The development of inflammatory arthritis following SARS-CoV-2 infection: a systematic review of the literature.

BACKGROUND: Given the widespread impact of COVID-19, it is important to explore any atypical presentations and long-term sequelae associated with this viral infection, including the precipitation of inflammatory arthritis. OBJECTIVE: To identify and summarize clinical reports of acute inflammatory arthritis associated with COVID-19. METHODS: A systematic review of the PubMed (MEDLINE), Google Scholar, and Cochrane Central databases through January 31, 2022 was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. The inclusion criteria were: human subjects and English language. Data extraction and qualitative synthesis of the demographics, clinical presentations, treatments, and outcomes were performed. Quality assessment was performed using the Joanna-Briggs Institute critical appraisal tools. RESULTS: A total of 37 articles collectively describing the cases of 54 patients were included. The mean age was 48.2 years (6-78 years). 53.7% of patients were male and 46.3% were female. The onset of articular symptoms varied considerably, and the majority of cases were described as polyarticular (29). The classification of inflammatory arthritis in the included studies was as follows: reactive (19), post-viral (13), new-onset rheumatoid arthritis (RA) (8), crystal-proven arthropathy flare (4), acute viral (2), new-onset psoriatic arthritis (2), flare of preexisting RA (2), and other (4). Arthritis treatment regimens varied but consisted largely of NSAIDs and corticosteroids with most patients experiencing improvement or resolution of their joint symptoms. CONCLUSION: There is limited low-level evidence suggesting that patients may develop acute arthritis during or after SARS-CoV-2 infection. This review highlights the need for further research to elucidate the relationship between COVID-19 and the development of inflammatory arthritis.

This review paper sought to explore the relationship between COVID-19 disease and acute joint pain/inflammation (arthritis) through a systematic search of the literature. This review found limited low-level evidence suggesting that patients may develop inflammatory arthritis during or after COVID-19 disease. However, there is a need for further research to improve our understanding of the relationship between COVID-19 and the development of inflammatory arthritis.

Research Advances of Germinal Matrix Hemorrhage: An Update Review.

Germinal matrix hemorrhage (GMH) refers to bleeding that derives from the subependymal (or periventricular) germinal region of the premature brain. GMH can induce severe and irreversible damage attributing to the vulnerable structure of germinal matrix and deleterious circumstances. Molecular mechanisms remain obscure so far. In this review, we summarized the newest preclinical discoveries recent years about GMH to distill a deeper understanding of the neuropathology, and then discuss the potential diagnostic or therapeutic targets among these pathways. GMH studies mostly in recent 5 years were sorted out and the authors generalized the newest discoveries and ideas into four parts of this essay. Intrinsic fragile structure of preterm germinal matrix is the fundamental cause leading to GMH. Many molecules have been found effective in the pathophysiological courses. Some of these molecules like minocycline are suggested active to reduce the damage in animal GMH model. However, researchers are still trying to find efficient diagnostic methods and remedies that are available in preterm infants to rehabilitate or cure the sequent injury. Merits have been obtained in the last several years on molecular pathways of GMH, but more work is required to further unravel the whole pathophysiology.

An update on promising therapies for CNS conditions.

In this special edition, we present five articles that explore various neurovascular and neurodegenerative diseases and update the readers on promising therapies. We discuss where the current focus of research on central nervous conditions is heading. The topics range from discussing different brain injury models simulate human physiology, to analyzing outcomes following subdural hematoma evacuation. In addition, this special issue discusses new therapeutic targets during the acute phase of brain injury. The ideas and expert analysis regarding different neurological topics set up readers to explore future research on the subject matter.

Simplex-Centroid mixture design applied to arsenic (V) removal from waters using synthetic minerals.

Arsenic (As) is a toxic and carcinogenic element. Therefore, it is necessary to carry out research on As-contaminated water management in order to achieve the World Health Organization (WHO) standard for drinking water (0.010 mg L-1). A Simplex-Centroid mixture design (SCMD) was used to determine the best mineral composition for both maximum adsorption capacity of As(V) (MAC-As) and residual concentration of As(V) (RC-As), using synthetic poorly crystallized aluminum hydroxide (pAlHyd), calcined layered double hydroxide (cLDH), and two-line ferrihydrite (2ℓFh). The analysis of variance results and the predicted values of models showed a good agreement with the experimental data, indicating that SCMD is a reliable method to optimize As removal through determination of the best mineral composition. The ability of pure synthetic minerals to remove As from water was different among those mixtures thereof, which indicate that the mineral components interacted with each other. Results showed that cLDH was the best As adsorbent. However, it showed a RC-As higher than the WHO standard. The pAlHyd and 2ℓFh exhibited smaller MAC-As, but they lowered RC-As to below 0.010 mg L-1, showing no direct relationship between high MAC-As and low RC-As. Therefore, mineral compositions which combine high adsorption capacity with low residual concentration should work better for removing As from drinking water, ensuring it meets the WHO potability standard. Ternary diagrams for MAC-As and RC-As showed that the best combination for maximizing MAC-As and reducing RC-As should be a mixture of 75-90% of cLDH, 10-20% of pAlHyd, and 0-5% of 2ℓFh.

Docosahexaenoic Acid Alleviates Oxidative Stress-Based Apoptosis Via Improving Mitochondrial Dynamics in Early Brain Injury After Subarachnoid Hemorrhage.

Mitochondrial dysfunction is considered a crucial therapeutic target for early brain injury following subarachnoid hemorrhage (SAH). Emerging evidence indicates that docosahexaenoic acid (DHA), an essential omega-3 fatty acid, protects mitochondria in various chronic diseases. This study aimed to investigate the neuroprotective effects of DHA on mitochondrial dynamic dysfunction after EBI using in vivo and in vitro approaches. For in vivo experiments, the rat endovascular perforation SAH model was performed, whereby DHA was administered intravenously 1 h after induction of SAH. Primary cultured neurons treated with oxyhemoglobin (OxyHb) for 24 h were used to mimic SAH in vitro. Our results demonstrated that DHA improved neurological deficits and reduced brain edema in rats with SAH, and attenuated OxyHb-induced neuronal death in primary cultured cells. DHA reduced the amount of reactive oxygen species-positive cells and improved cell viability when compared to the SAH + vehicle group in vitro. DHA attenuated malondialdehyde levels and superoxide dismutase stress, increased Bcl2 and Bcl-xl, and decreased Bax and cleaved caspase-3 in vivo. Additionally, DHA ameliorated mitochondrial dysfunction, upregulated the mitochondrial fusion-related protein Optic Atrophy 1, and downregulated the mitochondrial fission-related protein Dynamin-Related-Protein 1 (Drp1) and Serine 616 phosphorylated Drp1 after SAH both in vitro and in vivo. Taken together, our current study demonstrates that DHA might prevent oxidative stress-based apoptosis after SAH. The characterization of the underlying molecular mechanisms may further improve mitochondrial dynamics-related signaling pathways.

Recombinant Netrin-1 binding UNC5B receptor attenuates neuroinflammation and brain injury via PPARγ/NFκB signaling pathway after subarachnoid hemorrhage in rats.

Neuroinflammation is an essential mechanism involved in the pathogenesis of subarachnoid hemorrhage (SAH)-induced brain injury. Recently, Netrin-1 (NTN-1) is well established to exert anti-inflammatory property in non-nervous system diseases through inhibiting infiltration of neutrophil. The present study was designed to investigate the effects of NTN-1 on neuroinflammation, and the potential mechanism in a rat model of SAH. Two hundred and ninety-four male Sprague Dawley rats (weight 280-330 g) were subjected to the endovascular perforation model of SAH. Recombinant human NTN-1 (rh-NTN-1) was administered intravenously. Small interfering RNA (siRNA) of NTN-1 and UNC5B, and a selective PPARγ antagonist bisphenol A diglycidyl ether (BADGE) were applied. Post-SAH evaluations included neurobehavioral function, brain water content, Western blot analysis, and immunohistochemistry. Our results showed that endogenous NTN-1 and its receptor UNC5B level were increased after SAH. Administration of rh-NTN-1 reduced brain edema, ameliorated neurological impairments, and suppressed microglia activation after SAH, which were concomitant with PPARγ activation, inhibition of NFκB, and decrease in TNF-α, IL-6, and ICAM-1, as well as myeloperoxidase (MPO). Knockdown of endogenous NTN-1 increased expression of pro-inflammatory mediators and MPO, and aggravated neuroinflammation and brain edema. Moreover, knockdown of UNC5B using specific siRNA and inhibition of PPARγ with BADGE blocked the protective effects of rh-NTN-1. In conclusion, our findings indicated that exogenous rh-NTN-1 treatment attenuated neuroinflammation and neurological impairments through inhibiting microglia activation after SAH in rats, which is possibly mediated by UNC5B/PPARγ/NFκB signaling pathway. Exogenous NTN-1 may be a novel therapeutic agent to ameliorating early brain injury via its anti-inflammation effect.

Correction to: Increase in the prevalence of hypertension among adults exposed to the great Chinese famine during early life.

The 'Conclusion' section in the Abstract was published incorrectly in the original publication of the article [1] and is corrected with this erratum as below: "Fetal exposure to the Chinese famine may be associated with an increased risk of hypertension in adulthood in women."

Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury.

Cardiac arrest (CA) is a well-known cause of global brain ischemia. After CA and subsequent loss of consciousness, oxygen tension starts to decline and leads to a series of cellular changes that will lead to cellular death, if not reversed immediately, with brain edema as a result. The electroencephalographic activity starts to change as well. Although increased intracranial pressure (ICP) is not a direct result of cardiac arrest, it can still occur due to hypoxic-ischemic encephalopathy induced changes in brain tissue, and is a measure of brain edema after CA and ischemic brain injury. In this review, we will discuss the pathophysiology of brain edema after CA, some available techniques, and methods to monitor brain oxygen, electroencephalography (EEG), ICP (intracranial pressure), and microdialysis on its measurement of cerebral metabolism and its usefulness both in clinical practice and possible basic science research in development. With this review, we hope to gain knowledge of the more personalized information about patient status and specifics of their brain injury, and thus facilitating the physicians' decision making in terms of which treatments to pursue.

Increase in the prevalence of hypertension among adults exposed to the Great Chinese Famine during early life.

OBJECTIVE: This study aimed to assess the association between exposure to the Great Chinese Famine (1959-1961) during early life and hypertension in adulthood. METHODS: From July to September 2009, 1224 eligible adults were recruited in a cross-sectional survey using a multi-stage stratified random sampling method in Chongqing China. A questionnaire was used to collect information of hypertension and sociodemographic factors. Participants were categorized as childhood, fetal, and none exposure to famine based on the date of birth. RESULTS: Of the sample, 12.3% reported having hypertension. The prevalence of hypertension varied by famine status: 11.9% in childhood exposure, 16.1% in fetal exposure, and 10.2% in non-exposure group. After adjusting for sociodemographic and lifestyle factors, compared with non-exposure group, fetal exposure group had an increased likelihood of having hypertension with odds ratio of 1.79 (95%CI 1.13-2.84). Although there was no significant gender and famine interaction, the positive association between famine exposure and hypertension was stronger among women than men. CONCLUSION: Fetal exposure to the Chinese famine may be associated with an increased risk of hypertension in adulthood in women [corrected].

Phosphoinositide 3-Kinase Gamma Contributes to Neuroinflammation in a Rat Model of Surgical Brain Injury.

Neuroinflammation plays an important role in the pathophysiology of surgical brain injury (SBI). Phosphoinositide 3-kinase gamma (PI3Kγ), predominately expressed in immune and endothelial cells, activates multiple inflammatory responses. In the present study, we investigated the role of PI3Kγ and PI3Kγ-activated phosphodiesterase 3B (PDE3B) in neuroinflammation in a rat model of SBI. One hundred and fifty-two male Sprague Dawley rats (weight 280-350 g) were subjected to a partial right frontal lobe corticotomy model of SBI. A PI3Kγ pharmacological inhibitor (AS252424 or AS605240) was administered intraperitoneally. PI3Kγ siRNA, human recombinant active-PI3Kγ protein, or human recombinant active-PDE3B protein were administered intracerebroventricularly. Post-SBI assessments included neurobehavioral tests, brain water content, Western blot, and immunohistochemistry. Endogenous PI3Kγ levels were increased within peri-resection brain tissues after SBI, accompanied by increased brain water content and neurological functional deficits. There was a trend toward increased endogenous PDE3B phosphorylation after SBI. The selective PI3Kγ inhibitors AS252424 and AS605240 reduced brain water content surrounding corticotomy and improved neurological function after SBI. SBI increased and PI3Kγ inhibitor decreased levels of myeloperoxidase, cluster of differentiation 3, mast cell degranulation, E-selectin, and IL-1 in peri-resection brain tissues. Direct administration of human recombinant active-PI3Kγ protein and active-PDE3B protein countered the protective effect of AS252424. PI3Kγ siRNA reduced PI3Kγ levels, decreased brain water content within peri-resection brain tissues, and improved neurological function after SBI. Collectively, our findings suggest that PI3Kγ contributed to neuroinflammation after SBI. The use of selective PI3Kγ inhibitors may be a novel approach to ameliorating SBI via their anti-inflammation effects. Significance statement: Life-saving or elective neurosurgeries often involve unavoidable damages to neighboring, nondiseased brain tissues. Such surgical brain injury (SBI) is attributable exclusively to the neurosurgical procedure itself and may cause postoperative complications that exacerbate neurological function. Although the importance of this medical problem is fully acknowledged, intraoperative administration of adjunctive treatment such as steroids and mannitol to patients undergoing neurosurgery appear not to be efficient remedies for SBI. To date, the issue of perioperative neuroprotection specifically against SBI has not been well studied. Using a clinically relevant rat model of SBI, we are exploring a new neuroprotective strategy targeting phosphoinositide 3-kinase gamma (PI3Kγ). PI3Kγ activates multiple inflammatory responses. By attenuating neuroinflammation, selective PI3Kγ inhibition would limit postoperative complications and benefit neurological outcomes.

Prosody and reading in dyslexic children.

This study investigates the role of prosody in the reading aloud of dyslexic children. Ten dyslexic and 30 non-dyslexic control children (mean age 9.5 and 9.9 years, respectively) were recorded when reading a text of appropriate level and subsequently asked to retell it and tested on its comprehension. The data were analysed acoustically by the WinPitchPro programme. The temporal and intonational processing of reading of the two groups were contrasted and revealed unusual characteristics of the dyslexic group with respect to what follows: (1) temporal processing (reduced speeds of reading and articulation and alterations in the number and duration of pauses); (2) variation of the fundamental frequency (limited ability to vary the melody at the phrasal and phonemic level); and (3) vowel stress patterning (difficulty in producing typical stress patterns, and of marking the pre-stressed and stressed syllables). Fulfilling its objective, the present study promotes advances in the understanding of the functioning of prosody in reading aloud in dyslexia.

Neuroprotective Strategies after Neonatal Hypoxic Ischemic Encephalopathy.

Neonatal hypoxic ischemic encephalopathy (HIE) is a devastating disease that primarily causes neuronal and white matter injury and is among the leading cause of death among infants. Currently there are no well-established treatments; thus, it is important to understand the pathophysiology of the disease and elucidate complications that are creating a gap between basic science and clinical translation. In the development of neuroprotective strategies and translation of experimental results in HIE, there are many limitations and challenges to master based on an appropriate study design, drug delivery properties, dosage, and use in neonates. We will identify understudied targets after HIE, as well as neuroprotective molecules that bring hope to future treatments such as melatonin, topiramate, xenon, interferon-beta, stem cell transplantation. This review will also discuss some of the most recent trials being conducted in the clinical setting and evaluate what directions are needed in the future.

What's New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment.

Traumatic brain injury (TBI), defined as an alteration in brain functions caused by an external force, is responsible for high morbidity and mortality around the world. It is important to identify and treat TBI victims as early as possible. Tracking and monitoring TBI with neuroimaging technologies, including functional magnetic resonance imaging (fMRI), diffusion tensor imaging (DTI), positron emission tomography (PET), and high definition fiber tracking (HDFT) show increasing sensitivity and specificity. Classical electrophysiological monitoring, together with newly established brain-on-chip, cerebral microdialysis techniques, both benefit TBI. First generation molecular biomarkers, based on genomic and proteomic changes following TBI, have proven effective and economical. It is conceivable that TBI-specific biomarkers will be developed with the combination of systems biology and bioinformation strategies. Advances in treatment of TBI include stem cell-based and nanotechnology-based therapy, physical and pharmaceutical interventions and also new use in TBI for approved drugs which all present favorable promise in preventing and reversing TBI.

Effect of WeChat-based intervention on food safety knowledge, attitudes and practices among university students in Chongqing, China: a quasi-experimental study.

BACKGROUND: Food safety is of global importance and has been of concern in university settings in recent years. However, effective methods to conduct food safety education are limited. This study aims to evaluate the effects of an intervention on food safety knowledge, attitudes and practices (KAP) by social media, WeChat, among university students. METHODS: A quasi-experimental study was conducted in Chongqing, China. Two departments were recruited randomly from a normal university and a medical university. One department from each university was randomly selected as the intervention group and the other as the control group. All freshmen students in each selected department were chosen to participate in this study. One thousand and twenty-three students were included at baseline, and 444 students completed the study. This intervention was conducted through food safety-related popular science articles with an average of three articles per week released by WeChat official accounts called "Yingyangren" for two months to the intervention group. No intervention was conducted in the control group. An independent t-test was used to test statistical differences in the food safety KAP scores between the two groups. A paired t-test was used to test statistical differences in the food safety KAP scores between before and after the intervention. And quantile regression analysis was conducted to explore the difference between the two groups across the quantile levels of KAP change. RESULTS: After the intervention, compared with control group, participants in the intervention group did not score significant higher on knowledge (p = 0.98), attitude (p = 0.13), and practice (p = 0.21). And the scores of food safety knowledge and practices slightly improved after the intervention both in the intervention group (p = 0.01 and p = 0.01, respectively) and in the control group (p = 0.0003 and p = 0.0001, respectively). Additionally, the quantile regression analysis showed that the intervention had no effect on improving the food safety KAP scores. CONCLUSIONS: The intervention using the WeChat official account had limited effects on improving the food safety KAP among the university students. This study was an exploration of food safety intervention using the WeChat official account; valuable experience can be provided for social media intervention in future study. TRIAL REGISTRATION: ChiCTR-OCH-14004861.

Assisted Synthesis of Coated Iron Oxide Nanoparticles for Magnetic Hyperthermia.

Magnetite nanoparticles were synthesized by the co-precipitation method with and without the assistance of an additive, namely, gelatin, agar-agar or pectin, using eco-friendly conditions and materials embodying a green synthesis process. X-ray diffraction and transmission electron microscopy were used to analyze the structure and morphology of the nanoparticles. Magnetic properties were investigated by SQUID magnetometry and 57Fe Mössbauer spectroscopy. The results show that the presence of the additives implies a higher reproducibility of the morphological magnetic nanoparticle characteristics compared with synthesis without any additive, with small differences associated with different additives. To assess their potential for magnetic hyperthermia, water-based suspensions of these nanoparticles were prepared with and without citric acid. The stable solutions obtained were studied for their structural, magnetic and heating efficiency properties. The results indicate that the best additive for the stabilization of a water-based emulsion and better heating efficiency is pectin or a combination of pectin and agar-agar, attaining an intrinsic loss power of 3.6 nWg-1.

Practical Strategies and Tools for Use by Occupational and Environmental Medicine Departments During COVID-19 Pandemic Surges.

OBJECTIVES: Occupational and environmental medicine (OEM) departments in healthcare institutions can be quickly overwhelmed when COVID-19 infection rates rapidly and simultaneously increase in the workforce and the patients served. Our goal is to present a detailed toolkit of practical approaches for use by front-line OEM specialists to address workforce management tasks during pandemic surges. METHODS: Specific focus is on tasks related to employee symptom triage, exposure risk assessment, workplace contact tracing, and work restrictions. RESULTS: Tools include strategies used by customer call centers, two decision support algorithms (exposure due to cohabitation or non-cohabitation), a color-coded employee case tracking tool, a contact tracing protocol, and documentation templates that serve as memory aids for encounters. CONCLUSIONS: These tools are created with commonly used software. Implementation is feasible in most front-line OEM settings, including those with limited resources.

Treatment outcomes of peri-articular steroid injection for patients with work-related sacroiliac joint pain and lumbar para-spinal muscle strain.

OBJECTIVES: Evaluating treatment outcomes of local corticosteroid injections for work-related lower back pain (LBP) as the current evidence for the American College of Occupational and Environmental Medicine guidelines is considered insufficient to recommend this practice. MATERIAL AND METHODS: The authors conducted a retrospective study involving the patients who were treated with peri-articular and lower lumbar corticosteroid injections for work-related LBP at their occupational medicine clinic. RESULTS: Sixty-four patients met the inclusion criteria. The average pain level was reduced from M±SD 5.1±2.0 to M±SD 3.1±2.3 after the corticosteroid injection (p < 0.0001). Thirty-five patients (55%) were discharged to regular duty; 23 (36%) were transferred to orthopedics due to persistent pain; and 6 (9%) were lost to follow-up. CONCLUSIONS: Corticosteroid injections for work-related LBP are effective in reducing pain and enhancing discharge to regular duty. Nonetheless, larger prospective trials are needed to validate these findings. Int J Occup Med Environ Health. 2021;34(1):111-20.

Mitophagy in Cerebral Ischemia and Ischemia/Reperfusion Injury.

Ischemic stroke is a severe cerebrovascular disease with high mortality and morbidity. In recent years, reperfusion treatments based on thrombolytic and thrombectomy are major managements for ischemic stroke patients, and the recanalization time window has been extended to over 24 h. However, with the extension of the time window, the risk of ischemia/reperfusion (I/R) injury following reperfusion therapy becomes a big challenge for patient outcomes. I/R injury leads to neuronal death due to the imbalance in metabolic supply and demand, which is usually related to mitochondrial dysfunction. Mitophagy is a type of selective autophagy referring to the process of specific autophagic elimination of damaged or dysfunctional mitochondria to prevent the generation of excessive reactive oxygen species (ROS) and the subsequent cell death. Recent advances have implicated the protective role of mitophagy in cerebral ischemia is mainly associated with its neuroprotective effects in I/R injury. This review discusses the involvement of mitochondria dynamics and mitophagy in the pathophysiology of ischemic stroke and I/R injury in particular, focusing on the therapeutic potential of mitophagy regulation and the possibility of using mitophagy-related interventions as an adjunctive approach for neuroprotective time window extension after ischemic stroke.

Dihydrolipoic acid enhances autophagy and alleviates neurological deficits after subarachnoid hemorrhage in rats.

Autophagy is a crucial pathological process in early brain injury (EBI) after subarachnoid hemorrhage (SAH). In this study, we investigated the role of dihydrolipoic acid (DHLA) on enhancing autophagy and alleviating neurological deficits after SAH. SAH was induced by endovascular perforation in male Sprague-Dawley rats. DHLA (30 mg/kg) was administered intraperitoneally 1 h (h) after SAH. Small interfering ribonucleic acid (siRNA) for lysosome-associated membrane protein-1 (LAMP1) was administered through intracerebroventricular (i.c.v) route 48 h before SAH induction. SAH grading score, neurological score, immunofluorescence staining, Fluoro-Jade C (FJC) staining, and Western blot were examined. DHLA treatment increased autophagy-related protein expression and downregulated the apoptosis-related protein expression 24 h after SAH. In addition, the DHLA treatment reduced neuronal cell death and alleviated neurological deficits after SAH. Furthermore, knockdown of LAMP1 abolished the neuroprotective effects of DHLA. These results indicate that LAMP1 may participate in autophagy after SAH. DHLA treatment can enhance autophagy, attenuate apoptosis, and alleviate neurofunctional deficits in EBI after SAH. It may provide an effective alternative method for the treatment of EBI after SAH.

Stem Cell Therapy in Brain Ischemia: The Role of Mitochondrial Transfer.

Mitochondrial dysfunction is an important pathological process in the setting of ischemic brain injury. Stem cell-mediated mitochondrial transfer provides an efficient intercellular process to supply additional mitochondria in the ischemic brain tissues. In this review, we summarize the mitochondrial pathology associated with brain ischemia, mechanisms of stem cell-mediated mitochondrial transfer, and in vitro/in vivo experimental findings of mitochondrial transfer from stem cells to ischemic vascular endothelial cells/neurons as potential therapeutic strategy in the management of ischemic brain injury.