Cytokine storm is a general term applied to maladaptive cytokine release in response to infection and other stimuli. The pathogenesis is complex but includes loss of regulatory control of proinflammatory cytokine production, both at local and systemic levels. The disease progresses rapidly, and the mortality is high. Some evidence shows that, during the coronavirus disease 2019 (COVID-19) epidemic, severe deterioration in some patients has been closely associated with dysregulated and excessive cytokine release. This article reviews what we know of the mechanism and treatment strategies of the COVID-19 virusinduced inflammatory storm in an attempt to provide some background to inform future guidance for clinical treatment.

In addition to the typical respiratory response, new coronavirus pneumonia (COVID-19) is also associated with very common gastrointestinal symptoms. Cases with gastrointestinal symptoms are more likely to be complicated by liver injury and acute respiratory distress syndrome (ARDS), and diarrhea can also lead to electrolyte disturbances, causing nausea and vomiting, headache, fatigue, etc. If not treated in time, coma and circulatory failure may ensue. As SARS-CoV-2 infects the human body through the combination of ACE2 in the gastrointestinal tract, the mechanism underlying the gastrointestinal symptoms may involve damage to the intestinal mucosal barrier and promotion of the production of inflammatory factors, causing cytokine storms. Indeed, after cells in the lungs become infected by SARS-CoV-2, effector CD4+ T cells reach the small intestine through the gut-lung axis, causing intestinal immune damage and diarrhea; early extensive use of antibacterial and antiviral drugs can also lead to diarrhea in patients. Thus, treatment options for COVID-19 patients should be promptly adjusted when they have gastrointestinal symptoms. Additionally, when drug-induced diarrhea occurs, drugs should be withdrawn or reduced, and microecological regulators should be applied to maintain the intestinal microecological balance and prevent secondary bacterial infections. To guarantee effective treatment, attention should be paid to the patient's enteral nutrition and digestive tract function. As SARS-CoV-2 has been detected in the feces of COVID-19 patients, future prevention and control efforts must consider the possibility of fecal-oral transmission of the virus.

The rapid spread of the epidemic has aroused widespread concern in the international community. Severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) was first reported in China, with bats as the likely original hosts and pangolins as potential intermediate hosts. The current source of the disease is mainly patients infected with SARS-COV-2. Patients in the incubation period may also become sources of infection. The virus is mainly transmitted via respiratory droplets and contact, and the population is generally susceptible. The epidemic has progressed through the local outbreak stage and community transmission stage due to exposure at Wuhan's Huanan wholesale seafood market and is now in the stage of large-scale transmission due to the spread of the epidemic. The basic productive number (R0) at the beginning of the epidemic was 2.2, with an average incubation period of 5.2 days. The proportion of critically ill patients was 23.4%, the mortality rate was lower than those of SARS and Middle East respiratory syndrome, and 96.5% of deaths occurred in Hubei Province, where the outbreak occurred first. Among them, elderly men with underlying diseases had a higher mortality rate. Chinese medical staff have summarized a set of effective strategies and methods in the diagnosis and treatment of this disease that are worthy of reference for their international counterparts. With powerful government intervention and the efforts of Chinese medical staff, China's outbreak has gradually improved.

To develop a 3D MR technique to simultaneously acquire proton multiparametric maps (T 1 , T 2 , and proton density) and sodium density weighted images over the whole brain. Methods:We implemented a 3D stack-of-stars MR pulse sequence which consists of interleaved proton ( 1 H) and sodium ( 23 Na) excitations, tailored slice encoding gradients that can encode the same slice for both nuclei, and simultaneous readout with different radial trajectories ( 1 H, full-radial; 23 Na, center-out radial).The receive chain of our 7T scanner was modified to enable simultaneous acquisition of 1 H and 23 Na signal. A heuristically optimized flip angle train was implemented for proton MR fingerprinting (MRF). The SNR and the accuracy of proton T 1 and T 2 were evaluated in phantoms. Finally, in vivo application of the method was demonstrated in five healthy subjects. Results:The SNR for the simultaneous measurement was almost identical to that for the single-nucleus measurements (<2% change). The proton T 1 and T 2 maps remained similar to the results from a reference 2D MRF technique (normalized RMS error in T 1 ≈ 4.2% and T 2 ≈ 11.3%). Measurements in healthy subjects corroborated these results and demonstrated the feasibility of our method for in vivo application. The in vivo T 1 values measured using our method were lower than the results measured by other conventional techniques.Conclusions: With the 3D simultaneous implementation, we were able to acquire sodium and proton density weighted images in addition to proton T 1 , T 2 , and B + 1 from 1 H MRF that covers the whole brain volume within 21 min.

Background: Chemotherapy remains a primary treatment method for advanced pancreatic cancer. However, chemotherapy resistance can influence the therapeutic effect of pancreatic cancer. The resistance mechanism of chemotherapeutic agents such as gemcitabine, which is an agent typically used to treat pancreatic cancer, is complicated and can be influenced by genes and the environment. Oridonin is a tetracyclic diterpenoid compound extracted from the traditional Chinese herb Rabdosia labtea . Oridonin may overcome drug resistance in pancreatic cancer, but researching pancreatic cancer drug resistance of chemotherapy by oridonin is not completely understood. Purpose: The present study aimed to assess the impact of oridonin on multidrug resistance proteins, apoptosis-associated proteins and energy metabolism in gemcitabine-resistant PANC-1 (PANC-1/Gem) pancreatic cancer cells. Methods: Gemcitabine resistance in PANC-1/Gem cells was induced using a concentration gradient of gemcitabine. Cell Counting Kit-8 assays were used to detect the impact of gemcitabine and oridonin on the proliferation of PANC-1 and PANC-1/Gem cells. Western blot analysis and immunofluorescence were used to detect the expression of multidrug resistance proteins, apoptosis-associated proteins and low-density lipoprotein receptor protein 1 (LRP1) proteins in PANC-1/Gem cells. The effects of gemcitabine and oridonin on PANC-1/Gem cells apoptosis were detected using flow cytometry. Animal xenograft tumor assays were used to detect the effect of gemcitabine and oridonin on pancreatic cancer in vivo. Furthermore, the ATP Assay kit was used to determine the effects of gemcitabine and oridonin on ATP levels in PANC-1/Gem cells. Immunofluorescence assays were used to detect the effects of gemcitabine and oridonin on the expression of low-density lipoprotein receptor protein 1 (LRP1) in PANC-1/Gem cells. In addition, LRP1 expression was knocked down in PANC-1/Gem cells via lentiviral vector-mediated RNA silencing. Clone formation assays and Western blot analysis were used to detect the effect of LRP1 knockdown on the proliferation of PANC-1/Gem cells. Results: The present results demonstrate that oridonin overcomes PANC-1/Gem cells gemcitabine reistance by regulating GST pi and LRP1/ERK/JNK signaling. Conclusion: In conclusion, the present study indicated that oridonin could overcome gemcitabine resistance in PANC-1/Gem cells by regulating GST pi and LRP1/ ERK/JNK signaling, inducing cell apoptosis. Therefore, oridonin with gemcitabine may be a promising preoperative treatment for patients who suffer from pancreatic cancer.

With ongoing research, it was found that asymptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection was widespread in coronavirus disease 2019 (COVID-19) populations. Studies have confirmed asymptomatic patients with COVID-19 have potential infectivity, and most of the transmission occurred before symptoms appear. Asymptomatic infection rates varied widely in different countries and regions. Identifying the asymptomatic infected persons and cutting off the infection source is an effective way to prevent the spread of this disease. However, asymptomatic patients have hidden clinical symptoms, and screening based only on the clinical symptoms of COVID-19 can easily lead to a missed diagnosis. Therefore, determining asymptomatic infection patients by SARS-CoV-2 nucleic acid testing is the gold standard. A series of prevention and control measures adopted by the Chinese government, especially the "Four Early" policy, have achieved outstanding achievements, which are worth learning from by other countries.

The objective of the current study was to design and build a dual-tuned coil array for simultaneous 23 Na/ 1 H MRI of the human brain at 7 T. Quality factor, experimental B 1 + measurements, and electromagnetic simulations in prototypes showed that setups consisting of geometrically interleaved 1 H and 23 Na loops performed better than or similar to 1 H or 23 Na loops in isolation. Based on these preliminary findings, we built a transmit/receive eight-channel 23 Na loop array that was geometrically interleaved with a transmit/receive eight-channel 1 H loop array. We assessed the performance of the manufactured array with mononuclear signal-to-noise ratio (SNR)and B 1 + measurements, along with multinuclear magnetic resonance fingerprinting maps and images. The 23 Na array within the developed dual-tuned device provided more than 50% gain in peripheral SNR and similar B 1 + uniformity and coverage as a reference birdcage coil of similar size. The 1 H array provided good B 1 + uniformity in the brain, excluding the cerebellum and brain stem. The integrated 23 Na and 1 H arrays were used to demonstrate truly simultaneous quantitative 1 H mapping and 23 Na imaging. K E Y W O R D S magnetic resonance fingerprinting, simultaneous multinuclear MRI, sodium ( 23 Na) MRI, ultrahigh field MRI 1 | INTRODUCTION Multinuclear proton ( 1 H) and sodium ( 23 Na) MRI can provide complementary anatomical and biochemical information to characterize various soft-tissue neuropathologies, such as traumatic brain injury, cancer, and multiple sclerosis, where sodium metabolic dysfunction is believed to play a key role. Two challenges in 23 Na MRI are its low NMR sensitivity (9.2% that of proton) and the low concentration of 23 Na ions in vivo

Recent studies have demonstrated that the expression of the long non-coding RNA (lncRNA) AFAP1-AS1 in pancreatic cancer is negatively correlated with survival and prognosis. However, the effects of oridonin and lncRNA AFAP1-AS1 on the epithelial-to-mesenchymal transition (EMT) and migration of pancreatic cancer cells have not been fully elucidated. Surgery is the only potentially curative method for pancreatic cancer, but postoperative recurrence and metastasis are common. The aim of the present study was to assess the effect of oridonin and lncRNA AFAP1-AS1 silencing on pancreatic cancer cells. The pancreatic cancer cell lines BxPC-3 and PANC-1 cells were transfected with siAFAP1-AS1 and its negative control (siNC). After that, oridonin was used to treat the siAFAP1-AS1-transfected cells. The expression of lncRNA AFAP1-AS1 was downregulated in the pancreatic cancer cell lines BxPC-3 and PANC-1. The apoptosis and cell cycle progression of pancreatic cancer cells were evaluated by flow cytometry and Hoechst 33258 staining. Metastasis and invasion of BxPC-3 and PANC-1 cells were detected by transwell migration assay, real-time cell analysis, and western blot analysis. Cells were transfected with the lentiviral siAFAP1-AS1 and siNC, and tumorigenesis was evaluated in BALB/C nude mice. Immunohistochemical examination was used to verify the effects of oridonin and siAFAP1-AS1 on pancreatic cancer. The results demonstrated that the combination of oridonin and siAFAP1-AS1 inhibited pancreatic cancer cell proliferation, induced apoptosis, arrested cell cycle progression, prevented the migration, regulated EMT-related protein expression in BxPC-3 and PANC-1 cells, and inhibited pancreatic cancer cell tumorigenicity and EMT in nude mice.