Measuring Rural Poverty in China: a Case Study Approach

This paper measures rural poverty in Hubei Province and Inner Mongolia in China. The poverty lines we derived by Ravallion's method differ from the official Chinese poverty lines. The official pan-country poverty line underestimates rural poverty in Hubei Province and overestimates rural poverty in Inner Mongolia. Poverty determinants are estimated by Logit as well as Probit models. The study notes that factors such as living in a mountainous area, lack of better irrigation conditions, a large family size, few fixed assets, few land owned and sole dependence on agriculture as a livelihood source would make a rural household more vulnerable to poverty. On the other hand, a rural household whose members are either better educated or trained laborers would statistically be less poor. The growth-redistribution decomposition reveals that for all the three FGT indexes in Hubei province, income growth contributed much to the alleviation of poverty, while the redistribution or inequality effects counteracted the growth effects and worsened poverty. The poverty incidence decomposition results reveal that about one third of the growth effects had been counteracted by the redistribution effects. This implies that future anti-poverty programs should pay more attention to solving the inequality problem in China. Poverty dominance analysis also helps us better understand the poverty situation. It reveals that rural poverty in Inner Mongolia is more severe than that in Hubei, and that poverty incidence in Hubei has lessened from 1997 to 2003, which are the same findings as those drawn from deriving poverty lines.Rural Poverty Line, Poverty Determinants, Growth Redistribution Decomposition, Poverty Dominance, China

N-(Naphthalen-1-yl)benzamide

In the title compound, C17H13NO, the N—H and C=O bonds are anti with respect to each other. The dihedral angle between the naphthalene ring system and the phenyl ring is 86.63 (5)°. In the crystal, N—H⋯O hydrogen bonds link mol­ecules into chains along [010]

Non-genetic adaptive resistance to KRASG12C inhibition: EMT is not the only culprit.

Adaptions to therapeutic pressures exerted on cancer cells enable malignant progression of the tumor, culminating in escape from programmed cell death and development of resistant diseases. A common form of cancer adaptation is non-genetic alterations that exploit mechanisms already present in cancer cells and do not require genetic modifications that can also lead to resistance mechanisms. Epithelial-to-mesenchymal transition (EMT) is one of the most prevalent mechanisms of adaptive drug resistance and resulting cancer treatment failure, driven by epigenetic reprogramming and EMT-specific transcription factors. A recent breakthrough in cancer treatment is the development of KRASG12C inhibitors, which herald a new era of therapy by knocking out a unique substitution of an oncogenic driver. However, these highly selective agents targeting KRASG12C, such as FDA-approved sotorasib (AMG510) and adagrasib (MRTX849), inevitably encounter multiple mechanisms of drug resistance. In addition to EMT, cancer cells can hijack or rewire the sophisticated signaling networks that physiologically control cell proliferation, growth, and differentiation to promote malignant cancer cell phenotypes, suggesting that inhibition of multiple interconnected signaling pathways may be required to block tumor progression on KRASG12C inhibitor therapy. Furthermore, the tumor microenvironment (TME) of cancer cells, such as tumor-infiltrating lymphocytes (TILs), contribute significantly to immune escape and tumor progression, suggesting a therapeutic approach that targets not only cancer cells but also the TME. Deciphering and targeting cancer adaptions promises mechanistic insights into tumor pathobiology and improved clinical management of KRASG12C-mutant cancer. This review presents recent advances in non-genetic adaptations leading to resistance to KRASG12C inhibitors, with a focus on oncogenic pathway rewiring, TME, and EMT

A Breakthrough Brought about by Targeting KRASG12C: Nonconformity Is Punished.

KRAS is the most frequently mutated oncogene in lung carcinomas, accounting for 25% of total incidence, with half of them being KRASG12C mutations. In past decades, KRAS enjoyed the notorious reputation of being untargetable-that is, until the advent of G12C inhibitors, which put an end to this legend by covalently targeting the G12C (glycine to cysteine) substitution in the switch-II pocket of the protein, inhibiting the affinity of the mutant KRAS with GTP and subsequently the downstream signaling pathways, such as Raf/MEK/ERK. KRASG12C-selective inhibitors, e.g., the FDA-approved AMG510 and MRTX849, have demonstrated potent clinical efficacy and selectivity in patients with KRASG12C-driven cancers only, which spares other driver KRAS mutations (e.g., G12D/V/S, G13D, and Q61H) and has ushered in an unprecedented breakthrough in the field in recent decades. However, accumulating evidence from preclinical and clinical studies has shown that G12C-targeted therapeutics as single agents are inevitably thwarted by drug resistance, a persistent problem associated with targeted therapies. A promising strategy to optimize G12C inhibitor therapy is combination treatments with other therapeutic agents, the identification of which is empowered by the insightful appreciation of compensatory signaling pathways or evasive mechanisms, such as those that attenuate immune responses. Here, we review recent advances in targeting KRASG12C and discuss the challenges of KRASG12C inhibitor therapy, as well as future directions

Psychometric Properties of the Chinese version of UPPS-P Impulsive Behavior Scale.

OBJECTIVE: The present study aimed to assess the psychometric properties of a Chinese version of the UPPS-P Impulsive Behavior Scale. The associations between the UPPS-P scale and impulsivity choice, gender, smoking, and drinking status were also assessed. METHODS: A total of 127 adults ranging from 21 to 65 years old participated in the study. Participants were administered with the Chinese version of the UPPS-P Impulsive Behavior Scale, Beck Depression Inventory II (BDI-II), and State-Trait Anxiety Inventory (STAI). Impulsivity choice tasks were also tested including the Delay Discounting Task (DDT), Balloon Analogue Risk Task (BART), and Beads Task (Beads). RESULTS: A new version of the UPPS-P Impulsive Behavior Scale was formed that includes 40 items. The scores of the UPPS-P Impulsive Behavior Scale demonstrated adequate internal consistency on five subscales but less sufficient structure validity in the present sample. In addition, positive urgency was negatively related to the Beads task; negative urgency and positive urgency were positively related to the DDT and BART. Moreover, positive and negative urgency were positively correlated with depression; all five subscales were positively correlated with anxiety; sensation seeking was higher in males than females and in alcohol drinkers than non-drinkers; and lack of premeditation and lack of perseverance were higher in nonsmokers than smokers. CONCLUSIONS: The present study supports the reliability but not the structure validity of the UPPS-P Impulsive Behavior Scale. The impulsivity personality trait assessed by the UPPS-P scale was associated with impulsivity choice, depression, anxiety, gender, and drinking and smoking status. Further studies should be conducted to explore the structure of impulsivity in the Chinese population