Rapid review: A review of methods and recommendations based on current evidence.

Rapid review (RR) could accelerate the traditional systematic review (SR) process by simplifying or omitting steps using various shortcuts. With the increasing popularity of RR, numerous shortcuts had emerged, but there was no consensus on how to choose the most appropriate ones. This study conducted a literature search in PubMed from inception to December 21, 2023, using terms such as "rapid review" "rapid assessment" "rapid systematic review" and "rapid evaluation". We also scanned the reference lists and performed citation tracking of included impact studies to obtain more included studies. We conducted a narrative synthesis of all RR approaches, shortcuts and studies assessing their effectiveness at each stage of RRs. Based on the current evidence, we provided recommendations on utilizing certain shortcuts in RRs. Ultimately, we identified 185 studies focusing on summarizing RR approaches and shortcuts, or evaluating their impact. There was relatively sufficient evidence to support the use of the following shortcuts in RRs: limiting studies to those published in English-language; conducting abbreviated database searches (e.g., only searching PubMed/MEDLINE, Embase, and CENTRAL); omitting retrieval of grey literature; restricting the search timeframe to the recent 20 years for medical intervention and the recent 15 years for reviewing diagnostic test accuracy; conducting a single screening by an experienced screener. To some extent, the above shortcuts were also applicable to SRs. This study provided a reference for future RR researchers in selecting shortcuts, and it also presented a potential research topic for methodologists.

Spatiotemporal dynamics and potential ecological drivers of acute respiratory infectious diseases: an example of scarlet fever in Sichuan Province.

OBJECT: Scarlet fever is an acute respiratory infectious disease that endangers public health and imposes a huge economic burden. In this paper, we systematically studied its spatial and temporal evolution and explore its potential ecological drivers. The goal of this research is to provide a reference for analysis based on surveillance data of scarlet fever and other acute respiratory infectious illnesses, and offer suggestions for prevention and control. METHOD: This research is based on a spatiotemporal multivariate model (Endemic-Epidemic model). Firstly, we described the epidemiology status of the scarlet fever epidemic in Sichuan Province from 2016 to 2019. Secondly, we used spatial autocorrelation analysis to understand the spatial pattern. Thirdly, we applied the endemic-epidemic model to analyze the spatiotemporal dynamics by quantitatively decomposing cases into endemic, autoregressive, and spatiotemporal components. Finally, we explored potential ecological drivers that could influence the spread of scarlet fever. RESULTS: From 2016 to 2019, the incidence of scarlet fever in Sichuan Province varied much among cities. In terms of temporal distribution, there were 1-2 epidemic peaks per year, and they were mainly concentrated from April to June and October to December. In terms of transmission, the endemic and temporal spread were predominant. Our findings imply that the school holiday could help to reduce the spread of scarlet fever, and a standard increase in Gross Domestic Product (GDP) was associated with 2.6 folds contributions to the epidemic among cities. CONCLUSION: Scarlet fever outbreaks are more susceptible to previous cases, as temporal spread accounted for major transmission in many areas in Sichuan Province. The school holidays and GDP can influence the spread of infectious diseases. Given that covariates could not fully explain heterogeneity, adding random effects was essential to improve accuracy. Paying attention to critical populations and hotspots, as well as understanding potential drivers, is recommended for acute respiratory infections such as scarlet fever. For example, our study reveals GDP is positively associated with spatial spread, indicating we should consider GDP as an important factor when analyzing the potential drivers of acute infectious disease.

Impact of mTORC1 inhibition on keratinocyte proliferation during skin tumor promotion in wild-type and BK5.AktWT mice.

In this study, we examined the impact of rapamycin on mTORC1 signaling during 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced keratinocyte proliferation and skin tumor promotion in both wild-type (FVB/N) and BK5.Akt(WT) mice. TPA activated mTORC1 signaling in a time-dependent manner in cultured primary mouse keratinocytes and a mouse keratinocyte cell line. Early activation (15-30 min) of mTORC1 signaling induced by TPA was mediated in part by PKC activation, whereas later activation (2-4 h) was mediated by activation of EGFR and Akt. BK5.Akt(WT) transgenic mice, where Akt1 is overexpressed in basal epidermis, are highly sensitive to TPA-induced epidermal proliferation and two-stage skin carcinogenesis. Targeting mTORC1 with rapamycin effectively inhibited TPA-induced epidermal hyperplasia and hyperproliferation as well as tumor promotion in a dose-dependent manner in both wild-type and BK5.Akt(WT) mice. A significant expansion (∼threefold) of the label retaining cell (LRC) population per hair follicle was observed in BK5.Akt(WT) mice compared to FVB/N mice. There was also a significant increase in K15 expressing cells in the hair follicle of transgenic mice that coincided with expression of phospho-Akt, phospho-S6K, and phospho-PRAS40, suggesting an important role of mTORC1 signaling in bulge-region keratinocyte stem cell (KSC) homeostasis. After 2 weeks of TPA treatment, LRCs had moved upward into the interfollicular epidermis from the bulge region of both wild-type and BK5.Akt(WT) mice. TPA-mediated LRC proliferation and migration was significantly inhibited by rapamycin. Collectively, the current data indicate that signaling through mTORC1 contributes significantly to the process of skin tumor promotion through effects on proliferation of the target cells for tumor development.

Dietary energy balance modulates prostate cancer progression in Hi-Myc mice.

Male Hi-Myc mice were placed on three dietary regimens [30% calorie restriction (CR), overweight control (modified AIN76A with 10 kcal% fat), and a diet-induced obesity regimen (DIO) 60 kcal% fat]. All diet groups had approximately similar incidence of hyperplasia and low-grade prostatic intraepithelial neoplasia in the ventral prostate at 3 and 6 months of age. However, 30% CR significantly reduced the incidence of in situ adenocarcinomas at 3 months compared with the DIO group and at 6 months compared with both the overweight control and DIO groups. Furthermore, the DIO regimen significantly increased the incidence of adenocarcinoma with aggressive stromal invasion, as compared with the overweight control group (96% vs. 65%, respectively; P = 0.02) at the 6-month time point. In addition, at both 3 and 6 months, only in situ carcinomas were observed in mice maintained on the 30% CR diet. Relative to overweight control, DIO increased whereas 30% CR reduced activation of Akt, mTORC1, STAT3, and NFκB (p65) in ventral prostate. DIO also significantly increased (and 30% CR decreased) numbers of T-lymphocytes and macrophages in the ventral prostate compared with overweight control. The mRNA levels for interleukin (IL) 1α, IL1ß, IL6, IL7, IL23, IL27, NFκB1 (p50), TNFα, and VEGF family members were significantly increased in the ventral prostate of the DIO group compared with both the overweight control and 30% CR diet groups. Collectively, these findings suggest that enhanced growth factor (Akt/mTORC1 and STAT3) and inflammatory (NFκB and cytokines) signaling may play a role in dietary energy balance effects on prostate cancer progression in Hi-Myc mice.