X-Eval: Generalizable Multi-aspect Text Evaluation via Augmented Instruction Tuning with Auxiliary Evaluation Aspects

Natural Language Generation (NLG) typically involves evaluating the generated text in various aspects (e.g., consistency and naturalness) to obtain a comprehensive assessment. However, multi-aspect evaluation remains challenging as it may require the evaluator to generalize to any given evaluation aspect even if it's absent during training. In this paper, we introduce X-Eval, a two-stage instruction tuning framework to evaluate the text in both seen and unseen aspects customized by end users. X-Eval consists of two learning stages: the vanilla instruction tuning stage that improves the model's ability to follow evaluation instructions, and an enhanced instruction tuning stage that exploits the connections between fine-grained evaluation aspects to better assess text quality. To support the training of X-Eval, we collect AspectInstruct, the first instruction tuning dataset tailored for multi-aspect NLG evaluation spanning 27 diverse evaluation aspects with 65 tasks. To enhance task diversity, we devise an augmentation strategy that converts human rating annotations into diverse forms of NLG evaluation tasks, including scoring, comparison, ranking, and Boolean question answering. Extensive experiments across three essential categories of NLG tasks: dialogue generation, summarization, and data-to-text coupled with 21 aspects in meta-evaluation, demonstrate that our X-Eval enables even a lightweight language model to achieve a comparable if not higher correlation with human judgments compared to the state-of-the-art NLG evaluators, such as GPT-4.Comment: 17 pages, 5 figures, 14 table

Epiphytic bryophyte biomass estimation on tree trunks and upscaling in tropical montane cloud forests

Epiphytic bryophytes (EB) are some of the most commonly found plant species in tropical montane cloud forests, and they play a disproportionate role in influencing the terrestrial hydrological and nutrient cycles. However, it is difficult to estimate the abundance of EB due to the nature of their “epiphytic” habitat. This study proposes an allometric scaling approach implemented in twenty-one 30 × 30 m plots across an elevation range in 16,773 ha tropical montane cloud forests of northeastern Taiwan to measure EB biomass, a primary metric for indicating plant abundance and productivity. A general allometry was developed to estimate EB biomass of 100 cm2 circular-shaped mats (n = 131) with their central depths. We developed a new point-intercept instrument to rapidly measure the depths of EB along tree trunks below 300 cm from the ground level (sampled stem surface area (SSA)) (n = 210). Biomass of EB of each point measure was derived using the general allometry and was aggregated across each SSA, and its performance was evaluated. Total EB biomass of a tree was estimated by referring to an in-situ conversion model and was interpolated for all trees in the plots (n = 1451). Finally, we assessed EB biomass density at the plot scale of the study region. The general EB biomass-depth allometry showed that the depth of an EB mat was a salient variable for biomass estimation (R2 = 0.72, p < 0.001). The performance of upscaling from mats to SSA was satisfactory, which allowed us to further estimate mean (±standard deviation) EB biomass of the 21 plots (272 ± 104 kg ha−1). Since a significant relationship between tree size and EB abundance is commonly found, regional EB biomass may be mapped by integrating our method and three-dimensional remotely sensed airborne data

Liver angiosarcoma, a rare liver malignancy, presented with intraabdominal bleeding due to rupture- a case report

Liver angiosarcoma is a rare disease, however it still ranks as the third of most common primary liver maligancies. The prognosis of liver angiosarcoma is very poor with almost all patients with this kind of disease die within 2 years after diagnosis. No specific symptoms and signs are closely associated with this disease. Here, we report a case presenting shock status at first due to rupture of liver angiosarcoma- induced internal bleeding. After emergent transarterial embolization (TAE), she received partial hepatectomy two weeks later. 4 months after operation, she is still with a good performance status without obvious recurrence or metastasis identified

Examination of effects of GSK3β phosphorylation, β-catenin phosphorylation, and β-catenin degradation on kinetics of Wnt signaling pathway using computational method

<p>Abstract</p> <p>Background</p> <p>Recent experiments have explored effects of activities of kinases other than the well-studied GSK3β, in wnt pathway signaling, particularly at the level of β-catenin. It has also been found that the kinase PKA attenuates β-catenin degradation. However, the effects of these kinases on the level and degradation of β-catenin and the resulting downstream transcription activity remain to be clarified. Furthermore, the effect of GSK3β phosphorylation on the β-catenin level has not been examined computationally. In the present study, the effects of phosphorylation of GSK3β and of phosphorylations and degradation of β-catenin on the kinetics of the wnt signaling pathway were examined computationally.</p> <p>Methods</p> <p>The well-known computational Lee-Heinrich kinetic model of the wnt pathway was modified to include these effects. The rate laws of reactions in the modified model were solved numerically to examine these effects on β-catenin level.</p> <p>Results</p> <p>The computations showed that the β-catenin level is almost linearly proportional to the phosphorylation activity of GSK3β. The dependence of β-catenin level on the phosphorylation and degradation of free β-catenin and downstream TCF activity can be analyzed with an approximate, simple function of kinetic parameters for added reaction steps associated with effects examined, rationalizing the experimental results.</p> <p>Conclusion</p> <p>The phosphorylations of β-catenin by kinases other than GSK3β involve free unphorphorylated β-catenin rather than GSK3β-phosphorylated β-catenin*. In order to account for the observed enhancement of TCF activity, the β-catenin dephosphorylation step is essential, and the kinetic parameters of β-catenin phosphorylation and degradation need to meet a condition described in the main text. These findings should be useful for future experiments.</p

Intracellular mechanisms underlying the nicotinic enhancement of LTP in the rat dentate gyrus

We have previously shown that activation of nicotinic acetylcholine receptors (nAChRs) enhanced long-term potentiation (LTP) in the rat dentate gyrus in vitro via activation of α7 nAChR. In the present studies, mechanisms underlying the acute and chronic nicotinic enhancement of LTP were examined. In particular, the involvement of activation of intracellular kinases was examined using selective kinase antagonists, and the effects of enhancing cholinergic function with positive allosteric modulators of the α7 nAChR and with acetylcholinesterase (AChE) inhibitors were also investigated. Activation of extracellular signal-regulated kinase (ERK) and cAMP-dependent protein kinase (PKA) was found to be involved in the induction of the acute nicotinic enhancement of LTP, although not control LTP. In contrast, activation of the tyrosine kinase Src, Ca2+-calmodulin-dependent protein kinase II, Janus kinase 2 and p38 mitogen-activated protein kinase was not involved in the acute nicotinic enhancement of LTP, although Src activation was necessary for control LTP. Moreover, activation of phosphoinositide 3-kinase was involved in the acute nicotinic enhancement of LTP to a much lesser extent than in control LTP. Chronic nicotine enhancement of LTP was found to be dependent on PKA, ERK and Src kinases. Acute nicotinic enhancement of LTP was occluded by chronic nicotine treatment. The positive allosteric modulator PNU-120596 was found to strongly reduce the threshold for nicotinic enhancement of LTP, an affect mediated via the α7 nAChR as it was blocked by the selective antagonist methyllycaconitine. The AChE inhibitors tacrine and physostigmine enhanced control LTP

The incidence of liver injury in Uyghur patients treated for TB in Xinjiang Uyghur autonomous region, China, and its association with hepatic enzyme polymorphisms nat2, cyp2e1, gstm1 and gstt1.

BACKGROUND AND OBJECTIVE: Of three first-line anti-tuberculosis (anti-TB) drugs, isoniazid is most commonly associated with hepatotoxicity. Differences in INH-induced toxicity have been attributed to genetic variability at several loci, NAT2, CYP2E1, GSTM1and GSTT1, that code for drug-metabolizing enzymes. This study evaluated whether the polymorphisms in these enzymes were associated with an increased risk of anti-TB drug-induced hepatitis in patients and could potentially be used to identify patients at risk of liver injury. METHODS AND DESIGN: In a cross-sectional study, 2244 tuberculosis patients were assessed two months after the start of treatment. Anti-TB drug-induced liver injury (ATLI) was defined as an ALT, AST or bilirubin value more than twice the upper limit of normal. NAT2, CYP2E1, GSTM1 and GSTT1 genotypes were determined using the PCR/ligase detection reaction assays. RESULTS: 2244 patients were evaluated, there were 89 cases of ATLI, a prevalence of 4% 9 patients (0.4%) had ALT levels more than 5 times the upper limit of normal. The prevalence of ATLI was greater among men than women, and there was a weak association with NAT2*5 genotypes, with ATLI more common among patients with the NAT2*5*CT genotype. The sensitivity of the CT genotype for identifying patients with ATLI was 42% and the positive predictive value 5.9%. CT ATLI was more common among slow acetylators (prevalence ratio 2.0 (95% CI 0.95,4.20) )compared to rapid acetylators. There was no evidence that ATLI was associated with CYP2E1 RsaIc1/c1genotype, CYP2E1 RsaIc1/c2 or c2/c2 genotypes, or GSTM1/GSTT1 null genotypes. CONCLUSIONS: In Xinjiang Uyghur TB patients, liver injury was associated with the genetic variant NAT2*5, however the genetic markers studied are unlikely to be useful for screening patients due to the low sensitivity and low positive predictive values for identifying persons at risk of liver injury

When a tree dies in the forest : scaling climate-driven tree mortality to ecosystem water and carbon fluxes

Altres ajuts: COST FP1106 network STReESS.Drought- and heat-driven tree mortality, along with associated insect outbreaks, have been observed globally in recent decades and are expected to increase in future climates. Despite its potential to profoundly alter ecosystem carbon and water cycles, how tree mortality scales up to ecosystem functions and fluxes is uncertain. We describe a framework for this scaling where the effects of mortality are a function of the mortality attributes, such as spatial clustering and functional role of the trees killed, and ecosystem properties, such as productivity and diversity. We draw upon remote-sensing data and ecosystem flux data to illustrate this framework and place climate-driven tree mortality in the context of other major disturbances. We find that emerging evidence suggests that climate-driven tree mortality impacts may be relatively small and recovery times are remarkably fast (~4 years for net ecosystem production). We review the key processes in ecosystem models necessary to simulate the effects of mortality on ecosystem fluxes and highlight key research gaps in modeling. Overall, our results highlight the key axes of variation needed for better monitoring and modeling of the impacts of tree mortality and provide a foundation for including climate-driven tree mortality in a disturbance framework