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Biology subjects

Bennett, L. A.

Publications and source records attributed to Bennett, L. A..

4 recordsLinked to original sources

Discrimination of Annonaceae using herbarium leaf reflectance spectra under limited sample size conditions

PremiseHerbarium collections offer an unparalleled archive of plant biodiversity, but their use for species identification through spectral data remains constrained by uncertain effects of preservation histories. This study assesses whether barium specimens can reliably predict species based on its leaf reflectance spectrum, despite variations in age, geographic origin, or conservation method under limited sample size conditions. MethodsWe scanned herbarium specimens of different ages and geographic distribution of 14 species of the pantropical Annonaceae. In addition, we used a second dataset of 9 species where some specimens were conserved in alcohol prior to drying and some not. We used five supervised classification models frequently used for high-dimensional data such as spectroscopy. ResultsAll models achieved high accuracy (>80%) when trained on multiple specimens per species. However, when using only one specimen per species, accuracy varied substantially depending on the taxon. DiscussionOur findings demonstrate that herbarium specimens often retain a strong taxonomic signal in their spectra, however, inter-individual variability affects accuracy in some taxa. These findings confirm the usefulness of herbarium spectroscopy as a non-destructive tool for species identification and offer a promising avenue for digitizing historical biodiversity data into high-dimensional trait space.

plant biology↗

Chronic pain mediated changes in the appetitive value of affective touch in mice

The existence of skin-to-brain circuits for rewarding gentle touch highlight its critical nature across species. However, this gentle affective touch is not always appetitive and can produce aversion or negative affect in disorders such as chronic pain. Sensory neurons expressing the protein MrgprB4 detect gentle stroking in mice and their activation of these neurons known to be positively reinforcing. Here we assess whether activation of channelrhodopsin (ChR2) expressing MrgprB4 afferents signal positively valenced tactile information and whether this is altered in models of chronic pain. We further interrogate how this this sensory information is reflected in the downstream circuits recruited. Optogenetic activation of MrgprB4 lineage afferents was found to be appetitive in control and capsaicin sensitized mice but not nerve injured mice, indicating that the appetitive value is diminished in neuropathic pain. Remarkably, this appetitive value was partially recovered in male nerve injured mice by treatment with the analgesic gabapentin. These behavioral changes were also accompanied by different patterns of neuronal activity throughout the brain, including altered activation of sites that receive direct projections from the spinal cord between sham and nerve injured mice. Together, these findings highlight the plastic nature of these affective tactile circuits under pathological conditions.

neuroscience↗

Spinal reconsolidation engages non-ionotropic NMDA receptor signaling to reverse pain hypersensitivity

Reconsolidation enables the activity-dependent modification of memory traces and has been used to reverse addiction, fear memory, and pain hypersensitivity in animal models. We demonstrate that non-ionotropic NMDA receptor signalling in the spinal dorsal horn is sufficient to reverse pain hypersensitivity and necessary for pain modulation by spinal reconsolidation. These findings reveal a key process by which reconsolidation disrupts memory traces that may be exploited in the treatment of pain and other disorders.

neuroscience↗

Cytoprotective effects of combination of gypenosides and Costus pictus D.Don extract in BRIN-BD11 β-cells

Ethnopharmacological RelevanceGypenosides and Costus pictus D.Don are used as an anti-diabetic herbal remedy in China and India respectively. However, the synergistic effect of these two extracts on {beta}-cell protection is not yet elucidated. IntroductionIn Type 2 diabetes mellitus (T2DM), pro-inflammatory cytokines and lipotoxicity are known causes of pancreatic {beta}-cell dysfunction and impaired insulin secretion and eventually {beta}-cell death. Thus, any cytoprotective drug supplements can protect the {beta}-cell and may help in T2DM treatment. Gypenosides, extracted from the Chinese medicinal herb Gynostemma pentaphyllum and the leaf extract from an Indian medicinal herb Costus pictus D. Don are used in traditional medicine due to their insulin secretory properties. In our previous studies, both extracts have shown significant cytoprotective effects in insulin-secreting BRIN-BD11 cells. In the present study, we aim to investigate the synergistic effects of a combination of these extracts on BRIN-BD11 {beta}-cell protection. MethodsCombination of extracts was prepared by adding Gypenosides with Costus pictus at 2:1 to a concentration of 18.75mg/ml. Cell viability was determined by MTT assay following treatment with combination and/or palmitate and cytokine cocktail for 24-48h. Following 24h treatment, proliferation was measured by Ki67 staining and cytoprotective gene expression was quantified by qPCR. ResultsCombination treatment of 25{micro}g/ml enhanced cell viability both at 24h (n=8; P<0.05) and 48h (n=8; P<0.0001) treatment. Over 24h, combination treatment (25&12.5 {micro}g/ml) showed a significant protective effect against 125{micro}M and 250{micro}M palmitate induced (P<0.0001) and cytokine cocktail-(TNF 1000U, IL-1{beta} 50U & IFN{gamma} 1000U) (P<0.0001 & P<0.01 respectively) induced toxicity. Combination treatment over 24h increased expression of antioxidant genes Nrf2 (P<0.001), Cat (P<0.001) and Sod1 (P<0.05) along with pro-proliferative Erk1 (P<0.01) while pro-inflammatory Nfkb1 expression was reduced(P<0.001). ConclusionThe results suggest that a combination of gypenosides and costus pictus may protect {beta}-cells against inflammatory cytokines and lipotoxicity caused by saturated free fatty acids associated with obesity and diabetes.

pharmacology and toxicology↗