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Auto-biological beliefs—beliefs about one’s own biology—are an understudied component of personal identity. Research participants who are led to believe they are biologically vulnerable to affective disorders report more symptoms and less ability to control their mood; however, little is known about the impact of self-originating beliefs about risk for psychopathology, and whether such beliefs correspond to empirically derived estimates of actual vulnerability. Participants in a neuroimaging study (n = 1256) completed self-report measures of affective symptoms, perceived stress, and neuroticism, and an emotional face processing task in the scanner designed to elicit threat responses from the amygdala. A subsample (n = 63) additionally rated their own perceived neural response to threat (i.e., amygdala activity) compared to peers. Self-ratings of neural threat response were uncorrelated with actual threat-related amygdala activity measured via BOLD fMRI. However, self-ratings predicted subjective distress across a variety of self-report measures. In contrast, in the full sample, threat-related amygdala activity was uncorrelated with self-report measures of affective distress. These findings suggest that beliefs about one’s own biological threat response—while unrelated to measured neural activation—may be informative indicators of psychological functioning.
Childhood maltreatment is robustly associated with increased risk of poor mental health outcome and changes in brain function. The authors investigated whether childhood experience of abuse (e.g. physical, emotional and sexual abuse) and neglect (physical and emotional deprivation) was differentially associated with neural reactivity to threat.
Participants were drawn from an existing study and allocated to one of four groups based on self-report of childhood maltreatment experience: individuals with childhood abuse experiences (n = 70); individuals with childhood neglect experiences (n = 87); individuals with combined experience of childhood abuse and neglect (n = 50); and non-maltreated individuals (n = 207) propensity score matched (PSM) on gender, age, IQ, psychopathology and SES. Neural reactivity to facial cues signalling threat was compared across groups, allowing the differential effects associated with particular forms of maltreatment experience to be isolated.
Brain imaging analyses indicated that while childhood abuse was associated with heightened localised threat reactivity in ventral amygdala, experiences of neglect were associated with heightened reactivity in a distributed cortical fronto-parietal network supporting complex social and cognitive processing as well as in the dorsal amygdala. Unexpectedly, combined experiences of abuse and neglect were associated with hypo-activation in several higher-order cortical regions as well as the amygdala.
Different forms of childhood maltreatment exert differential effects in neural threat reactivity: while the effects of abuse are more focal, the effects of neglect and combined experiences of abuse are more distributed. These findings are relevant for understanding the range of psychiatric outcomes following childhood maltreatment and have implications for intervention.
Hill (Twin Research and Human Genetics, Vol. 21, 2018, 84–88) presented a critique of our recently published paper in Cell Reports entitled ‘Large-Scale Cognitive GWAS Meta-Analysis Reveals Tissue-Specific Neural Expression and Potential Nootropic Drug Targets’ (Lam et al., Cell Reports, Vol. 21, 2017, 2597–2613). Specifically, Hill offered several interrelated comments suggesting potential problems with our use of a new analytic method called Multi-Trait Analysis of GWAS (MTAG) (Turley et al., Nature Genetics, Vol. 50, 2018, 229–237). In this brief article, we respond to each of these concerns. Using empirical data, we conclude that our MTAG results do not suffer from ‘inflation in the FDR [false discovery rate]’, as suggested by Hill (Twin Research and Human Genetics, Vol. 21, 2018, 84–88), and are not ‘more relevant to the genetic contributions to education than they are to the genetic contributions to intelligence’.
UK guidelines recommend routine HIV testing in high prevalence emergency departments (ED) and targeted testing for HBV and HCV. The ‘Going Viral’ campaign implemented opt-out blood-borne virus (BBV) testing in adults in a high prevalence ED, to assess seroprevalence, uptake, linkage to care (LTC) rates and staff time taken to achieve LTC. Diagnosis status (new/known/unknown), current engagement in care, and severity of disease was established. LTC was defined as patient informed plus ⩾1 clinic visit. A total of 6211/24 981 ED attendees were tested (uptake 25%); 257 (4.1%) were BBV positive (15 co-infected), 84 (33%) required LTC. 100/147 (68%) HCV positives were viraemic; 44 (30%) required LTC (13 new, 16 disengaged). 26/54 (48%) HBV required LTC (seven new, 11 disengaged). 16/71 (23%) HIV required LTC (10 new, five disengaged). 26/84 (31%) patients requiring LTC had advanced disease (CD4 <350, APRI (AST-to-Platelet Ratio Index) >1, Fibroscan F3/F4 or liver cancer), including five with AIDS-defining conditions and three hepatocellular carcinomas. There were five BBV-related deaths. BBV prevalence was high (4.1%); most were HCV (2.4%). HIV patients were more successfully and quickly LTC than HBV or HCV patients. ED testing was valuable as one-third of those requiring LTC (new, disengaged or unknown status patients) had advanced disease.
While phantosmia-induced phantogeusia has been described (Ahmed, 20173), the reverse, phantogeusia-induced phantosmia, has not heretofore been described. Such a case is presented.
Case Study: A 39-yr-old left-handed (pathological) male, six years prior to presentation, noted a sudden onset of phantogeusia of roast cooking, pizza, fruit, strawberries, or a sour taste, and shortly thereafter he would develop unpleasant phantosmias which would sometimes combine with the ambient aroma. These would occur 3-10 times per week and would last for the duration of the phantogeusia, for as long as 1-2 hours. Occasionally the phantosmia would occur first and then induce the phantogeusia of asour taste.
Abnormalities in Neurologic examination: Mental status examination: Immediate recall: Digit span: 6 digits forward and 3 digits backwards. CN XI, X: Decreased gag bilaterally. Motor Examination: Drift: left pronator drift with right abductor digiti minimi sign and right cerebellar spooning. Gait Examination: Tandem Gait: unstable. Cerebellar Examination: Holmes Rebound Phenomena: bilaterally positive, left greater than the right. Sensory Examination: Ipswich Touch Test: decreased in left lower extremity. Temperature: decreased in left lower extremity. Rydel-Seiffer Vibratory Test: bilateral upper extremities 5, bilateral lower extremities 3. Reflexes: upper extremities 1+, absent lower extremities. Neuropsychiatric Examination: Go-No-Go Test: 6/6 (normal). Animal Fluency Test: 15 (normal). Clock Drawing Test: 3 (abnormal). Center for Neurologic Study Lability Scale: 16 (Pseudobulbar affect).
Close connection of the tertiary smell and taste integration areas, where smell and taste converge, in the posterior orbitofrontal cortex, anterior to the insular taste cortex, and posterior to the granular orbitofrontal cortex may have allowed activation of memory engrams connecting these two (Rolls, 19944). Alternatively, electrical discharge from the primary taste area may have spread to involve the cortical representation of smell. Since the cortical area involved in the interpretation and hedonics of taste co-localize with the area involving olfactory hedonics, spread from one area to the other area may occur. As a result of electrical discharge (from an epileptiform focus) or as a result of well-connected and developed memory engrams with associated hedonics, phantom tastes may induce phantom smells. Alternatively, this may represent a distorted retronasal smell whereby the olfactory component of the gustatory hallucination causes a discharge of the olfactory epithelium (a pseudoretronasal smell).
Given the above, treatment of those with both phantosmia and phantogeusia may respond to treatment of phantogeusia alone. Under this construct, the phantosmia is the slave of the phantogeusia whereby management of the taste hallucination will thus eliminate the smell hallucination.
Smell and Taste Treatment and Research Foundation.
The experience of childhood maltreatment is a significant risk factor for the development of depression. This risk is particularly heightened after exposure to additional, more contemporaneous stress. While behavioral evidence exists for this relation, little is known about biological correlates of these stress interactions. Identifying such correlates may provide biomarkers of risk for later depression.
Here, we leverage behavioral, experiential, and neuroimaging data from the Duke Neurogenetics Study to identify potential biomarkers of stress exposure. Based on the past research, we were specifically interested in reward-related connectivity and the interaction of early and more recent stress. We examined psychophysiological interactions between the ventral striatum and other brain regions in relation to these stress variables, as well as measures of internalizing symptomatology (n = 926, participant age range = 18–22 years of age).
We found relatively increased reward-related functional connectivity between the left ventral striatum and the medial prefrontal cortex in individuals exposed to greater levels of childhood maltreatment who also experienced greater levels of recent life stress (β = 0.199, p < 0.005). This pattern of functional connectivity was further associated with elevated symptoms of depression (β = 0.089, p = 0.006). Furthermore, using a moderated mediation framework, we demonstrate that this functional connectivity provides a biological link between cumulative stress exposure and internalizing symptomatology.
These findings suggest a novel biomarker linking cumulative stress exposure with the later experience of depressive symptoms. Our results are discussed in the context of past research examining stress exposure in relation to depression.
Cognitive impairment has been identified as an important aspect of major depressive disorder (MDD). We tested two theories regarding the association between MDD and cognitive functioning using data from longitudinal cohort studies. One theory, the cognitive reserve hypothesis, suggests that higher cognitive ability in childhood decreases risk of later MDD. The second, the scarring hypothesis, instead suggests that MDD leads to persistent cognitive deficits following disorder onset. We tested both theories in the Dunedin Study, a population-representative cohort followed from birth to midlife and assessed repeatedly for both cognitive functioning and psychopathology. We also used data from the Environmental Risk Longitudinal Twin Study to test whether childhood cognitive functioning predicts future MDD risk independent of family-wide and genetic risk using a discordant twin design. Contrary to both hypotheses, we found that childhood cognitive functioning did not predict future risk of MDD, nor did study members with a past history of MDD show evidence of greater cognitive decline unless MDD was accompanied by other comorbid psychiatric conditions. Our results thus suggest that low cognitive functioning is related to comorbidity, but is neither an antecedent nor an enduring consequence of MDD. Future research may benefit from considering cognitive deficits that occur during depressive episodes from a transdiagnostic perspective.
B-cell non-Hodgkin lymphoma (B-cell NHL) is the second commonest malignancy in the stomach. We determined the distribution of Helicobacter pylori outer membrane protein Q (HopQ) allelic type, cytotoxin-associated gene (cag)-pathogenicity activity island (cag-PAI) and vacuolation activating cytotoxin A (vacA) genes, respectively, in patients with B-cell NHL. We also compared them with their distribution in non-ulcer dyspepsia (NUD). H. pylori was cultured from gastric biopsy tissue obtained at endoscopy. Polymerase chain reaction was performed. Of 170 patients enrolled, 114 (63%) had NUD and 56 (37%) had B-cell NHL. HopQ type 1 was positive in 66 (58%) in NUD compared with 46 (82%) (P = 0·002) in B-cell NHL; HopQ type 2 was positive in 93 (82%) with NUD compared with 56 (100%) (P < 0·001) in B-cell NHL. Multiple HopQ types were present in 46 (40%) in NUD compared with 46 (82%) (P < 0·001) in B-cell NHL. CagA was positive in 48 (42%) in NUD vs. 50 (89%) (P < 0·001) in B-cell NHL; cagT was positive in 35 (31%) in NUD vs. 45 (80%) (P < 0·001) in B-cell NHL; left end of the cagA gene (LEC)1 was positive in 23 (20%) in NUD vs. 43 (77%) (P < 0·001) in B-cell NHL. VacAs1am1 positive in B-cell NHL in 48 (86%) (P < 0·001) vs. 50 (44%) in NUD, while s1am2 was positive in 20 (17%) in NUD vs. 46 (82%) (P < 0·001) in B-cell NHL. H. pylori strains with multiple HopQ allelic types, truncated cag-PAI evidenced by expression of cagA, cagT and cag LEC with virulent vacAs1 alleles are associated with B-cell NHL development.
Avian influenza virus (AIV) type A subtype H9N2 usually causes mild asymptomatic infections, and is mostly undetected and is, therefore, under-reported. This has allowed the virus to rapidly evolve via mutations and reassortments in its genome with other avian influenza subtypes especially H1N1, H5N1 and H7N3 thereby introducing new variant strains and producing severe disease. It has been reported that the AIV H9N2 donated its internal genes for the devastating 1997 Hong Kong outbreak and furthermore, it may be the cause of the next influenza pandemic. There are many factors such as its wide host range, ability to cross the species barrier, ecological diversity, antiviral resistance and zoonotic importance that make it an excellent candidate for the next influenza pandemic. These and other factors like ineffective vaccination, negative immunological pressures, lack of surveillance, which contribute to its continuous persistence and evolutionary dynamics are discussed in this paper. It is important to take the necessary measures to control and prevent its unchecked circulation to prevent the future outbreaks.