Executive summary In September 2015, the member states of the United Nations endorsed sustainable development goals (SDG) for 2030 that aspire to human rights-centered approaches to ensuring the health and well-being of all people. The SDGs embody both the UN Charter values of rights and justice for all and the responsibility of states to rely on the best scientific evidence as they seek to better humankind. In April 2016, these same states will consider control of illicit drugs, an area of social policy that has been fraught with controversy, seen as inconsistent with human rights norms, and for which scientific evidence and public health approaches have arguably played too limited a role. The previous UN General Assembly Special Session (UNGASS) on drugs in 1998 – convened under the theme “a drug-free world, we can do it!” – endorsed drug control policies based on the goal of prohibiting all use, possession, production, and trafficking of illicit drugs. This goal is enshrined in national law in many countries. In pronouncing drugs a “grave threat to the health and well-being of all mankind,” the 1998 UNGASS echoed the foundational 1961 convention of the international drug control regime, which justified eliminating the “evil” of drugs in the name of “the health and welfare of mankind.” But neither of these international agreements refers to the ways in which pursuing drug prohibition itself might affect public health. The “war on drugs” and “zero-tolerance” policies that grew out of the prohibitionist consensus are now being challenged on multiple fronts, including their health, human rights, and development impact. The Johns Hopkins – Lancet Commission on Drug Policy and Health has sought to examine the emerging scientific evidence on public health issues arising from drug control policy and to inform and encourage a central focus on public health evidence and outcomes in drug policy debates, such as the important deliberations of the 2016 UNGASS on drugs. The Johns Hopkins-Lancet Commission is concerned that drug policies are often colored by ideas about drug use and drug dependence that are not scientifically grounded. The 1998 UNGASS declaration, for example, like the UN drug conventions and many national drug laws, does not distinguish between drug use and drug abuse. A 2015 report by the UN High Commissioner for Human Rights, by contrast, found it important to emphasize that “[d]rug use is neither a medical condition nor does it necessarily lead to drug dependence.” The idea that all drug use is dangerous and evil has led to enforcement-heavy policies and has made it difficult to see potentially dangerous drugs in the same light as potentially dangerous foods, tobacco, alcohol for which the goal of social policy is to reduce potential harms. Health impact of drug policy based on enforcement of prohibition The pursuit of drug prohibition has generated a parallel economy run by criminal networks. Both these networks, which resort to violence to protect their markets, and the police and sometimes military ...

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Summary Background Reincarceration in prison or jail correlates with non-sustained HIV viral suppression, but HIV treatment outcomes in released prisoners who are reincarcerated have not recently been systematically assessed despite advances in antiretroviral treatment (ART) potency, simplicity, and tolerability. Methods In a retrospective cohort of reincarcerated inmates with HIV in Connecticut (2005–12), we used longitudinally linked demographic, pharmacy, and laboratory databases to examine correlates of viral suppression. The primary outcome was viral suppression on reincarceration, defined as viral load lower than 400 RNA copies per mL. Findings Of 497 prisoners and jail detainees with HIV, with 934 reincarcerations, individuals were mostly unmarried, uninsured, and black men prescribed a protease-inhibitor-based ART regimen. During the median 329 days (IQR 179–621) between prison release and reincarceration, the proportion of incarceration periods with viral suppression decreased significantly from 52% to 31% (mean HIV-RNA increased by 0·4 log10; p<0·0001), lower than Connecticut’s HIV-infected prison population and those prescribed ART nationally. 158 (51%) of 307 individuals with viral suppression on release had viral suppression on reincarceration. Viral suppression on reincarceration was associated with increasing age (adjusted odds ratio [aOR] 1·04, 95% CI 1·01–1·07), being prescribed non-nucleoside reverse transcriptase inhibitor-based regimens (1·63, 1·14–2·34), and having higher levels of medical or psychiatric comorbidity (1·16, 1·03–1·30). Interpretation Identification of individuals most at risk for recidivism and loss of viral suppression might mitigate the risk that repeated reincarceration poses to systems of public health and safety. Funding Bristol-Myers Squibb Virology, Patterson Trust, and National Institute on Drug Abuse.

We assessed video directly observed therapy (VDOT) for monitoring tuberculosis treatment in 5 health districts in California, USA, to compare adherence between 174 patients using VDOT and 159 patients using in-person directly observed therapy (DOT). Multivariable linear regression analyses identified participant-reported sociodemographics, risk behaviors, and treatment experience associated with adherence. Median participant age was 44 (range 18–87) years; 61% of participants were male. Median fraction of expected doses observed (FEDO) among VDOT participants was higher (93.0% [interquartile range (IQR) 83.4%–97.1%]) than among patients receiving DOT (66.4% [IQR 55.1%–89.3%]). Most participants (96%) would recommend VDOT to others; 90% preferred VDOT over DOT. Lower FEDO was independently associated with US or Mexico birth, shorter VDOT duration, finding VDOT difficult, frequently taking medications while away from home, and having video-recording problems (p<0.05). VDOT cost 32% (range 6%–46%) less than DOT. VDOT was feasible, acceptable, and achieved high adherence at lower cost than DOT.

Background Injection drug use, infectious disease, and incarceration are inextricably linked in Russia. We aimed to identify factors associated with time to relapse (first opioid injection after release from prison) and using a non-sterile, previously used syringe at relapse in a sample of people who inject drugs in St. Petersburg. Methods We collected data on time from release to relapse among individuals with a history of incarceration, a subsample of a larger study among people who inject drugs. Proportional hazards and logistic regression were used to identify factors associated with time to relapse and injection with a non-sterile previously used syringe at relapse, respectively. Results The median time to relapse after release was 30 days. Factors that were independently associated with relapsing sooner were being a native of St. Petersburg compared to not being native (AHR: 1.64; 95% CI 1.15 – 2.33), unemployed at relapse compared to employed (AHR: 4.49; 95% CI 2.96 – 6.82) and receiving a previous diagnosis of HBV and HCV compared to no previous diagnosis (AHR: 1.49; 95% CI 1.03 – 2.14). Unemployment at relapse was also significant in modeling injection with a non-sterile, previously used syringe at relapse compared to those who were employed (AOR: 6.80; 95% CI 1.96 – 23.59). Conclusions Unemployment was an important correlate for both resuming opioid injection after release and using a non-sterile previously used syringe at relapse. Linkage to medical, harm reduction, and employment services should be developed for incarcerated Russian people who inject drugs prior to release.

Previous studies in our lab have identified Pre-B-cell colony enhancing factor as a novel biomarker in acute lung injury. This study continues to elucidate the underlying molecular mechanism of Pre-B-cell colony enhancing factor (PBEF) in the pathogenesis of acute lung injury in pulmonary cell culture models. Our results revealed that IL-1β induced PBEF expression in pulmonary vascular endothelial cells at the transcriptional level and a -1535 T-variant in the human PBEF gene promoter significantly attenuated its binding to an IL-1β induced unknown transcription factor. This may underlie the reduced expression of PBEF and thus the less susceptibility to acute lung injury in those -1535T carriers. Furthermore, overexpression of PBEF significantly augmented IL-8 secretion and mRNA expression by more than 6 fold and 2 fold in A549 cells and HPAEC, respectively. It also significantly augmented IL-1β mediated cell permeability by 44% in A549 cells and 65% in endothelial cells. The knockdown of PBEF expression significantly inhibited IL-1β-stimulated IL-8 secretion and mRNA level by 60% and 70%, respectively; and the knockdown of PBEF expression also significantly attenuated IL-1β-induced cell permeability by 29% in epithelial cells and 24% in endothelial cells. PBEF expression also affected the expression of two other inflammatory cytokines (IL-16 and CCR3 genes). These results suggest that PBEF is critically involved in pulmonary vascular and epithelial inflammation and permeability, which are hallmark features in the pathogenesis of acute lung injury. This study lend further support that PBEF is a potential new target in acute lung injury.