Molecular mechanism and therapeutic significance of essential amino acids in metabolically associated fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD), also known as metabolically associated fatty liver disease (MAFLD), is a systemic metabolic disease characterized by lipid accumulation in the liver, lipid toxicity, insulin resistance, intestinal dysbiosis, and inflammation that can progress from simple steatosis to nonalcoholic steatohepatitis (NASH) and even cirrhosis or cancer. It is the most prevalent illness threatening world health. Currently, there are almost no approved drug interventions for MAFLD, mainly dietary changes and exercise to control weight and regulate metabolic disorders. Meanwhile, the metabolic pathway involved in amino acid metabolism also influences the onset and development of MAFLD in the body, and most amino acid metabolism takes place in the liver. Essential amino acids are those amino acids that must be supplemented from outside the diet and that cannot be synthesized in the body or cannot be synthesized at a rate sufficient to meet the body's needs, including leucine, isoleucine, valine (collectively known as branched-chain amino acids), tryptophan, phenylalanine (which are aromatic amino acids), histidine, methionine, threonine and lysine. The metabolic balance of the body is closely linked to these essential amino acids, and essential amino acids are closely linked to the pathophysiological process of MAFLD. In this paper, we will focus on the metabolism of essential amino acids in the body and further explore the therapeutic strategies for MAFLD based on the studies conducted in recent years.

Novel Bis-pyrazoline Fluorescent Probe for Cu2+ and Fe3+ Detection and Application in Cell Imaging.

A fluorescent probe Y((1,1'-([1,1'-biphenyl]-4,4'-diylbis(3-(2-hydroxyphenyl)-4,5-dihydro-1H-pyrazole-5,1-diyl)) bis(ethan-1-one))) was designed and synthesized, which could be used to Cu2+ and Fe3+ sensors. Through the study of optical properties, the probe Y shows good selectivity and sensitivity to Cu2+ and Fe3+ in aqueous tetrahydrofuran solution [10.0 mM HEPES, pH 7.4, THF-H2O = 9:1(v/v)] with has excellent anti-interference performance, and its detection limits were 0.931 uΜ for Cu2+ and 0.401uΜ for Fe3+. The coordination mechanism of probe Y with Cu2+ and Fe3+ was speculated and verified at DFT level and HRNM. By Hela cytotoxicity and imaging tests, probe Y not only has good biocompatibility, but also can be used for sensing Cu2+ in cells.

Bis-chalcone Fluorescent Probe for Hydrazine Ratio Sensing in Environment and Organism.

In this paper, four novel hydrazine fluorescent probes X1-X4 with bis-chalcone structure were designed and synthesized. Through the measurement of its optical properties, it is found that it can quickly identify hydrazine, high sensitivity, low detection limit, and good anti-interference ability. The recognition of hydrazine by probes X1-X4 is not affected in the pH range of 4-10, X2 has the highest sensitivity, and the detection limit is as low as 0.336 × 10-7 M. Through Gaussian quantization calculation of probe molecules and their reaction products with hydrazine, it is speculated that the recognition mechanism is the closure of intramolecular charge transfer effect. In addition, the cytotoxicity and imaging of HeLa cells were tested, which showed that probes X1-X4 could be used to detect hydrazine in cells.

[Retracted] TGF­ß1 induces peritoneal fibrosis by activating the Smad2 pathway in mesothelial cells and promotes peritoneal carcinomatosis.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the fluorescence microscopy data shown in Fig. 6A and B were strikingly similar to data appearing in different form in Fig. 7 in a previously published paper [Lv Z­D, Na D, Liu F­N, Du Z­M, Sun Z, Li Z, Ma X­Y, Wang Z­N and Xu H­M: Induction of gastric cancer cell adhesion through transforming growth factor­beta1­mediated peritoneal fibrosis. J Exp Clin Cancer Res 29: 139, 2010], which featured some of the same authors, although the data were shown to portray results obtained under different experimental conditions. Furthermore, the data in Fig. 7A for the 'TGF­ß1' and the 'TGF­ß1 + siRNAcon' experiments contained an overlapping section, such that these data appeared to have been derived from the same original source, even though they were intended to show the results from differently performed experiments. Owing to the fact that the contentious data in the above article had already been published prior to its submission to International Journal of Molecular Medicine, and due to a lack of overall confidence in the presented data, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 29: 373­379, 2012; DOI: 10.3892/ijmm.2011.852].

Effect of Sr2+ ions on the structure, up-conversion emission and thermal sensing of Er3+, Yb3+ co-doped double perovskite Ba(2-x)SrxMgWO6 phosphors.

Investigating the effect of different phases on the optical performance is crucial for thermal sensing phosphor materials. Ba(2-x)SrxMgWO6:Er3+, Yb3+, K+ double perovskite phosphors were successfully prepared using a high-temperature solid-phase method. The dominant up-conversion luminescent (UCL) mechanism was deduced by analyzing the power-dependence spectra and energy level diagrams. By X-ray diffraction tests and tolerance factor calculations, it was demonstrated that the substitution of Sr2+ ions for Ba2+ ions led to the phase changing from cubic to tetragonal. The phase transition led to a decrease in the crystallographic symmetry of the compounds and changes in the optical thermometric properties. The optical temperature sensing properties were investigated using the fluorescence intensity ratio of thermally coupled energy levels (2H11/2 and 4S3/2 to the ground state energy level 4I15/2) of Er3+ ions in Ba2MgWO6, BaSrMgWO6 and Sr2MgWO6. The maximum absolute sensitivities obtained for Ba2MgWO6, BaSrMgWO6 and Sr2MgWO6 doped with 7% Er3+, 2% Yb3+ and 9% K+ were 6.77 × 10-4 K-1, 10.09 × 10-4 K-1 and 23.4 × 10-4 K-1, respectively. The comparison revealed that the phase transition caused an increase in the luminescence intensity and absolute sensitivity. This provides a useful pathway for modulating the subsequent thermometric performance.

Sr/Ba substitution induced higher thermal stability far red-emitting Ba1-ySryLaLiWO6:Mn4+ phosphors for plant growth applications.

A series of red-emitting BaLaLiWO6:Mn4+ (BLLW:Mn4+) phosphors were successfully synthesized by a high-temperature solid-state reaction method. The crystal structure and luminescence properties of the obtained samples were systematically investigated. The emission spectra exhibited a deep red emission band peaking at 716 nm with a full width at half-maximum (FWHM) of 44 nm under 340 nm excitation. The optimal Mn4+ molar concentration was about 1.2%. In addition, the luminescence mechanism was analyzed using a Tanabe Sugano energy level diagram. With the substitution of Sr for Ba, there was a red shift in the emission spectrum and a blue shift in the excitation spectrum. The emission intensity of BLLW:1.2%Mn4+ at 150 °C was about 22% of the initial value at room temperature. In contrast, the emission intensity of SrLaLiWO6:1.2%Mn4+ still maintained 79% of the initial emission intensity at room temperature at 150 °C. This was due to the fact that with the substitution of Sr for Ba, the W-O bond length gradually decreases, which gradually enhanced the crystal field strength of Mn4+.

ATG5-Mediated Autophagy May Inhibit Pyroptosis to Ameliorate Oleic Acid-Induced Hepatocyte Steatosis.

Despite activated autophagy ameliorating hepatocyte steatosis and metabolic associated fatty liver disease (MAFLD), mechanisms underlying the beneficial roles of autophagy in hepatic deregulation of lipid metabolism remain undefined. We explored whether autophagy can ameliorate oleic acid (OA)-induced hepatic steatosis by suppressing pyroptosis. Pyroptosis is involved in hepatocyte steatosis induced by OA. In addition, autophagy flux was blocked in OA-treated hepatocytes. Treatment with OA induced lipid accumulation in liver cell line L-02, which was attenuated by rapamycin (Rap), an autophagy agonist, while aggravated by autophagy inhibitor bafilomycin A1 (Baf A1). Inversely, treatment with pyroptotic agonist Nigericin aggravated OA-induced hepatic steatosis, while pyroptosis antagonist disulfiram ameliorated this effect. Mechanistically, treatment with Rap downregulated the expression of pyroptosis-related proteins, including NLRP3, Caspase-1, IL-18, GSDMD expression evoked by OA, thus improving pyroptosis in hepatic steatosis. Significantly, overexpression of ATG5 obviously downregulated cleaved caspase-1 expressions without altering the total caspase1 expressions in hepatic cell steatosis. Taken together, our studies strongly demonstrated that the activation of ATG5 inhibits pyroptosis to improve hepatic steatosis and suggest autophagy activation as a potential therapeutic strategy for pyroptosis-mediated MAFLD.

Relationship between the stroke mechanism of symptomatic middle cerebral artery atherosclerotic diseases and culprit plaques based on high-resolution vessel wall imaging.

Purpose: For patients with symptomatic middle cerebral artery (MCA) atherosclerotic stenosis, identifying the potential stroke mechanisms may contribute to secondary prevention. The purpose of the study is to explore the relationship between stroke mechanisms and the characteristics of culprit plaques in patients with atherosclerotic ischemic stroke in the M1 segment of the middle cerebral artery (MCA) based on high-resolution vessel wall imaging (HR-VWI). Methods: We recruited 61 patients with acute ischemic stroke due to MCA atherosclerotic stenosis from Shenzhen Bao'an District People's Hospital. According to prespecified criteria based on infarct topography and magnetic resonance angiography, possible stroke mechanisms were divided into parent artery atherosclerosis occluding penetrating artery (P), artery-to-artery embolism (A), hypoperfusion (H), and mixed mechanisms (M). The correlation between the characteristics of MCA M1 culprit plaque and different stroke mechanisms was analyzed using HR-VWI. The indicators included plaque surface irregularity, T1 hyperintensity, location, plaque burden (PB), remodeling index (RI), enhancement rate, and stenosis rate. Results: Parental artery atherosclerosis occluding penetrating artery was the most common mechanism (37.7%). The proposed criteria showed substantial to excellent interrater reproducibility (κ, 0.728; 0.593-0.863). Compared with the P group, the surface irregularity, T1 hyperintensity, and obvious enhancement of the culprit plaque in the A group were more common (p < 0.0125). Compared with the other stroke mechanisms, positive remodeling of culprit plaques was more common (p < 0.0125), the RI was greater (p < 0.05), and the PB was the smallest (p < 0.05) in the P group. The enhancement ratio (ER) was smaller in the P group (p < 0.05). Compared with the A group, T1 hyperintensity of the culprit plaque was more common in the H group (p < 0.0125), and the stenosis rate was greater (p < 0.05). After adjustment for clinical demographic factors in the binary logistic regression analysis, the enhancement level (odds ratio [OR] 0.213, 95% CI (0.05-0.91), p = 0.037) and PB of culprit plaque (OR 0, 95% CI (0-0.477), p = 0.034) were negatively associated with P groups. Conclusion: The culprit plaque characteristics of patients with symptomatic MCA atherosclerotic in different stroke mechanisms may be evaluated using HR-VWI. The plaque characteristics of different stroke mechanisms may have clinical value for the selection of treatment strategies and prevention of stroke recurrence. Clinical trial registration: Identifier: ChiCTR1900028533.

Aberrant blood cell division cycle 42 expression and its correlation with disease severity, inflammation and mortality risk in patients with acute pancreatitis.

Cell division cycle 42 (CDC42) can inhibit inflammation by regulating the activity of macrophage and T cells, which contributes to the pathophysiology of acute pancreatitis (AP). Therefore, CDC42 may have application as a potential biomarker for AP. The present study aimed to explore this possibility. Peripheral blood mononuclear cells (PBMCs) were collected from 149 patients with AP and 50 healthy controls (HCs). Subsequently, CDC42 expression in the PBMCs was measured using RT-qPCR; C-reactive protein (CRP), TNF-α and IL-6 in the serum of patients with AP were measured using ELISA. Meanwhile, Mann-Whitney U test, Kruskal-Wallis test, and Spearman's rank correlation test were performed on the data. The CDC42 expression levels were lower in patients with AP compared with those in HCs (P<0.001). CDC42 expression was declined in patients with moderate-severe AP (MSAP) vs. patients with mild AP (MAP) (P=0.029), and in patients with severe AP (SAP) vs. patients with MAP (P=0.004). CDC42 expression correlated negatively with the Ranson's score (P<0.001), APACEH II score (P=0.011) and SOFA score (P<0.001) in patients with AP. CDC42 expression also correlated negatively with CRP (P<0.001) and TNF-α (P=0.004) levels but not with IL-6 levels (P=0.177). Furthermore, CDC42 expression was lower in deceased patients with AP vs. AP survivors (P<0.001) and in deceased patients with SAP vs. SAP survivors (P=0.026). CDC42 had good potential in predicting mortality from AP, with AUC of 0.829 and a 95% CI of 0.731-0.927, and it also had certain potential in predicting mortality from SAP and MSAP, with AUC (95% CI) of 0.794 (0.616-0.973) and 0.757 (0.558-0.956), respectively. In conclusion, data from the present study suggest that lower CDC42 expression levels correlate with higher disease susceptibility, disease severity, inflammation, and mortality risk in patients with AP.

Targeting Thyroid Hormone/Thyroid Hormone Receptor Axis: An Attractive Therapy Strategy in Liver Diseases.

Thyroid hormone/thyroid hormone receptor (TH/TR) axis is characterized by TH with the assistance of plasma membrane transporters to combine with TR and mediate biological activities. Growing evidence suggests that TH/TR participates in plenty of hepatic metabolism. Thus, this review focuses on the role of the TH/TR axis in the liver diseases. To be specific, the TH/TR axis may improve metabolic-associated fatty liver disease, hepatitis, liver fibrosis, and liver injury while exacerbating the progression of acute liver failure and alcoholic liver disease. Also, the TH/TR axis has paradoxical roles in hepatocellular carcinoma. The TH/TR axis may be a prospecting target to cure hepatic diseases.

Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases.

Nuclear lamins, known as type 5 intermediate fibers, are composed of lamin A, lamin C, lamin B1, and lamin B2, which are encoded by LMNA and LMNB genes, respectively. Importantly, mutations in nuclear lamins not only participate in lipid disorders but also in the human diseases, such as lipodystrophy, metabolic-associated fatty liver disease, and dilated cardiomyopathy. Among those diseases, the mechanism of lamin has been widely discussed. Thereby, this review mainly focuses on the regulatory mechanism of the mutations in the lamin gene in lipid alterations and the human diseases. Considering the protean actions, targeting nuclear lamins may be a potent therapeutic avenue for lipid metabolic disorders and human diseases in the future.

Targetting ferroptosis for blood cell-related diseases.

Ferroptosis is an iron-dependent cell death pathway and participates in various diseases. Current evidence suggests that ferroptosis can obviously affect the function of blood cells. This paper aims to elaborate the role of ferroptosis in blood cells and related diseases. First, abnormal ferroptosis damages the developing red blood cells by breaking systemic iron homeostasis, leading to erythropoiesis suppression and anaemia. Ferroptosis mediates neutrophils recruitment and neutrophil extracellular trap formation (NETosis). In T-cells, ferroptosis induces a novel point of synergy between immunotherapy and radiotherapy. Additionally, ferroptosis may mediate B cells differentiation, antibody responses and lymphoma. Nevertheless, increased ferroptosis can ameliorate acute myeloid leukaemia and T-cell leukaemia/lymphoma by inducing iron-dependent cancer cells death. Besides, ferroptosis activates platelets by increasing P-selectin, thus causing thromboembolism. Ferroptosis mediates virus infection and parasite infection by driving T-cell death and preventing T-cell immunity. Interestingly, ferroptosis is also considered as a critical player in COVID-19 infections, while targetting ferroptosis may also improve thromboembolism and prognosis in patients with COVID-19 infection. Overall, the crucial role of ferroptosis in blood cells will show a new therapeutic potential in blood cell-related diseases.HighlightsFerroptosis shows a new therapeutic potential for blood cell-related diseases.Ferroptosis damages erythropoiesis and thus induces anaemia.Ferroptosis induces platelet activation and leads to thromboembolism.Ferroptosis regulates T-cell and B-cell immunity, which participant in infectious diseases.Inversely, ferroptosis ameliorates acute myeloid leukaemia and T-cell leukaemia.

PPFIA4 Promotes Colon Cancer Cell Proliferation and Migration by Enhancing Tumor Glycolysis.

Dysregulated glycolysis is one of the mechanisms employed by cancer cells to facilitate growth and metastasis. Here we aimed to characterize the PPFIA4 gene, as a glycolysis-related oncogene in promoting the proliferation and migration of colon cancer cells. Using bioinformatical tools including The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA), we found that PPFIA4 expression and methylation levels were higher in colon cancer tissues of different stages than in normal tissues. Higher PPFIA4 level was also positively correlated with poorer survival of patients. PPFIA4 upregulation also correlated with poor prognosis and higher clinical stages of colon cancer patients. Colon cancer cell viability, migration and migration were enhanced after PPFIA4 overexpression. EMT markers and glycolysis were upregulated after PPFIA4 overexpression. PPFIA4 expression was found to be positively correlated with PFKFB3 and ENO2 levels, while knockdown of PFKFB3 and ENO2 reduced cell proliferation, migration, invasion and glycolysis. PPFIA4 upregulation is a potential biomarker in colon cancer which promotes proliferation, migration, invasion and glycolysis. The upregulation of PFKFB3/ENO2 signaling by PPFIA4 is a potential mechanism underlying the oncogenic effects of PPFIA4.

Mitochondrial unfolded protein response: A novel pathway in metabolism and immunity.

Mitochondrial unfolded protein response (mitoUPR) is a mitochondria stress response to maintain mitochondrial proteostasis during stress. Increasing evidence suggests that mitoUPR participates in diverse physiological processes especially metabolism and immunity. Although mitoUPR regulates metabolism in many aspects, it is mainly reflected in the regulation of energy metabolism. During stress, mitoUPR alters energy metabolism via suppressing oxidative phosphorylation (OXPHOS) or increasing glycolysis. MitoUPR also alters energy metabolism and regulates diverse metabolic diseases such as diabetes, cancers, fatty liver and obesity. In addition, mitoUPR also participates in immune process during stress. MitoUPR can induce innate immune response during various infections and may regulate inflammatory response during diverse inflammations. Considering the pleiotropic actions of mitoUPR, mitoUPR may supply diverse therapeutic targets for metabolic diseases and immune diseases.

Photogenerated charge separation and recombination path modification in monocline Lu2WO6via lattice transition and Bi-O antibonding states.

Monoclinic Lu2WO6 undergoes diphase-to-perovskite BiLuWO6 transition via selective occupancy of Bi in three Lu sites. The transformation mechanism, process, and structure stabilities are revealed by variable cell nudged elastic band method, video, and phonon spectrum. Lattice transition brings about photogenerated charge separation in BiLuWO6. This is verified by indirect band gap transition, high electron migration rate, weak exciton binding energy, large photocurrent response, and small impedance. The electron-hole life time is elongated to produce abundant superoxide and hydroxyl radicals for the degradation of rhodamine B and phenol molecules. Bi-O antibonding states serve as immediate energy levels to change the recombination path, inducing 340 nm excitation band and 510 nm green light emission of Lu2WO6. Furthermore, multicolor emission of 1 at% Bi3+ + RE3+ (RE = Sm/Eu/Dy)-codoped Lu2WO6 is acquired via synergistic modification of the Bi-O antibonding state and RE3+ 4f states. Thus, the photogenerated charge motion in Lu2WO6 is tuned to expand application fields.

Functions of nuclear receptors SUMOylation.

The nuclear receptor superfamily is a family of ligand-activated transcription factors that play a key role in cell metabolism and human diseases. They can be modified after translation, such as acetylation, ubiquitination, phosphorylation and SUMOylation. Crosstalk between SUMO and ubiquitin, phosphorylation and acetylation regulates a variety of metabolic and physiological activities. Nuclear receptors play an important role in lipid metabolism, inflammation, bile acid homeostasis and autophagy. SUMOylation nuclear receptors can regulate their function and affect cell metabolism. It also provides a potential therapeutic target for atherosclerosis, tumor and other metabolic and inflammation-related diseases. This review focuses on the function of SUMOylation nuclear receptors.

Quantitative and Qualitative Analysis of Atherosclerotic Stenosis in the Middle Cerebral Artery Using High-Resolution Magnetic Resonance Imaging.

PURPOSE: We analyzed and compared the imaging characteristics of the vessel wall of the middle cerebral artery (MCA) in symptomatic and asymptomatic patients using a 3.0-T high-resolution magnetic resonance imaging (HR-MRI) protocol, including a 3-dimensional T1-sampling perfection with application-optimized contrasts using different flip angle evolutions sequence. METHODS: Fifty-three patients with atherosclerotic stenosis of the MCA underwent 3.0-T HR-MRI examinations. The characteristics of atherosclerotic plaques in 53 patients (28 symptomatic, 25 asymptomatic) were analyzed, including plaque distribution and signal intensity. Plaque burden (PB), stenosis degree, and the remodeling index were measured and compared between symptomatic and asymptomatic patients. RESULTS: The PB of the symptomatic group was significantly higher than that of the asymptomatic group (P = .006), and moderate-severe stenosis was more common (P = .01). The remodeling index of the symptomatic group was also lower (P = .015) and negative remodeling (NR) was more common (P = .043). Binary logistic regression analysis showed that stenosis degree was a risk factor in symptomatic patients (odds ratio = 135, P = .023). CONCLUSION: There is a trend that some characteristics of plaques and vessels, including the moderate-severe stenosis, larger PB, and NR, were observed more frequently among patients with symptomatic atherosclerotic stenosis of the MCA than among asymptomatic patients.

Sumoylation in liver disease.

Small ubiquitin-like modifiers (SUMO) are highly conserved post-translational modification proteins that are present in eukaryotic cells. They are extensively expressed in diverse tissues, including the heart, liver, kidney, and lungs. SUMOylation, a crucial post-translational modification, exhibits a strong effect on DNA repair, transcriptional regulation, protein stability and cell cycle progression. Increasing evidence has demonstrated that SUMOylation is closely related to the development of liver disease. Therefore, the effects of SUMOylation in liver diseases, such as Hepatocellular carcinoma (HCC), viral hepatitis, non-alcoholic fatty liver disease (NAFLD), cirrhosis and primary biliary cirrhosis (PBC) were reviewed in this study. Specifically, SUMO1 was found to promote the invasion and metastasis of HCC and may promote hypoxia-mediated P65 nuclear transport while accelerating the progression of HCC. In addition, SUMO1-modified centrosomal P4.1-associated protein (CAPA) was observed to be overexpressed in Hepatitis B virus (HBV)-related HCC in response to TNF-α stimulation. Furthermore, SUMOylated CAPA was found to induce HBX-triggered NF-κB activation. Considering the diversity and significance of SUMOylation, targeting of the SUMOylation pathway may serve as an effective approach in the treatment of liver diseases.

Epidemiological and clinical characteristics of COVID-19 patients in Hengyang, Hunan Province, China.

BACKGROUND: In December 2019, an ongoing outbreak of coronavirus disease 2019 (COVID-19) was first identified in Wuhan, China. The characteristics of COVID-19 patients treated in local hospitals in Wuhan are not fully representative of patients outside Wuhan. Therefore, it is highly essential to analyze the epidemiological and clinical characteristics of COVID-19 in areas outside Wuhan or Hubei Province. To date, a limited number of studies have concentrated on the epidemiological and clinical characteristics of COVID-19 patients with different genders, clinical classification, and with or without basic diseases. AIM: To study the epidemiological and clinical characteristics of COVID-19 patients in Hengyang (China) and provide a reliable reference for the prevention and control of COVID-19. METHODS: From January 16 to March 2, 2020, a total of 48 confirmed cases of COVID-19 were reported in Hengyang, and those cases were included in this study. The diagnostic criteria, clinical classification, and discharge standard related to COVID-19 were in line with the Diagnosis and Treatment Protocol for Novel Coronavirus Pneumonia (Trial Version 7) released by National Health Commission and National Administration of Traditional Chinese Medicine. The presence of SARS-CoV-2 in pharyngeal swab specimens was detected by quantitative reverse transcription polymerase chain reaction. All the data were imported into the excel worksheet and statistically analyzed by using SPSS 25.0 software. RESULTS: A total of 48 cases of COVID-19 were collected, of which 1 was mild, 38 were moderate, and 9 were severe. It was unveiled that there were 31 (64.6%) male patients and 17 (35.4%) female patients, with a female-to-male ratio of 1.82:1. The range of age of patients with COVID-19 was dominantly 30-49 years old [25 (52.1%) of 48], followed by those aged over 60 years old [11 (22.9%)]. Besides, 29.2% (14 of 48) of patients had basic diseases, and 57.2% (8 of 14) of patients with basic diseases were aged over 60 years old. The occupations of 48 COVID-19 patients were mainly farmers working in agricultural production [15 (31.5%) of 48], rural migrant workers from Hengyang to Wuhan [15 (31.5%)], and service workers operating in the service sector [8 (16.7%)]. The mean latent period was 6.86 ± 3.57 d, and the median was 7 [interquartile range (IQR): 4-9] d. The mean time from onset of symptoms to the first physician visit was 3.38 ± 2.98 (95%CI: 2.58-9.18) d, with a median of 2 (IQR: 1-5) d, and the mean time from hospital admission to confirmed diagnosis was 2.29 ± 2.11 (95%CI: 1.18-6.42) d, with a median of 2 (IQR: 1-3) d. The main symptoms were fever [43 (89.6%) of 48], cough and expectoration [41 (85.4%)], fatigue [22 (45.8%)], and chills [22 (45.8%)]. Other symptoms included poor appetite [13 (27.1%)], sore throat [9 (18.8%)], dyspnea [9 (18.8%)], diarrhea [7 (14.6%)], dizziness [5 (10.4%)], headache [5 (10.4%)], muscle pain [5 (10.4%)], nausea and vomiting [4 (8.3%)], hemoptysis [4 (8.3%)], and runny nose [1 (2.1%)]. The numbers of peripheral blood leukocytes, lymphocytes, and eosinophils were significantly reduced in the majority of the patients. The levels of C-reactive protein, fibrinogen, blood glucose, lactate dehydrogenase, D-dimer, alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (γ-GT), myoglobin (MB), and creatine kinase (CK) were increased in 64.6%, 44.7%, 43.2%, 37.0%, 29.5%, 22.9%,20.8%, 21.6%, 13.6%, and 12.8% of patients, respectively. The incidence of ALT elevation in male patients was remarkably higher than that in females (P < 0.01), while the incidences of AST, CK, and blood glucose elevations in severe patients were remarkably higher than those in moderate patients (P < 0.05, respectively). Except for the mild patients, chest computed tomography showed characteristic pulmonary lesions. All the patients received antiviral drugs, 38 (79.2%) accepted traditional Chinese medicine, and 2 (4.2%) received treatment of human umbilical-cord mesenchymal stem cells. On March 2, 2020, 48 patients with COVID-19 were all cured and discharged. CONCLUSION: Based on our results, patients with COVID-19 often have multiple organ dysfunction or damage. The incidences of ALT elevation in males, and AST, CK, and blood glucose elevations in severe patients are remarkably higher.