Decreased T cell expression of H/ACA box small nucleolar RNA 12 promotes lupus pathogenesis in patients with systemic lupus erythematosus.

Objective To investigate whether the aberrant expression of non-coding RNAs (ncRNAs) in T cells from patients with systemic lupus erythematosus (SLE) could contribute to the pathogenesis of lupus. Methods Expression profiles of RNA transcripts in T cells from three patients with SLE and three controls were analyzed by microarray analysis. Potentially aberrant-expressed ncRNAs were validated using T cell samples from 23 patients with SLE and 17 controls. Transfection studies and microarray analyses were conducted to search for any gene expression that is regulated by specific ncRNAs. Results Initial analysis revealed differential expression of 18 ncRNAs in SLE T cells. After validation, decreased expression of H/ACA box small nucleolar RNA 12 (SNORA12) was confirmed in SLE T cells (0.69-fold, P = 0.007) compared with normal T cells, and its expression level was inversely associated with higher SLE disease activity scores. Jurkat cells transfected with a plasmid encoding SNORA12 showed increased expression of two genes and decreased expression of 15 genes in Jurkat cells. These changes of gene expression were significantly associated with the SLE pathway in the Kyoto Encyclopedia of Genes and Genomes map using microarray analysis. Overexpression of SNORA12 altered the expression of CD69, decreased the expression of histone cluster 1 H4 family member k (HIST1H4K), inhibited the secretion of interferon gamma and the expression of HIST1H4K was increased in SLE T cells. Conclusion Among the ncRNAs, we found that the expression level of SNORA12, which belongs to the family of small nucleolar RNAs, was lower in SLE T cells and affected T cell function. This novel finding suggests that aberrant-expressed snoRNAs lead to dysfunction of T cells and may be involved in the immunopathogenesis of SLE.

Relativistic jet activity from the tidal disruption of a star by a massive black hole.

Supermassive black holes have powerful gravitational fields with strong gradients that can destroy stars that get too close, producing a bright flare in ultraviolet and X-ray spectral regions from stellar debris that forms an accretion disk around the black hole. The aftermath of this process may have been seen several times over the past two decades in the form of sparsely sampled, slowly fading emission from distant galaxies, but the onset of the stellar disruption event has not hitherto been observed. Here we report observations of a bright X-ray flare from the extragalactic transient Swift J164449.3+573451. This source increased in brightness in the X-ray band by a factor of at least 10,000 since 1990 and by a factor of at least 100 since early 2010. We conclude that we have captured the onset of relativistic jet activity from a supermassive black hole. A companion paper comes to similar conclusions on the basis of radio observations. This event is probably due to the tidal disruption of a star falling into a supermassive black hole, but the detailed behaviour differs from current theoretical models of such events.

Hybrid 3D structures of ZnO nanoflowers and PdO nanoparticles as a highly selective methanol sensor.

The present study concerns the enhancement of methanol selectivity of three dimensional (3D) nanoflowers (NFs) of ZnO by dispersing nickel oxide (NiO) and palladium oxide (PdO) nanoparticles on the surface of the nanoflowers to form localized hybrid nano-junctions. The nanoflowers were fabricated through a liquid phase deposition technique and the modification was achieved by addition of NiCl and PdCl2 solutions. In addition to the detailed structural (like X-ray diffraction (XRD), electron dispersive spectroscopy (EDS), X-ray mapping, XPS) and morphological characterization (by field emission scanning electron microscopy (FESEM)), the existence of different defect states (viz. oxygen vacancy) was also confirmed by photoluminescence (PL) spectroscopy. The sensing properties of the pristine and metal oxide nanoparticle (NiO/PdO)-ZnO NF hybrid sensor structures, towards different alcohol vapors (methanol, ethanol, 2-propanol) were investigated in the concentration range of 0.5-700 ppm at 100-350 °C. Methanol selectivity study against other interfering species, viz. ethanol, 2-propanol, acetone, benzene, xylene and toluene was also investigated. It was found that the PdO-ZnO NF hybrid system offered enhanced selectivity towards methanol at low temperature (150 °C) compared to the NiO-ZnO NF and pristine ZnO NF counterparts. The underlying mechanism for such improvement has been discussed with respective energy band diagram and preferential dissociation of target species on such 3D hybrid structures. The corresponding improvement in transient characteristics has also been co-related with the proposed model.

[Pedigree survey in a family with hereditary protein S deficiency].

Objective: To observe the clinical feature of familiar hereditary protein S deficiency(HPSD), and to explore the related gene mutations. Methods: A total of seven family members were enrolled in this study and examined during the June to September 2015. Medical histories of the families were analyzed to detect HPSD according to the diagnostic criteria. PROS1 genes of the proband and her family were analyzed. DNA was extracted from peripheral blood. The 15 exons and their intron-exon boundaries of PROS1 were amplified with PCR, and the PCR products were sequenced and analyzed to identify potential mutations. Medical histories from the family members died prior this study were also obtained. Results: Four out of 7 family members of 2 generations were diagnosed as HPSD. The proband suffered from pulmonary embolism, her elder brother suffered from cerebral infarction and her niece suffered from deep vein thrombosis. A missense mutation at the 1063 bp of cDNA(c.1063C>T)was detected in the exon 10 of PROS1, which resulted in arginine 355 to cysteine replacement in the first ball domain of laminin of the protein S(p.R355C). Conclusion: HPSD is an autosomal dominant genetic disease, patients often suffer from recurring vein thrombosis and pulmonary embolism. A missense mutation(c.1063C>T, p. R355C)of PROS1 was discovered in this Chinese family with HPSD, thus, this mutation might be the genetic basis responsible for these family members with HPSD .

Increased prevalence of JC polyomavirus viruria was associated with arthritis/arthralgia in patients with systemic lupus erythematosus.

OBJECTIVE: The objective of this paper is to investigate the prevalence of reactivation of the human polyomavirus John Cunningham virus (JCV) in patients with systemic lupus erythematosus (SLE) and its associated clinical manifestations. METHODS: Sixty-one patients with SLE and 22 controls were enrolled. Urine JCV viral load was quantified by real-time polymerase chain reaction (PCR). Length variants of the VP1 gene were analyzed using capillary electrophoresis. RESULTS: The prevalence of JCV viruria (63.9% vs. 18.2%, p < 0.001) and urine JCV viral load (2.92 ± 2.76 vs. 0.81 ± 1.85 copies/ml by log10 scale, p < 0.001) were significantly higher in patients with SLE compared with controls. JCV viruria (+) SLE patients had a higher occurrence of arthritis/arthralgia compared with JCV viruria (-) SLE patients (64.1% vs. 22.7%, p = 0.003). In SLE patients, the urine JCV viral load was significantly associated with the occurrence of arthritis/arthralgia. SLE patients with urine JCV viral load >10,000 copies/ml exhibited a 12.75-fold (95% confidence interval 2.88-56.40) risk in clinical arthritis/arthralgia, 18.90-fold (95% confidence interval 2.10-170.39) risk in persistent arthritis, and significantly greater number of length variants in the VP1 gene of JCV compared with JCV viruria (-) SLE patients. CONCLUSION: Reactivation of JCV in the urinary tract of SLE patients was very common. Both JCV viruria and urine JCV viral load were associated with the occurrence of arthritis/arthralgia in patients with SLE. High urine JCV viral load also was associated with the genetic variant in the VP1 gene.

Genetic characterization of red-colored heartwood genotypes of Chinese fir using simple sequence repeat (SSR) markers.

The present study investigated the genetic characterization of red-colored heartwood Chinese fir [Cunninghamia lanceolata (Lamb.) Hook.] in Guangxi using 21 simple sequence repeat (SSR) markers and analyzes of the genetic variation (N = 149) in samples obtained from five sites in Guangxi Province, China. The number of different alleles and the Shannon's information index per locus ranged from 3 to 12 and from 0.398 to 2.258 with average values of 6 and 1.211, respectively, indicating moderate levels of genetic diversity within this germplasm collection. The observed and expected heterozygosity ranged from 0.199 to 0.827 and from 0.198 to 0.878 with an average of 0.562 and 0.584, respectively. Although, the mean fixation index was 0.044, indicative of a low level of genetic differentiation among germplasms, analysis of molecular variance revealed considerable differentiation (99%) within the samples. The neighbor-joining dendrogram revealed that the majority of red-colored Chinese fir genotypes were apparently not associated with their geographic origins. Further analysis by STRUCTURE showed that this Guangxi germplasm collection could be divided into three genetic groups comprising 76, 37, and 36 members, respectively; these were classified into mixed groups with no obvious population structure. These results were consistent with those of the cluster analysis. On the whole, our data provide a starting point for the management and conservation of the current Guangxi germplasm collection as well as for their efficient use in Chinese fir-breeding programs.

Decreased microRNA(miR)-145 and increased miR-224 expression in T cells from patients with systemic lupus erythematosus involved in lupus immunopathogenesis.

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with abnormal T cell immune responses. We hypothesized that aberrant expression of microRNAs (miRNAs) in T cells may contribute to the pathogenesis of SLE. First, we analysed the expression profiles of 270 human miRNAs in T cells from five SLE patients and five healthy controls and then validated those potentially aberrant-expressed miRNAs using real-time polymerase chain reaction (PCR). Then, the expression of mRNAs regulated by these aberrant-expressed miRNAs was detected using real-time PCR. Finally, miRNA transfection into Jurkat T cells was conducted for confirming further the biological functions of these miRNAs. The initial analysis indicated that seven miRNAs, including miR-145, miR-224, miR-513-5p, miR-150, miR-516a-5p, miR-483-5p and miR-629, were found to be potentially abnormally expressed in SLE T cells. After validation, under-expressed miR-145 and over-expressed miR-224 were noted. We further found that STAT1 mRNA targeted by miR-145 was over-expressed and apoptosis inhibitory protein 5 (API5) mRNA targeted by miR-224 was under-expressed in SLE T cells. Transfection of Jurkat cells with miR-145 suppressed STAT1 and miR-224 transfection suppressed API5 protein expression. Over-expression of miR-224 facilitates activation-induced cell death in Jurkat cells. In the clinical setting, the increased transcript levels of STAT1 were associated significantly with lupus nephritis. In conclusion, we first demonstrated that miR-145 and miR-224 were expressed aberrantly in SLE T cells that modulated the protein expression of their target genes, STAT1 and API5, respectively. These miRNA aberrations accelerated T cell activation-induced cell death by suppressing API5 expression and associated with lupus nephritis by enhancing signal transducer and activator of transcription-1 (STAT)-1 expression in patients with SLE.

Thermal response of a dental tissue induced by femtosecond laser pulses.

This paper reports a theoretical and experimental study for thermal transport in a thin slice of human tooth induced by a 120 fs, 800 nm pulse laser at a repetition rate of 1 kHz. The surface reflectivity of enamel and the convection heat transfer coefficient were determined using an inverse heat transfer analysis. Instead of a fully three-dimensional modeling, two simplified two-dimensional (2D) planar and axisymmetric heat conduction models were proposed to simulate the temperature fields. The temperature responses obtained from the 2D planar and axisymmetric model agree well with the experimental measurements. On the other hand, the one-dimensional (1D) result significantly differs from the 2D axisymmetric one, suggesting that care should be taken when a 1D thermal model is considered for estimating temperature response.

Augmentation of mouse natural killer activity and induction of interferon by tumor cells in vivo.

Conventional and nude mice inoculated with syngeneic or allogenic tumor cells developed a rapid rise in serum interferon (IF) levels, peaking within 24 h. Within the same period, natural killer (NK) activity was readily boosted in the spleen. Both activities usually declined at 3 d. Cells that lacked the ability to augment NK activity also failed to induce detectable levels of IF. The boosting of IF and NK functions did not appear to be a result of contamination of the tumor lines by viruses because inoculation of several type C viruses into normal mice had no effect, and other viruses, like lymphocytic choriomeningitis virus and influenza, elevated IF and NK levels with a significantly later kinetics, peaking 3-4 d. The IF induced by tumor cells was heat and acid labile, species specific, and appeared to be in the type II class, although it was susceptible to antisera against Newcastle disease virus-induced IF. These data suggest that an early, nonthymus-dependent consequence of tumor-cell recognition is the production of IF, which, in turn, activates NK cells to lyse the tumor cells.

Interferon induced by Plasmodium berghei.

An inhibitor of virus is demonstrable in the serums of mice infected with Plasmodium berghei. The titer of the inhibitor, detectable within 10 hours after injection of parasitized blood, increases rapidly until 30 to 40 hours when it levels off or decreases slightly before reaching a plateau. The factor that induces production of the antiviral substance is not present in the plasma of the infected blood, and the inhibitor is not detectable in serums of mice injected with nonparasitized mouse erythrocytes. The inhibitor fulfills the essential require ments of an interferon.

Rare coexistence of gouty and septic arthritis: a report of 14 cases.

OBJECTIVES: To analyse the characteristic features of patients with coexistence of gouty arthritis and pyarthrosis at our university hospital in southern Taiwan, an area with high prevalence of hyperuricemia and gout. METHODS: A retrospective chart review was performed for patients who had concomitant gouty and septic arthritis from July 1998 to June 2008. Clinical and laboratory data of these patients were analysed. Furthermore, a comparison was made with published cases in English literature. RESULTS: Fourteen cases with coexistence of gouty arthritis and pyarthrosis have been identified during the past 10 years. There were 13 male and 1 female, all of Han Chinese in ethnicity, with ages ranging from 45 to 85 and an average of 63.7 years. At disease presentation, there were 11 oligoarticular cases (78.6%), 2 monoarticular cases (14.3%) and 1 polyarticular case (7.1%). Ankle and knee joints were most commonly involved. Bacteriological analyses demonstrated gram-positive cocci in 12 cases, of these 10 were oxacillin-sensitive Staphylococcus aureus (71.4%). Multiple tophi deposition was noted in 13 patients (92.9%) and among them 11 patients (84.6%) had associated chronic kidney disease. CONCLUSION: Different clinical presentations and bacteriological characteristics have been identified in the present series. While the mechanisms responsible for such a coexistence remain to be elucidated, these cases underline the importance of thorough evaluation of the aspirated synovial fluid. Our report adds a novel insight into the understanding of the clinical and microbiological manifestations of such a rare concurrence of gouty and septic arthritis.

Low-loss propagation in Cr4+:YAG double-clad crystal fiber fabricated by sapphire tube assisted CDLHPG technique.

Cr4+:YAG double-clad crystal fiber with an uniform 10-microm core was fabricated by using a sapphire tube as a heat capacitor to stabilize the power fluctuation of the CO2 laser in the co-drawing laser-heated pedestal growth system. The uniformity of the fiber core showed a factor of 3 improvement compared to that without the use of sapphire tube. The variation of the core diameter is within the +/-1.35-degree adiabatic criterion and has a autocorrelation length of 1.7 mm. The measured propagation loss is only 0.02 dB/cm. The sapphire tube also reduces the vertical temperature gradient during the crystal fiber growth process so the 10-microm crystal core exhibits a smooth perimeter. The sapphire tube assisted system can be applied to the growth of many other optical crystal materials.

TGF-ß upregulates the translation of USP15 via the PI3K/AKT pathway to promote p53 stability.

Crosstalk between transforming growth factor beta (TGF-ß) signaling and p53 has a critical role in cancer progression. TGF-ß signals via Smad and non-Smad pathways. Under normal conditions, wild-type p53 forms a complex with Smad2/3 and co-activates transcription of a variety of tumor suppressor genes, resulting in tumor suppressive effects. Thus, p53 stability is essential in progression of tumor suppressive responses mediated by TGF-ß signaling. However, it remains unknown whether p53 stability is regulated by TGF-ß. In the current study, we identify that USP15 binds to and stabilizes p53 through deubiquitination in U2OS and HEK293 cells. TGF-ß promotes the translation of USP15 through activation of mammalian target of rapamycin by the phosphoinositide 3-kinase/AKT pathway. Upregulation of USP15 translation links the crosstalk between TGF-ß signaling and p53 stability, allowing this cytokine to have a critical role in cancer progression.

NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial-mesenchymal transition.

The transcription factor NKX6.1 (NK6 homeobox 1) is important in the development of pancreatic ß-cells and neurons. Although recent publications show that NKX6.1 is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the metastasis suppressor function of human NKX6.1 using cell, animal and clinical analyses. Our data show that NKX6.1 represses tumor formation and metastatic ability both in vitro and in vivo. Mechanistically, NKX6.1 suppresses cell invasion by inhibiting the epithelial-to-mesenchymal transition (EMT). NKX6.1 directly enhances the mRNA level of E-cadherin by recruiting BAF155 coactivator and represses that of vimentin and N-cadherin by recruiting RBBP7 (retinoblastoma binding protein 7) corepressor. Clinical cancer tumors with metastasis show low NKX6.1 protein expression coinciding with low E-cadherin and high vimentin expression. Our results demonstrate that NKX6.1 functions as an EMT suppressor by interacting with different epigenetic modifiers, making it a potential novel therapeutic option.

Risk of cataract for people with tuberculosis: results from a population-based cohort study.

BACKGROUND: Tuberculosis (TB) is an infectious disease involving multiple organs, including the eyes. We examined the risk of cataract among patients with TB using population data. METHOD: Using data from the National Health Insurance (NHI) system of Taiwan, we established a TB cohort with 6994 patients newly diagnosed between 2000 and 2010. For each TB patient, four subjects without TB were randomly selected for the non-TB cohort, frequency matched by age, sex and diagnosis years. The incidence of cataract was measured by the end of 2011. The hazard ratio (HR) of cataract was estimated using Cox proportional hazards regression analysis. RESULTS: The overall incidence rate of cataract was 21% greater in the TB cohort than in the non-TB cohort (22.9 vs. 18.8/1000 person-years, P < 0.001), with an adjusted HR (aHR) of 1.26 (95%CI 1.16-1.37). Cataract incidence increased with age, and was higher in men than women and much higher for those with comorbidity. The hazard of cataract was higher in the first 6 months after TB diagnosis. CONCLUSION: TB patients are at elevated risk of developing cataract. Although the incidence decreased with time, the aHR remains statistically significant through the follow-up years.

The risk of chronic kidney disease in tuberculosis: a population-based cohort study.

BACKGROUND: The relationship between tuberculosis (TB) and subsequent chronic kidney disease (CKD) remains unclear. Therefore, we examined the risk of CKD among patients with TB in a nationwide study. METHODS: We conducted a retrospective cohort study using data from the National Health Insurance system of Taiwan. The cohort included 8735 patients who were newly diagnosed with TB. Patients were recruited between 1998 and 2002, and the date of diagnosis was defined as the index date. Each patient was randomly matched with four people from the general population without TB, according to age, gender and the index year. The occurrence of CKD was followed up until the end of 2011. The relative risks of CKD were estimated using the Cox proportional hazard model after adjusting for age, gender, index year and comorbidities. RESULTS: The overall incidence of CKD was 1.27-fold greater in the TB cohort than in the non-TB cohort. The adjusted hazard ratio (HR) of CKD associated with TB was higher in women (1.72; 95% confidence interval [CI]: 1.33-2.22), those aged <50 years (1.67; 95% CI: 1.15-2.41) and those without comorbidities (1.39; 95% CI: 1.06-1.83). In addition, patients with more comorbidities among hypertension, diabetes and hyperlipidemia have a greater risk of developing CKD in both cohorts, and the adjusted HRs were higher in the TB cohort than in the non-TB cohort. CONCLUSION: TB patients had a significantly higher risk of developing CKD than the general population. The detailed mechanisms need further investigation.

Differential distribution of apolipoprotein E in young and aged spontaneously hypertensive and stroke-prone rats.

OBJECTIVES: To evaluate whether the differential distribution of apolipoprotein E among lipoprotein fractions and hepatic expression of the apolipoprotein E gene are causal factors in the regulation of lipid metabolism and physiological functions in young and aged spontaneously hypertensive and stroke-prone rats. DESIGN AND METHODS: Biochemical analyses were performed on serum and hepatic specimens from young (2-month-old) and aged (8-month-old) spontaneously hypertensive rats, stroke-prone spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. Levels of apolipoprotein E among various lipoprotein fractions were determined using sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Liver concentrations of apolipoprotein E mRNA were analyzed by Northern blotting and relative levels of apolipoprotein E mRNA in different strains of rats were compared. Statistical analysis was performed by measuring correlations between hepatic apolipoprotein E mRNA levels and biological parameters. RESULTS: Levels of apolipoprotein E in high-density and low-density lipoproteins were significantly lower in hypertensive rats than in age-matched normotensive Wistar- Kyoto rats. Although there was a significant increase in high-density lipoprotein apolipoprotein E contents in all aged animals, the elevation in aged hypertensive rats was much less than that in aged normotensive rats. Levels of apolipoprotein E in the very-low-density lipoprotein fraction were diminished in young stroke-prone rats but were remarkably high in aged rats. Steady-state levels of apolipoprotein E mRNA increased with age in all strains of rats, whereas aged hypertensive rats exhibited lower apolipoprotein E mRNA levels than aged normotensive rats. CONCLUSIONS: The distribution of apolipoprotein E among various lipoprotein fractions was dramatically altered with age, and the alteration varied among different strains of rats. The differential distribution of apolipoprotein E in young and aged spontaneously hypertensive and stroke-prone rats suggests that apolipoprotein E could be a causal factor that disturbs the homeostasis of lipids and lipoproteins and perturbs physiological functions in hypertensive rats.

Prevalence of nonreporting behavior of sharps injuries in Taiwanese health care workers.

BACKGROUND: Health care workers (HCWs) were surveyed to identify factors associated with nonreporting behavior of sharps injuries (SIs) in Taiwan. METHODS: We surveyed 10,469 full-time medical, nursing, technical, and supporting personnel employed at 16 randomly selected hospitals from 132 available accredited teaching hospitals in Taiwan. Information about the most recent injury and reporting behavior after an SI were collected from July 1996 to June 1997 by using a pretested structured questionnaire. Eleven categories, including an open-ended option, were provided for participants to explain their nonreporting behavior. RESULTS: Questionnaires were completed by 82.6% (8645) of our sample, of whom 87.3% reported to have experienced a recent SI. A used item was the most commonly (P <. 001) involved item in an SI, and SIs with a used item were significantly more likely (odds ratio 3.6; CI 95%, 3.03-4.26; P <. 001) to be reported compared with an SI that involved unused items. A total of 81.8% of injuries were not reported, with job category significantly affecting reporting behavior (P <.001). Medical staff had the highest nonreporting rate (85.2%). Although attendees of a prevention program were statistically more likely (P <.001) to report an injury compared with nonattendees, the level of reporting in both groups was not encouraging (21.3% and 17.2%, respectively). All reasons given for nonreporting were disconcerting, but none more so than the use of subjective assessment of risk by 21.7% of HCWs who did not report their injuries. Other reasons for not reporting SIs included that the item was unused (34%) and that the HCW was too busy to report the SI (14.9%), unaware of reporting requirements (14. 4%), or immune to hepatitis B virus (12.4%). CONCLUSIONS: With 82% of SIs in Taiwanese HCWs going unreported, the expected national incidence will be seriously underestimated and impact the appropriateness of prevention programs. The very low rate of reporting suggests that the current reporting system requires simplification. Because most injuries involved used items, the reporting systems also should include a more responsive management component. The results also suggest that the current prevention programs, currently provided by the general nursing department, require expert content knowledge in infection control if nonreporting and SIs are to be reduced.

Sharps injuries among hospital support personnel.

Sharps injuries (SIs) among support personnel in hospitals have received little attention in the scientific literature. A cross-sectional study was undertaken to measure the incidence of SIs in Taiwanese support personnel. All support personnel, including laundry workers, cleaners, porters and central supply workers, from 16 hospitals were surveyed for SIs, sustained between June 1996 and July 1997. Either a questionnaire or face-to-face interviews, for those staff with a literacy problem, were used. Of the 862 persons eligible for study, 79.4% (684) were evaluable. Few staff (30.4%) had attended a prevention programme and 61% had suffered an SI in the past year. Few (25.4%) reported their injury. Hollow-bore needles, of which 72.2% had been used, were associated with 42.2% of injuries. Cleaners sustained the majority (65.7%) of injuries, and inappropriate disposal was associated with 54.7% of all injuries. For those staff employed for more than four years, the risk of sustaining an injury increased significantly with length of employment (P<0.001). Most of the injuries were sustained by cleaners handling sharps inappropriately disposed of by clinical staff. A safer environment for support staff could be achieved with the co-operation of clinical staff to correctly dispose of sharps to ensure single handling of sharps. A formal orientation of support staff in the reporting of SIs would enable clinical assessment and management of injuries, as well as an evaluation of needle and sharps safety in the healthcare setting.