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This article provides an examination of the evolution of networking in China and the Arab world over two decades and provides an update to, and new insights arising from, an article called Guanxi and Wasta; A Comparison, published in Thunderbird International Business Review in 2006. This article highlights the continued theoretical and practical importance of guanxi in China and wasta in the Arab World and how research, understanding, and practice of guanxi and wasta have developed over 20 years including integrating (limited) focus on diversity, equity, and inclusion. As well as presenting the 'dark' and 'light' sides of guanxi and wasta, the article explores how institutional development has weakened use of informal networks but to a greater extent for guanxi than wasta. The article provides practical insights into managing informal networks in international business. The article suggests future directions for research and practice in guanxi and wasta in respect to responding to major foci of business internationally including digitalisation, artificial intelligence, and diversity and inclusion.
Prior research on the victim-offender overlap has largely focused on Western societies and community-based settings, with limited attention to juvenile correctional facilities in East Asian contexts. This study examines institutional misconduct, victimization, and the victim-offender overlap in Taiwan's juvenile correctional facilities using data collected in 2015 from a nationwide survey of incarcerated youth. Drawing on importation and deprivation perspectives, we employ bivariate probit regression models to assess the joint association between misconduct and victimization and to identify shared and distinct risk factors. Results indicate a significant overlap between institutional misconduct and victimization. Gang membership, prior victimization in society, and in-facility environmental stress are significantly associated with both outcomes, supporting the relevance of both theoretical perspectives. These findings highlight the importance of addressing pre-incarceration vulnerabilities and institutional conditions in efforts to reduce misconduct and improve safety in juvenile correctional facilities.
Despite the substantial interest in mass imprisonment, limited research has studied how mass incarceration has occurred across the 3000 city and county jails in the United States. Using Bureau of Justice Statistics surveys and censuses of US jails, we investigate patterns of jail construction over the last 50 years and ask whether these infrastructural changes represent expanding carceral capacity or simply capacity restructuring, whereby jails were consolidated and renovated rather than multiplied. Despite consistent numbers of jails over time, jail populations have increased substantially, suggesting that mass incarceration has functioned differently in jails than in prisons. We posit a theory of "jailization," whereby jails have permeated the membranes of different arms of the criminal legal system to serve as a catchment center or "lobby," and argue for dedicated studies of jails' unique and flexible roles. This contributes to the literature on penal change by showing that changes to jails during the era of mass incarceration look markedly different than that of prisons, underscoring the importance of studying them as unique criminal legal institutions.
BACKGROUND:Tumor evolution is a spatiotemporal dynamic process orchestrated by the interplay of genetic mutations, epigenetic reprogramming, and bidirectional microenvironmental interactions, which collectively generate the phenotypic diversity necessary for cancer progression, metastasis, and therapeutic resistance. Foundational models - linear, branched, neutral, and parallel evolution - provide complementary, albeit incomplete, frameworks to illustrate how tumors diversify through the accumulation of gradual mutations or catastrophic genomic events (e.g., chromosomal instability, disruptions in topologically associating chromatin domains). The applicability of each model is context-dependent, shaped by the specific selective pressures present across space and time. These evolutionary processes are fundamental to clonal heterogeneity, immune evasion, and the establishment of adaptive cellular ecosystems. CONTENT:Somatic mutations, including single-base substitutions and structural variations, function as evolutionary barcodes that trace tumor lineage. Beyond the genetic code, epigenetic dysregulation-encompassing DNA hypermethylation that silences tumor suppressors and dynamic RNA modifications (e.g., m6A) that fine-tune mRNA stability-confers a layer of phenotypic plasticity. This allows for rapid, often reversible, adaptation to therapeutic and microenvironmental stresses without altering the underlying DNA sequence, thereby generating non-genetic heterogeneity. Non-coding RNAs, including microRNAs that post-transcriptionally fine-tune gene expression and circular RNAs that can function as miRNA sponges or encode peptides, comprise a critical regulatory network. They orchestrate oncogenic signaling, metastasis, and immune suppression, often in response to signals from the tumor microenvironment, thereby integrating diverse cues to shape evolutionary trajectories. The tumor microenvironment transcends a passive supportive role to act as a dynamic and decisive orchestrator of evolution: hypoxia stabilizes HIFs to drive angiogenic and metabolic reprogramming; lactate accumulation in acidic niches polarizes immunosuppressive macrophages; and neural-tumor crosstalk promotes perineural invasion. These bi-directional interactions create distinct ecological niches that exert spatially heterogeneous selection pressures, fundamentally shaping the clonal landscape. Treatment pressures (e.g., chemotherapy, radiotherapy, immunotherapy, etc.) impose evolutionary bottlenecks, selecting resistant clones and fostering cross-resistance through shared pathways. Emerging technologies - single-cell sequencing, spatial multi-omics, and liquid biopsies - now decode intra-tumoral heterogeneity, map cellular ecosystems, and monitor clonal dynamics in real time and multiple dimensions. CONCLUSION:Integrating evolutionary models with multi-omics data reveals the complexity of tumor adaptation, emphasizing the need for temporally adaptive therapeutic strategies. Current preclinical models inadequately recapitulate human tumor-microenvironment interactions, necessitating advanced systems to bridge this translational gap. Looking forward, the convergence of artificial intelligence and dense, longitudinal biomarker profiling holds the potential to move personalized oncology beyond static genomic matching. The future lies in refining dynamic interventions that simultaneously target the dual pillars of malignancy: the molecular hallmarks of cancer cells and the ecological hallmarks of the tumor ecosystem, thereby aiming to control the process of evolution itself.
