财经类院校贫困生心理健康状况及述情障碍

目的：评估财经类院校贫困生心理状况,探讨财经类院校贫困生的心理状况与述情障碍的关系,为更好解决贫困生的心理问题提供依据。方法：对298名贫困学生进行症状自评量表（SymptomChecklist-90,SCL-90）多伦多述情障碍量表（Twenty-ItemTorontoAlexithymiaScale,TAS．20）的测量并与320名非贫困生对照组的结果进行比较。结果：①贫困生组的抑郁、焦虑、人际关系敏感、精神病性、偏执因子分及SCL．90总分因子高于对照组,贫困生组的F1因子明显高于对照组;②述情障碍组SCL-90总分和各因子得分明显高于非述情组;③述情量表总分及各因子分与症状自评量表总分及各因子分显著相关（P〈0．01或P〈0．05）。结论：①与非贫困学生相比,贫困生具有较多的心身症状,主要表现在抑郁、焦虑、人际关系敏感、精神病性、偏执。②述情障碍与心理健康密切相关,述情障碍个体倾向于更容易出现心身症状。③F1（缺乏识别情感的能力）是一个较其它因子更敏感的述情障碍的鉴定指标。     

Developmental and behavioural phenotype in Noonan syndrome?

Developmental and behavioural phenotype in Noonan syndrome? Noonan syndrome is characteristic by facial dysmorphology, congenital heart defects, short stature, developmental retardation and severe early feeding disorders in many cases. Data from a postal survey on physical development, feeding difficulties, developmental problems and behavioural aspects in 26 children are reported. The findings suggest developmental and behavioural difficulties in 46 per cent, but do not support the notion of a behavioural phenotype specific to Noonan syndrome. Having to cope with early surgery, feeding, developmental and behavioural problems establishes a need for psychological counseling for families receiving a diagnosis of Noonan syndrome.     

PTPN11 gene analysis in 74 Brazilian patients with Noonan syndrome or Noonan-like phenotype

Mutations in the PTPN11 gene are known to cause a large fraction of the cases of Noonan syndrome. The objective of this study was to determine the PTPN11 gene mutation rate in a cohort of clinically well-characterized Brazilian patients with Noonan or Noonan-like syndromes and to study the genotype-phenotype correlation. Fifty probands with Noonan syndrome ascertained according to well-established diagnostic criteria, 3 with LEOPARD syndrome, 5 with Noonan-like/multiple giant cell lesion syndrome, and 3 with neurofibromatosis/ Noonan were enrolled in this study. Mutational analysis was performed using denaturing high-performance liquid chromatography (DHPLC) followed by sequencing of amplicons with an aberrant elution profile. We detected missense mutations in the PTPN11 gene in 21 probands with Noonan syndrome (42%), in all 3 patients with LEOPARD syndrome, and in 1 case with Noonan-like/multiple giant cell lesion syndrome. One patient with neurofibromatosis-Noonan syndrome had a mutation in both the PTPN11 and NF1 genes. The only anomalies that reached statistical significance when comparing probands with and without mutations were the hematological abnormalities. Our data confirms that Noonan syndrome is a genetically heterogeneous disorder, with mutations in the PTPN11 gene responsible for roughly 50% of the cases. A definitive genotype-phenotype correlation has not been established, but the T73I mutation seems to predispose to a myeloproliferative disorder. Regarding Noonan-like syndromes, mutation of the PTPN11 gene is the main causal factor in LEOPARD syndrome, and it also plays a role in neurofibromatosis-Noonan syndrome. Noonan- like/multiple giant cell lesion syndrome, part of the spectrum of Noonan syndrome, is also heterogeneous.     

Neonatal Noonan syndrome with a molluscoid cutaneous excess over the scalp.

The Noonan syndrome is a multiple congenital anomalies syndrome with variable expressivity and autosomal dominant inheritance. We report an observation of a newborn with Noonan syndrome and an unusual molluscoid cutaneous excess over the scalp that might represent a new skin manifestation in Noonan Syndrome rather than a consequence of lymphatic dysplasia.     

Genetics and variation in phenotype in Noonan syndrome

Noonan syndrome is a well-known clinical entity comprising multiple congenital anomalies characterized by typical facial features, short stature and congenital heart defect. Approximately 50% of cases are sporadic. Familial cases are generally autosomal dominant. In 2001 a gene responsible for Noonan syndrome, PTPN11, encoding for the non-receptor protein tyrosine phosphatase SHP-2, was identified. Mutation analysis of the PTPN11 gene was carried out in Nijmegen in 150 patients with Noonan syndrome. Mutations were found in 68 patients (45%), the most common being A922G in exon 8. In exon 4 a mutation was found that encoded the C-SH2 domain of the PTPN11 gene in two unique patients who shared some uncommon features. A 218C-->T mutation was found in exon 3 in one patient with Noonan syndrome and mild juvenile myelomonocytic leukaemia.     

Depression and Anxiety Correlate Differently with Salivary Free Cortisol in the Morning in Patients with Functional Somatic Syndrome

Patients presenting with functional somatic syndrome (FSS) are common, and the symptoms are persistent and difficult to treat for doctors and costly for society. The aim of this study was to clarify the common pathophysiology of FSS, especially the relationship between hypothalamic-pituitary-adrenal (HPA) axis function and psychological characteristics of patients with FSS. The subjects were 45 patients with FSS and 29 healthy controls. Salivary free cortisol was measured in the morning, and psychological tests examining depression, anxiety and quality of life (QOL) were performed on the same day. In patients with FSS, depressive scores showed a significant negative correlation with salivary free cortisol in the morning, although in healthy controls, cortisol showed a significant positive correlation with depressive scores. In addition, the correlation between other psychological test scores and cortisol secretion in patients with FSS contrasted with that of controls. The relationship between cortisol and depression, anxiety or QOL, suggests that the HPA axis of patients with FSS is dysfunctional and does not function properly when patients with FSS are under stress. This dysfunction may explain the pathology of medically unexplained persistent symptoms of patients with FSS.     

Interaction between Neuroanatomical and Psychological Changes after Mindfulness-Based Training

Several cross-sectional studies have documented neuroanatomical changes in individuals with a long history of meditation, while a few evidences are available about the interaction between neuroanatomical and psychological changes even during brief exposure to meditation. Here we analyzed several morphometric indexes at both cortical and subcortical brain level, as well as multiple psychological dimensions, before and after a brief -8 weeks- Mindfulness Based Stress Reduction (MBSR) training program, in a group of 23 meditation naïve-subjects compared to age-gender matched subjects. We found a significant cortical thickness increase in the right insula and the somatosensory cortex of MBSR trainees, coupled with a significant reduction of several psychological indices related to worry, state anxiety, depression and alexithymia. Most importantly, an interesting correlation between the increase in right insula thickness and the decrease in alexithymia levels during the MBSR training were observed. Moreover, a multivariate pattern classification approach allowed to identify a cluster of regions more responsive to MBSR training across subjects. Taken together, these findings documented the significant impact of a brief MBSR training on brain structures, as well as stressing the idea of MBSR as a valuable tool for alexithymia modulation, also originally providing a plausible neurobiological evidence of a major role of right insula into mediating the observed psychological changes.     

Mouse model of Noonan syndrome reveals cell type- and gene dosage-dependent effects of Ptpn11 mutation

Noonan syndrome is a common human autosomal dominant birth defect, characterized by short stature, facial abnormalities, heart defects and possibly increased risk of leukemia. Mutations of Ptpn11 (also known as Shp2), which encodes the protein-tyrosine phosphatase Shp2, occur in approximately 50% of individuals with Noonan syndrome, but their molecular, cellular and developmental effects, and the relationship between Noonan syndrome and leukemia, are unclear. We generated mice expressing the Noonan syndrome-associated mutant D61G. When homozygous, the D61G mutant is embryonic lethal, whereas heterozygotes have decreased viability. Surviving Ptpn11(D61G/+) embryos ( approximately 50%) have short stature, craniofacial abnormalities similar to those in Noonan syndrome, and myeloproliferative disease. Severely affected Ptpn11(D61G/+) embryos ( approximately 50%) have multiple cardiac defects similar to those in mice lacking the Ras-GAP protein neurofibromin. Their endocardial cushions have increased Erk activation, but Erk hyperactivation is cell and pathway specific. Our results clarify the relationship between Noonan syndrome and leukemia and show that a single Ptpn11 gain-of-function mutation evokes all major features of Noonan syndrome by acting on multiple developmental lineages in a gene dosage-dependent and pathway-selective manner.     

Shp2 knockdown and Noonan/LEOPARD mutant Shp2-induced gastrulation defects

Shp2 is a cytoplasmic protein-tyrosine phosphatase that is essential for normal development. Activating and inactivating mutations have been identified in humans to cause the related Noonan and LEOPARD syndromes, respectively. The cell biological cause of these syndromes remains to be determined. We have used the zebrafish to assess the role of Shp2 in early development. Here, we report that morpholino-mediated knockdown of Shp2 in zebrafish resulted in defects during gastrulation. Cell tracing experiments demonstrated that Shp2 knockdown induced defects in convergence and extension cell movements. In situ hybridization using a panel of markers indicated that cell fate was not affected by Shp2 knock down. The Shp2 knockdown-induced defects were rescued by active Fyn and Yes and by active RhoA. We generated mutants of Shp2 with mutations that were identified in human patients with Noonan or LEOPARD Syndrome and established that Noonan Shp2 was activated and LEOPARD Shp2 lacked catalytic protein-tyrosine phosphatase activity. Expression of Noonan or LEOPARD mutant Shp2 in zebrafish embryos induced convergence and extension cell movement defects without affecting cell fate. Moreover, these embryos displayed craniofacial and cardiac defects, reminiscent of human symptoms. Noonan and LEOPARD mutant Shp2s were not additive nor synergistic, consistent with the mutant Shp2s having activating and inactivating roles in the same signaling pathway. Our results demonstrate that Shp2 is required for normal convergence and extension cell movements during gastrulation and that Src family kinases and RhoA were downstream of Shp2. Expression of Noonan or LEOPARD Shp2 phenocopied the craniofacial and cardiac defects of human patients. The finding that defective Shp2 signaling induced cell movement defects as early as gastrulation may have implications for the monitoring and diagnosis of Noonan and LEOPARD syndrome.     

Shp2 Knockdown and Noonan/LEOPARD Mutant Shp2–Induced Gastrulation Defects

Shp2 is a cytoplasmic protein-tyrosine phosphatase that is essential for normal development. Activating and inactivating mutations have been identified in humans to cause the related Noonan and LEOPARD syndromes, respectively. The cell biological cause of these syndromes remains to be determined. We have used the zebrafish to assess the role of Shp2 in early development. Here, we report that morpholino-mediated knockdown of Shp2 in zebrafish resulted in defects during gastrulation. Cell tracing experiments demonstrated that Shp2 knockdown induced defects in convergence and extension cell movements. In situ hybridization using a panel of markers indicated that cell fate was not affected by Shp2 knock down. The Shp2 knockdown–induced defects were rescued by active Fyn and Yes and by active RhoA. We generated mutants of Shp2 with mutations that were identified in human patients with Noonan or LEOPARD Syndrome and established that Noonan Shp2 was activated and LEOPARD Shp2 lacked catalytic protein-tyrosine phosphatase activity. Expression of Noonan or LEOPARD mutant Shp2 in zebrafish embryos induced convergence and extension cell movement defects without affecting cell fate. Moreover, these embryos displayed craniofacial and cardiac defects, reminiscent of human symptoms. Noonan and LEOPARD mutant Shp2s were not additive nor synergistic, consistent with the mutant Shp2s having activating and inactivating roles in the same signaling pathway. Our results demonstrate that Shp2 is required for normal convergence and extension cell movements during gastrulation and that Src family kinases and RhoA were downstream of Shp2. Expression of Noonan or LEOPARD Shp2 phenocopied the craniofacial and cardiac defects of human patients. The finding that defective Shp2 signaling induced cell movement defects as early as gastrulation may have implications for the monitoring and diagnosis of Noonan and LEOPARD syndrome.     

Gain-of-Function Mutations in RIT1 Cause Noonan Syndrome,a RAS/MAPK Pathway Syndrome

RAS GTPases mediate a wide variety of cellular functions, including cell proliferation, survival, and differentiation. Recent studies have revealed that germline mutations and mosaicism for classical RAS mutations, including those in HRAS, KRAS, and NRAS, cause a wide spectrum of genetic disorders. These include Noonan syndrome and related disorders (RAS/mitogen-activated protein kinase [RAS/MAPK] pathway syndromes, or RASopathies), nevus sebaceous, and Schimmelpenning syndrome. In the present study, we identified a total of nine missense, nonsynonymous mutations in RIT1, encoding a member of the RAS subfamily, in 17 of 180 individuals (9%) with Noonan syndrome or a related condition but with no detectable mutations in known Noonan-related genes. Clinical manifestations in the RIT1-mutation-positive individuals are consistent with those of Noonan syndrome, which is characterized by distinctive facial features, short stature, and congenital heart defects. Seventy percent of mutation-positive individuals presented with hypertrophic cardiomyopathy; this frequency is high relative to the overall 20% incidence in individuals with Noonan syndrome. Luciferase assays in NIH 3T3 cells showed that five RIT1 alterations identified in children with Noonan syndrome enhanced ELK1 transactivation. The introduction of mRNAs of mutant RIT1 into 1-cell-stage zebrafish embryos was found to result in a significant increase of embryos with craniofacial abnormalities, incomplete looping, a hypoplastic chamber in the heart, and an elongated yolk sac. These results demonstrate that gain-of-function mutations in RIT1 cause Noonan syndrome and show a similar biological effect to mutations in other RASopathy-related genes.     

CFC syndrome: a syndrome distinct from Noonan syndrome

We report two children with a common pattern of birth defects. Both have very sparse, curly hair, nystagmus and mental retardation. The first one has Noonan syndrome habitus associated with keratosis plantaris and nystagmus; the second one has a slightly Noonan-like face, macrocephaly, keratosis pilaris, and hypertrophic cardiomyopathy. They represent the extreme of a spectrum of congenital defects recently reported independently as CFC syndrome by Reynolds and as "Noonan-like short stature syndrome with sparse hair" by Baraitser and Patton. The clinical features are reviewed and the autonomy of the syndrome with regards to Noonan syndrome, is disputed, since every sign seems to occur independently in Noonan syndrome. The father of the second case probably has a minor syndrome expression, pointing to probable autosomal dominant inheritance.     

Deletion of the proximal long arm of chromosome 3 in an infant with features of Turner syndrome

A case of deletion of the proximal one-fourth of chromosome 3 long arm is described. While the Turner syndrome phenotype was present neonatally, the patient has no structural or numerical abnormality of the sex chromosomes, and thus may represent an autosomal deletion with a clinical picture similar to Turner syndrome. Her score on the Noonan syndrome index of Duncan et al. (1981) is 27%, making Noonan syndrome unlikely.     

Attention-deficit/hyperactivity disorder and alexithymia: a pilot study

Although the relationship between alexithymia and psychopathology has been studied extensively in adults, research is lacking on alexithymia in childhood psychopathology. The aim of this study was to investigate the relationship between alexithymia and attention-deficit/hyperactivity disorder (ADHD). The Italian version of the Alexithymia Questionnaire for Children was administered to a sample of 50 children with a DSM-IV diagnosis of ADHD, as assessed by means of the K-SADS PL, and to 100 healthy, age- and sex-matched children without ADHD. The total alexithymia score as well as the difficulty in identifying feelings (DIF) and externally oriented thinking factors were significantly associated with ADHD. The total alexithymia score, the DIF, and the difficulty in describing feelings factors were also significantly associated with symptoms of hyperactivity/impulsivity. No significant relationship between alexithymia and inattentiveness symptoms emerged. Results provide preliminary data on the relationship between alexithymia and ADHD. Findings point to an association between difficulty in identifying emotions and hyperactivity/impulsivity. Future studies conducted on larger patient samples, as well as longitudinal designs, are warranted to confirm our findings.     

The Associations of Psychological Stress with Depressive and Anxiety Symptoms among Chinese Bladder and Renal Cancer Patients: The Mediating Role of Resilience

BackgroundThe prevalence of depressive and anxiety symptoms and their associated factors in bladder and renal cancer patients are not well evaluated in China. Given the growing attention to positive psychological constructs in the field of oncology, it is necessary to explore the effects of these constructs on depressive and anxiety symptoms. This study aims to explore the associations of psychological stress with depressive and anxiety symptoms among Chinese bladder and renal cancer patients and the mediating role of resilience in these relationships.MethodsA cross-sectional study was conducted at the First Affiliated Hospital of China Medical University in Liaoning province. 327 bladder cancer patients and 268 renal cancer patients completed questionnaires on demographic variables, the Center for Epidemiologic Studies Depression Scale, Zung Self-Rating Anxiety Scale, Resilience Scale-14, and Perceived Stress Scale-10 during the period from July 2013 to July 2014. Hierarchical linear regression analyses were performed to explore the mediating role of resilience.ResultsThe prevalence of depressive and anxiety symptoms was 78.0% and 71.3% in bladder cancer patients, and 77.6% and 68.3% in renal cancer patients. Psychological stress was positively related to depressive and anxiety symptoms, while resilience was negatively related to these symptoms. Resilience partially mediated the relations of psychological stress with depressive and anxiety symptoms.ConclusionsThe high prevalence of depressive and anxiety symptoms among Chinese bladder and renal cancer patients should receive more attention from medical institutions and government agencies. In addition to reducing depressive and anxiety symptoms, resilience development should be included in depression and anxiety prevention and treatment strategies in China.     

Morningness-eveningness and social anxiety symptoms: the influence of depression symptoms on the indirect effect through punishment sensitivity and experiential avoidance

Social anxiety has recently been linked to morningness-eveningness; however, the psychological mechanisms underlying this relationship are not well known. As such, the purpose of the current study is to propose a model by which morningness-eveningness is related to social anxiety symptoms through punishment sensitivity and experiential avoidance within an adult American, community sample recruited via Amazon’s Mechanical Turk (MTurk). It was hypothesized that experiential avoidance and punishment sensitivity would be associated with increased social anxiety symptoms and that morningness-eveningness would be negatively related to social anxiety symptoms. Furthermore, eveningness was hypothesized to be associated with increased punishment sensitivity and in turn, greater experiential avoidance. Lastly, the relationship between morningness-eveningness and social anxiety was hypothesized to be mediated by punishment sensitivity among the group with high depression levels, but not among the group with lesser depression symptoms. The results indicated that eveningness was related to social anxiety symptoms through experiential avoidance, and that depression symptoms influenced the relationship between morningness-eveningness and punishment sensitivity such that, in those high in depression symptoms, there was a significant association between eveningness and punishment sensitivity, but not among those with lower depression levels. The study findings build upon existing chronobiological research and addresses inconsistencies in previous literature.     

Alexithymia and the Processing of Emotional Facial Expressions (EFEs): Systematic Review, Unanswered Questions and Further Perspectives

Alexithymia is characterized by difficulties in identifying, differentiating and describing feelings. A high prevalence of alexithymia has often been observed in clinical disorders characterized by low social functioning. This review aims to assess the association between alexithymia and the ability to decode emotional facial expressions (EFEs) within clinical and healthy populations. More precisely, this review has four main objectives: (1) to assess if alexithymia is a better predictor of the ability to decode EFEs than the diagnosis of clinical disorder; (2) to assess the influence of comorbid factors (depression and anxiety disorder) on the ability to decode EFE; (3) to investigate if deficits in decoding EFEs are specific to some levels of processing or task types; (4) to investigate if the deficits are specific to particular EFEs. Twenty four studies (behavioural and neuroimaging) were identified through a computerized literature search of Psycinfo, PubMed, and Web of Science databases from 1990 to 2010. Data on methodology, clinical characteristics, and possible confounds were analyzed. The review revealed that: (1) alexithymia is associated with deficits in labelling EFEs among clinical disorders, (2) the level of depression and anxiety partially account for the decoding deficits, (3) alexithymia is associated with reduced perceptual abilities, and is likely to be associated with impaired semantic representations of emotional concepts, and (4) alexithymia is associated with neither specific EFEs nor a specific valence. These studies are discussed with respect to processes involved in the recognition of EFEs. Future directions for research on emotion perception are also discussed.     

Response to Propranolol and Diazepam in Somatic and Psychic Anxiety

A total of 12 chronically anxious psychiatric outpatients were treated with racemic propranolol (Inderal), diazepam (Valium), and placebo for one week each, using a balanced cross-over experimental design. Six patients had predominantly somatic anxiety, complaining mostly of bodily symptoms, and six had mainly psychic anxiety, complaining primarily of psychological symptoms. Clinical ratings of anxiety were made by patient and psychiatrist after each treatment. Though diazepam was in general more effective than propranolol or placebo in relieving anxiety, propranolol was more effective than placebo in patients with somatic anxiety but not in those with psychic anxiety. We suggest that propranolol should be reserved for patients whose anxiety symptoms are mainly somatic.     

The prevalence and pulmonary consequences of anxiety and depressive disorders in patients with asthma

The aim of this study was to determine the prevalence of anxiety and depression symptoms in outpatients with treated asthma and to determine the influence of anxiety and depression symptoms on lung function and asthma symptoms. The study was conducted in the pulmonary clinic of the Department of Pulmonary Diseases, Osijek University Hospital Centre, on 200 outpatients with asthma, aged 18-50 years, of which there were 65.5% women and 35.5% men. Each patient underwent a clinical examination with an extensive anamnesis and lung auscultation. The lung function was tested by spirometry. Demographic data and data on general and socioeconomic characteristics were evaluated using a questionnaire created internally for the purposes of this research, psychological status was assessed by HAD questionnaire, and Q test was used as a measure of asthma control. Based on the HAD questionnaire, 44.5% of asthma patients met the criteria for anxiety, and 24.5% of asthma patients met the criteria for depression. There was no significant correlation between asthma symptoms and the degree of anxiety or depression, while the pulmonary function of asthma patients negatively correlated with the degree of anxiety and depression. Pulmonary function in asthma patients with symptoms of anxiety and depression was significantly poorer than in asthma patients without anxiety and/or depression symptoms. The results show that among asthma patients there are large number of those who have symptoms of anxiety and depression. Asthma patients with symptoms of anxiety and depression have poorer lung function than patients with only asthma symptoms, however there is no significant correlation between the lung function and symptoms of asthma. We have confirmed that patients with anxiety symptoms visit general practitioners or EMS significantly more when compared to patients with depression symptoms.