Objective:To explore the expression changes of nerve growth factor (NGF)/tropomyosin receptor kinase A (TrkA) signaling pathway of dorsal root ganglia (DRG) in incisional rat remifentanil-induced hyperalgesia and its effect on the expression of membrane delta opioid receptor (DOR).Methods:A total of 48 SPF male SD rats were randomly divided into 6 groups based on body weight matching, with 8 in each group, which were control group (infusion of 0.9% NaCl solution via the tail vein), incision pain group (incision pain model established using the Brennan method), remifentanil group (infusion of remifentanil via the tail vein), incision pain+ remifentanil model group (incision pain model established using the Brennan method, followed by infusion of remifentanil via the tail vein), NGF group and TrkA inhibitor group(established incision pain+ remifentanil model after intrathecal injection of NGF (0.06 μg/g) or K252a (0.3 μg/g, TrkA inhibitor)). Mechanical paw withdrawal threshold (PWT) was used to assess pain sensitivity in rats. Western blot was employed to measure the expression of NGF, TrkA, and the total DOR(tDOR) and the membrane DOR(mDOR) in DRG tissues. Immunoelectron microscopy was used to detect subcellular DOR expression in DRG. Data were processed using SPSS 24.0 software. Multiple comparisons among groups were conducted by repeated measures ANOVA or one-way ANOVA, and post-hoc comparisons were performed using the Bonferroni test.Results:(1) The results of pain behavior showed that there was a significant interaction effect between time and group in the comparison of PWT among the six groups of rats before and after intervention ( F=345.817, P<0.001). At each time point after intervention, the PWTs of the incision pain+ remifentanil group were lower than those of the incision pain group and remifentanil group, the PWTs of the NGF group were lower than those of the incision pain+ remifentanil group, and the PWTs of the TrkA inhibitor group were higher than those of the incision pain+ remifentanil group and NGF group (all P<0.05). (2)The Western blot results showed that there were statistically significant differences in the relative levels of NGF, TrkA, and mDOR in the DRG tissues of the six groups of rats ( F=156.2, 163.8, 421.2, all P<0.001). The levels of NGF, TrkA, and mDOR proteins in the incision pain+ remifentanil group (1.45±0.07, 1.46±0.04, 3.01±0.20) were higher than those in the incision pain group (1.25±0.05, 1.24±0.04, 1.84±0.05) and remifentanil group (1.24±0.04, 1.26±0.03, 1.84±0.04) (all P<0.05). The levels of NGF, TrkA, and mDOR in the NGF group (1.57±0.03, 1.58±0.07, 3.74±0.25) were higher than those in the incision pain+ remifentanil group (all P<0.05). The relative expression levels of TrkA, and mDOR in the TrkA inhibitor group (1.25±0.04, 1.68±0.07) were lower than those in the incision pain+ remifentanil group and the NGF group (all P<0.05). (3)The results of immunoelectron microscopy showed that there were statistically significant differences in the localization of DOR in the cell membrane, subcellular sites of synthesis pathways, and subcellular localization of degradation pathways among the six groups of rat DRG tissues ( F=140.3, 60.63, 60.28, all P<0.01). The DOR of the synthesis pathway of incision pain+ remifentanil group was higher than that of the incision pain group and remifentanil group, while the DOR of the synthesis pathway of NGF was higher than that of the incision pain+ remifentanil group.The DOR of the synthesis pathway of TrkA inhibitor group was lower than that of the incision pain+ remifentanil group and NGF group (both P<0.05). The DOR of the degradation pathway in the incision pain+ remifentanil group was lower than that in the incision pain group and remifentanil group, the DOR of the degradation pathway in the NGF group was lower than that in the incision pain+ remifentanil group, and the DOR of the degradation pathway in the TrkA inhibitor group was higher than that in the incision pain+ remifentanil group and NGF group (both P<0.05). Conclusion:The NGF/TrkA signaling pathway is involved in rat incisional pain-remifentanil hyperalgesia by upregulating the delta opioid receptor of the dorsal root ganglia.

Objective:To explore the expression changes of nerve growth factor (NGF)/tropomyosin receptor kinase A (TrkA) signaling pathway of dorsal root ganglia (DRG) in incisional rat remifentanil-induced hyperalgesia and its effect on the expression of membrane delta opioid receptor (DOR).Methods:A total of 48 SPF male SD rats were randomly divided into 6 groups based on body weight matching, with 8 in each group, which were control group (infusion of 0.9% NaCl solution via the tail vein), incision pain group (incision pain model established using the Brennan method), remifentanil group (infusion of remifentanil via the tail vein), incision pain+ remifentanil model group (incision pain model established using the Brennan method, followed by infusion of remifentanil via the tail vein), NGF group and TrkA inhibitor group(established incision pain+ remifentanil model after intrathecal injection of NGF (0.06 μg/g) or K252a (0.3 μg/g, TrkA inhibitor)). Mechanical paw withdrawal threshold (PWT) was used to assess pain sensitivity in rats. Western blot was employed to measure the expression of NGF, TrkA, and the total DOR(tDOR) and the membrane DOR(mDOR) in DRG tissues. Immunoelectron microscopy was used to detect subcellular DOR expression in DRG. Data were processed using SPSS 24.0 software. Multiple comparisons among groups were conducted by repeated measures ANOVA or one-way ANOVA, and post-hoc comparisons were performed using the Bonferroni test.Results:(1) The results of pain behavior showed that there was a significant interaction effect between time and group in the comparison of PWT among the six groups of rats before and after intervention ( F=345.817, P<0.001). At each time point after intervention, the PWTs of the incision pain+ remifentanil group were lower than those of the incision pain group and remifentanil group, the PWTs of the NGF group were lower than those of the incision pain+ remifentanil group, and the PWTs of the TrkA inhibitor group were higher than those of the incision pain+ remifentanil group and NGF group (all P<0.05). (2)The Western blot results showed that there were statistically significant differences in the relative levels of NGF, TrkA, and mDOR in the DRG tissues of the six groups of rats ( F=156.2, 163.8, 421.2, all P<0.001). The levels of NGF, TrkA, and mDOR proteins in the incision pain+ remifentanil group (1.45±0.07, 1.46±0.04, 3.01±0.20) were higher than those in the incision pain group (1.25±0.05, 1.24±0.04, 1.84±0.05) and remifentanil group (1.24±0.04, 1.26±0.03, 1.84±0.04) (all P<0.05). The levels of NGF, TrkA, and mDOR in the NGF group (1.57±0.03, 1.58±0.07, 3.74±0.25) were higher than those in the incision pain+ remifentanil group (all P<0.05). The relative expression levels of TrkA, and mDOR in the TrkA inhibitor group (1.25±0.04, 1.68±0.07) were lower than those in the incision pain+ remifentanil group and the NGF group (all P<0.05). (3)The results of immunoelectron microscopy showed that there were statistically significant differences in the localization of DOR in the cell membrane, subcellular sites of synthesis pathways, and subcellular localization of degradation pathways among the six groups of rat DRG tissues ( F=140.3, 60.63, 60.28, all P<0.01). The DOR of the synthesis pathway of incision pain+ remifentanil group was higher than that of the incision pain group and remifentanil group, while the DOR of the synthesis pathway of NGF was higher than that of the incision pain+ remifentanil group.The DOR of the synthesis pathway of TrkA inhibitor group was lower than that of the incision pain+ remifentanil group and NGF group (both P<0.05). The DOR of the degradation pathway in the incision pain+ remifentanil group was lower than that in the incision pain group and remifentanil group, the DOR of the degradation pathway in the NGF group was lower than that in the incision pain+ remifentanil group, and the DOR of the degradation pathway in the TrkA inhibitor group was higher than that in the incision pain+ remifentanil group and NGF group (both P<0.05). Conclusion:The NGF/TrkA signaling pathway is involved in rat incisional pain-remifentanil hyperalgesia by upregulating the delta opioid receptor of the dorsal root ganglia.

Objective:To evaluate the role of sphingosine-1-phospho-1 receptor 1 (S1PR1) in remifentanil-induced hyperalgesia in rats with incisional pain and the relationship with KCNQ2/3 potassium channels in the dorsal root ganglia (DRG).Methods:Forty-eight male Sprague-Dawley rats with successful caudal vein catheterization, aged 2-3 months, weighing 260-280 g, were divided into 6 groups ( n=8 each) using a random number table method: control group (group C), S1PR1 inhibitor group (FTY720) group (group F), remifentanil group (group R), remifentanil + S1PR1 inhibitor (FTY720) group (group RF), remifentanil + incision pain group (group RI) and remifentanil + incision pain + S1PR1 inhibitor (FTY720) group (group RIF). In group C, normal saline 0.1 ml· kg -1·min -1 was intravenously infused for 60 min. In group F, FTY720 3 nmol was intrathecally injected at 10 min before normal saline injection, and 0.1 ml · kg -1·min -1 normal saline was infused into the caudal vein for 60 min. Remifentanil 1.0 μg· kg -1·min -1 was infused for 60 min through the caudal vein in group R. In RF group, FTY720 (3 nmol) was intrathecally injected, and 10 min later remifentanil 1.0 μg· kg -1·min -1 was infused via the caudal vein for 60 min. The incisional pain model was established, and remifentanil 1.0 μg· kg -1·min -1 was infused via the caudal vein for 60 min in RI group. In RIF group, FTY720 3 nmol was intrathecally injected at 10 min before remifentanil infusion, then the incisional pain model was developed, and remifentanil 1.0 μg· kg -1·min -1 was infused via the caudal vein at the same time for 60 min. The mechanical paw withdraw threshold (MWT) and thermal paw withdraw latency (TWL) were measured at 24 h before remifentanil or normal saline infusion (T 0) and 2, 6, 24 and 48 h after remifentanil or normal saline infusion (T 1-4). The rats were sacrificed after the last measurement of pain threshold, and the L 4-6 segments of the DRG were taken for determination of the expression of S1PR1, KCNQ2 and KCNQ3 protein and mRNA in the DRG by Western blot and real-time polymerase chain reaction. Results:Compared with group C, the MWT was significantly decreased, and the TWL was shortened at T 1-4, the expression of S1PR1 protein and mRNA in the DRG was up-regulated, the expression of KCNQ2 and KCNQ3 protein and mRNA in the DRG was down-regulated ( P<0.05), and no significant change was found in each parameter in R and RI groups ( P>0.05). Compared with group R, the MWT was significantly decreased, and the TWL was shortened at T 1-4, the expression of S1PR1 protein and mRNA in the DRG was up-regulated, and the expression of KCNQ2 and KCNQ3 protein and mRNA in the DRG was down-regulated in group RI, and the MWT was significantly increased, and the TWL was prolonged at T 1-4, the expression of S1PR1 protein and mRNA in the DRG was down-regulated, and the expression of KCNQ2 and KCNQ3 protein and mRNA in the DRG was up-regulated in group RF ( P<0.05). Compared with group RI, the MWT was significantly increased, and the TWL was prolonged at T 1-4, the expression of S1PR1 protein and mRNA in the DRG was down-regulated, and the expression of KCNQ2 and KCNQ3 protein and mRNA in the DRG was up-regulated in group RIF ( P<0.05). Conclusions:S1PR1 is involved in the process of remifentanil-induced hyperalgesia in rats with incisional pain, which is related to the inhibition of KCNQ2/3 potassium channel expression in the DRG.

Objective:To investigate the reproductive toxicity of cadmium sulfide nanoparticles (Nano-CdS) with different particle sizes on male mice.Methods:In January 2019, 30 SPF grade male mice were randomly divided into a control group, an experimental group[CdS Ⅰ group (particle size approximately 5 nm), and a CdS Ⅱ group (particle size approximately 50 nm) ], with 10 mice in each group. The experimental group was orally gavaged with 100 mg/kg, once a day, while the control group was gavaged with an equal volume of physiological saline for 45 consecutive days. After 45 days, levels of cadmium accumulation in testis were determined directly by AAS, deformity and testicular histopathological changes were also observed. Serum testosterone levels were measured by enzyme-linked immunosorbentassay (ELISA), expression levels of P450scc, 17β-HSD and P450c17 mRNA were determined by real-time PCR. P450c17 protein was determinated by Western Blot.Results:The histopathological results showed that the testes of the experimental group mice showed varying degrees of damage; Ultrastructural observation showed that the ultrastructure of mouse testicular cells in each experimental group showed varying degrees of mitochondrial expansion and disappearance of cristae, as well as irregular nuclear membranes. The degree of damage in CdS Ⅰ group was milder than that in CdS Ⅱ group. Compared with the control group, the cadmium content in the testes of the CdS Ⅰ and CdS Ⅱ groups significantly increased ( P=0.001, 0.001), and the CdS Ⅱ group was higher than the CdS Ⅰ group ( P=0.001). Compared with the control group, the levels of testosterone in the CdS Ⅰ and CdS Ⅱ groups decreased with statistical significance ( P=0.001, 0.001). Real time fluorescence quantitative PCR results showed that compared with the control group, the experimental group's P450scc, 17β-HSD. The expression levels of 17β-HSD and P450c17 mRNA were significantly reduced, with statistically significant differences ( P=0.001, 0.001, 0.001), and CdS Ⅱ group 17β-HSD. The expression levels of 17β-HSD and P450c17 mRNA were significantly lower than those of CdS Ⅰ group ( P=0.001, 0.036). The Western Blot assay results showed that the expression levels of P450c17 protein in the testes of CdS Ⅰ and CdS Ⅱ groups of mice were significantly reduced, with statistical significance ( P=0.001, 0.001) ; And the CdS Ⅱ group was significantly lower than the CdS Ⅰ group ( P=0.001). According to Spearman correlation analysis, testosterone levels are correlated with P450scc, P450c17, 17β-HSD mRNA. There is a highly positive correlation between 17β-HSD mRNA levels, with statistically significant differences ( rs=0.88, 0.80, 0.70, P=0.001, 0.001, 0.004) . Conclusion:Nano cadmium sulfide may induce reproductive toxicity by reducing the expression levels of key enzyme genes and enzyme protein activity in testosterone and its synthesis in mice, and the CdS Ⅱ group has a stronger toxic effect.

Objective:To investigate the reproductive toxicity of cadmium sulfide nanoparticles (Nano-CdS) with different particle sizes on male mice.Methods:In January 2019, 30 SPF grade male mice were randomly divided into a control group, an experimental group[CdS Ⅰ group (particle size approximately 5 nm), and a CdS Ⅱ group (particle size approximately 50 nm) ], with 10 mice in each group. The experimental group was orally gavaged with 100 mg/kg, once a day, while the control group was gavaged with an equal volume of physiological saline for 45 consecutive days. After 45 days, levels of cadmium accumulation in testis were determined directly by AAS, deformity and testicular histopathological changes were also observed. Serum testosterone levels were measured by enzyme-linked immunosorbentassay (ELISA), expression levels of P450scc, 17β-HSD and P450c17 mRNA were determined by real-time PCR. P450c17 protein was determinated by Western Blot.Results:The histopathological results showed that the testes of the experimental group mice showed varying degrees of damage; Ultrastructural observation showed that the ultrastructure of mouse testicular cells in each experimental group showed varying degrees of mitochondrial expansion and disappearance of cristae, as well as irregular nuclear membranes. The degree of damage in CdS Ⅰ group was milder than that in CdS Ⅱ group. Compared with the control group, the cadmium content in the testes of the CdS Ⅰ and CdS Ⅱ groups significantly increased ( P=0.001, 0.001), and the CdS Ⅱ group was higher than the CdS Ⅰ group ( P=0.001). Compared with the control group, the levels of testosterone in the CdS Ⅰ and CdS Ⅱ groups decreased with statistical significance ( P=0.001, 0.001). Real time fluorescence quantitative PCR results showed that compared with the control group, the experimental group's P450scc, 17β-HSD. The expression levels of 17β-HSD and P450c17 mRNA were significantly reduced, with statistically significant differences ( P=0.001, 0.001, 0.001), and CdS Ⅱ group 17β-HSD. The expression levels of 17β-HSD and P450c17 mRNA were significantly lower than those of CdS Ⅰ group ( P=0.001, 0.036). The Western Blot assay results showed that the expression levels of P450c17 protein in the testes of CdS Ⅰ and CdS Ⅱ groups of mice were significantly reduced, with statistical significance ( P=0.001, 0.001) ; And the CdS Ⅱ group was significantly lower than the CdS Ⅰ group ( P=0.001). According to Spearman correlation analysis, testosterone levels are correlated with P450scc, P450c17, 17β-HSD mRNA. There is a highly positive correlation between 17β-HSD mRNA levels, with statistically significant differences ( rs=0.88, 0.80, 0.70, P=0.001, 0.001, 0.004) . Conclusion:Nano cadmium sulfide may induce reproductive toxicity by reducing the expression levels of key enzyme genes and enzyme protein activity in testosterone and its synthesis in mice, and the CdS Ⅱ group has a stronger toxic effect.

Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis and insulin resistance and there are currently no approved drugs for its treatment. Hyperactivation of mTOR complex 1 (mTORC1) and subsequent impairment of the transcription factor EB (TFEB)-mediated autophagy-lysosomal pathway (ALP) are implicated in the development of NAFLD. Accordingly, agents that augment hepatic TFEB transcriptional activity may have therapeutic potential against NAFLD. The objective of this study was to investigate the effects of nuciferine, a major active component from lotus leaf, on NAFLD and its underlying mechanism of action. Here we show that nuciferine activated ALP and alleviated steatosis, insulin resistance in the livers of NAFLD mice and palmitic acid-challenged hepatocytes in a TFEB-dependent manner. Mechanistic investigation revealed that nuciferine interacts with the Ragulator subunit hepatitis B X-interacting protein and impairs the interaction of the Ragulator complex with Rag GTPases, thereby suppressing lysosomal localization and activity of mTORC1, which activates TFEB-mediated ALP and further ameliorates hepatic steatosis and insulin resistance. Our present results indicate that nuciferine may be a potential agent for treating NAFLD and that regulation of the mTORC1-TFEB-ALP axis could represent a novel pharmacological strategy to combat NAFLD.

Objective:To explore the risks of cardiovascular disease (CVD) and influencing factors in human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) patients with long-term combination anti-retroviral therapy (cART).Methods:The baseline data from the multi-center prospective cohort of HIV/AIDS patients who received long-term cART from 2018 to 2020 were collected. cART-naive HIV/AIDS patients were matched by age and gender using the propensity score matching (PSM) as controls. Data collection adverse events of anti-human immunodeficiency virus drugs reduced model (D: A: D[R]) score, Framingham risk score (FRS) and atherosclerotic cardiovascular disease (ASCVD) risk score were used to assess the 10-year CVD risk in patients with long-term cART treatment and in cART-naive patients. Logistic regression analysis was used to assess the risk factors related to high 10-year CVD risk.Results:A total of 301 HIV/AIDS patients received long-term cART and 300 cART-naive HIV/AIDS patients were included, with an average age of 39.8 years old. There were 490 male accounting for 81.5%. Based on the D: A: D [R] score, 4.3%(13/301) of patients in the long-term cART group had a 10-year CVD risk assessment of ≥10%, and 6.3%(19/300) of patients in the cART-naive group. Based on the FRS, 13.4%(36/269) of patients in the long-term cART group had a 10-year CVD risk assessment of ≥10%, and 10.6%(28/264) in the cART-naive group. Based on the ASCVD risk score, 10.4%(14/135) of patients in the long-term cART group had a 10-year CVD risk assessment of ≥7.5%, and 13.8%(17/123) in the cART-naive group. There was no significant difference in the prevalence of high 10-years CVD risk between the long-term cART group and the cART-naive group assessed by any of risk equations (all P>0.050). By multivariate logistic regression analysis, the risk factors associated with 10-year CVD risk ≥10% assessed by D: A: D[R] model were age≥50 years, smoking, hypertension, diabetes, dyslipidemia and CD4 + T lymphocyte count <200×10 6 cells/L (adjusted odds ratio ( AOR)=697.48, 4 622.28, 23.11, 25.95, 27.72 and 18.25, respectively, all P<0.010). The risk factors associated with 10-year CVD risk ≥10% assessed by FRS were age≥50 years, male, smoking, hypertension, diabetes and dyslipidemia ( AOR=53.51, 4.52, 36.93, 36.77, 6.15 and 3.84, respectively, all P<0.050). The risk factors associated with 10-year CVD risk ≥7.5% assessed by ASCVD risk score were age≥50 years, male, smoking, hypertension, diabetes ( AOR=18.48, 14.11, 14.81, 13.42 and 12.41, respectively, all P<0.050). Conclusions:Long-term cART has no significant effect on the 10-year CVD risk in HIV/AIDS patients. Higher CVD risk in HIV/AIDS patients are mainly associated with CD4 + T lymphocyte counts<200×10 6 cells/L and traditional CVD risk factors, including age≥50 years old, smoking, hypertension, diabetes and dyslipidemia.

Objective To analyze the clinical features of patients with acute stage brucellosis in Shenzhen,and provide a scientific basis for prevention and control of brucellosis in immigrant city.Methods A retrospective analysis was conducted to collect clinical data of patients with brucellosis admitted to the Department of Infectious Diseases,Shenzhen People's Hospital from May 2013 to May 2018.The patient's epidemiology manifestations,pathogen and laboratory examination results,diagnosis and treatment outcomes and prognosis were analyzed.Results Among the 39 patients with brucellosis,males were predominant,with a male to female ratio of 1.4 ∶ 1.0 (23 ∶ 16),an age of (44.91 ± 17.18) years and 24 cases were non-Guangdong natives.There were 23 cases with epidemiological history,including 14 cases with mutton,sheep viscera and goat milk history;the disease occurred throughout the year,mainly from February to July,a total of 26 cases.The clinical manifestations of the patients were mainly fever,sweating,fatigue,joint and muscle pain,weight loss,and liver or spleen or lymph nodes swelling.The blood culture was identified as 38 cases of Brucella melitensis and 1 case of Brucella suis.All strains were sensitive to common antibiotics in vitro.All cases were diagnosed as acute stage of brucellosis,2 cases with orchitis,1 case with brucellosis meningoencephalitis,3 cases with spondylitis,and 3 cases with misdiagnosis.Thirty-nine patients were cured according to the "Brucellosis Diagnosis and Treatment Guidelines (Trial)" and were followed up for 1 year.Conclusions Patients with brucellosis in Shenzhen are mainly infected with Brucella melitensis;fever,sweating,joint and muscle pain are the main clinical symptoms;the patient's efficacy and prognosis are better after treatment;for the occurrence of occasional misdiagnosis,it is recommended that in immigrant cities,medical staff should strengthen their understanding of brucellosis.

Objective: To understand the epidemiological and clinical features of patients with hemorrhagic fever and renal syndrome (HFRS) in Shenzhen, and to accumulate experience in the diagnosis and treatment of HFRS in this area. Methods: A retrospective analysis was conducted by collecting the clinical data from 46 patients who were confirmed with HFRS and admitted to the Department of Infectious Diseases of Shenzhen People's Hospital from January 2015 to December 2018. The demographic characteristics, epidemiological, clinical manifestations, examinations, treatments and prognosis, and other characteristics were analyzed. Results: All the 46 patients with HFRS were residens in Shenzhen, with a male-to-female ratio of 6.67∶1.00(40∶6), aged (40.18 ± 15.63) years old, and 38 patients (82.61%) aged 23-45 years old. There were 41 patients (89.13%) with a history of HFRS epidemiology, and there were mice in their houses or workplaces. The houses of 39 patients (84.78%) were rented, and 34 patients(87.18%) rented their houses in urban villages. There were morbidity throughout the year, and 33 patients (71.74%) were ill from January to June. In clinical classification, 44 cases (95.65%) were mild, 2 cases (4.35%) were medium, and there were no severe or critical cases. The clinical manifestations were that all patients were hospitalized due to fever mainly with hyperthermia. Thirty-nine patients (84.78%) were presented with systemic aches, headaches, low back pain and eyelid pain, and 28 patients (60.87%) had skin and mucous membrane hyperemia flushing. Clinical stages showed that all patients had pyretogenesis stage and polyuria stage, including pyretogenesis stage [(7.34 ± 6.82) d], polyuria stage [(9.94 ± 5.77) d], only 4.35% (2/46) patients with hypotension shock stage, all patients did not have oliguric stage. On the next day of admission, the number of white blood cells in 46 patients was (8.17 ± 3.19) × 10⁹/L, and 38 cases (82.61%) in the normal range; platelet was (61.92 ± 32.53) × 10⁹/L, and 42 cases (91.30%) were decreased; the procalcitonin was (1.62 ± 0.38) ng/ml, and 41 cases (89.13%) were increased; C-reactive protein was (74.33 ± 30.48) mg/L, and 46 patients (100.00%) were elevated; creatinine was (176.25 ± 55.15) μmol/L, and 19 cases (41.30%) were increased. Abnormal liver function was manifested by increased enzymology, alanine aminotransferase was (137.58 ± 46.76) U/L, and aspartate aminotransferase was (129.82 ± 40.29) U/L. All patients were positive for Hantavirus IgM. B-ultrasound results showed that in 58.70% (27/46) patients, both kidneys were plump and the parenchymal echo was enhanced. Liver injury occurred in 39 patients (84.78%) and sinus bradycardia in 2 patients (4.35%). All the 46 patients were clinically cured. Conclusion The epidemiological characteristics of patients with HFRS in Shenzhen are typical, the clinical manifestations are mild, and the curative effect and prognosis are good.