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California's fruit and nut tree crops represent one-third of the state's cash farm receipts and 70% of U.S. fruit and nut production. Advances in crop biotechnology and genetic engineering could help protect these valuable crops from pests and diseases and improve productivity. However, due to the difficulty of genetically engineering woody tree crops, as well as intellectual property concerns, regulatory hurdles and public perceptions about genetic engineering, biotechnology has not gained a foothold in this area of agriculture. Our survey of published genetic engineering research and issued field trial permits between 2000 and 2011 revealed that citrus and grape are the focus of most current work, and that walnut — not the more widely planted almond — is the focus among nut crops. Matching publicly funded genetic engineering research projects to a survey of the industry's top needs, we found that far less than half of the funded research has focused on the top-identified pest and disease threats. The most promising genetic engineering technology for fruit and nut tree crops may be transgrafting, which could address consumer concerns and benefit growers.

The regulatory implications of using transgrafted plants are currently unknown. A plant's vascular system can selectively transport across graft junctions endogenous elements such as full-length RNAs, sRNAs, proteins, hormones, metabolites and vitamins, and even elicit epigenetic effects, heritably changing the way genes are expressed without changing the actual DNA sequence. However, not all of these elements are transported freely, and they either require specific molecular signals or cellular transporters to aid in their movement through a plant's vascular system.

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The vagal afferent pathway is important in short-term regulation of food intake, and decreased activation of this neural pathway with long-term ingestion of a high-fat diet may contribute to hyperphagic weight gain. We tested the hypothesis that expression of genes encoding receptors for orexigenic factors in vagal afferent neurons are increased by long-term ingestion of a high-fat diet, thus supporting orexigenic signals from the gut. Obesity-prone (DIO-P) rats fed a high-fat diet showed increased body weight and hyperleptinemia compared with low-fat diet-fed controls and high-fat diet-induced obesity-resistant (DIO-R) rats. Expression of the type I cannabinoid receptor and growth hormone secretagogue receptor la in the nodose ganglia was increased in DIO-P compared with low-fat diet-fed controls or DIO-R rats. Shifts in the balance between orexigenic and anorexigenic signals within the vagal afferent pathway may influence food intake and body weight gain induced by high fat diets. cholecystokinin; diet-induced obesity; ghrelin

Introduction: Recurrent major depressive disorder (MDD) has been associated with cognitive impairment and hippocampus atrophy. Additionally, in older adults it is related to increased dementia risk, as well as being dementia's prodromal syndrome. Case Report: A 68-year-old female patient, with a history of MDD beginning in 2014, has been under the care of the Psychogeriatrics service at HC-UFMG. In 2015, she was 60-year-old and underwent her first MRI scan. At that time, the Medial Temporal Atrophy Score (MTA) was 2 and she had a treatment resistant depression (TRD). She began multimodal treatments, including ECT, achieving only partial remission. Since then, the patient had recurrences of depression without the remission of cognitive impairment. In 2021, her MTA Score was still 2 with TDR symptoms. Currently, she is on Venlafaxine 150mg, Mirtazapine 30mg, Lithium 300mg, Olanzapine 5mg, Clonazepam 0.25mg and maintenance ECT every 45 days. The patient remains with cognitive impairment that leads to disabilities but had not significantly progressed. On the other hand, the main impact in functionality is related to depressive symptoms, especially to the loss of interest and apathy. Discussion: This case stands out due to the combination of hippocampal atrophy at a relatively young age and severe depression with cognitive impairment that has not progressed to dementia in 9 years. Severe depression can lead to significant cognitive deficits, as well as, hippocampus atrophy. While depression is related to hippocampus atrophy, it has not been related to TRD in a review study with Voxel-Based Morphometry. Conversely, Alzheimer's Disease is related to MTA ≥2 scores, as well as depressive symptoms. MTA 2 in a person of 60 years of age is not considered normal. When combined with cognitive impairment, these findings are generally related to neurodegeneration. Since both MTA and cognitive deficits were relatively stable, the hypothesis of a cognitive impairment and hippocampus atrophy due to depression were more likely. Conclusions: MDD leads to cognitive impairment in older adults, as well as hippocampus atrophy. Nevertheless, depression and age are important risk factors for dementia and, therefore, a progression to dementia due to a neurodegenerative disease is still possible. [ABSTRACT FROM AUTHOR]

Abstract: Cholecystokinin (CCK), released by lipid in the intestine, initiates satiety by acting at cholecystokinin type 1 receptors (CCK1Rs) located on vagal afferent nerve terminals located in the wall of the gastrointestinal tract. In the present study, we determined the role of the CCK1R in the short term effects of a high fat diet on daily food intake and meal patterns using mice in which the CCK1R gene is deleted. CCK1R−/− and CCK1R+/+ mice were fed isocaloric high fat (HF) or low fat (LF) diets ad libitum for 18 h each day and meal size, meal frequency, intermeal interval, and meal duration were determined. Daily food intake was unaltered by diet in the CCK1R−/− compared to CCK1R+/+ mice. However, meal size was larger in the CCK1R−/− mice compared to CCK1R+/+ mice when fed a HF diet, with a concomitant decrease in meal frequency. Meal duration was increased in mice fed HF diet regardless of phenotype. In addition, CCK1R−/− mice fed a HF diet had a 75% decrease in the time to 1st meal compared to CCK1R+/+ mice following a 6 h fast. These data suggest that lack of the CCK1R results in diminished satiation, causing altered meal patterns including larger, less frequent meals when fed a high fat diet. These results suggest that the CCK1R is involved in regulating caloric intake on a meal to meal basis, but that other factors are responsible for regulation of daily food intake. [Copyright &y& Elsevier]