Rodents and shrews are major reservoirs of various pathogens that are related to zoonotic infectious diseases. The purpose of this study was to investigate co-infections of zoonotic pathogens in rodents and shrews trapped in four provinces of China. We sampled different rodent and shrew communities within and around human settlements in four provinces of China and characterised several important zoonotic viral, bacterial, and parasitic pathogens by PCR methods and phylogenetic analysis. A total of 864 rodents and shrews belonging to 24 and 13 species from RODENTIA and EULIPOTYPHLA orders were captured, respectively. For viral pathogens, two species of hantavirus (Hantaan orthohantavirus and Caobang orthohantavirus) were identified in 3.47% of rodents and shrews. The overall prevalence of Bartonella spp., Anaplasmataceae, Babesia spp., Leptospira spp., Spotted fever group Rickettsiae, Borrelia spp., and Coxiella burnetii were 31.25%, 8.91%, 4.17%, 3.94%, 3.59%, 3.47%, and 0.58%, respectively. Furthermore, the highest co-infection status of three pathogens was observed among Bartonella spp., Leptospira spp., and Anaplasmataceae with a co-infection rate of 0.46%. Our results suggested that species distribution and co-infections of zoonotic pathogens were prevalent in rodents and shrews, highlighting the necessity of active surveillance for zoonotic pathogens in wild mammals in wider regions.

Objectives: Central-line–associated bloodstream infection (CLABSI) has been the leading cause of healthcare-associated infections (HAIs) in the intensive care unit (ICU) setting. Previous studies have shown that a care bundle is effective in reducing CLABSI rates; however, the data on long-term sustainability and cost savings of bundled care are limited. Methods: From January 2011 to December 2020, a prospective surveillance was performed to monitor CLABSI at a university hospital in northern Taiwan. To reduce the CLABSI rate, a hospital-wide bundled care program for CLABSI prevention was implemented in 2013. We evaluated the long-term effect of the care bundle on CLABSI incidence and length of stay in the ICU. Results: During the study period, the overall CLABSI incidence decreased from 8.22 per 1,000 catheter days before the care bundle was implemented to 6.33 per 1,000 catheter days in 2020 (P for trend <.01). The most common pathogens causing CLABSI were gut organisms (1,420 of 2,363, 60.1%), followed by environmental organisms (734 of 2,363, 31.1%) and skin organisms (177 of 2,363, 7.5%). The decreasing trend was statistically significant in the incidence of CLABSI caused by skin organisms (P for trend < .01), but not in the incidence of CLABSI caused by environmental organisms (P for trend = .86) or gut organisms (P for trend = .06). In the multivariable analysis, implementation of this care bundle was independently associated with a decrease in the CLABSI rate (RR, 0.77; 95% CI, 0.66–0.88). Compared with patients without CLABSI, patients with CLABSI had a longer average ICU length of stay (27 vs 17 days). Conclusions: A sustainable reduction in the incidence of CLABSI caused by common commensals could be achieved through a cost-saving bundled care program.

Many studies have suggested that folate-related one-carbon metabolism-related nutrients may play a role in certain cancer risks, but few studies have assessed their associations with the risk for nasopharyngeal carcinoma (NPC). In this study, we investigated the association between four folate-related one-carbon metabolism-related nutrients (folate, vitamin B6, vitamin B12 and methionine) and NPC risk in Chinese adults. A total of 600 patients newly diagnosed (within 3 months) with NPC were individually matched with 600 hospital-based controls by age, sex and household type (urban v. rural). Folate, vitamin B6, vitamin B12 and methionine intakes were measured using a validated seventy-eight-item FFQ. A higher dietary folate or vitamin B6 intake was associated with a lower NPC risk after adjusting for potential confounders. The adjusted OR of NPC for quartiles 2–4 (v. 1) were 0·66 (95 % CI 0·48, 0·91), 0·52 (95 % CI 0·37, 0·74) and 0·34 (95 % CI 0·23, 0·50) (P trend<0·001) for folate and 0·72 (95 % CI 0·52, 1·00), 0·55 (95 % CI 0·39, 0·78) and 0·44 (95 % CI 0·30, 0·63) (P trend<0·001) for vitamin B6. No significant association with NPC risk was observed for dietary vitamin B12 or methionine intake. The risk for NPC with dietary folate intake was more evident in the participants who were not exposed to toxic substances than in those who were exposed (P interaction=0·014). This study suggests that dietary folate and vitamin B6 may be protective for NPC in a high-risk population.

Introduction: The mortality of Parkinson’s disease (PD) and its associated risk factors among clinically definite PD patients in China has been rarely investigated. Our study aimed to identify the mortality rates and predictors of death in PD patients in China. Methods: 157 consecutive, clinically definite PD patients from the urban area of Shanghai were recruited from a central hospital based movement disorder clinic in 2006. All patients were regularly followed up at the clinic until December 31, 2011, or death. Mortality and associations with baseline demographics, health and medical factors were then determined within the cohort. Results: After 5 years, 11(7%) patients had died. The standardised mortality ratio was 0.62 (95% CI 0.32 to 1.07, P=0.104). The main causes of death were pneumonia (54.5%, 6/11) and digestive disorders (18.2%, 2/11), respectively. Age at onset, independent living, the mini mental state examination score, the Parkinson’s disease sleep scale score and the Epworth sleepiness scale score at baseline were statistically significantly different between the survival group and the deceased group (P<0.05). Across all participants, risk factors for death included low mini mental state examination score, and high Epworth sleepiness scale score according to a binary variable logistic regression analysis. Conclusions: This study confirms the similar survival of patients with PD to the control population up to a follow-up of 5 years. Interventions tailored to potential risk factors associated with death may offer further benefits.

Prophylaxis and treatment with oseltamivir effectively controlled a community outbreak of pandemic influenza A (H1N1) in China. The genetic makeup of strains of different generations seemed to be stable. Travel in confined settings might accelerate the transmission of pandemic influenza in a community outbreak.

The testosterone-inducible regulator (teiR) gene was cloned from Comamonas testosteroni chromosomal DNA, and introduced into plasmids pKtac2 (containing a tac promoter) and pK18 to yield plasmids pKtac2-teiR and pKteiR100. The recombinant plasmids were transformed into competent Escherichia coli HB101 and total protein was extracted to detect the TeiR protein expression level using enzyme-linked immunosorbent assay (ELISA). E. coli transformed by pKtac2-teiR and pKteiR100 produced 6.65 and 5.93 μg/mg of TeiR protein, respectively. Recombinant plasmids were also co-transformed into competent E. coli HB101 with plasmid p6 [containing hsdA gene (3α-HSD/CR, 3α-hydroxysteroid dehydrogenase/carbonyl reductase encoding gene)] to reveal the relationship between 3α-HSD/CR and TeiR by ELISA. The amounts of TeiR protein expressed by E. coli containing pKtac2-teiR and pKteiR100 were 5.94 μg/mg and 5.33 μg/mg, respectively, and these increased up to 6.81 μg/mg and 6.10 μg/mg after inducing with 1 mmol/l isopropyl-β-d-thiogalactoside (IPTG). Interestingly, 3α-HSD/CR protein expression level, after co-transformation with plasmids pKtac2-teiR and p6, was lower than that observed in the co-transformation with pKteiR100 and p6. The first co-transformation induced 1.20 μg/mg 3α-HSD/CR protein and the second 1.71 μg/mg. These values rose to 1.42 and 1.80 μg/mg, respectively, after treatment with 1 mmol/l IPTG. Our results proved that the tac promoter was more efficient than the lacZ promoter and that the teiR gene could act as an activator for hsdA gene expression.

Little is known about the biological effect of folate in the protection against mitochondrial (mt) oxidative decay. The objective of the present study was to examine the consequence of folate deprivation on mt oxidative degeneration, and the mechanistic link underlying the relationship. Male Wistar rats were fed with an amino acid-defined diet containing either 8 (control) or 0 (folate-deficient, FD) mg folic acid/kg diet. After a 4-week FD feeding period, significant elevation in oxidative stress was observed inside the liver mitochondria with a 77 % decrease in mt folate level (P < 0·001), a 28 % reduction in glutathione peroxidase activity (P = 0·0333), a 1·2-fold increase of mt protein carbonyls (P = 0·0278) and an accumulated 4834 bp large-scale deletion in mtDNA. The elicited oxidative injuries in FD liver mitochondria were associated with 30 % reduction of cytochrome c oxidase (CcOX) activity (P = 0·0264). The defective CcOX activity in FD hepatocytes coincided with mt membrane potential dissipation and intracellular superoxide elevation. Exposure of FD hepatocytes to pro-oxidant challenge (32 μm-copper sulphate for 48 h) led to a further loss in CcOX activity and mt membrane potential with a simultaneous increase in superoxide production. Preincubation of pro-oxidant-treated FD hepatocytes with supplemental folic acid (10–1000 μm) reversed the mt oxidative defects described earlier and diminished superoxide overproduction. Increased supplemented levels of folic acid strongly correlated with decreased lipid peroxidation (γ − 0·824, P = 0·0001) and protein oxidative injuries (γ − 0·865, P = 0·0001) in pro-oxidant-challenged FD liver mitochondria. Taken together, the results demonstrated that folate deprivation induces oxidative stress in liver mitochondria, which is associated with CcOX dysfunction, membrane depolarization and superoxide overproduction. The antioxidant activity of supplemental folic acid may partially, if not fully, contribute to the amelioration of pro-oxidant-elicited mt oxidative decay.

In this paper, we measured and analyzed the operation lifetime of a high efficiency blue OLED which consists of N,N' –Vdiphenyl -N,N'-bis(1-napthyl) -1,1'-biphenyl-4,4'- diamine (NPB) as the hole-transport layer (HTL), 4,4'-bis[2-(4-(N,N-diphenylamino)phenyl)vinyl]biphenyl (DPAVBi) doped in 9,10-bis(2';-naphthyl) anthracene (ADN) as the emitting layer (EML), and bis(10-hydroxyben-zo[h]quinolinato)beryllium (Bebq2) as the electron-transport layer (ETL). Due to the high electron mobility of the ETL (one order of magnitude higher than Alq3), the carrier balance is achieved and a blue OLED with a high external quantum efficiency of 8.32% is obtained. The device structure of our blue OLED device is ITO /HTL (40nm)/EML (45nm, 4% dopant)/ETL (15nm)/ LiF(1.2nm)/Al (100nm). In our operation lifetime measurement, we fixed the initial luminescence of the blue OLEDs at 12500, 10000, 7000, 5000 cd/m2 with a constant current driving. The resulting half-lifetime are 5.58, 16.56, 27, 109.819 hours, respectively. To estimate the half-lifetime of this device, we use a well-known relation in our fitting: L*t1/2n= constant where n is the acceleration coefficient, and t1/2 is the half-lifetime. In our blue OLED, the n value is 3.088. By using the equation, we can calculate that the estimated half lifetime at an initial luminance of 1000 cd/m2 achieves 15611 hours in our device. For further investigating the lifetime mechanism in our blue OLED, we fit all the luminance versus time curves obtained under different driving condition. We found that luminance is inversely proportional to the square of the time, rather than a typically stretched exponential decay which means the luminance decay is a second-order reaction in our blue OLED.