Crowdsourced and crowdfunded: the future of forensic DNA?

ABSTRACT

Forensic DNA analysis is dependent on comparing the known and the unknown. Expand the number of known profiles, and the likelihood of a successful match increases. Forensic use of DNA is moving towards comparing samples of unknown origin with publicly available genetic data, such as the records held by genetic genealogy providers. Use of forensic genetic genealogy has yielded a number of recent high-profile successes but has raised ethical and privacy concerns. Navigating family trees is complex, even more so when combined with a comparison of genetic relationships. This intelligence-gathering process has led to occasional false leads, and its use also risks a public backlash, similar to concerns over Cambridge Analytica. A cautious approach to use of this technique is therefore warranted.     

软组织损伤引起慢性疼痛的治疗

目的：综述运动系统软组织损伤引起慢性疼痛的各种治疗方法的研究进展。资料来源：应用计算机检索Medline1980—01／2006—04与运动系统软组织损伤引起慢性疼痛的治疗相关文章，检索词“Soft tissue injury，pain．chronic，comprehensive therapy”，并限定文章语言种类为“English”；同时计算机检索中国期刊全文数据库1994—01／2006-04期间的相关文章，检索词“软组织损伤、慢性疼痛、治疗方法”，并限定语言种类为中文。同时手工查阅相关书籍。资料选择：对资料进行初审，所选文献内容符合：①软组织损伤引起的慢性疼痛药物治疗的研究。②软组织损伤引起的慢性疼痛微创治疗的研究。③软组织损伤引起的慢性疼痛运动疗法的研究。④软组织损伤引起的慢性疼痛心理治疗的研究。⑤软组织损伤引起的慢性疼痛其他疗法的研究。排除重复性研究的文献。资料提炼：共收集到40篇关于软组织损伤引起的慢性疼痛治疗方法的文献，均为全文，23篇符合纳入标准，排除17篇重复性研究。同时录入书籍3本。资料综合：软组织损伤引起的慢性疼痛的产生是生理、心理及社会因素复杂结合的结果，个体表现差异较大，目前尚无特效治疗方法，常用的治疗方法有：药物治疗、微创治疗、运动疗法、心理治疗、物理疗法及其他疗法。结论：对于软组织损伤引起的慢性疼痛的治疗必须以整体的观点对其进行合理的评估和个体化治疗，才能收到良好的效果。     

The role of complementary and alternative therapies in cardiac rehabilitation: a systematic evaluation.

BACKGROUND: Presently, complementary and alternative medicine, including both therapies and herbal/oral supplements, is used globally. Few studies have examined the use of specific therapies, separate from herbal/oral supplements, in cardiac rehabilitation. This paper presents a systematic evaluation of current research evidence related to use of specific complementary and alternative medicine therapies in secondary prevention of cardiovascular disease, with a view to making recommendations for cardiac rehabilitation. DESIGN AND METHODS: A literature search was conducted using complementary and alternative medicine websites, Medline, Allied and Complementary Medicine, CINAHL, Cochrane databases, EMBASE, SportDiscus, Clinical Evidence, and Evidence-Based Practice to locate research-based scientific evidence related to the use of complementary and alternative medicine in cardiac rehabilitation. Search keywords included heart, cardiac, cardiovascular, coronary, myocardial and rehabilitation, combined with particular therapies. Herbal/oral supplements were not included in this evaluation. RESULTS: Some complementary and alternative medicine therapies may be useful to patients by themselves or coupled with traditional cardiac rehabilitation. Tai chi, as a complement to existing exercise interventions, can be utilized for low and intermediate risk patients. transcendental meditation may be used as a stress reduction technique. There was insufficient evidence found for the use of acupuncture or chelation therapy in cardiac rehabilitation or secondary prevention. CONCLUSIONS: Some complementary and alternative medicine therapies hold promise for patients in cardiac rehabilitation. Further research is essential, however, in all areas of complementary and alternative medicine to confirm its usefulness as an adjunct to cardiac rehabilitation.     

9/11 and the New York City Office of Chief Medical Examiner

On September 11, 2001 two hijacked airplanes struck the Twin Towers at the World Trade Center in New York City. All of the remains (19,915) were examined by the Office of Chief Medical Examiner (OCME) of New York City. The major goals of the OCME were to accurately identify the decedents and to promptly issue death certificates. As of September 2005, there were 1594 identifications of a total of 2749 people reported missing. Of these, 976 were identified by a single means, which included DNA analysis in 852 of the victims. Use of legal statues can assist in the timely issuance of death certificates in mass fatalities, which benefit surviving family members. DNA analysis markedly improves the ability to identify remains and has become the standard method for identification in these types of disasters. Certain postmortem tissue samples are better suited for DNA analysis and yield better results than others.     

Hepatic gene downregulation following acute and subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to lead to the development of hepatotoxicity and carcinogenicity in the liver of female rats. In this study, we investigated hepatic gene downregulation in response to acute and subchronic TCDD exposure. We identified 61 probes which exhibited a downregulation of twofold or greater following subchronic (13 weeks) exposure to TCDD. Comparative analysis of the hepatic expression of these 61 probes was conducted with rats subchronically exposed to PeCDF, PCB126, PCB153, and a mixture of PCB126 and PCB153. PCB153 produced little or no alteration in these probes, while the binary mixture mimicked most closely the downregulation observed with TCDD. To discern if the repression of genes within this probe set occur as a primary response to TCDD exposure, we analyzed the early responsiveness of 11 genes at 6, 24, and 72 h following a single exposure to TCDD. We observed early repression of the 11 genes within this early time course, indicating that the repression of this subset of genes occurs as a primary response to TCDD exposure and not as a secondary response to 13 weeks of subchronic treatment. In addition, the gender, species, and AhR dependence of these responses were also investigated. Gender- and species-dependent repression was observed within this subset of genes. Furthermore, utilizing AhR knockout mice, we were able to determine the AhR-dependent downregulation of seven of 11 genes. Together these results assist efforts to understand the multitude of effects imposed by TCDD and AhR ligands on gene expression.     

Hippocampal damage and cytoskeletal disruption resulting from impaired energy metabolism

To determine if impaired energy metabolism might contribute to some aspects of Alzheimer disease (AD), including the vulnerability of the CA1 region of the hippocampal formation and the altered cytoskeleton evident in neurofibrillary tangles, we examined the effects of metabolic poisons on neuronal damage and cytoskeletal disruption in the hippocampal formation. Intrahippocampal injection of 3-nitropropionic acid (3-NP) and malonic acid resulted in neuronal death, particularly in CA1. Cytoskeletal disruption included loss of dendritic MAP2, but sparing of axonal τ. MK-801 (a noncompetitive NMDA receptor antagonist) did not atenuate the lesions produced by intrahippocampal injection of malonate. MK-801, however, was effective against intrastriatal malonate. Acute systemic 3-NP resulted in neuronal damage and cytoskeletal disruption in the CA1 region of the hippocampal formation, including an extensive loss of MAP2 immuno-reactivity, but sparing of τ. The neuronal loss in CA1 was delayed as compared to striatum. Chronic intraventricular infusion of 3-NP produced a different pattern of neuronal damage. Loss of τ-1 immuno-reactivity was observed in CA3 and CA1 s. oriens, whereas MAP2 immunostaining was preserved. These results demonstrate that chronic and acute administration of metabolic inhibitors produce distinct patterns of neuronal damage and cytoskeletal disruption. The results further suggest a differential involvement of the NMDA receptor in malonate-induced neuronal damage in striatum as compared to the hippocampus. The pattern of neuronal damage and cytoskeletal disruption observed following acute metabolic impairment resembled some aspects of neurofibrillary pathology in AD, but did not result in τ hyperphosphorylation.     

Experimental animal models of pancreatic carcinogenesis and metastasis

Pancreatic cancer is a lethal disease characterized by early metastasis, local invasion, and resistance to conventional therapies. To understand its etiology and eventually make prevention of it possible and effective, appropriate carcinogenesis models will certainly help us understand the effects of environmental and genetic elements on pancreatic carcinogenesis. The development of new treatment strategies to control cancer metastasis is of immediate urgency. Fulfillment of this task relies on our knowledge of the cellular and molecular biology of pancreatic cancer metastasis and the availability of biologically and clinically relevant model systems. Many of the existing pancreatic cancer carcinogenesis and metastasis animal models are described in this review. The advantages and disadvantages of each model and their clinical implications are discussed, and special attention is focused on experimental therapeutic strategies targeting pancreatic cancer metastasis.     

Turboprop: improved PROPELLER imaging.

A variant of periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER) MRI, called turboprop, is introduced. This method employs an oscillating readout gradient during each spin echo of the echo train to collect more lines of data per echo train, which reduces the minimum scan time, motion-related artifact, and specific absorption rate (SAR) while increasing sampling efficiency. It can be applied to conventional fast spin-echo (FSE) imaging; however, this article emphasizes its application in diffusion-weighted imaging (DWI). The method is described and compared with conventional PROPELLER imaging, and clinical images collected with this PROPELLER variant are shown.