Parkinson's disease (PD) is a neurodegenerative disorder, which primarily impacts the nervous system, marked by its immune and inflammatory characteristics. The interleukin-2 (IL-2) cytokine family has a crucial role in regulating both neuroinflammation and immune activity, positioning it as one of the critical immune pathways in PD. Balancing pro-inflammatory and anti-inflammatory signals in PD heavily depends on the IL-2 cytokine family, that includes IL-2, IL-4, IL-7, IL-9, IL-15 and IL-21. This balance is vital for neuron survival and resistance to degeneration. Disruptions in IL-2 signaling can upset the equilibrium among regulatory T cells (Tregs) and pro-inflammatory T cells, such as Th1 and Th17, further aggravating the chronic neuroinflammation typical of PD. In PD, a decline in IL-2 or receptor dysfunction can hinder Treg activity, leading to increased inflammation and neurodegeneration. Similarly, IL-15 and IL-21 supports cytotoxic immune cell function, including natural killer (NK) cells and CD8+ T cells, which may exacerbate neuronal damage by sustaining pro-inflammatory processes. Moreover, IL-4 and IL-7 have anti-inflammatory roles in maintaining T cell homeostasis, and their dysregulation can contribute to interruption of the blood-brain barrier and increased infiltration of immune cells into the central nervous system. Targeting the IL-2 cytokine family in Parkinson's disease has shown therapeutic potential by expanding Tregs, which reduce neuroinflammation and promote dopaminergic neuron survival. Recombinant IL-2 and IL-2/anti-IL-2 complexes have demonstrated efficacy in animal models, enhancing Treg function and leading to improved neuroprotection. Additionally, IL-4-based therapies have been explored for their ability to shift microglia toward a neuroprotective phenotype, further enhancing neuronal survival by modulating inflammatory responses and cellular metabolism. Current research is exploring how to optimize cytokine delivery while minimizing immune side effects, with the goal of developing more targeted therapies for PD.

The COVID-19 disease has spread rapidly across the world within just six months, affecting 169 million people and causing 3.5 million deaths globally (2021). The most affected countries include the USA, Brazil, India, and several European countries such as the UK and Russia. Healthcare professionals face new challenges in finding better ways to manage patients and save lives. In this regard, more comprehensive research is needed, including genomic and proteomic studies, personalized medicines and the design of suitable treatments. However, finding novel molecular entities (NME) using a standard or de novo strategy to drug development is a time-consuming and costly process. Another alternate strategy is discovering new therapeutic uses for old/existing/available medications, known as drug repurposing. There are a variety of computational repurposing methodologies, and some of them have been used to counter the coronavirus disease pandemic of 2019 (COVID-19). This review article compiles recently published data on the origin, transmission, pathogenesis, diagnosis, and management of the coronavirus by drug repurposing and vaccine development approach. We have attempted to screen probable drugs in clinical trials by using literature survey. This systematic review aims to create priorities for future research of drugs repurposed and vaccine development for COVID-19.

Dengue hemorrhagic fever (DHF) is an infectious disease caused by the presence of the dengue virus that is spread worldwide regardless of age. An X-coded gene on the chromosome regulates the immune system. The gene can control the immune system which causes females to have higher amounts of CD4+ T cells and less susceptibility to inflammation, making them not easily infected with viruses. In this paper, we construct and analyze the model of DHF transmission by classifying the sex of human populations. The model parameters are estimated based on DHF data in West Java Province, Indonesia using the least-squares method. The results of the model analysis obtained two equilibria, namely the disease-free equilibrium (locally and globally asymptotically stable if [Formula: see text]) and the endemic equilibrium in special cases (globally asymptotically stable if [Formula: see text]). We then extend an optimal control model for dengue transmission, which includes fumigation and prevention as the control variables. The Pontryagin maximum principle is utilized to find the optimal control conditions. Next, based on the ICER calculation, implementing control in the form of a combination of fumigation and prevention is the best strategy in eliminating DHF cases and cost efficiency. We also suggest that prevention efforts should be differentiated between male and female due to the significant impact in eliminating DHF sufferers.

This research attempted to compare the immune response of Pfizer, Sinovac, and Influvac tetra vaccines in addition to comparing their effects on the submandibular glands (SMGs) and associated lymph nodes in albino rats.

Forty rats were allocated into four groups: group Ι (control), group II (Pfizer), group III (Sinovac) and group IV (Influvac tetra). Serum immunoglobulins G and A (IgG and IgA) were measured. Then, animals were sacrificed. Histological and immunohistochemical examinations were performed on the dissected SMGs and associated lymph nodes.

The Pfizer group had the highest mean IgG and IgA readings, followed by the Sinovac, Influenza and control groups, with a significant variation between every 2 groups. Histopathological examination of the SMGs of all groups showed nearly normal gland architecture resembling the control group. However, mild changes were observed in vaccinated groups. Lymph nodes' histopathological examination revealed inactive primary lymphoid follicles in the control group. However, all vaccinated groups revealed active lymph nodes with secondary lymphoid follicles. Regarding the area percentage of CD3 immunoexpression, the greatest value was reported in Pfizer group, followed by Sinovac, Influenza and control groups, with a significant difference between Pfizer and both Sinovac and influenza groups. However, no substantial variation was observed between Sinovac and Influenza groups.

All vaccines administered were effective. The Pfizer vaccination had the most T cells and the highest serum concentrations of IgG and IgA. All vaccines generally had a satisfactory safety profile with no impact on salivary gland histology.

Diabetes mellitus is a chronic metabolic disorder that affects multiple organs, including the stomach. This research examines the effects of naringin and/or zinc on stomach and pancreatic tissues of streptozotocin-induced diabetic rats. Type 2 diabetes is induced by intraperitoneal injection of nicotinamide and streptozotocin. Three weeks after diabetes induction, rats receive eight weeks of treatment. Malondialdehyde and total antioxidant capacity are estimated colorimetrically. Asprosin and P-selectin levels are assessed via ELISA. Quantitative RT-PCR analysis of nuclear factor kappa B (NF-кB), peroxisome proliferator-activated receptor gamma (PPAR γ), and nuclear factor erythroid 2-related factor 2 (Nrf-2) genes is carried out. Tumor necrosis factor-alpha (TNF-α) is assessed immunohistochemically, and stomach and pancreatic tissues are examined histologically. Combined naringin and zinc treatment significantly reduces gastric Malondialdehyde, serum asprosin, and P-selectin levels in serum, stomach, and pancreas compared to diabetic rats. Additionally, gastric NF-кB expression is significantly lower, while PPAR γ and Nrf-2 expressions are significantly higher compared to diabetic rats. Immunohistochemical analysis and histopathological examination confirm these findings. In conclusion, combined naringin and zinc treatment significantly improves gastric alterations in diabetic rats by reducing oxidative stress and inflammation. Nonetheless, it shows no additional impacts on pancreatic tissue compared to naringin or zinc alone.

Coronavirus disease-2019 (COVID-19) can cause not only respiratory symptoms but also facial paralysis. Lianhua Qingwen (LHQW) has been reported to have therapeutic effects on COVID-19 and facial neuritis (FN). We explored the potential mechanism of LHQW in the treatment of COVID-19 and FN through a network-pharmacology approach.

Active compounds and relevant targets of LHQW were obtained from the databases of Traditional Chinese Medicine Systems Pharmacology Database, HERB, UniProt Knowledge Base, SwissADME, and Swiss Target Prediction. Disease targets of COVID-19 and FN were acquired from Gene Cards. Database For Annotation, Visualization And Integrated Discovery and Metascape were used to search the biological functions of intersecting targets. After identifying the core targets and their corresponding ingredients, KEGG Mapper analyzes the localization of core targets in key pathways. AutoDock were employed to conduct molecular docking of the core targets and their corresponding ingredients.

We obtained four core genes: interleukin (IL)-8, IL-1B, IL-6, and tumor necrosis factor (TNF)-α. Database searching revealed the anti-inflammatory and antiviral effects of LHQW may be related to the action of aleo-emodin, hyperforin, kaempferol, luteolin, and quercetin on these four genes by regulating the pathways of IL-17 and NOD-like receptor. The molecular-docking results of the four core targets and their corresponding active ingredients showed good binding activity between receptors and ligands.

We uncovered the active ingredients, potential targets, and biological pathways of LHQW for COVID-19 and FN coinfection. Our data provide a theoretical basis for further exploration of the mechanism of action of LHQW in treatment of COVID-19 and FN.

Porphyra sp. (nori), a species of red seaweed, has garnered attention for its rich nutritional profile and diverse bioactive compounds. This review synthesizes current research on Porphyra nori, focusing on its composition, bioactive components, health benefits, and potential applications in functional foods and therapeutics. Key bioactives identified include polysaccharides, peptides, phenolics, and vitamins, each contributing to antioxidant, anti-inflammatory, and anticancer properties and also modulating the immune responses, supporting cardiovascular health, and influencing metabolic pathways. Furthermore, it serves as a valuable source of vitamin B12 and plays a crucial function in the synthesis of DNA, the generation of red blood cells, and the cognitive development of the neurological system. It reduces dependence on animal-derived sources for vitamin B12, whereas innovations in cultivation and processing methods significantly improve its absorption and market potential. Future research directions include elucidating molecular mechanisms, optimizing extraction methods, and exploring synergistic effects with other foods or pharmaceuticals. Porphyra nori emerges as a promising source of bioactive compounds, poised to contribute to personalized nutrition and preventive healthcare strategies.

The widespread impact of the coronavirus disease 2019 (COVID-19) epidemic on human health causes sudden lifestyle changes, through social distancing and isolation at home, with social and economic consequences. This qualitative study aimed to identify the lived experiences of recovered adult patients from COVID-19 in Iran.

This qualitative research was conducted using a national phenomenological approach. The participants were patients who recovered from COVID-19 through their treatment period in the hospital or at home. Semi-structured in-depth interviews were applied for 45 participants who were invited using purposeful sampling and continued to achieve data saturation. The five-stage inductive process to analyze the structure of lived experience (IPSE) approach was used to analyze the data using MAXQDA 2020 software.

According to the statements of the participants in the study, five types of experiences extracted during the period of suffering from the disease: nutritional problems, physical problems, the psychological burden caused by the disease, the supporting role of others in the disease tolerance, and the unpleasant and better experiences of the disease.

Patients with COVID-19 disease experience many physical and psychosocial consequences which affect their quality of life. Therefore, sociopsychological support provided by psychologists and family members can have ameliorating effects in reducing disease consequences. Further interventional studies were needed to capture these aspects of diseases.

The present study evaluated the antioxidant and anti-inflammatory properties of Cleome arabica (CA) fruit extract against bisphenol A (BPA)-induced ovarian injury in female Wistar rats. The antioxidant activity was estimated by the total antioxidant capacity (TAC) and superoxide radical (NBT) content. For the in vivo analyses, 24 animals were divided into the following 4 groups: the control group; the BPA group (50 mg/kg BW BPA for 30 days); the BPA  + CA group (50 mg/kg BW BPA and 50 mg/kg BW CA); and the CA group (50 mg/kg BW CA). The in vitro results demonstrated that CA exhibited strong antioxidant activity and scavenged O2•- radicals. . Pharmacokinetic properties were also explored, reflecting the physiological dynamics of the five active molecules (quercetin, catechin, kaempferol, rosmarinic acid, and naringenin). The in vivo findings revealed a significant increase in body weight associated with a significant increase in plasma C-reactive protein (CRP), proinflammatory cytokines (IL-1, IL-6, and TNF-α), and testosterone levels (p < 0.01). In addition, ovarian histological disruption was observed. However, co-administration of CA extract significantly improved ovarian histological integrity and attenuated inflammatory and androgenic disturbances. Moreover, in silico investigations showed that CA compounds interacted more strongly with the active sites of IL-1β, IL-6, or TNF-α. The best binding energy was observed between catechin (five H-bonds) and IL-1β and IL-6, at -6.0 and -6.1 kcal/mol, respectively, and between rosmarinic acid (four H-bonds) and TNF-α, at -6.4 kcal/mol. The present study supports the use of Cleome arabica in the treatment of infertility for female polycystic ovary syndrome (PCOS) patients.

Various COVID-19 vaccines can affect the immune system. Discrepancies have been noted in immune system characteristics, such as T-lymphocyte levels, between vaccinated and non-vaccinated individuals. This study investigates the variations in immune responses among the four administered COVID-19 vaccines, influencing factors, and clinical outcomes in Jordan. A total of 350 adults, who were at least two doses vaccinated, were interviewed and blood samples were collected for subsequent laboratory analyses. The study involved the quantification of T-cells specifically targeting anti-SARS CoV-2 using Flow cytometry analysis. BNT162b2 (Pfizer) recipients displayed significantly higher CD3+/CD4+ T-helper cell responses (90.84%, 87.46% - 94.22%) compared to non-Pfizer-BioNTech recipients {BBIBP-CorV (Sinopharm) and Sputnik V (Gamaleya Research Institute), then ChAdOx1 nCoV-19 (AstraZeneca)} (83.62%, 77.91% - 89.33%). The CD3+/CD8+ (T cytotoxic) level was notably elevated in non-Pfizer-BioNTech recipients {Sinopharm and Sputnik V then ChAdOx1 nCoV-19 AstraZeneca (73.94%, 69.38% - 78.49%) compared to BNT162b2 (Pfizer) recipients (58.26%, 53.07% - 63.44%). The CD3+ (T-cells) level showed no significant difference between BNT162b2 recipients (73.74%) and non-Pfizer-BioNTech recipients (77.83%), with both types generating T-cells. Comparing two doses of non-Pfizer-BioNTech vaccines with the third dose of BNT162b2 recipients (Pfizer), no difference in the type of immune reaction was observed, with non-Pfizer-BioNTech recipients still stimulating endogenous pathways like cell-mediated cytotoxic effects for cells. All COVID-19 vaccines administered in Jordan were effective, with respect to the total number of T cells. Non-Pfizer-BioNTech had higher in toxic T-cells and Pfizer-BioNTech was higher in helper T-cells that stimulate plasma cells to produce antibodies.

The pandemic COVID-19 (coronavirus disease 2019) is caused by the severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), which devastated the global economy and healthcare system. The infection caused an unforeseen rise in COVID-19 patients and increased the mortality rate globally. This study gives an overall idea about host-pathogen interaction, immune responses to COVID-19, recovery status of infection, targeted organs and complications associated, and comparison of post-infection immunity in convalescent subjects and non-infected individuals. The emergence of the variants and episodes of COVID-19 infections made the situation worsen. The timely introduction of vaccines and precautionary measures helped control the infection's severity. Later, the population that recovered from COVID-19 grew significantly. However, understanding the impact of healthcare issues resulting after infection is paramount for improving an individual's health status. It is now recognised that COVID-19 infection affects multiple organs and exhibits a broad range of clinical manifestations. So, post COVID-19 infection creates a high risk in individuals with already prevailing health complications. The identification of post-COVID-19-related health issues and their appropriate management is of greater importance to improving patient's quality of life. The persistence, sequelae and other medical complications that normally last from weeks to months after the recovery of the initial infection are involved with COVID-19. A multi-disciplinary approach is necessary for the development of preventive measures, techniques for rehabilitation and strategies for clinical management when it comes to long-term care.

One of the main efforts of scientists to study drug development is the discovery of novel antiviral agents that could be beneficial in the struggle against viruses that cause diseases in humans. Natural products are complex metabolites that are designed and synthesised by different sources in an attempt to optimise nature. Recently, natural products are still a source of biologically active molecules, facilitating drug discovery. A p21-activating kinase PAK1 is a key regulator of cytoskeletal actin assembly, phenotypic signalling, and transcription process which affects a wide range of cellular processes such as cell motility, invasion, metastasis, cell growth, angiogenesis, and cell cycle progression. Most recently, PAK1 was shown to be involved in the progression of coronavirus-caused pulmonary inflammation (lung fibrosis), but clinical data is not currently available yet. This review highlights the naturally occurring compounds that inhibit the oncogenic, melanogenic, and ageing kinase PAK1. Additionally, the potent anti-inflammatory effects of natural products in an attempt to prevent pulmonary fibrosis in COVID-19 have also been discussed.

With the rapid development of immunotherapy in recent years, cytokine storm has been recognized as a common adverse effect of immunotherapy. The emergence of COVID-19 has renewed global attention to it. The cytokine storm's inflammatory response results in infiltration of large amounts of monocytes/macrophages in the lungs, heart, spleen, lymph nodes, and kidneys. This infiltration leads to secondary tissue damage, acute respiratory distress syndrome (ARDS), organismal damage, and even death. However, there is currently no designated treatment for cytokine storm and the resulting ARDS. Consequently, there is a pressing need to identify a pharmaceutical agent that can effectively mitigate cytokine storms. Ebosin is a new exopolysaccharide generated by Streptomyces sp.139 and pharmacological activity for cytokine storm is investigated in vivo. The results show that Ebosin significantly augments the survival rates of mice, and its effectiveness increases with higher doses. It significantly inhibited the expression of cytokines IL-5, IL-6, IL-9 and chemokine Eotaxin in serum and lung tissues. Ebosin can alleviate the pathological damage in the lungs, liver, and spleen caused by LPS. Additionally, it can inhibit the phosphorylation of IKKα/β, Stat3 and NF-κB p65 upon LPS stimulation in vitro. We hypothesized that Ebosin may decrease cytokine release by inhibiting the phosphorylation of IKKα/β, Stat3, and NF-κB p65, neutrophil infiltration in animals. The article preliminarily elucidated the activity and mechanism of Ebosin against cytokine storm, which provides a reference for the study of anti-cytokine storm activity of microbial natural products.

It is not always possible to differentiate between influenza and COVID-19 based on symptoms alone. This is a topic of significant importance as it aims to determine whether there are specific hematological parameters that can be used to distinguish between influenza and COVID-19 in children.

Two hundred thirty-one children between the ages of 1 month and 18 years who presented to the children's outpatient clinic between June 2021 and June 2022 with similar symptoms and were tested with an influenza test and a COVID-19 PCR test were included in the study. Of the patients included in the study, 130 tested positive for COVID-19 and 101 positive for influenza. The patients were evaluated for hematological parameters.

Age, eosinophils and monocyte factors were shown to be statistically significantly effective in COVID-19. The risk of COVID-19 increased 1,484-fold with age, 10,708-fold with increasing eosinophil count, and 1,591-fold with increasing monocyte count. The performance of the monocyte count and eosinophil count was assessed by receiver operating characteristic curve (ROC) analysis. According to the performed ROC analysis, the area under the curve (AUC) value was observed to be 0.990 for monocytes. According to the cutoff point >1.50, the sensitivity value was determined as 98.4% and the specificity value as 97.0%. AUC significance for eosinophils was found to be 0.989. According to the cutoff point >0.02, the sensitivity value was determined as 99.2% and the specificity value as 93.1%.

In the diagnosis of COVID-19, the eosinophil count and monocyte count are easily accessible, inexpensive, and important parameters in terms of differential diagnosis and can help in the differentiation of COVID-19 from influenza during seasonal outbreaks of the latter. Developing parameters for clinicians to use in diagnosing COVID-19 and influenza can facilitate their work in practice.

The review discusses the pathophysiological mechanisms of SARS-CoV-2, the modes of transmission, and the long-term health consequences of COVID-19, emphasizing the importance of research and successful public health initiatives.

COVID-19 taxonomy, pathophysiology, symptomatology, and epidemiological importance are the key objects of this research paper. This review explains how COVID-19 affects different systems of the body, including respiratory, cardiovascular, and reproductive systems of the human body. It describes the modes of entry of the virus into the cell; more precisely, ACE2 and TMPRSS2 in viral entry. In addition, the present study analyzes the situation of COVID-19 in India regarding vaccine development and the transmission rate related to socioeconomic factors.

The manifestation of COVID-19 presents a lot of symptoms and post-acute problems, issues which are seriously impacting mental health and physical health as well. The present review summarizes current research into pathogenicity and the mode of virus transmission, together with immunological responses. Coupled with strong vaccination programs, public health initiatives should hold the key to fighting this pandemic.

Long-term effects and the development of treatment methods will need further study, as ambiguities on COVID-19 remain. Multidisciplinary collaboration across healthcare sectors in this respect is of paramount importance for the prevention of further spread and protection of public health.

Immunotherapy and associated immune regulation strategies gained huge attraction in order to be utilized for treatment and prevention of respiratory diseases. Engineering specifically nanomedicines can be used to regulate host immunity in lungs in the case of respiratory diseases including coronavirus disease 2019 (COVID-19) infection. COVID-19 causes pulmonary embolisms, thus new therapeutic options are required to target thrombosis, as conventional treatment options are either not effective due to the complexity of the immune-thrombosis pathophysiology. In this review, we discuss regulation of immune response in respiratory diseases especially COVID-19. We further discuss thrombosis and provide an overview of some antithrombotic nanoparticles, which can be used to develop nanomedicine against thrombo-inflammation induced by COVID-19 and other respiratory infectious diseases. We also elaborate the importance of immunomodulatory nanomedicines that can block pro-inflammatory signalling pathways, and thus can be recommended to treat respiratory infectious diseases.

The host immune response might confer differential vulnerability to SARS-CoV-2 infection. The Toll-like receptor 8 (TLR8), could participated for severe COVID-19 outcomes. To investigated the relationship of TLR8 rs3764879-C/G, rs3764880-A/G, and rs3761624-A/G with COVID-19 outcomes and with biochemical parameters. A cross-sectional study of 830 laboratory-confirmed COVID-19 patients was performed, and classified into mild, severe, critical, and deceased outcomes. The TLR8 rs3764879-C/G, rs3764880-A/G, and rs3761624-A/G polymorphisms were genotyped. A logistic regression analysis was performed to determinate the association with COVID-19. A stratified analysis was by alleles was done with clinical and metabolic markets. In all outcomes, men presented the highest ferritin levels compared to women (P < 0.001). LDH levels were significantly different between sex in mild (P = 0.003), severe (P < 0.001) and deceased (P = 0.01) COVID-19 outcomes. The GGG haplotype showed an Odds Ratio of 1.55 (Interval Confidence 95% 1.05-2.32; P = 0.03) in men. Among patients with severe outcome, we observed that the carriers of the GGG haplotype had lower Ferritin, C-reactive protein and LDH levels than the CAA carriers (P < 0.01). After further stratified by sex, these associations were also seen in the male patients, except for D-dimer. Interestingly, among men patients, we could observe associations between TLR8 haplotypes and Ferritin (P < 0.001), D-dimer (P = 0.04), C-reactive protein, and Lactate dehydrogenase in mild (P = 0.04) group. Our results suggest that even though TLR8 haplotypes show a significant association with COVID-19 outcomes, they are associated with clinical markers in COVID-19 severity.

An increasing number of studies have highlighted the existence of a sex-specific immune response, wherein men experience a worse prognosis in cases of acute inflammatory diseases. Initially, this sex-dependent inflammatory response was attributed to the influence of sex hormones. However, a growing body of evidence has shifted the focus toward the influence of chromosomes rather than sex hormones in shaping these inflammatory sex disparities. Notably, certain pattern recognition receptors, such as Toll-like receptors (TLRs), and their associated immune pathways have been implicated in driving the sex-specific immune response. These receptors are encoded by genes located on the X chromosome. TLRs are pivotal components of the innate immune system, playing crucial roles in responding to infectious diseases, including bacterial and viral pathogens, as well as trauma-related conditions. Importantly, the TLR-mediated inflammatory responses, as indicated by the production of specific proteins and cytokines, exhibit discernible sex-dependent patterns. In this review, we delve into the subject of sex bias in TLR activation and explore its clinical implications relatively to both the X chromosome and the hormonal environment. The overarching objective is to enhance our understanding of the fundamental mechanisms underlying these sex differences.

Emergency use of remdesivir was approved for COVID-19 in some countries. Based on the promising results of remdesivir, the most common side effects were nausea, worsening respiratory failure, increased alanine aminotransferase levels, and constipation. The aim of this study was to determine the incidence of elevated liver enzymes in patients with COVID-19 receiving remdesivir.

In this retrospective study, information was collected from patients' files. The study population included patients with moderate to severe COVID-19 who were admitted to Rouhani Babol Hospital. For daily patient selection, the list of patients was extracted from the system, and based on the census, the patient file was selected. Data were analyzed using Stata 16.

620 patients suffering from moderate to severe COVID-19 were included in this study, 43% of whom were men. Of these patients, 120 were selected as the control group who did not receive remdesivir. The increase in liver enzymes in patients receiving remdesivir compared with the control, for alanine transaminase (ALT) and aspartate transaminase (AST), respectively, was 6.20 and 3.64 times, but it was not statistically significant for alkaline phosphatase (ALP). Also, the increase in bilirubin levels in patients receiving remdesivir was not statistically significant.

The recipients of remdesivir had high liver enzymes, which is one of the possible side effects of this drug. The intensity of the enzymes was mild and moderate, and they were not dangerous to the health of any of the consumers. Deaths in patients with COVID-19 were not due to drug-induced liver complications but to other factors such as disease-related complications.

This study investigated the modulatory effect of Ginkgo biloba extract on lead acetate-induced endothelial dysfunction. Animals were administered GBE (50 mg/kg and 100 mg/kg orally) after exposures to lead acetate (25 mg/kg orally) for 14 days. Aorta was harvested after euthanasia, the tissue was homogenised, and supernatants were decanted after centrifuging. Oxidative, nitrergic, inflammatory, and anti-apoptotic markers were assayed using standard biochemical procedure, ELISA, and immunohistochemistry, respectively. GBE reduced lead-induced oxidative stress by increasing SOD, GSH, and CAT as well as reducing MDA levels in endothelium. Pro-inflammatory cytokines (TNF-α and IL-6) were reduced while increasing Bcl-2 protein expression. GBE lowered endothelin-I and raised nitrite levels. Histological changes caused by lead acetate were normalised by GBE. Our findings suggest that Ginkgo biloba extract restored endothelin-I and nitric oxide functions by increasing Bcl-2 protein expression and reducing oxido-inflammatory stress in endothelium.

Trauma, a significant global cause of mortality and disability, often leads to fractures and hemorrhagic shock, initiating an exaggerated inflammatory response, which harms distant organs, particularly the lungs. Elderly individuals are more vulnerable to immune dysregulation post-trauma, leading to heightened organ damage, infections, and poor health outcomes. This study investigates the role of NF-κB and inflammasomes in lung damage among aged mice post-trauma.

Twelve male C57BL/6J mice underwent hemorrhagic shock and a femoral fracture (osteotomy) with external fixation (Fx) (trauma/hemorrhage, THFx), while another 12 underwent sham procedures. Mice from young (17-26 weeks) and aged (64-72 weeks) groups (n=6) were included. After 24h, lung injury was assessed by hematoxylin-eosin staining, prosurfactant protein C (SPC) levels, HMGB1, and Muc5ac qRT-PCR. Gene expression of Nlrp3 and Il-1β, and protein levels of IL-6 and IL-1β in lung tissue and bronchoalveolar lavage fluid were determined. Levels of lung-infiltrating polymorphonuclear leukocytes (PMNL) and activated caspase-3 expression to assess apoptosis, as well as NLRP3, ASC, and Gasdermin D (GSDMD) to assess the expression of inflammasome components were analyzed via immunostaining. To investigate the role of NF-κB signaling, protein expression of phosphorylated and non-phosphorylated p50 were determined by western blot.

Muc5ac, and SPC as lung protective proteins, significantly declined in THFx versus sham. THFx-aged exhibited significantly lower SPC and higher HMGB1 levels versus THFx-young. THFx significantly increased activated caspase-3 versus both sham groups, and THFx-aged had significantly more caspase-3 positive cells versus THFx-young. IL-6 significantly increased in both sham and THFx-aged groups versus corresponding young groups. THFx significantly enhanced PMNL in both groups versus corresponding sham groups. This increase was further heightened in THFx-aged versus THFx-young. Expression of p50 and phosphorylated p50 increased in all aged groups, and THFx-induced p50 phosphorylation significantly increased in THFx-aged versus THFx-young. THFx increased the expression of inflammasome markers IL-1β, NLRP3, ASC and GSDMD versus sham, and aging further amplified these changes significantly.

This study's findings suggest that the aging process exacerbates the excessive inflammatory response and damage to the lung following trauma. The underlying mechanisms are associated with enhanced activation of NF-κB and increased expression of inflammasome components.

Virus infection is one of the greatest threats to human life and health. In response to viral infection, the host's innate immune system triggers an antiviral immune response mostly mediated by inflammatory processes. Among the many pathways involved, the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome has received wide attention in the context of viral infection. The NLRP3 inflammasome is an intracellular sensor composed of three components, including the innate immune receptor NLRP3, adaptor apoptosis-associated speck-like protein containing CARD (ASC), and the cysteine protease caspase-1. After being assembled, the NLRP3 inflammasome can trigger caspase-1 to induce gasdermin D (GSDMD)-dependent pyroptosis, promoting the maturation and secretion of proinflammatory cytokines such as interleukin-1 (IL-1β) and interleukin-18 (IL-18). Recent studies have revealed that a variety of viruses activate or inhibit the NLRP3 inflammasome via viral particles, proteins, and nucleic acids. In this review, we present a variety of regulatory mechanisms and functions of the NLRP3 inflammasome upon RNA viral infection and demonstrate multiple therapeutic strategies that target the NLRP3 inflammasome for anti-inflammatory effects in viral infection.

SARS-CoV-2 unsparingly impacts all areas of medicine. Pregnant women are particularly affected by the pandemic and COVID-19 related liver damage seems to be another threat to maternal and fetal health. The aim of this study is to define liver damage profile including bile acids serum levels in COVID-19 pregnant patients and to determine predictors of disease aggravation and poor obstetrics outcomes.

This study has been carried out in the Obstetrics and Gynecology Department, at the National Medical Institute in Warsaw, Poland between 01.02.2021 and 01.11.2022 The study cohort comprises 148 pregnant patients with COVID-19 and 102 pregnant controls who has been tested negative for SARS-CoV-2.

COVID-19 pregnant patients presented liver involvement at admission in 41,9%. Hepatotoxic damage accounted for 27 (19.85%), cholestatic type was diagnosed in 11 (8.09%) and mixed type of liver injury was presented in 19 (13.97%) of patients. Higher serum levels of AST, ALT, GGT, total bilirubin and bile acids as well as mixed type of liver injury at admission were correlated with severe form of an illness. AST and ALT above upper reference limit as well as hepatotoxic type of liver damage predisposed pregnant patients with COVID-19 to poor obstetrics outcomes.

Hepatic damage in pregnant women with COVID-19 is a common, mild, transaminase-dominant, or mixed type of injury, and often correlates with elevated inflammatory markers. SARS-CoV-2 test should be performed as a part of differential diagnosis in elevated liver function tests. Although bile acids serum levels were commonly elevated they seems to be clinically irrelevant in terms of pregnancy outcomes. Video Abstract.

Introduction Kidney transplant recipients (KTRs) are prone to coronavirus disease 2019 (COVID-19) disease secondary to chronic immunosuppressive therapy. There have been differences in mortality and morbidity amongst the general population with different COVID-19 waves. This study is done to understand the effects of different COVID-19 waves amongst KTRs. Methods This was a retrospective single-centre trial from a high-volume transplant centre in North India. The immunosuppression protocol was changed according to national guidelines, and predictors of survival were evaluated. Results A total of 62 patients got infected during the first COVID-19 wave (March 2020 to February 2021) and 50 patients during the second COVID-19 wave (March 2021 to December 2021). Analysis showed a higher incidence of severe COVID-19 disease (79% vs. 50%) in the first wave, while the rest of the baseline parameters were similar in both waves. Mortality was similar in both groups. In both groups, severe COVID-19 disease, the requirement of hospitalisation, invasive oxygen therapy, and CT score findings were significant predictors of survival. There was no change in survival with respect to immunosuppression modification. Allograft dysfunction was more common in the second wave (7 vs. 1). Baseline creatinine was significantly associated with allograft dysfunction in follow-up. Conclusion Patients had severe COVID-19 disease during the first wave; however, poor availability of healthcare services during the second wave led to more patients with allograft dysfunction. Though immunosuppression change is necessary to prevent flare-ups of COVID-19 infection, it is not associated with survival benefits.

In coronavirus disease (COVID-19), inflammation takes center stage, with a cascade of cytokines released, contributing to both inflammation and lung damage. The objective of this study is to identify biomarkers for diagnosing and predicting the severity of COVID-19.

Cytokine levels were determined in the serum from venous blood samples collected from 100 patients with COVID-19 and 50 healthy controls. COVID-19 patients classified based on the Modified Early Warning (MEWS) score. Cytokine concentrations were determined with a multiplex ELISA kit (Bio-Plex Pro™ Human Cytokine Screening Panel).

The concentrations of all analyzed cytokines were elevated in the serum of COVID-19 patients relative to the control group, but no significant differences were observed in interleukin-9 (IL-9) and IL-12 p70 levels. In addition, the concentrations of IL-1α, IL-1β, IL-1ra, IL-2Rα, IL-6, IL-12 p40, IL-18, and tumor necrosis factor alpha (TNFα) were significantly higher in symptomatic patients with accompanying pneumonia without respiratory failure (stage 2) than in asymptomatic/mildly symptomatic patients (stage 1).

The study revealed that IL-1ra, IL-2Rα, IL-6, IL-8, IL-12 p40, IL-16, and IL-18 levels serve as potential diagnostic biomarkers in COVID-19 patients. Furthermore, elevated IL-1α levels proved to be valuable in assessing the severity of COVID-19.

The immune responses of kidney transplant recipients against SARS-CoV-2 remains under studied.

In this prospective pilot study, we performed comprehensive immune profiling using cellular, proteomic, and serologic assays on a cohort of 9 kidney transplant recipients and 12 non-transplant individuals diagnosed with COVID-19.

Our data show that in addition to having reduced SARS-CoV-2 specific antibody levels, kidney transplant recipients exhibited significant cellular differences including a decrease in naïve-but increase in effector T cells, a high number of CD28+ CD4 effector memory T cells, and increased CD8 T memory stem cells compared with non-transplant patients. Furthermore, transplant patients had lower concentrations of serum cytokine MIP-1β as well as a less diverse T cell receptor repertoire.

Overall, our results show that compared to non-transplant patients, kidney transplant recipients with SARS-CoV-2 infection exhibit an immunophenotype that is reminiscent of the immune signature observed in patients with severe COVID-19.

The COVID-19 pandemic ignited research centered around the identification of robust biomarkers and therapeutic targets. SARS-CoV-2, the virus responsible, hijacks the metabolic machinery of the host cells. It relies on lipids and lipoproteins of host cells for entry, trafficking, immune evasion, viral replication, and exocytosis. The infection causes host cell lipid metabolic remodelling. Targeting lipid-based processes is thus a promising strategy for countering COVID-19. Here, we review the role of lipids in the different steps of the SARS-CoV-2 pathogenesis and identify lipid-centric targetable avenues. We discuss lipidome changes in infected patients and their relevance as potential clinical diagnostic or prognostic biomarkers. We summarize the emerging direct and indirect therapeutic approaches for targeting COVID-19 using lipid-inspired approaches. Given that viral protein-targeted therapies may become less effective due to mutations in emerging SARS-CoV-2 variants, lipid-inspired interventions may provide additional and perhaps better means of combating this and future pandemics.

Life expectancy is increasing throughout the world and coincides with a rise in non-communicable diseases (NCDs), especially for metabolic disease that includes diabetes mellitus (DM) and neurodegenerative disorders. The debilitating effects of metabolic disorders influence the entire body and significantly affect the nervous system impacting greater than one billion people with disability in the peripheral nervous system as well as with cognitive loss, now the seventh leading cause of death worldwide. Metabolic disorders, such as DM, and neurologic disease remain a significant challenge for the treatment and care of individuals since present therapies may limit symptoms but do not halt overall disease progression. These clinical challenges to address the interplay between metabolic and neurodegenerative disorders warrant innovative strategies that can focus upon the underlying mechanisms of aging-related disorders, oxidative stress, cell senescence, and cell death. Programmed cell death pathways that involve autophagy, apoptosis, ferroptosis, and pyroptosis can play a critical role in metabolic and neurodegenerative disorders and oversee processes that include insulin resistance, β-cell function, mitochondrial integrity, reactive oxygen species release, and inflammatory cell activation. The silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), AMP activated protein kinase (AMPK), and Wnt1 inducible signaling pathway protein 1 (WISP1) are novel targets that can oversee programmed cell death pathways tied to β-nicotinamide adenine dinucleotide (NAD+), nicotinamide, apolipoprotein E (APOE), severe acute respiratory syndrome (SARS-CoV-2) exposure with coronavirus disease 2019 (COVID-19), and trophic factors, such as erythropoietin (EPO). The pathways of programmed cell death, SIRT1, AMPK, and WISP1 offer exciting prospects for maintaining metabolic homeostasis and nervous system function that can be compromised during aging-related disorders and lead to cognitive impairment, but these pathways have dual roles in determining the ultimate fate of cells and organ systems that warrant thoughtful insight into complex autofeedback mechanisms.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), later renamed coronavirus disease 2019 (COVID-19), was first identified in Wuhan, China, in early December 2019. Initially, the China office of the World Health Organization was informed of numerous cases of pneumonia of unidentified etiology in Wuhan, Hubei Province at the end of 2019. This would subsequently result in a global pandemic with millions of confirmed cases of COVID-19 and millions of deaths reported to the WHO. We have analyzed most of the data published since the beginning of the pandemic to compile this comprehensive review of SARS-CoV-2. We looked at the core ideas, such as the etiology, epidemiology, pathogenesis, clinical symptoms, diagnostics, histopathologic findings, consequences, therapies, and vaccines. We have also included the long-term effects and myths associated with some therapeutics of COVID-19. This study presents a comprehensive assessment of the SARS-CoV-2 virology, vaccines, medicines, and significant variants identified during the course of the pandemic. Our review article is intended to provide medical practitioners with a better understanding of the fundamental sciences, clinical treatment, and prevention of COVID-19. As of May 2023, this paper contains the most recent data made accessible.

COVID-19 caused by SARS-CoV-2 virus is characterized by respiratory compromise and immune system involvement, even leading to serious disorders, such as cytokine storm.

We then conducted a literature review on the topic of sepsis and covid-19, and in parallel conducted an experimental study on the histological finding of patients who died from SARS-Covid 19 infection and a control group.

Sepsis associated with covid-19 infection has some similarities and differences from that from other causes.

In this paper the complex interplay between the 2 disorders was discussed, focusing on the similarities and on the effect that one could have on the other. A preliminary experimental section that demonstrates the multisystemic involvement in subjects who die from SARS-CoV-2 is also proposed.

Understanding COVID-19's onset and clinical effects requires knowing host immune responses.

To investigate the presence of IgM, IgG, and cytokine levels (IL-2 and IL-6) in individuals with COVID-19 who have had their diagnosis confirmed by PCR.

This cross-sectional research included 70 adult ICU patients from King Abdullah Hospital in Bisha, Saudi Arabia. Subjects gave two blood samples. After hospital release, only 21 patients provided the second sample. Each patient provided a sample upon admission. Quantitative ELISAs evaluated IL-2, IL-6, and SARS-CoV-2-specific IgM and IgG antibodies.

All patients were critically ill and unvaccinated against COVID-19. 46 (65.7%) of the patients were male, and their age range was 33-98 years (with a mean age of 66.5); 24.3%) were 51-61 years old. IgG was positive in all patients, although IgM predominated in 57/70 (81.4%) (6-1200 IU/mL). Total data analysis yielded these results. IL-6 was calculated at 10-1900 ng/mL, whereas IL-2 was 4-280. Discharged hospital patients had a statistically significant increase in IgM and IgG (P = 0.01, 0.004) but a statistically insignificant decline in IL-6 and IL-2 (P = 0.761, 0.071). Low IgM levels increased hospital stays. The study found lengthier hospital stays with higher IgG levels.

The identification of IgM and IgG antibodies, greater IL-6 levels, and lower IL-2 levels can help diagnose and monitor COVID-19 infection.

To establish a prediction model of pneumonia risk in SARS-CoV-2-infected patients to reduce unnecessary chest CT scans.

The model was constructed based on a retrospective cohort study. We selected SARS-CoV-2 test-positive patients and collected their clinical data and chest CT images from the outpatient and emergency departments of Hunan Provincial People's Hospital, China. Univariate and multivariate logistic regression and least absolute shrinkage and selection operator (LASSO) regression were utilized to identify predictors of pneumonia risk for patients infected with SARS-CoV-2. These predictors were then incorporated into a nomogram to establish the model. To ensure its performance, the model was evaluated from the aspects of discrimination, calibration, and clinical validity. In addition, a smoothed curve was fitted using a generalized additive model (GAM) to explore the association between the pneumonia grade and the model's predicted probability of pneumonia.

We selected 299 SARS-CoV-2 test-positive patients, of whom 205 cases were in the training cohort and 94 cases were in the validation cohort. Age, CRP natural log-transformed value (InCRP), and monocyte percentage (%Mon) were found to be valid predictors of pneumonia risk. This predictive model achieved good discrimination of AUC in the training and validation cohorts which was 0.7820 (95% CI: 0.7254-0.8439) and 0.8432 (95% CI: 0.7588-0.9151), respectively. At the cut-off value of 0.5, it had a sensitivity and specificity of 70.75% and 66.33% in the training cohort and 76.09% and 73.91% in the validation cohort, respectively. With suitable calibration accuracy shown in calibration curves, decision curve analysis indicated high clinical value in predicting pneumonia probability in SARS-CoV-2-infected patients. The probability of pneumonia predicted by the model was positively correlated with the actual pneumonia classification.

This study has developed a pneumonia risk prediction model that can be utilized for diagnostic purposes in predicting the probability of pneumonia in patients infected with SARS-CoV-2.

Coronavirus disease 2019 (COVID-19) is a highly contagious respiratory disease that has posed a serious threat to people's daily lives and caused an unprecedented challenge to public health and people's health worldwide. Lung squamous cell carcinoma (LUSC) is a common type of lung malignancy with a highly aggressive nature and poor prognosis. Patients with LUSC could be at risk for COVID-19, We conducted this study to examine the potential for naringenin to develop into an ideal medicine and investigate the underlying action mechanisms of naringenin in COVID-19 and LUSC due to the anti-viral, anti-tumor, and anti-inflammatory activities of naringenin.

LUSC related genes were obtained from TCGA, PharmGKB, TTD,GeneCards and NCBI, and then the transcriptome data for COVID-19 was downloaded from GEO, DisGeNET, CTD, DrugBank, PubChem, TTD, NCBI Gene, OMIM. The drug targets of Naringenin were revealed through CTD, BATMAN, TCMIP, SymMap, Chemical Association Networks, SwissTargetPrediction, PharmMapper, ECTM, and DGIdb. The genes related to susceptibility to COVID-19 in LUSC patients were obtained through differential analysis. The interaction of COVID-19/LUSC related genes was evaluated and demonstrated using STRING to develop a a COX risk regression model to screen and evaluate the association of genes with clinical characteristics. To investigate the related functional and pathway analysis of the common targets of COVID-19/LUSC and Naringenin, KEGG and GO enrichment analysis were employed to perform the functional analysis of the target genes. Finally, The Hub Gene was screened and visualized using Cytoscape, and molecular docking between the drug and the target was performed using Autodock.

We discovered numerous COVID-19/LUSC target genes and examined their prognostic value in LUSC patients utilizing a variety of bioinformatics and network pharmacology methods. Furthermore, a risk score model with strong predictive performance was developed based on these target genes to assess the prognosis of LUSC patients with COVID-19. We intersected the therapeutic target genes of naringenin with the LUSC, COVID-19-related targets, and identified 354 common targets, which could be used as potential target genes for naringenin to treat COVID-19/LUSC. The treatment of COVID-19/LUSC with naringenin may involve oxidative stress, anti-inflammatory, antiviral, antiviral, apoptosis, immunological, and multiple pathways containing PI3K-Akt, HIF-1, and VEGF, according to the results of the GO and KEGG enrichment analysis of these 354 common targets. By constructing a PPI network, we ascertained AKT1, TP53, SRC, MAPK1, MAPK3, and HSP90AA1 as possible hub targets of naringenin for the treatment of COVID-19/LUSC. Last but not least, molecular docking investigations showed that naringenin has strong binding activity in COVID-19/LUSC.

We revealed for the first time the pharmacological targets and potential molecular processes of naringenin for the treatment of COVID-19/LUSC. However, these results need to be confirmed by additional research and validation in real LUSC patients with COVID-19.

The novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is primarily a respiratory virus. However, an increasing number of neurologic complications associated with this virus have been reported, e.g., transverse myelitis (TM). We report a case of a 39-year-old man admitted to Namazi Hospital affiliated with Shiraz University of Medical Sciences, Shiraz, Iran. In December 2020, the patient was infected with Coronavirus Disease 2019 (COVID-19). During hospitalization, the patient suffered from sudden onset of paraplegia, and urinary retention, and had a T6-T7 sensory level. TM was diagnosed and an extensive workup was performed to rule out other etiologies. Eventually, para-infectious TM associated with COVID-19 was concluded. The patient received pulse methylprednisolone therapy of 1 g/day for 10 consecutive days followed by seven sessions of plasma exchange without a favorable response. The patient then underwent regular physical rehabilitation and tapering oral administration of prednisolone 1 mg/Kg. As a result, weakness in the lower extremities improved slightly after six months. Overall, we suspect a correlation between COVID-19 and TM, however, further studies are required to substantiate the association.

We aimed to propose a mortality risk prediction model using on-admission clinical and laboratory predictors. We used a dataset of confirmed COVID-19 patients admitted to three general hospitals in Tehran. Clinical and laboratory values were gathered on admission. Six different machine learning models and two feature selection methods were used to assess the risk of in-hospital mortality. The proposed model was selected using the area under the receiver operator curve (AUC). Furthermore, a dataset from an additional hospital was used for external validation. 5320 hospitalized COVID-19 patients were enrolled in the study, with a mortality rate of 17.24% (N = 917). Among 82 features, ten laboratories and 27 clinical features were selected by LASSO. All methods showed acceptable performance (AUC > 80%), except for K-nearest neighbor. Our proposed deep neural network on features selected by LASSO showed AUC scores of 83.4% and 82.8% in internal and external validation, respectively. Furthermore, our imputer worked efficiently when two out of ten laboratory parameters were missing (AUC = 81.8%). We worked intimately with healthcare professionals to provide a tool that can solve real-world needs. Our model confirmed the potential of machine learning methods for use in clinical practice as a decision-support system.

The coronavirus disease 2019 (COVID-19) pandemic has psychological consequences such as increased risk of depression, anxiety, and stress problems, exacerbating human health disparities. This study aimed to analyze depression and its causes in COVID-19-recovered patients in Bangladesh. A cross-sectional study was conducted on COVID-19-recovered patients who attended follow-up visits after 14 days to 3 months at Dhaka Medical College Hospital (DMCH) and Dhaka North City Corporation Hospital (DNCCH), Dhaka, Bangladesh, from 1 January to 31 December 2021. Respondents were face-to-face interviewed with a semistructured questionnaire after written agreement. The Patient Health Questionnaire (PHQ-9) was used to assess respondents' depression, and data were analyzed using SPSS version 23, with a P value of <0.05 indicating statistical significance. A total of 325 COVID-19-recovered patients aged from 15 to 65 years (mean, 44.34 ± 13.87 years) were included in this study, the highest proportion (23.1%) of them were aged 46 to 55 years, and the majority (61.5%) of them were male. There were 69.5% of respondents who had no signs of depression while 31% of them did have signs, with 26.7% being mildly depressed, 2.5% being extremely depressed, and 1.2% being severely depressed. Diabetes mellitus, hospitalization duration, social distancing, social media posts on COVID-19, loss of employment, family damage, and fear of reinfection were significantly associated with depression level of respondents. This study gives us a glimpse into the psychological health of COVID-19-recovered patients, and its findings highlight the imperative of alleviating their psychological anguish in Bangladesh. IMPORTANCE The COVID-19 pandemic had a significant psychological impact on healthy populations, with increased depression, perceived stress, posttraumatic stress disorder, and insomnia reported. The COVID-19 pandemic affects people's mental health by instilling fear of infection and depression. In the post-COVID-19 syndrome, depressive symptoms and clinically significant depression may have serious consequences for quality-of-life outcomes. To combat the spread of COVID-19, the Bangladesh government has implemented a number of measures, including lockdown, social distancing, self-isolation, and quarantine. Given the negative consequences, it is critical to investigate potential factors and mechanisms that may shed light on mental health improvement. The purpose of the study is to determine the level of depression in patients 3 months after recovering from acute COVID-19. The study's findings highlight the need for COVID-19-infected people in Bangladesh to receive health education and interventions.

The clinical efficacy of matrine in treating coronavirus disease (COVID-19) has been confirmed; however, its underlying mechanism of action remains unknown.

TCMSP, SwissTargetPrediction, SEA, GeneCards, CTD, and TTD were used to identify potential targets for matrine in SARS-CoV-2. Cytoscape software was used to determine the target-pathway network for topographical analysis. The online STRING analysis platform and Cytoscape were together used to generate a PPI network and for GO and KEGG pathway enrichment analysis. Finally, molecular docking simulations were performed to study matrine-Mpro, matrine-ACE2, and matrine-RdRp interactions.

Ten common matrine targets were obtained, particularly including TNF-α, IL-6, and CASP3. GO and KEGG pathway enrichment analysis revealed five significantly enriched signalling pathways involved in cell proliferation, apoptosis, programmed cell death, and immune responses.

During COVID-19 treatment, matrine regulates viral replication, host cell apoptosis, and inflammation by targeting the TNF-α, IL-6, and CASP3 in the TNF signalling pathway.

The coronavirus disease 2019 (COVID-19) represents a global health and economic challenge. Hepatic injuries have been approved to be associated with severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection. The viral tropism pattern of SARS-CoV-2 can induce hepatic injuries either by itself or by worsening the conditions of patients with hepatic diseases. Besides, other factors have been reported to play a crucial role in the pathological forms of hepatic injuries induced by SARS-CoV-2, including cytokine storm, hypoxia, endothelial cells, and even some treatments for COVID-19. On the other hand, several groups of people could be at risk of hepatic COVID-19 complications, such as pregnant women and neonates. The present review outlines and discusses the interplay between SARS-CoV-2 infection and hepatic injury, hepatic illness comorbidity, and risk factors. Besides, it is focused on the vaccination process and the role of developed vaccines in preventing hepatic injuries due to SARS-CoV-2 infection.

Background Coronavirus disease-19 (COVID-19) patients often deteriorate rapidly based on viral infection-related inflammation and the subsequent cytokine storm. The clinical symptoms were found to be inconsistent with laboratory findings. There is a need to develop biochemical severity score to closely monitor COVID-19 patients. Methods This study was conducted in the department of biochemistry at All India Institute of Medical Sciences (AIIMS) Bhubaneswar in collaboration with the intensive care unit. Laboratory data of 7,395 patients diagnosed with COVID-19 during the first three waves of the pandemic were analyzed. The serum high sensitivity high-sensitivity C-reactive protein (hs-CRP, immuno-turbidity method), lactate dehydrogenase (LDH, modified Wacker et al. method), and liver enzymes (kinetic-UV method) were estimated by fully automated chemistry analyzer. Serum ferritin and interleukin-6 (IL-6) were measured by one-step immunoassay using chemiluminescence technology. Three models were used in logistic regression to check for the predictive potential of biochemical parameters, and a COVID-19 biochemical severity score was calculated using a non-linear regression algorithm. Results The receiver operating characteristic curve found age, urea, uric acid, CRP, ferritin, IL6, and LDH with the highest odds of predicting ICU admission for COVID-19 patients. COVID-19 biochemical severity scores higher than 0.775 were highly predictive (odds ratio of 5.925) of ICU admission (AUC=0.740, p<0.001) as compared to any other individual parameter. For the validation, 30% of the total dataset was used as testing data (n=2095) with a sensitivity of 68.3%, specificity of 74.5%, and odds ratio of 6.304. Conclusion Age, urea, uric acid, ferritin, IL6, LDH, and CRP-based predictive probability algorithm calculating COVID-19 severity was found to be highly predictive of ICU admission for COVID-19 patients.

Patients with psychiatric disorders are exposed to high risk of COVID-19 and increased mortality. In this study, we set out to assess the clinical features and outcomes of patients with current psychiatric disorders exposed to COVID-19.

This multi-center prospective study was conducted in 22 psychiatric wards dedicated to COVID-19 inpatients between 28 February and 30 May 2020. The main outcomes were the number of patients transferred to somatic care units, the number of deaths, and the number of patients developing a confusional state. The risk factors of confusional state and transfer to somatic care units were assessed by a multivariate logistic model. The risk of death was analyzed by a univariate analysis.

In total, 350 patients were included in the study. Overall, 24 (7%) were transferred to medicine units, 7 (2%) died, and 51 (15%) patients presented a confusional state. Severe respiratory symptoms predicted the transfer to a medicine unit [odds ratio (OR) 17.1; confidence interval (CI) 4.9-59.3]. Older age, an organic mental disorder, a confusional state, and severe respiratory symptoms predicted mortality in univariate analysis. Age >55 (OR 4.9; CI 2.1-11.4), an affective disorder (OR 4.1; CI 1.6-10.9), and severe respiratory symptoms (OR 4.6; CI 2.2-9.7) predicted a higher risk, whereas smoking (OR 0.3; CI 0.1-0.9) predicted a lower risk of a confusional state.

COVID-19 patients with severe psychiatric disorders have multiple somatic comorbidities and have a risk of developing a confusional state. These data underline the need for extreme caution given the risks of COVID-19 in patients hospitalized for psychiatric disorders.