for SGA and 40,531 pounds for SHOX-D. The probability of treatment of each of the conditions being cost-effective at 30,000 pounds was: 95% for GHD, 19% for TS, 1% for PWS, 16% for CRI, 38% for SGA and 15% for SHOX-D.