Pasteurella multocida and Aeromonas hydrophila are rare human pathogens,and zoonotic infections caused by bites of big cats are rarely reported.This paper reported the first case of wound infection caused by Pas-teurella multocida and Aeromonas hydrophila after tiger bites in China.Strain identification and drug susceptibility testing were conducted by BD PHOENIXTM100 automatic microbial analyzer.The patient was discharged with a good prognosis after wound debridement,surgical intervention and combined antimicrobial treatment.This paper aims to advise emergency physicians to consider the possibility of co-infection of Pasteurella multocida and Aero-monas hydrophila when encountering rare big cat bites.

Aim To investigate whether polydatin re-duces airway inflammation in asthmatic mouse model and explore whether this pathway is related to p38 MAPK/Nrf2/HO-1 . Methods After the establish-ment of the OVA-induced asthmatic mouse model, the animals were injected with 30 mg·kg-1 and 45 mg· kg-1 of polydatin diluted in 0. 2 mL normal saline, while the control group was replaced by normal saline. HE, PAS and Masson staining were used to observe the pathological changes of lung tissue. Diff-Quick staining was used to classify and count the number of inflamma-tory cells in BALF. ELISA was used to detect IgE ex-pressions in BALF. The content of ROS in BALF cells was detected by DHR-123 . The activities of antioxidant enzymes SOD, CAT and MDA in BALF were detected by the enzyme-linked immunosorbent assay kit. The expression of HO-1 in lung tissue was detected by im-munohistochemistry. The protein and mRNA expres-sions of Nrf2 and HO-1 in lung tissue of mice were de-tected by Western blot and RT-PCR. Results Poly-datin treatment significantly reduced inflammatory cell infiltration mucosal secretion, goblet cell proliferation and collagen deposition in the lung tissue of mice, and decreased the number of inflammatory cells and the ex-pression of total IgE and ROS in BALF. It also in-creased the levels of antioxidant enzymes such as SOD and CAT, and lowered the level of MDA. Polydatin re-duced the phosphorylation of p38 MAPK in the lung tissue of mice, enhanced the levels of mRNA and pro-tein expressions of Nrf2 and HO-1 and promoted the nuclear transfer of Nrf2 . The above effects of polydatin were dose-dependent. Conclusions Polydatin exerts anti-oxidative effects in OVA-induced asthmatic mouse model via anti-oxidant pathway. The mechanism may be achieved through the p38 MAPK/Nrf2/HO-1 path-way.

Background/Aims: Accumulating evidence indicates that L-carnitine (LC) protects against multiorgan damage through its antioxidant properties and preservation of the mitochondria. Little information is available about the effects of LC on renal fibrosis. This study examined whether LC treatment would provide renoprotection in a rat model of unilateral ureteral obstruction (UUO) and in vitro. Methods: Sprague-Dawley rats that underwent UUO were treated daily with LC for 7 or 14 days. The influence of LC on renal injury caused by UUO was evaluated by histopathology, and analysis of gene expression, oxidative stress, mitochondrial function, programmed cell death, and phosphatidylinositol 3-kinase (PI3K)/ AKT/forkhead box protein O 1a (FoxO1a) signaling. In addition, H2O2-exposed human kidney cells (HK-2) were treated with LC. Results: LC treatment inhibited expression of proinflammatory and profibrotic cytokines, and was followed by a significant attenuation of tubulointerstitial inflammation and fibrosis. The increased oxidative stress caused by UUO was associated with mitochondrial dysfunction and excessive apoptosis and autophagy via PI3K/AKT/FoxO1a-dependent signaling, and this was abrogated by administration of LC. In H2O2-exposed HK-2 cells, LC decreased intracellular production of reactive oxygen species, and suppressed expression of profibrotic cytokines and reduced the number of apoptotic cells. Conclusions LC protects against the progression of tubulointerstitial fibrosis in an obstructed kidney.

Background/Aims: Cigarette smoking is an important modifiable risk factor in kidney disease progression. However, the underlying mechanisms for this are lacking. This study aimed to assess whether nicotine (NIC), a major toxic component of cigarette smoking, would exacerbates tacrolimus (TAC)-induced renal injury. Methods: Sprague-Dawley rats were treated daily with NIC, TAC, or both drugs for 4 weeks. The influence of NIC on TAC-caused renal injury was examined via renal function, histopathology, oxidative stress, mitochondria, endoplasmic reticulum (ER) stress, and programmed cell death (apoptosis and autophagy). Results: Both NIC and TAC significantly impaired renal function and histopathology, while combined NIC and TAC treatment aggravated these parameters beyond the effects of either alone. Increased oxidative stress, ER stress, mitochondrial dysfunction, proinf lammatory and profibrotic cytokine expressions, and programmed cell death from either NIC or TAC were also aggravated by the two combined. Conclusions Our observations suggest that NIC exacerbates chronic TAC nephrotoxicity, implying that smoking cessation may be beneficial for transplant smokers taking TAC.

As the incidence of diabetes mellitus is rapidly increasing worldwide,that of related complications,such as diabetic kidney disease(DKD),also increases,conferring a heavy economic burden on the patients,families,society,and government.Diabetes mellitus complicated with chronic kidney disease(CKD)includes DKD and the CKD caused by other reasons.Because of the insufficient knowledge about CKD,the assessment of diabetes mellitus complicated with CKD remains to be improved.The therapies for diabetes mellitus complicated with CKD focus on reducing the risk factors.In clinical practice,DKD may not be the CKD caused by diabetes.According to clinical criteria,some non-diabetic kidney disease may be misdiagnosed as DKD and not be treated accurately.This review summarizes the status quo and research progress in the assessment,diagnosis,and treatment of diabetes mellitus complicated with CKD and predicts the directions of future research in this field.
Humans ; Diabetes Mellitus, Type 2/complications* ; Diabetic Nephropathies/etiology* ; Renal Insufficiency, Chronic/therapy* ; Risk Factors ; Diabetes Mellitus/therapy*