Differentiation of Bacteroides ovatus and Bacteroides thetaiotaomicron by means of bacteriophage.

Two members of the Bacteroides fragilis group, B. ovatus and B. thetaiotaomicron, are difficult to distinguish by biochemical methods. They are currently identified on the basis of their variable ability to ferment salicin. We studied a method of identification for these two species by using cell lysis by bacteriophages. A total of 38 bacteriophages were used to distinguish the two species. Identification by bacteriophages was compared with species identification by prereduced anaerobically sterilized biochemical testing with salicin as the differentiating test. A total of 215 clinical isolates biochemically identified as B. ovatus or B. thetaiotaomicron were tested. A total of 100% of the strains identified as B. ovatus by bacteriophages produced strong acid in salicin (pH less than or equal to 5.4). However, 40% of the strains identified as B. thetaiotaomicron by bacteriophages also produced strong acid in salicin, and an additional 39% produced weak acid (pH 5.5 to 5.7). This study demonstrates that salicin fermentation is an inadequate test for the differentiation of B. ovatus and B. thetaiotaomicron.     

Stigma apprehension among adolescents discharged from brief psychiatric hospitalization

This study explores stigma apprehension (fear of being devalued or rejected) and its correlates among 102 adolescents, interviewed within 7 days of discharge from their first psychiatric hospitalization. Components of the Model of Stigma-Induced Identity Threat by Major and O'Brien (Annu Rev Psychol 56:393-421, 2005) comprise the study model, including collective stigma representations and group and domain identification; additional clinical, personal, and contextual characteristics such as social affiliation, interpersonal support, self-identification as having a mental disorder, and perceived need for others' approval were added to the model. We found that, on average, the participants reported "a little" stigma apprehension, and 21% reported substantial stigma apprehension. Multivariate analysis demonstrated that higher stigma apprehension was most associated with the female sex, younger age at initiation of mental health treatment, lower self-esteem, greater need for others' approval, more experiences with personal stigmatization, and not identifying or affiliating with peers who have mental health or behavior challenges. These factors collectively accounted for 46% of the variance. The study's findings particularly highlight the role of social context and external contingencies of self-worth in determining adolescents' perceptions of stigma-related threat.     

Short-chain acyl-CoA dehydrogenase gene mutation (c.319C>T) presents with clinical heterogeneity and is candidate founder mutation in individuals of Ashkenazi Jewish origin

We report 10 children (7 male, 3 female), 3 homozygous for c.319C>T mutation and 7 heterozygous for c.319C>T on one allele and c.625G>A variant on the other in the short-chain acyl-CoA dehydrogenase (SCAD) gene (ACADS). All were of Ashkenazi Jewish origin in which group we found a c.319C>T heterozygote frequency of 1:15 suggesting the presence of a founder mutation or selective advantage. Phenotype was variable with onset from birth to early childhood. Features included hypotonia (8/10), developmental delay (8/10), myopathy (4/10) with multicore changes in two and lipid storage in one, facial weakness (3/10), lethargy (5/10), feeding difficulties (4/10) and congenital abnormalities (3/7). One female with multiminicore myopathy had progressive external ophthalmoplegia, ptosis and cardiomyopathy with pneumonia and respiratory failure. Two brothers presented with psychosis, pyramidal signs, and multifocal white matter abnormalities on MRI brain suggesting additional genetic factors. Two other infants also had white matter changes. Elevated butyrylcarnitine (4/8), ethylmalonic aciduria (9/9), methylsuccinic aciduria (6/7), decreased butyrate oxidation in lymphoblasts (2/4) and decreased SCAD activity in fibroblasts or muscle (3/3) were shown. Expression studies of c.319C>T in mouse liver mitochondria showed it to be inactivating. c.625G>A is a common variant in ACADS that may confer disease susceptibility. Five healthy parents were heterozygous for c.319C>T and c.625G>A, suggesting reduced penetrance or broad clinical spectrum. We conclude that the c.319C>T mutation can lead to wide clinical and biochemical phenotypic variability, suggesting a complex multifactorial/polygenic condition. This should be screened for in individuals with multicore myopathy, particularly among the Ashkenazim.     

Activation of descending pain-facilitatory pathways from the rostral ventromedial medulla by cholecystokinin elicits release of prostaglandin-E₂ in the spinal cord

Cholecystokinin (CCK) has been suggested to be both pro-nociceptive and “anti-opioid” by actions on pain-modulatory cells within the rostral ventromedial medulla (RVM). One consequence of activation of RVM CCK₂ receptors may be enhanced spinal nociceptive transmission; but how this might occur, especially in states of pathological pain, is unknown. Here, in vivo microdialysis was used to demonstrate that levels of RVM CCK increased by approximately 2-fold after ligation of L₅/L₆ spinal nerves (SNL). Microinjection of CCK into the RVM of naïve rats elicited hypersensitivity to tactile stimulation of the hindpaw. In addition, RVM CCK elicited a time-related increase in (prostaglandin-E₂) PGE₂ measured in cerebrospinal fluid from the lumbar spinal cord. The peak increase in spinal PGE₂ was approximately 5-fold and was observed at approximately 80 minutes post-RVM CCK, a time coincident with maximal RVM CCK-induced mechanical hypersensitivity. Spinal administration of naproxen, a nonselective COX-inhibitor, significantly attenuated RVM CCK-induced hindpaw tactile hypersensitivity. RVM-CCK also resulted in a 2-fold increase in spinal 5-hydroxyindoleacetic acid (5-HIAA), a 5-hydoxytryptophan (5-HT) metabolite, as compared with controls, and mechanical hypersensitivity that was attenuated by spinal application of ondansetron, a 5-HT₃ antagonist. The present studies suggest that chronic nerve injury can result in activation of descending facilitatory mechanisms that may promote hyperalgesia via ultimate release of PGE₂ and 5-HT in the spinal cord.     

Family, peer, and individual correlates of depressive symptomatology among U.S. and Chinese adolescents

This study examined the correlates of symptoms of depressed mood among adolescents in 2 dramatically different cultures (n = 502 in Tianjin, People's Republic of China; n = 201 in greater Los Angeles). Gender, stressful life events, perceived parental warmth, and conflict with parents were associated in the expected direction with depressive symptoms in each cultural setting. As predicted, regression analyses showed that the quality of family relationships and grades in school had significantly stronger associations with depressive symptoms among Chinese youths than among U.S. youths, whereas gender differences in depressive symptoms were greater among the U.S. youths. Peer warmth moderated the effects of particular risk factors for depressive symptoms in each cultural setting.     

Glycogen storage disease type 1a in Israel: Biochemical,clinical, and mutational studies

Glycogen storage disease type 1a (von Gierke disease, GSD 1a) is caused by the deficiency of microsomal glucose-6-phosphatase (G6Pase) activity which catalyzes the final common step of glycogenolysis and gluconeogenesis. The recent cloning of the G6Pase cDNA and characterization of the human G6Pase gene enabled the characterization of the mutations causing GSD 1a. This, in turn, allows the introduction of a noninvasive DNA-based diagnosis that provides reliable carrier testing and prenatal diagnosis. In this study, we report the biochemical and clinical characteristics as well as mutational analyses of 12 Israeli GSD 1a patients of different families, who represent most GSD 1a patients in Israel. The mutations, G6Pase activity, and glycogen content of 7 of these patients were reported previously. The biochemical data and clinical findings of all patients were similar and compatible with those described in other reports. All 9 Jewish patients, as well as one Muslim Arab patient, presented the R83C mutation. Two Muslim Arab patients had the V166G mutation which was not found in other patients' populations. The V166G mutation, which was introduced into the G6Pase cDNA by site-directed mutagenesis following transient expression in COS-1 cells, was shown to cause complete inactivation of the G6Pase. The characterization of all GSD 1a mutations in the Israeli population lends itself to carrier testing in these families as well as to prenatal diagnosis, which was carried out in 2 families. Since all Ashkenazi Jewish patients harbor the same mutation, our study suggests that DNA-based diagnosis may be used as an initial diagnostic step in Ashkenazi Jews suspected of having GSD 1a, thereby avoiding liver biopsy. Am. J. Med. Genet. 72:286–290, 1997. © 1997 Wiley-Liss, Inc.     

The efficacy of treadmill training on balance dysfunction in individuals with chronic stroke: a systematic review

Background: Physical activity and exercise interventions are useful in facilitating the functional recovery of those with chronic stroke and, routinely, are gait-specific. While treadmill training has proven useful in gait performance recovery post-stroke, its efficacy on balance dysfunction has not been systematically reviewed.

Objectives: The purpose of this systematic review was to determine the effect of treadmill training (TT) interventions on balance dysfunction in individuals with chronic stroke.

Methods: A systematic literature search of PubMed, EMBASE, and CINAHL was performed. Eligible randomized controlled trials were published between 2007 and 2016. Selected trials investigated TT interventions in persons with chronic stroke and implemented at least one objective balance measure. Methodological quality was assessed using PEDro criteria.

Results: Eight studies met eligibility criteria and were included in the qualitative analysis. Studies differed in TT implementation and use of adjunctive treatments; however, all trials demonstrated improvements in balance measures that were as effective, if not more so, than conventional physical therapy treatments, including targeted balance training.

Conclusions: This review recognized moderate evidence in favor of TT interventions in balance and stroke rehabilitation programs. With TT, intensity may be a more critical factor than specificity and may offer additional carryover to recovery parameters of postural control and balance, beyond gait performance. It is recommended that clinicians utilizing TT incorporate objective measures of balance to assess the potential for skill transference and improvements in balance. Higher quality studies and additional research are needed to denote critical parameters by which improvements in balance may be optimized.