Epidemiological investigation on the local epidemic situation in Zhengzhou High-Tech Zone caused by SARS-CoV-2 Delta variant / 中华预防医学杂志

This study collected epidemic data of COVID-19 in Zhengzhou from January 1 to January 20 in 2022. The epidemiological characteristics of the local epidemic in Zhengzhou High-tech Zone caused by the SARS-CoV-2 Delta variant were analyzed through epidemiological survey and big data analysis, which could provide a scientific basis for the prevention and control of the Delta variant. In detail, a total of 276 close contacts and 599 secondary close contacts were found in this study. The attack rate of close contacts and secondary close contacts was 5.43% (15/276) and 0.17% (1/599), respectively. There were 10 confirmed cases associated with the chain of transmission. Among them, the attack rates in close contacts of the first, second, third, fourth and fifth generation cases were 20.00% (5/25), 17.86% (5/28), 0.72% (1/139) and 14.81% (4/27), 0 (0/57), respectively. The attack rates in close contacts after sharing rooms/beds, having meals, having neighbor contacts, sharing vehicles with the patients, having same space contacts, and having work contacts were 26.67%, 9.10%, 8.33%, 4.55%, 1.43%, and 0 respectively. Collectively, the local epidemic situation in Zhengzhou High-tech Zone has an obvious family cluster. Prevention and control work should focus on decreasing family clusters of cases and community transmission.

Application of the time series model in prediction of incidence of hand-foot-mouth disease from 2008 to 2016 in China / 中华疾病控制杂志

Objective To predict the monthly incidence of hand-foot-mouth disease (HFMD) in China by using autoregressive integrated moving average (ARIMA) model and provide evidence for prevention and control of HFMD. Methods The monthly incidence data of HFMD in China from 2008 to 2016 were collected from the Public Health Science data Center. The incidence database was established by Excel 2007 and graphed. SAS 9.1 was used to construct the ARIMA model, based on the data of the monthly reported incidence of HFMD in China from January 2008 to December 2015, and then the data in 2016 were used to verify the predicted results. The monthly incidence in 2017 was predicted in the same way.The difference was statistically significant when P<0.05. Result The model predicting monthly incidence of HFMD in China is ARIMA ((12), 2, 0) sparse coefficient and residuals is white noise. The parameters were as follows: moted mean squared error=3.6490, mean absolute error=2.62, mean absolute percentage error=28.24%. Conclusion The sparse coefficient model could well simulate the trend of HFMD case in time series, which has good reference of early warning and prevention of HFMD.

Bacterial magnetosomes-based nanocarriers for co-delivery of cancer therapeutics in vitro.

In recent times, co-delivery of therapeutics has emerged as a promising strategy for treating dreadful diseases such as cancer. MATERIALS AND METHODS: In this study, we developed a novel nanocarrier based on bacterial magnetosomes (BMs) that co-loaded with siRNA and doxorubicin (DOX) using polyethyleneimine (PEI) as a cross-linker (BMs/DP/siRNA). The delivery efficiency of siRNA as well as the pH-responsive release of DOX, and synergistic efficacy of these therapeutics in vitro were systematically investigated. RESULTS: The structure of DOX-PEI (DP) conjugates that synthesized via hydrazone bond formation was confirmed by 1H nuclear magnetic resonance (NMR). The in vitro release experiments showed that the DP conjugate (DOX-loading efficiency - 5.77%±0.08%) exhibited the long-term release behavior. Furthermore, the optimal BMs/DP/siRNA particle size of 107.2 nm and the zeta potential value of 31.1±1.0 mV facilitated enhanced cellular internalization efficiency. Moreover, the agarose gel electrophoresis showed that the co-delivery system could protect siRNA from degradation in serum and RNase A. In addition, the cytotoxicity assay showed that BMs/DP/siRNA could achieve an excellent synergistic effect compared to that of siRNA delivery alone. The acridine orange (AO)/ethidium bromide (EB) double staining assay also showed that BMs/DP/siRNA complex could induce cells in a stage of late apoptosis and nanocomplex located in the proximity of the nucleus. CONCLUSION: The combination of gene and chemotherapeutic drug using BMs is highly efficient, and the BMs/DP/siRNA would be a promising therapeutic strategy for the future therapeutics.

Low expression of lncRNA-GAS5 promotes epithelial-mesenchymal transition of breast cancer cells in vitro / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the role of long non-coding RNA growth arrest-specific transcript 5 (lncRNA-GAS5) in breast cancer progression and epithelial-mesenchymal transition (EMT) of the cancer cells.</p><p><b>METHODS</b>Real-time quantitative PCR (qRT-PCR) was used to detect the expression of lncRNA-GAS5 in 37 pairs of breast cancer and adjacent non-tumor tissues and in parental MCF-7 cells and paclitaxel-resistant MCF-7 (MCF-7/PR) cells, and the correlation of lncRNA-GAS5 expression with the clinical stage and lymph node metastasis of breast cancer was investigated. The expressions of the genes related with cell cycle and EMT at both the mRNA and protein levels were detected using qRT-PCR, Western blotting and immunohistochemistry. The changes in the biological behaviors and morphology of breast cancer cells with either lncRNA-GAS5 knockdown or overexpression were observed. Nude mouse models were established bearing breast cancer xenografts derived from MCF-7/PR cells or MCF-7/PR cells over-expressing lncRNA-GAS5, and the inhibitory effect of paclitaxel on tumor growth was evaluated.</p><p><b>RESULTS</b>The transcriptional levels of lncRNA-GAS5 were significantly lower in breast cancer tissues than in the adjacent non-tumor tissues (P<0.05), and decreased lncRNA-GAS5 expression was significantly correlated with TNM stage and lymph node metastasis of breast cancer (P<0.05). lncRNA-GAS5 expression was also significantly lowered in paclitaxel-resistant breast cancer cells and showed a positive correlation with P21 expression and a negative correlation with CDK6. MCF-7 cells during EMT presented with a lowered expression of lncRNA-GAS5, whereas lncRNA-GAS5 over-expression strongly suppressed MCF-7/PR cell migration and invasion, and increased the susceptibility of the cells to paclitaxel. In the tumor-bearing nude mouse models, lncRNA-GAS5 overexpression in the tumor cells obviously enhanced the inhibitory effect of paclitaxel on tumor growth and lung metastasis by reversing the EMT marker proteins.</p><p><b>CONCLUSION</b>A decreased expression of lncRNA-GAS5 promotes lung metastasis of breast cancer by inducing EMT, suggesting the potential of lncRNA-GAS5 as a therapeutic target in breast cancer.</p>

Osteopontin Deficiency Alters Biliary Homeostasis and Protects against Gallstone Formation.

The precipitation of excess biliary cholesterol as solid crystals is a prerequisite for cholesterol gallstone formation, which occurs due to disturbed biliary homeostasis. Biliary homeostasis is regulated by an elaborate network of genes in hepatocytes. If unmanaged, the cholesterol crystals will aggregate, fuse and form gallstones. We have previously observed that the levels of osteopontin (OPN) in bile and gallbladder were reduced in gallstone patients. However, the role and mechanism for hepatic OPN in cholesterol gallstone formation is undetermined. In this study, we found that the expression of hepatic OPN was increased in gallstone patients compared with gallstone-free counterparts. Then, we observed that OPN-deficient mice were less vulnerable to cholesterol gallstone formation than wild type mice. Further mechanistic studies revealed that this protective effect was associated with alterations of bile composition and was caused by the increased hepatic CYP7A1 expression and the reduced expression of hepatic SHP, ATP8B1, SR-B1 and SREBP-2. Finally, the correlations between the expression of hepatic OPN and the expression of these hepatic genes were validated in gallstone patients. Taken together, our findings reveal that hepatic OPN contributes to cholesterol gallstone formation by regulating biliary metabolism and might be developed as a therapeutic target for gallstone treatments.

Loss of angiotensin-converting enzyme 2 promotes growth of gallbladder cancer.

The aim of this study is to investigate the role of angiotensin-converting enzyme 2 (ACE2) in gallbladder cancer (GBC) and the therapeutic potential of angiotensin receptor blocker in GBC. Human gallbladder epithelial cells (HGBEC) together with GBC cells and tissue samples were used. In vitro studies were carried out to investigate the role of ACE2 in GBC cells. ACE2 levels were studied in in vivo GBC mouse models subject to ARB treatment. ACE2 level was decreased in GBC cells compared with that in normal gallbladder cells. Replenishment of angiotensin II (A2) promoted tumour cell growth, which could be mitigated by ACE2 supplement. ARB blocked A2-induced GBC cell growth and activated ERK. Activity of mTOR was not altered with different ACE2 status. ARB inhibited tumour growth in xenograft mouse models. In vivo study also showed that decreased expression of ACE2 was associated with enlarged tumour size. By genetic replenishment of ACE2 and pharmaceutical use of ARB, restored ACE2 level mitigated GBC growth. Our results supported the rationale for the use of ARB in GBC patients for potential therapeutic benefit.

Inhibition of mTOR pathway attenuates migration and invasion of gallbladder cancer via EMT inhibition.

Gallbladder cancer (GBC) is an aggressive disease in which epithelial-mesenchymal transition (EMT) plays a critical role. Whether inhibition of mTOR effects via EMT reversal in GBC remains unclear. Using genetic and pharmacologic inhibitions of mTOR, we investigated the changes of EMT levels in GBC cells. Expressions of EMT related genes were also studied. Migration and invasion assays were carried out and in vivo tumour metastasis mouse models were established. Circulating tumour DNA was quantified. We used EMT index (ratio of Vimentin/Ecadherin expression) to profile EMT levels. We found that inhibition of mTOR using shRNAs and rapamycin inhibited EMT in GBC-SD gallbladder cancer cells. Inhibition of mTOR inhibited EMT in GBC-SD cells in TGF-ß-dependent manner, which was contributed majorly by mTORC2 inhibition. Rapamycin decreased invasiveness and migration of GBC-SD cells in vitro and in vivo. We have in the current study shown that rapamycin diminishes the ability of invasion and migration of GBC via inhibition of TGF-ß-dependent EMT. Our findings contribute to the understanding of the carcinogenesis of GBC.

Do hyperechoic thyroid nodules on B-ultrasound represent calcification?

OBJECTIVE: To explore the correlation between hyperechoic thyroid nodules observed on B-ultrasound and histological calcification seen in paraffin-wax sections. METHODS: Records of patients who underwent surgical removal of thyroid nodules diagnosed on preoperative B-ultrasound were analysed retrospectively. Calcification present on B-ultrasound was compared with calcification seen in postoperative pathology specimens. RESULTS: Of the 1,655 patients included in the study, 518 had malignant and 1,137 had benign thyroid nodules. Calcification on B-ultrasound was seen in 366 patients with malignant, and 414 with benign nodules. Calcification was confirmed on histology in 209 and 127 of these patients, respectively, giving a sensitivity and specificity for B-ultrasound in diagnosing calcification (compared with histology) of 95.87% and 47.67%, respectively, in thyroid cancer and 90.71%, and 71.21% respectively in benign thyroid nodules. Microcalcification was seen in 483 patients on B-ultrasound and in 186 on histology, of whom 294 (60.87%) and 152 (81.72%), respectively, had thyroid cancer. CONCLUSIONS: B-ultrasound is a useful and accurate test for detecting calcification in thyroid nodules, with a high sensitivity. There is a close association between calcification (especially microcalcification) and thyroid cancer on both B-ultrasound and pathological examination.

Therapeutic effect of Tripterygium wilfordii Hook F multiglycosides on gut barrier dysfunction in rats with acute necrotizing pancreatitis.

The aim of the current study was to investigate the therapeutic effect of Tripterygium wilfordii Hook F multiglycosides (TWG) on gut barrier dysfunction in rats with acute necrotizing pancreatitis (ANP). ANP was induced in rats using 3.5% sodium taurocholate. The rats were divided into 3 groups: the sham operation (SO), ANP and ANP+TWG groups. Biochemical and pathological change of pancreatic tissue and ileal mucosa, bacterial cultures and the survival rate were measured following surgery and treatment. TWG treatment significantly decreased amylase and lipase activities and plasma endotoxin and D-lactate levels. Edema and inflammation in the pancreas and ileal mucosa were alleviated. Positive bacterial cultures were significantly reduced. The survival rate of the rats in the ANP+TWG group was higher than that of the rats in the ANP group. TWG treatment showed beneficial effects by protecting the pancreas from bacterial infection caused by gut barrier dysfunction and improving the outcomes of the rats with ANP.

Comparative proteomic analysis of gallbladder bile proteins related to cholesterol gallstones.

BACKGROUND: Nucleation of cholesterol monohydrate crystals following the aggregation and fusion of cholesterol-enriched vesicles is a critical procedure in the formation of cholesterol gallstone. Biliary proteins play important roles in the process. It is inefficient to screen pro-nucleating or anti-nucleating proteins with routine physiochemical techniques, by which we discovered several pro-nucleating proteins. METHODOLOGY/PRINCIPAL FINDINGS: Based on comparative proteomic technologies, we investigated the differentially expressed proteins between the cholesterol gallstone and control groups, and between the vesicular phase and micellar phase. There are 401±75 spots detected on the cholesterol gallstone group and 389±94 spots on the control group gels, 120±24 spots detected on vesicular phase and 198±37 on micellar phase gels, and accordingly 22 and 8 differentially expressed proteins were identified successfully, respectively. Three of them, HSA, Profilin and Retinol Binding Protein, were validated by Western blot. CONCLUSION/SIGNIFICANCE: Some of the identified proteins are in good agreement with proteins reported to be involved in the gallstone formation before. The information from this study might provide some important clues to uncover the key proteins involved in the formation of cholesterol gallstone.

Serologic and molecular biological detection of rare B(A) blood group / 中国实验血液学杂志

This study was aimed to investigate one case with rare type B(A) in ABO blood group by using serological and molecular biological methods, and analyze the cause of inconsistency resulting from multiple detections. The serological method was used to identify the serum type of ABO blood group, at the same time the PCR sequencing method was used to detect the genotypes. The results indicated that the group typing and reverse typing for the blood donor were inconsistent, the group typing was AB, the reverse typing was B. The ABO genotype was B(A) 04 /001. This genotype was involved in nt640A > G point mutation which caused valine replacing methionine at 214. It is concluded that the sample inconsistent between the group typing and reverse typing could be typed by molecular biological method, and the molecular basis of weak expression of ABO blood group is elucidated too.

Rare blood group B (A) detection and safe transfusion / 中国实验血液学杂志

This study was aimed to investigate the genetic characteristics, identification method and transfusion strategy of rare blood type B(A). The rare blood group B(A) was typed by serological technique, PCR-SSP genotyping and sequencing of exon 6, 7 of ABO blood group. The genetic characteristics and molecular mechanism of B(A) blood group were also analyzed. Blood group compatibility test was conducted between blood donors of B(A) and recipients by clinical transfusion. The results showed that both forward and reverse grouping did not match the 3 cases of serological result in their family survey, while all of the 3 cases were grouped as AB blood group by forward grouping, B blood group by reverse grouping with serological result and B(A)04/001 group were genotyped by ABO genotyping. The patient of B blood group was transfused by 1 bag of washed red blood cells of donor of B(A) under closely monitoring, the patient's condition changed, and a mild adverse transfusion reaction was appeared. Washed red blood cell of O blood group was transfused into B(A) patient without blood transfusion reaction. It is concluded that the forward ABO serological grouping and reverse ABO serological grouping are not compatible, that may be verified by family survey and molecular biological methods. If in some cases transfusion therapy was applied, and group B(A) can not be transfused to the patient with group B or AB. Thus, transfusion compatibility or autologous transfusion can be adopted to transfuse to the patient from group B(A).

Inhibition of arterial allograft intimal hyperplasia using recipient dendritic cells pretreated with B7 antisense peptide.

BACKGROUND: Low expression or absence of dendritic cell (DC) surface B7 molecules can induce immune tolerance or hyporesponse. Whether DCs could induce indirect allogeneic-specific cross-tolerance or hyporesponse to recipient T cells remains unclear. METHODS: Generated from C3H/He mice bone marrow cells pulsed with donor antigen from C57BL/6 mice, recipient DCs were incubated with B7 antisense peptide (B7AP). Immune regulatory activities were examined in vitro by a series of mixed lymphocyte reactions. Murine allogeneic carotid artery orthotopic transplantation was performed from C57BL/6 to C3H/He. Recipients were given B7AP-treated DCs 7 days before transplantation. Allograft pathological analysis was done 2 months after transplantation. RESULTS: B7AP-pretreated DCs markedly inhibited T-cell proliferation compared with untreated group. Pretreated T cells exhibited markedly reduced response to alloantigen versus third-party antigen. Pathological analysis of arterial allografts demonstrated significant reduction of intimal hyperplasia in B7-AP pretreated group versus control. CONCLUSION: Blockade of B7 molecules by B7AP could induce indirect allogeneic-specific hyporesponse and inhibit arterial allograft intimal hyperplasia, which may be involved in future strategies for human allograft chronic rejection.

The association of polymorphisms on TGFBR1 and colorectal cancer risk: a meta-analysis.

Epidemiological studies found inconsistent results on the association of two variants on TGFBR1 (TGFBR1*6A and Int7G24A) with colorectal cancer (CRC) risk. The present study was aimed to evaluate the association of these two variants with CRC susceptibility via the meta-analysis methods. For variant TGFBR1*6A, nine reports including 6,765 CRC patients and 8,496 unrelated controls were identified. The heterozygotes *6A/*9A showed a significant increased risk of CRC with the pooled OR was 1.12 (95% CI = 1.02-1.23), and the pooled OR for the homozygotes *6A/*6A was 1.13 (95% CI = 0.80-1.58) compared to the homozygotes *9A/*9A. However, under the dominant effect model, the TGFBR1*6A carriers showed a significantly increased CRC risk (pooled OR = 1.12, 95% CI = 1.03-1.23, *6A/*6A and *6A/*9A vs. *9A/*9A). For variant Int7G24A, three case-control studies with 1,074 cases and 1,945 controls were found. Although no significant association was found for heterozygosity Int7G24A carriers with CRC risk (pooled OR = 0.97, 95% CI = 0.67-1.42), the homozygosity A/A carriers showed a significant elevated risk of CRC (pooled OR = 1.68, 95% CI = 1.14-2.47) compared to G/G homozygotes. Under the recessive effect model, homozygotes A/A showed a 71% increase of CRC risk compared to the A/G and G/G genotype carriers (pooled OR = 1.71, 95% CI = 1.17-2.51). These data strongly suggested that the two polymorphisms of TGFBR1 may confer low-penetrance susceptibility of CRC risk.

Osteopontin and integrin are involved in cholesterol gallstone formation.

BACKGROUND: This study aimed to investigate the role of osteopontin and its receptor, integrin αv, in gallstone formation using human tissue specimens and a guinea pig lithogenic model. MATERIAL/METHODS: The nucleation role of osteopontin was determined in patients' and normal gallbladder bile samples in vitro. Normal gallbladder was the control, and gallstone gallbladders were divided into group I (with normal epithelia) and group II (with degenerated epithelia) based on pathology change. Immunostaining, mRNA and protein expressions of osteopontin and integrin αv were analyzed. The animals were randomly divided into a lithogenic diet group and a normal diet group; the osteopontin mRNA expression in gallbladder and liver and osteopontin concentrations were determined. RESULTS: Osteopontin prolonged nucleation time and inhibited the pro-nucleating role induced by calcium in human bile in vitro. Immunostaining for osteopontin and integrin αv in human gallbladder tissues showed a higher reactivity in Group I than control group and Group II. The immunostaining in Group II was weaker than control group; similar results were observed for mRNA and protein expression of osteopontin and integrin αv. In the animal assay, the mRNA expression and concentration of osteopontin in gallbladder and liver gradually increased at initial stages and decreased in later stages. The concentrations of osteopontin in bile and serum of guinea pig showed similar trends. CONCLUSIONS: Our results suggest that osteopontin is involved in cholesterol gallstone formation, and the role of osteopontin might correlate with integrin αv and calcium.

A randomized trial of somatostatin to regulate the VEGFs/VEGFRs in patients with gastric cancer.

BACKGROUND/AIMS: Angiogenesis and lymphangiogenesis are essential for tumor growth and metastasis. Vascular endothelial growth factors and their receptors (VEGFs/VEGFRs) are important to modulate vasculogenesis. Disregulation of the VEGFs/VEGFRs are closely related to tumor progression and prognosis. METHODOLOGY: We established an open-label, randomized trial to assess the effect of somatostatin on the patients with primary gastric cancer and total gastrectomy. All the 60 patients were randomly divided into somatostatin pretreatment and placebo groups and we used ELISA, real-time PCR and immunohistochemistry analysis to identify the level of VEGFs. RESULTS: The results showed that the patients pretreated with somatostatin had a significant decrease in serum VEGF level, but not in the tissue mRNA level, and the decrease in serum VEGF was partially dependent on the synthesis and degradation of the protein but not the transcription of mRNA. We also found the tissue Flt-4 (VEGFR-3) protein decreased in somatostatin pretreatment group. CONCLUSIONS: We concluded that somatostatin exerts its anti-vasculogenesis effect by downregulating the serum VEGFs and Flt-4 level. Somatostatin can be used as an important adjuvant to improve the survival of gastric cancer patients.

Preliminary screening and identification of stem cell-like sphere clones in a gallbladder cancer cell line GBC-SD.

This paper aims to screen and identify sphere clone cells with characteristics similar to cancer stem cells in human gallbladder cancer cell line GBC-SD. GBC-SD cells were cultured in a serum-free culture medium with different concentrations of the chemotherapeutic drug cisplatin for generating sphere clones. The mRNA expressions of stem cell-related genes CD133, OCT-4, Nanog, and drug resistance genes ABCG2 and MDR-1 in sphere clones were detected by quantitative real-time polymerase chain reaction (PCR). Stem cell markers were also analyzed by flow cytometry and immunofluorescent staining. Different amounts of sphere clones were injected into nude mice to test their abilities to form tumors. Sphere clones were formed in serum-free culture medium containing cisplatin (30 µmol/L). Flow cytometry results demonstrated that the sphere clones expressed high levels of stem cell markers CD133(+) (97.6%) and CD44(+) (77.9%) and low levels of CD24(+) (2.3%). These clones also overexpressed the drug resistance genes ABCG2 and MDR-1. Quantitative real-time PCR showed that sphere clones expressed stem cell genes Nanog and OCT-4 284 and 266 times, respectively, more than those in the original GBC-SD cells. Immunofluorescent staining showed that sphere clones overexpressed OCT-4, Nanog, and SOX-2, and low expressed MUC1 and vimentin. Tumor formation experiments showed that 1×10(3) sphere clone cells could induce much larger tumors in nude mice than 1×10(5) GBC-SD cells. In conclusion, sphere clones of gallbladder cancer with stem cell-like characteristics can be obtained using suspension cultures of GBC-SD cells in serum-free culture medium containing cisplatin.

Osteopontin plays an anti-nucleation role in cholesterol gallstone formation.

AIM: To investigate the role of osteopontin in cholesterol gallstone formation. METHODS: Nucleation time was determined in model and human gallbladder bile in vitro. Effect of osteopontin on vesicles of bile was investigated via transmission electron microscopy. The mRNA and protein expression of osteopontin were detected in human calculus and normal gallbladder tissues, and then lipid compositions of human bile were determined via commercial kits. RESULTS: Osteopontin could prolong the nucleation time in a dose-dependent manner, and inhibit the pro-nucleation effect induced by calcium ion. Cholesterol crystal growth was inhibited by osteopontin in a dose-dependent manner in model and human gallbladder bile, but not affected by calcium. Furthermore, the formation, aggregation and fusion of vesicles were suppressed by osteopontin in model and human bile as demonstrated by transmission electron microscopy. The mRNA and protein expression of osteopontin in calculus gallbladder tissues were lower than those in normal tissues. The concentrations of cholesterol, phospholipid and bile acids, and cholesterol saturated index were higher and the contents of osteopontin and calcium, nevertheless, were found to be lower in lithogenic bile than those in normal controls. CONCLUSION: These findings indicated that osteopontin could inhibit the cholesterol gallstone formation as an anti-nucleation factor, which may be involved in the pathogenesis of cholesterol gallstone formation.

Bibliometric analysis of pressure ulcer research: 1990-2009.

PURPOSE: Bibliometric evaluation provides a method for evaluating trends in publications related to a specific topic. This search focused on pressure ulcer (PU) care; journals and authors with the greatest contribution and impact were emphasized. DESIGN: Bibliometric evaluation. METHODS: Data encompassing the period from 1990 to 2009 were extracted from the Science Citation Index online version. We analyzed selected documents with "pressure ulcer" as a part of the title, abstract, or key words and reported the following parameters: trends of publication output, document types, subject category, journal pattern, authorship, and research in nursing disciplines. RESULTS: The annual number of articles on PUs grew at a rapid rate, from approximately 39 in 1991 to 259 in 2009. The main subject categories in which research on PUs was conducted were surgery and nursing, each of which accounted for more than 10% of total articles. The United States was the dominant country in terms of volume of articles. The relationship between nurse staffing and PU-related outcomes is currently the major focus of PU nursing research, followed by risk assessment scale evaluations. CONCLUSION: We found that the number of PU-related publications has grown at a rapid rate over the past 20 years, reflecting an increasing awareness of the importance of PU prevention and management.