At the end of the Korean War, only one third of the approximately 21,000 Chinese prisoners of war were repatriated to Communist China; the remaining two thirds, or more than 14,300 prisoners, went to Nationalist Taiwan in a propaganda coup. These Chinese POWs were at the center of contention in the second half of the war. Utilizing previously untapped archival sources and oral history interviews in China, Taiwan, and the U.S., this study examines how Chinese prisoners, individually and collectively, made divergent decisions in the process of "voluntary repatriation." This research demonstrates that the Chinese prisoners' decisions and actions in UN prisons were directly related to their divergent pre-Korean War experiences in China under both the Nationalist and Communist regimes. The mini-civil war between the pro- Communist and pro-Nationalist prisoners revealed much of the suppressed social tension within China in 1949 and 1950, which exploded into life-and-death struggles in prison camps in Korea. Second, conflicting U.S. policies and the lack of a coherent and consistent policy on Chinese prisoners created much uncertainty and confusion among the prisoners. Out of fear and anxiety, both pro- and anti-Communist prisoners took increasingly aggressive and violent actions against their opponents, and against the prison authorities in the case of the pro-Communist prisoners. Third, while a small number of Nationalist interpreters and teachers hired by General MacArthur and his successors provided the vital communication channel between anti-Communist prisoners and Taipei, most fundamentally, the large number of prisoners controlled by a core of anti-Communist prisoners was a result of U.S. policy mistakes. By the time prisoner repatriation became an issue in armistice talks, the U.S. found itself riding a tiger that was impossible to dismount. In the end, only Chiang Kai-shek could tame the tiger by taking it to Taiwan in triumph

INTRODUCTION: There are limited data on comparative risk of infections with various biologic agents in older adults with inflammatory bowel diseases (IBDs). We aimed to assess the comparative safety of biologic agents in older IBD patients with varying comorbidity burden. METHODS: We used data from a large, national commercial insurance plan in the United States to identify patients 60 years and older with IBD who newly initiated tumor necrosis factor-α antagonists (anti-TNF), vedolizumab, or ustekinumab. Comorbidity was defined using the Charlson Comorbidity Index (CCI). Our primary outcome was infection-related hospitalizations. Cox proportional hazards models were fitted in propensity score-weighted cohorts to compare the risk of infections between the different therapeutic classes. RESULTS: The anti-TNF, vedolizumab, and ustekinumab cohorts included 2,369, 972, and 352 patients, respectively, with a mean age of 67 years. The overall rate of infection-related hospitalizations was similar to that of anti-TNF agents for patients initiating vedolizumab (hazard ratio [HR] 0.94, 95% confidence interval [CI] 0.84-1.04) and ustekinumab (0.92, 95% CI 0.74-1.16). Among patients with a CCI of >1, both ustekinumab (HR: 0.66, 95% CI: 0.46-0.91, p-interaction <0.01) and vedolizumab (HR: 0.78, 95% CI: 0.65-0.94, p-interaction: 0.02) were associated with a significantly lower rate of infection-related hospitalizations compared with anti-TNFs. No difference was found among patients with a CCI of ≤1. DISCUSSION: Among adults 60 years and older with IBD initiating biologic therapy, both vedolizumab and ustekinumab were associated with lower rates of infection-related hospitalizations than anti-TNF therapy for those with high comorbidity burden.

Comorbidities that promote the progression of Alzheimer's disease (AD) remain to be uncovered and evaluated in animal models. Because elderly individuals are vulnerable to viral and bacterial infections, these microbial agents may be considered important comorbidities that could potentiate an already existing and tenuous inflammatory condition in the brain, accelerating cognitive decline, particularly if the cellular and molecular mechanisms can be defined. Researchers have recently demonstrated that triggering inflammation in the brain exacerbates tau pathological characteristics in animal models. Herein, we explore whether inflammation induced via viral infection, compared with inflammation induced via bacterial lipopolysaccharide, modulates AD-like pathological features in the 3xTg-AD mouse model and provide evidence to support the hypothesis that infectious agents may act as a comorbidity for AD. Our study shows that infection-induced acute or chronic inflammation significantly exacerbates tau pathological characteristics, with chronic inflammation leading to impairments in spatial memory. Tau phosphorylation was increased via a glycogen synthase kinase-3β-dependent mechanism, and there was a prominent shift of tau from the detergent-soluble to the detergent-insoluble fraction. During chronic inflammation, we found that inhibiting glycogen synthase kinase-3β activity with lithium reduced tau phosphorylation and the accumulation of insoluble tau and reversed memory impairments. Taken together, infectious agents that trigger central nervous system inflammation may serve as a comorbidity for AD, leading to cognitive impairments by a mechanism that involves exacerbation of tau pathological characteristics.