Neurophysiological mechanisms underlying face processing within and beyond the temporal cortical visual areas.

The ways in which information about faces is represented and stored in the temporal lobe visual areas of primates, as shown by recordings from single neurons in macaques, are considered. Some neurons that respond primarily to faces are found in the cortex in the anterior part of the superior temporal sulcus (in which neurons are especially likely to be tuned to facial expression and to face movement involved in gesture), and in the TE areas more ventrally forming the inferior temporal gyrus (in which neurons are more likely to have responses related to the identity of faces). Quantitative studies of the responses of the neurons that respond differently to the faces of different individuals show that information about the identity of the individual is represented by the responses of a population of neurons, that is, ensemble encoding rather than 'grandmother cell' encoding is used. It is argued that this type of tuning is a delicate compromise between very fine tuning, which has the advantage of low interference in neuronal network operations but the disadvantage of losing the useful properties (such as generalization, completion and graceful degradation) of storage in neuronal networks, and broad tuning, which has the advantage of allowing these properties of neuronal networks to be realized but the disadvantage of leading to interference between the different memories stored in an associative network. There is evidence that the responses of some of these neurons are altered by experience so that new stimuli become incorporated in the network. It is shown that the representation that is built in temporal cortical areas shows considerable invariance for size, contrast, spatial frequency and translation. Thus the representation is in a form which is particularly useful for storage and as an output from the visual system. It is also shown that one of the representations that is built is object based, which is suitable for recognition and as an input to associative memory, and that another is viewer centred, which is appropriate for conveying information about gesture. Ways are considered in which such cortical representations might be built by competitive self-organization aided by back projections in the multi-stage cortical processing hierarchy which has convergence from stage to stage.     

Responses of Primate Taste Cortex Neurons to the Astringent Tastant Tannic Acid

In order to advance knowledge of the neural control of feeding,we investigated the cortical representation of the taste oftannic acid, which produces the taste of astringency. It isa dietary component of biological importance particularly toarboreal primates. Recordings were made from 74 taste responsiveneurons in the orbitofrontal cortex. Single neurons were foundthat were tuned to respond to 0.001 M tannic acid, and representeda subpopulation of neurons that was distinct from neurons responsiveto the tastes of glucose (sweet), NaCl (salty), HCI (sour),quinine (bitter) and monosodium glutamate (umami). In addition,across the population of 74 neurons, tannic acid was as wellrepresented as the tastes of NaCI, HCI quinine or monosodiumglutamate. Multidimensional scaling analysis of the neuronalresponses to the tastants indicates that tannic acid lies outsidethe boundaries of the four conventional taste qualities (sweet,sour, bitter and salty). Taken together these data indicatethat the astringent taste of tannic acid should be consideredas a distinct taste quality, which receives a separate representationfrom sweet, salt, bitter and sour in the primate cortical tasteareas. Chem. Senses 21: 135–145, 1996.     

Hepatitis C Transmission and Treatment in Contact Networks of People Who Inject Drugs

Hepatitis C virus (HCV) chronically infects over 180 million people worldwide, with over 350,000 estimated deaths attributed yearly to HCV-related liver diseases. It disproportionally affects people who inject drugs (PWID). Currently there is no preventative vaccine and interventions feature long treatment durations with severe side-effects. Upcoming treatments will improve this situation, making possible large-scale treatment interventions. How these strategies should target HCV-infected PWID remains an important unanswered question. Previous models of HCV have lacked empirically grounded contact models of PWID. Here we report results on HCV transmission and treatment using simulated contact networks generated from an empirically grounded network model using recently developed statistical approaches in social network analysis. Our HCV transmission model is a detailed, stochastic, individual-based model including spontaneously clearing nodes. On transmission we investigate the role of number of contacts and injecting frequency on time to primary infection and the role of spontaneously clearing nodes on incidence rates. On treatment we investigate the effect of nine network-based treatment strategies on chronic prevalence and incidence rates of primary infection and re-infection. Both numbers of contacts and injecting frequency play key roles in reducing time to primary infection. The change from “less-” to “more-frequent” injector is roughly similar to having one additional network contact. Nodes that spontaneously clear their HCV infection have a local effect on infection risk and the total number of such nodes (but not their locations) has a network wide effect on the incidence of both primary and re-infection with HCV. Re-infection plays a large role in the effectiveness of treatment interventions. Strategies that choose PWID and treat all their contacts (analogous to ring vaccination) are most effective in reducing the incidence rates of re-infection and combined infection. A strategy targeting infected PWID with the most contacts (analogous to targeted vaccination) is the least effective.     

The effect of large portion sizes on energy intake is sustained for 11 days

Objective: A previous study showed that increasing the portion sizes of all foods led to an increase in energy intake that was sustained over 2 days. The objective of the present study was to determine whether participants would compensate for excess energy intake or continue to overeat when portion sizes were increased for 11 days. Research Methods and Procedures: Participants in the study were 23 normal‐weight and overweight participants (10 women and 13 men). All of their foods and caloric beverages were provided during two different periods of 11 consecutive days, which were separated by a 2‐week interval. During one period, standard portions of all items were served; during the other, all portion sizes were increased by 50%. Results: The 50% increase in portion sizes resulted in a mean increase in daily energy intake of 423 ± 27 kcal (p < 0.0001), which did not differ significantly between women and men. This increase was sustained for 11 days and did not decline significantly over time, leading to a mean cumulative increase in intake of 4636 ± 532 kcal. A significant effect of portion size on intake was seen at all meals and in all categories of foods except fruit (as a snack) and vegetables. The effect of portion size on intake was not influenced by the body weight status of participants. Discussion: These results strengthen the evidence suggesting that increased portions contribute to the overconsumption of energy and to excess body weight.     

Heifer nutrition during early- and mid-pregnancy alters fetal growth trajectory and birth weight

Maternal nutrient intake during gestation can alter fetal growth. Whilst this has been studied extensively in the sheep, less is known about effects in the bovine. Composite-breed beef heifers were allocated to either a high (H/? = 76 MJ metabolisable energy (ME) and 1.4 kg crude protein (CP)) or low (L/? = 62 MJ ME and 0.4 kg CP daily) nutritional treatment at artificial insemination. Half of each nutritional group changed to an opposite nutritional group at the end of the first trimester (?/H = 82 MJ ME and 1.4 kg CP; ?/L = 62 MJ ME and 0.4 kg CP daily), resulting in 4 treatment groups: HH (n = 16); HL (n = 19); LH (n = 17); LL (n = 19). During the third trimester all heifers were fed the same diets. Fetuses were measured at 4-weekly intervals beginning at day 39 of gestation. Calves were also measured at birth for physical body variables. Low maternal nutrient intake was associated with decreased crown-rump length at day 39 (P < 0.01) and increased thoracic diameter at day 95 (P < 0.01). Umbilical cord diameter was reduced in L/? fetuses in the first trimester (P < 0.05) but was greater in ?/L fetuses in the second trimester compared to their respective H counterparts (P < 0.05). Calf birth weight was decreased in association with ?/L maternal diets (P < 0.05). In conclusion, fetal development of cattle may be affected by maternal nutrition as early as day 39 of gestation. This may be followed by either compensatory fetal growth, or alternatively, preferential fetal tissue growth that is dependant upon maternal nutrition. Clearly, calf birth weight may be altered by maternal nutrition during mid-gestation.     

Modulation of tissue-specific immune response to cardiac myosin can prolong survival of allogeneic heart transplants

The role of immune response to tissue-specific Ags in transplant rejection is poorly defined. We have previously reported that transplantation of cardiac allografts triggers a CD4(+) Th1 cell response to cardiac myosin (CM), a major contractile protein of the heart, and that pretransplant activation of proinflammatory CM-specific T cells accelerates rejection. In this study, we show that administration of CM together with IFA (CM/IFA) can prevent acute rejection of an allogeneic heart transplant. Prolongation of cardiac graft survival is associated with activation of CM- and allo-specific T cells secreting type 2 cytokines (IL-4, IL-5) and reduction of the frequency of proinflammatory IFN-gamma-secreting (type 1) alloreactive T cells. Blocking of IL-4 cytokine with Abs abrogates the prolongation. CM/IFA treatment prevents acute rejection of MHC class I-mismatched, but not fully mismatched grafts. However, if donor heart is devoid of MHC class II expression, CM-IFA administration delays rejection of fully allogeneic cardiac transplants. This finding suggests that the effect of CM modulation depends on the type (direct vs indirect) and strength of recipient's CD4(+) T cell alloresponse. Our results underscore the important role of host immunity to tissue-specific Ags in the rejection of an allograft. This study demonstrates that modulation of the immune response to a tissue-specific Ag can significantly prolong cardiac allograft survival, an observation that may have important implications for the development of novel selective immune therapies in transplantation.     

The glutathione-deficient, cadmium-sensitive mutant, cad2–1 , of Arabidopsis thaliana is deficient in γ-glutamylcysteine synthetase

This paper reports that the glutathione (GSH)-deficient mutant, cad2–1 , of Arabidopsis is deficient in the first enzyme in the pathway of GSH biosynthesis, γ-glutamylcysteine synthetase (GCS). The mutant accumulates a substrate of GCS, cysteine, and is deficient in the product, γ-glutamylcysteine. In vitro enzyme assays showed that the cad2–1 mutant has 40% of wild-type levels of GCS activity but is unchanged in the activity of the second enzyme in the pathway, GSH synthetase. The CAD2 locus maps to chromosome 4 and is tightly linked to a gene, GSHA , identified by a previously isolated cDNA. A genomic clone of GSHA complements both the phenotypic and biochemical deficiencies of the cad2–1 mutant. The nucleotide sequence of the gene has been determined and, in the mutant, this gene contains a 6 bp deletion within an exon. These data demonstrate that the CAD2 gene encodes GCS. The cad2–1 mutation is close to the conserved cysteine which is believed to bind the substrate glutamate and the specific inhibitor L-buthionine-[S,R] sulfoximine (BSO). Both root growth and GCS activity of the cad2–1 mutant was less sensitive than the wild-type to inhibition by BSO, indicating that the mutation may alter the affinity of the inhibitor binding site.