Human Papillomaviruses and Papillomatosis Lesions of the Female Lower Genital Tract

Objective: The objective of this study was to determine whether human papillomavirus (HPV) infections are involved in the development of papillomatosis lesions of the lower female genital tract

Health care systems in Sweden and China: Legal and formal organisational aspects

<p>Abstract</p> <p>Background</p> <p>Sharing knowledge and experience internationally can provide valuable information, and comparative research can make an important contribution to knowledge about health care and cost-effective use of resources. Descriptions of the organisation of health care in different countries can be found, but no studies have specifically compared the legal and formal organisational systems in Sweden and China.</p> <p>Aim</p> <p>To describe and compare health care in Sweden and China with regard to legislation, organisation, and finance.</p> <p>Methods</p> <p>Literature reviews were carried out in Sweden and China to identify literature published from 1985 to 2008 using the same keywords. References in recent studies were scrutinized, national legislation and regulations and government reports were searched, and textbooks were searched manually.</p> <p>Results</p> <p>The health care systems in Sweden and China show dissimilarities in legislation, organisation, and finance. In Sweden there is one national law concerning health care while in China the law includes the "Hygienic Common Law" and the "Fundamental Health Law" which is under development. There is a tendency towards market-orientated solutions in both countries. Sweden has a well-developed primary health care system while the primary health care system in China is still under development and relies predominantly on hospital-based care concentrated in cities.</p> <p>Conclusion</p> <p>Despite dissimilarities in health care systems, Sweden and China have similar basic assumptions, i.e. to combine managerial-organisational efficiency with the humanitarian-egalitarian goals of health care, and both strive to provide better care for all.</p

Cutaneous immunoprofiles of three spotted fever group Rickettsia cases

Spotted fever group rickettsia (SFGR) can cause mild to fatal illness. The early interaction between the host and rickettsia in skin is largely unknown, and the pathogenesis of severe rickettsiosis remains an important topic. A surveillance of SFGR infection by PCR of blood and skin biopsy specimens followed by sequencing and immunohistochemical (IHC) detection was performed on patients with a recent tick bite between 2013 and 2016. Humoral and cutaneous immunoprofiles were evaluated in different SFGR cases by serum cytokine and chemokine detection, skin IHC staining, and transcriptome sequencing (RNA-seq). A total of 111 SFGR cases were identified, including 79 “Candidatus Rickettsia tarasevichiae,” 22 Rickettsia raoultii, 8 Rickettsia sibirica, and 2 Rickettsia heilongjiangensis cases. The sensitivity to detect SFGR in skin biopsy specimens (9/24, 37.5%) was significantly higher than that in blood samples (105/2,671, 3.9%) (P 0.05). As early as 1 day after the tick bite, rickettsiae could be detected in the skin. R. sibirica infection was more severe than “Ca. Rickettsia” and R. raoultii infections. Increased levels of serum interleukin-18 (IL- 18), IP10, and monokine induced by gamma interferon (MIG) and decreased levels of IL-2 were observed in febrile patients infected with R. sibirica compared to those infected with “Ca. Rickettsia.” RNA-seq and IHC staining could not discriminate between SFGR-infected and uninfected tick bite skin lesions. However, the type I interferon (IFN) response was differently expressed between R. sibirica and R. raoultii infections at the cutaneous interface. It is concluded that skin biopsy specimens were more reliable for the detection of SFGR infection in human patients although the immunoprofile may be complicated by immunomodulators induced by the tick bite.The Natural Science Foundation of China (81621005 and 81773492) and the State Key Research Development Program of China (2016YFC 1200301).https://iai.asm.orgam2020Veterinary Tropical Disease

Molecular mechanisms and cellular functions of cGAS-STING signalling

The cGAS–STING signalling axis, comprising the synthase for the second messenger cyclic GMP–AMP (cGAS) and the cyclic GMP–AMP receptor stimulator of interferon genes (STING), detects pathogenic DNA to trigger an innate immune reaction involving a strong type I interferon response against microbial infections. Notably however, besides sensing microbial DNA, the DNA sensor cGAS can also be activated by endogenous DNA, including extranuclear chromatin resulting from genotoxic stress and DNA released from mitochondria, placing cGAS–STING as an important axis in autoimmunity, sterile inflammatory responses and cellular senescence. Initial models assumed that co-localization of cGAS and DNA in the cytosol defines the specificity of the pathway for non-self, but recent work revealed that cGAS is also present in the nucleus and at the plasma membrane, and such subcellular compartmentalization was linked to signalling specificity of cGAS. Further confounding the simple view of cGAS–STING signalling as a response mechanism to infectious agents, both cGAS and STING were shown to have additional functions, independent of interferon response. These involve non-catalytic roles of cGAS in regulating DNA repair and signalling via STING to NF-κB and MAPK as well as STING-mediated induction of autophagy and lysosome- dependent cell death. We have also learnt that cGAS dimers can multimerize and undergo liquid–liquid phase separation to form biomolecular condensates that could importantly regulate cGAS activation. Here, we review the molecular mechanisms and cellular functions underlying cGAS–STING activation and signalling, particularly highlighting the newly emerging diversity of this signalling pathway and discussing how the specificity towards normal, damage-induced and infection-associated DNA could be achieved

Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a

Long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) was recently identified as oncogene in several cancers. However, the role of MIAT on acquired resistance in lung cancer and the underlying mechanisms remain unclear. Here, we showed that the expression of MIAT in lung cancer tissues was upregulated compared with adjacent tissues. LncRNA MIAT expression was associated with tumor size, lymph node metastasis, distant metastasis and TNM stage. Univariate analysis and multivariate analysis revealed that the lncRNA MIAT to be an independent factor for predicating the prognosis of lung cancer patients. Low lncRNA MIAT have longer overall survival time and progression-free survival time than patients with high lncRNA MIAT expression. Moreover, the knockdown of MIAT significantly sensitized PC9 and gefitinib-resistant PC9 cells to gefitinib in vitro and in vivo, and increased the expression of miR-34a and inactivated PI3K/Akt signaling. MIAT interacted with miR-34a and epigenetically controlled the miR-34a expression by hyper-methylating its promotor. Taken together, our findings demonstrated that knockdown of MIAT by siRNA enhances lung cancer cells to gefitinib through the PI3K/Akt signaling pathway by epigenetically regulating miR-34a. Thus, MIAT may be a useful prognostic marker and therapeutic target for lung cancer patients