The relationship between family functioning and child and adolescent overweight and obesity: a systematic review.

There is mounting evidence that family functioning is linked to childhood overweight and obesity, and that both of these are associated with health-related behaviours and adverse health outcomes in children and adolescents. This paper systematically examines the peer-reviewed evidence regarding the relationship between child and adolescent overweight and obesity and family functioning. Peer-reviewed literature published between 1990 and 2011 hosted in Scopus, Pub Med or Psyc INFO were searched, in addition to the reference lists of included papers. Twenty-one studies met the selection criteria. Of the 17 identified cross-sectional and longitudinal studies, 12 reported significant associations between family functioning and childhood overweight and obesity. The instruments used to measure family functioning in the identified studies were heterogeneous. Poor family functioning was associated with increased risk of obesity and overweight in children and adolescents, and obese children and adolescents were more likely to come from families with poor family functioning. Aspects of family functioning which were associated with increased risk of child and adolescent obesity included poor communication, poor behaviour control, high levels of family conflict and low family hierarchy values. Half (2/4) of the identified intervention studies showed a significant relationship between family functioning and changes in child weight. The results demonstrate that family functioning is linked to obesity; however, higher level evidence and greater understanding of the mechanisms behind this relationship are required. The results indicate a need for a standardised family functioning measure applicable across populations. The results provide evidence of the value of considering family functioning in childhood obesity research and intervention.

The complete amino acid sequence of feline beta-lactoglobulin II and a partial revision of the equine beta-lactoglobulin II sequence.

The amino acid sequence of feline beta-lactoglobulin (designated II) has been determined. The protein chain is 163 amino acids long with a relative molecular mass of 18,558. The primary structure was determined by sequencing of native protein (residues 1-25), BPNS-skatole cleavage fragments and the peptides obtained by proteolytic cleavage with V8 proteinase and TPCK-trypsin. Feline beta-lactoglobulin II has 53 and 57% positional identities with bovine beta-lactoglobulin A and equine beta-lactoglobulin I, respectively, and approx. 68% with a revised sequence of equine beta-lactoglobulin II. The equine beta-lactoglobulin II sequence was re-examined between positions 78 and 122 resulting in a major revision in this area with only a single insertion to give a total of 163 residues.

Missense mutation in the lacI gene of Escherichia coli. Inferences on the structure of the repressor protein.

The lac repressor has been studied extensively but a precise three-dimensional structure remains unknown. Studies using mutational data can complement other information and provide insight into protein structure. We have been using the lacI gene-repressor protein system to study the mutational specificity of spontaneous and induced mutation. The sequencing of over 6000 lacI- mutations has revealed 193 missense mutations generating 189 amino acid replacements at 102 different sites within the lac repressor. Replacement sites are not distributed evenly throughout the protein, but are clustered in defined regions. Almost 40% of all sites and over one-half of all substitutions found occur within the amino-terminal 59 amino acid residues, which constitute the DNA-binding domain. The core domain (residues 60 to 360) is less sensitive to amino acid replacement. Here, substitution is found in regions involved in subunit aggregation and at sites surrounding residues that are implicated in sugar-binding. The distribution and nature of missense mutational sites directs attention to particular amino acid residues and residue stretches.

Inversions with deletions and duplications.

Complex mutational events, including de novo inversion with deletion and duplication of sequence, have been observed but are difficult to model. We propose that nascent leading-strand misalignment upon the lagging-strand template during DNA replication can result in the inversion of sequence. The positioning of this misalignment and of the realignment of the leading strand back into the leading-strand template will determine if the inversion is accompanied by deletion and duplication of sequence. We suggest that such strand misalignment-realignment events may occur at the replication fork during concurrent DNA replication.

Host-specificity of monogenean (platyhelminth) parasites: a role for anterior adhesive areas?

Monogeneans (flatworms) are among the most host-specific of parasites in general and may be the most host-specific of all fish parasites. Specificity, in terms of a restricted spatial distribution within an environment, is not unique to parasites and is displayed by some fungi, insects, birds, symbionts and pelagic larvae of free-living marine invertebrates. The nature of cues, how "habitats" are recognised and how interactions between partners are mediated and maintained is of interest across these diverse "associations". We review some experiments that demonstrate important factors that contribute to host-specificity at the level of infective stages (larvae of oviparous monogeneans; juveniles of viviparous gyrodactylids) and adult parasites. Recent research on immune responses by fish to monogenean infections is considered. We emphasise the critical importance of host epidermis to the Monogenea. Monogeneans live on host epidermis, they live in its products (e.g. mucus), monopisthocotyleans feed on it, some of its products are "attractants" and it may be an inhospitable surface because of its immunological activity. We focus attention on fish but reference is made to amphibian hosts. We develop the concept for a potential role in host-specificity by the anterior adhesive areas, either the specialised tegument and/or anterior secretions produced by monogeneans for temporary but firm attachment during locomotion on host epithelial surfaces. Initial contact between the anterior adhesive areas of infective stages and host epidermis may serve two important purposes. (1) Appropriate sense organs or receptors on the parasite interact with a specific chemical or chemicals or with surface structures on host epidermis. (2) A specific but instant recognition or reaction occurs between component(s) of host mucus and the adhesive(s) secreted by monogeneans. The chemical composition of fish skin is known to be species-specific and our preliminary analysis of the chemistry of some monogenean adhesives indicates they are novel proteins that display some differences between parasite families and species.

Preparation and characterization of polyclonal antibodies against human chaperonin 10.

Early pregnancy factor (EPF) has been identified as an extracellular homologue of chaperonin 10 (Cpn10), a heat shock protein that functions within the cell as a molecular chaperone. Here, we report the production of polyclonal antibodies directed against several different regions of the human Cpn10 molecule and their application to specific protein quantitation and localization techniques. These antibodies will be valuable tools in further studies to elucidate the mechanisms underlying the differential spatial and temporal localization of EPF and Cpn10 and in studies to elucidate structure and function.

Colony hybridisation in Escherichia coli: a rapid procedure for determining the distribution of specific classes of mutations among a number of preselected sites.

Colony probe oligonucleotide hybridisation was used for the unambiguous identification of DNA alterations and the determination of distributions and frequencies of forward mutation at the molecular level. To demonstrate the reliability and versatility of this technique, distributions of spontaneous and ethyl methanesulfonate (EMS)-induced mutations have been reproduced using a battery of oligonucleotide probes complementary to specific sites and classes of mutation. These studies are indicative of the diagnostic potential of oligonucleotide colony hybridisation to the characterisation of mutation; oligonucleotide hybridisation used in conjunction with a well studied mutational target provides a rapid and reliable alternative to DNA sequencing for the characterisation of all classes of mutations.

Increased wheeze but not bronchial hyperreactivity near power stations.

STUDY OBJECTIVE: In a previous study a higher than expected prevalence of asthma was found in Lake Munmorah, a coastal town near two power stations, compared with another coastal control town. This study aimed to compare atopy, bronchial hyperreactivity, and reported symptoms of asthma in the power station town and a second control area with greater socioeconomic similarity. DESIGN: A cross sectional survey was undertaken. SETTINGS: Lake Munmorah, a coastal town near two power stations, and Dungog, a country town in the Hunter Valley, NSW, Australia. PARTICIPANTS: All children attending kindergarten to year 6 at all schools in the two towns were invited to participate in 1990. The response rates for the questionnaire for reported symptoms and associated demographic data were 92% in Lake Munmorah and 93% in Dungog, with 84% and 90% of children respectively being measured for lung function, atopy, and bronchial reactivity. There were 419 boys and 432 girls aged 5 to 12 years. MEASUREMENTS AND MAIN RESULTS: Main outcome measures were current wheeze and bronchial hyper-reactivity, defined as a fall in forced expiratory volume in 1 second (FEV1) or peak expiratory flow (PEF) of 20% or more. Current wheeze was reported in 24.8% of the Lake Munmorah children compared with 14.6% of the Dungog children. Bronchial hyper-reactivity was similar for both groups--25.2% in Lake Munmorah and 22.3% in Dungog. The mean baseline FEV1 was lower in Lake Munmorah than in Dungog (p < 0.001). Dungog children were more likely to have positive skin test to house dust mite (Dungog 27.0%, Lake Munmorah 20.2%, p = 0.028) but there were no other differences in skin test atopy in the two towns. After adjusting for age, gender, any smoker in the house, and positive dust mite skin test, the odds of current wheeze in Lake Munmorah compared with Dungog was 2.16 (95% confidence interval 1.45, 3.15). CONCLUSIONS: Baseline lung function was lower and reported symptoms of asthma were higher in the power station town, but bronchial hyper-reactivity and skin test defined atopy were similar in the two communities. These results are consistent with the previous study and confirm the increased presence of reported symptomatic illness in the town near power stations.

Mechanisms of spontaneous mutation in DNA repair-proficient Escherichia coli.

This paper describes the DNA sequence analysis of 729 independent spontaneous lacI- mutations. This total is comprised of 478 novel mutations and 251 previously described events, and therefore should allow a more comprehensive view of spontaneous mutation in Escherichia coli. The spectrum is dominated by a hotspot (71% of all events). Mutations at this site consist of related addition and deletion events involving a number of repetitive sequences. Here we discuss how the frequency and proportion of these events vary in different DNA repair-deficient genetic backgrounds. The distribution of non-hotspot events includes base substitutions (38%), deletions (35%), frameshifts (14%), duplications (4%) and insertion elements (4%). G:C----A:T events dominate among base substitutions, while G:C----C:G events are the least common; the remaining types of base substitution are equally represented. Among deletions, a significant number do not display repeated sequences at their endpoints (26/72). However, almost all multiply recovered events (15/17) possess repeated sequences capable of accounting for the deletion endpoints. Similarly, over half of all duplications recovered (5/7) display repeated endpoints. Single-base frameshifts are equally divided between A:T and G:C sites, in each case (-) 1 events occur 3-fold more frequently that (+) 1 events. A comparative analysis of each mutational class recovered to lacI- spectra available in a variety of DNA repair/metabolism-deficient strains is presented here in an attempt to assess possible contributions from chemical, physical and enzymic sources of damage.

Severe hypoglycaemia and its association with psychological well-being in Australian adults with type 1 diabetes attending specialist tertiary clinics.

AIM: To investigate severe hypoglycaemia (SH) in adults with type 1 diabetes and its associations with impaired awareness of hypoglycaemia (IAH), clinical, psychological and socio-demographic factors. METHODS: Attendees of three specialist diabetes clinics in Melbourne, Australia completed questions about frequency of SH in the past six months; impaired awareness of hypoglycaemia (Gold score); and measures of general emotional well-being (WHO-5), diabetes-specific positive well-being (subscale of W-BQ28), diabetes-related distress (PAID) and fear of hypoglycaemia (HFS). RESULTS: Of 422 participants (mean ± SD age 37.5 ± 15.0 years; 54% women), 78 (18.5%) reported at least one SH event and 86 (20.5%) had IAH. SH and IAH frequencies were similar at all clinics. In total, 194 SH events were reported, with 10 people experiencing 40% of events. Compared with those without SH, participants with SH had longer diabetes duration, were younger at diabetes onset and more likely to have IAH (p<0.01). Those with SH had greater fear of hypoglycaemia and diabetes-related distress, poorer general emotional well-being, and lower diabetes-specific positive well-being, (p<0.01). There were no associations with age, gender, insulin regimen or HbA1c. CONCLUSIONS: This study has identified that SH and IAH in Australian adults with type 1 diabetes exist at similar levels to those reported in US and European research. SH was significantly associated with IAH and fear of hypoglycaemia. Assessment of hypoglycaemia, IAH and psychological well-being as part of a routine diabetes clinic visit was well accepted by attendees and enabled identification of those who may benefit from medical, educational or therapeutic interventions.

A controlled release pilocarpine buccal insert in the treatment of Sjögren's syndrome.

OBJECTIVES: To assess the efficacy of a novel hydrogel polymer buccal insert containing 5 mg pilocarpine in releasing the pilocarpine in a controlled fashion over a three hour period, and to assess the effects of this on quantitative tear and saliva production and the acceptability of the insert to the patient. DESIGN: This was an open, uncontrolled pilot study for which Ethics Committee approval was obtained prior to starting. Hydrogel buccal inserts containing 5 mg pilocarpine were used three times a day for seven days. SETTING: The Department of Oral Medicine, Glasgow Dental Hospital & School. SUBJECTS: Eight patients with Sjögren's syndrome. MAIN OUTCOME MEASURES: Changes over baseline in (1) Schirmer test, (2) whole saliva flow rate, (3) oral comfort score (VAS), (4) ocular comfort score (VAS), (5) patient acceptability. RESULTS: The buccal inserts successfully released in excess of 85% of their 5 mg pilocarpine load over three hours. There was a general improvement in oral and ocular comfort scores assessed by visual linear analogue scale, and saliva and tear production generally increased. The inserts were well tolerated by all patients except one (who wore dentures). Adverse events were few and none was serious. CONCLUSION: This novel form of buccal pilocarpine delivery demonstrated potential for use in treating patients with Sjögren's syndrome.

Genetic analysis of mutagenesis in aging Escherichia coli colonies.

Bacteria live in unstructured and structured environments, experiencing feast and famine lifestyles. Bacterial colonies can be viewed as model structured environments. SOS induction and mutagenesis have been observed in aging Escherichia coli colonies, in the absence of exogenous sources of DNA damage. This cAMP-dependent mutagenesis occurring in Resting Organisms in a Structured Environment (ROSE) is unaffected by a umuC mutation and therefore differs from both targeted UV mutagenesis and recA730 (SOS constitutive) untargeted mutagenesis. As a recB mutation has only a minor effect on ROSE mutagenesis it also differs from both adaptive reversion of the lacI33 allele and from iSDR (inducible Stable DNA Replication) mutagenesis. Besides its recA and lexA dependence, ROSE mutagenesis is also uvrB and polA dependent. These genetic requirements are reminiscent of the untargeted mutagenesis in lambda phage observed when unirradiated lambda infects UV-irradiated E. coli. These mutations, which are not observed in aging liquid cultures, accumulate linearly with the age of the colonies. ROSE mutagenesis might offer a good model for bacterial mutagenesis in structured environments such as biofilms and for mutagenesis of quiescent eukaryotic cells.

Editing DNA replication and recombination by mismatch repair: from bacterial genetics to mechanisms of predisposition to cancer in humans.

A hereditary form of colon cancer, hereditary non-polyposis colon cancer (HNPCC), is characterized by high instability of short repeated sequences known as microsatellites. Because the genes controlling microsatellite stability were known in bacteria and yeast, as was their evolutionary conservation, the search for human genes responsible for HNPCC became a 'targeted' search for known sequences. Mismatch-repair deficiency in bacteria and yeast produces multiple phenotypes as a result of its dual involvement in the editing of both replication errors and recombination intermediates. In addition, mismatch-repair functions are specialized in eukaryotes, characterized by specific mitotic (versus meiotic) functions, and nuclear (versus mitochondrial) localization. Given the number of phenotypes observed so far, we predict other links between mismatch-repair deficiency and human genetic disorders. For example, a similar type of sequence instability has been found in HNPCC tumours and in a number of neuro-muscular genetic disorders. Several human mitochondrial disorders display genomic instabilities reminiscent of yeast mitochondrial mismatch-repair mutants. In general, the process of mismatch repair is responsible for the constant maintenance of genome stability and its faithful transmission from one generation to the next. However, without genetic alteration, species would not be able to adapt to changing environments. It appears that nature has developed both negative and positive controls for genetic diversity. In bacteria, for example, an inducible system (sos) exists which generates genetic alterations in response to environmental stress (e.g. radiation, chemicals, starvation). Hence, the cost of generating diversity to adapt to changing conditions might be paid as sporadic gene alterations associated with disease.

The management of epiglottitis in a small paediatric intensive care unit.

The aim of this study was to examine the outcome of epiglottitis in a small paediatric institution. Over the 5 year period October 1986 to September 1991, 44 children (of whom 15 were retrieved) with epiglottitis were admitted to the only paediatric intensive care facility in the Hunter Region. The so-called classical features were often absent. Forty of the 44 children were intubated. The mean length of intubation was 22 h and the mean length of hospital stay was only 2 1/2 days. One child had a respiratory arrest prior to intubation but made a complete recovery; one child had a coexistent submental/submandibular fascial space infection; 16 (36%) had abnormal chest radiographs. Five children had post-extubation stridor with one of these children left with residual hoarseness. Epiglottitis can be managed safely in a small paediatric intensive care unit with acceptable short-term and long-term complications.