Nutrition Risk Screening 2002 for Adult Cancer Patients: A Systematic Review and Meta-Analysis.

It is critical to screen and assess malnutrition in cancer patients early. However, there is no uniform standard for nutritional risk screening and malnutrition assessment. We aimed to analyze the effects of the Nutrition Risk Screening 2002 (NRS2002) in screening for nutritional risk among adult cancer patients, using the Patient-Generated Subjective Global Assessment (PG-SGA) as the reference standard. A systematic search was performed using PubMed, Embase, Web of Science, the Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang Database, and China Science and Technology Journal Database (VIP). Studies comparing NRS2002 with PG-SGA in adult cancer patients were included. To assess the quality of the included studies, the Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2) was used. The combined sensitivity, specificity, diagnostic odds ratio (DOR), and the area under the receiver-operating characteristic curve (AUC) were calculated. In addition, sensitivity, subgroup, and publication bias analyses were performed. Thirteen articles involving 3,373 participants were included. The combined sensitivity, specificity, DOR, and AUC were 0.62 (95% CI, 0.60-0.64), 0.86 (95% CI, 0.84-0.88), 11.23 (95% CI, 8.26-15.27), and 0.85 (95% CI, 0.82-0.88), respectively. For adult cancer patients, NRS2002 has moderate sensitivity, high specificity, and high AUC in screening for nutritional risk.

Predictive value of NoSAS questionnaire combined with the modified Mallampati grade for hypoxemia during routine sedation for gastrointestinal endoscopy.

BACKGROUND: The incidence of hypoxemia during painless gastrointestinal endoscopy remains a matter of concem. To date, there is no recognized simple method to predict hypoxemia in digestive endoscopic anesthesia. The NoSAS (neck circumference, obesity, snoring, age, sex) questionnaire, an objective and simple assessment scale used to assess obstructive sleep apnea (OSA), combined with the modified Mallampati grade (MMP), may have certain screening value. This combination may allow anesthesiologists to anticipate, manage, and consequently decrease the occurrence of hypoxemia. METHODS: This study was a prospective observational trial. The primary endpoint was the incidence of hypoxaemia defined as pulse oxygen saturation (SpO2) < 95% for 10 s. A total of 2207 patients admitted to our hospital for painless gastrointestinal endoscopy were studied. All patients were measured for age, height, weight, body mass index, neck circumference, snoring, MMP, and other parameters. Patients were divided into hypoxemic and non-hypoxemic groups based on the SpO2. The ROC curve was plotted to evaluate the screening value of the NoSAS questionnaire separately and combined with MMP for hypoxemia. The total NoSAS score was evaluated at cut-off points of 8 and 9. RESULTS: With a NoSAS score ≥ 8 as the critical value for analysis, the sensitivity for hypoxemia was 58.3%, the specificity was 88.4%, and the area under the ROC was 0.734 (P < 0.001, 95% CI: 0.708-0.759). With a NoSAS score ≥ 9 as a critical value, the sensitivity for hypoxemia was 36.50%, the specificity rose to 96.16%, and the area under the ROC was 0.663 (P < 0.001, 95% CI: 0.639-0.688). With the NoSAS Score combined with MMP for analysis, the sensitivity was 78.4%, the specificity was 84%, and the area under the ROC was 0.859 (P < 0.001, 95%CI:0.834-0.883). CONCLUSIONS: As a new screening tool, the NoSAS questionnaire is simple, convenient, and useful for screening hypoxemia. This questionnaire, when paired withMMP, is likely to be helpful for the screening of hypoxemia.

Empagliflozin Attenuates Hyperuricemia by Upregulation of ABCG2 via AMPK/AKT/CREB Signaling Pathway in Type 2 Diabetic Mice.

Hyperuricemia (HUA) is a metabolic disease characterized by elevated serum uric acid (SUA). Empagliflozin, a kind of sodium-glucose cotransporter 2 inhibitors, has recently emerged as a new antidiabetic agent by facilitating glucose excretion in urine. Moreover, there was evidence of SUA reduction following treatment with empagliflozin in addition to glycaemic control, while the molecular mechanisms remain unknown. To investigate the potential mechanisms, the model of type 2 diabetes (T2DM) with HUA was established by combination of peritoneal injection of potassium oxonate and intragastric administration of hypoxanthine in KK-Ay mice. A series of method such as RT-PCR, western blot, immunochemistry, immunofluorescence were conducted to explore the mechanism. Our results showed that empagliflozin significantly ameliorated the levels of SUA and blood glucose in T2DM mice with HUA. Furthermore, in both kidney and ileum, empagliflozin obviously promoted protein expression of uric acid (UA) transporter ABCG2, p-AMPK, p-AKT and p-CREB. The same trend was observed in human tubular epithelial (HK-2) cells. Additionally, through application of an AMPK inhibitor (Compound C), it was further confirmed empagliflozin exerted its anti-hyperuricemic effects in an AMPK dependent manner. Meanwhile, with the help of ChIP assay and luciferase reporter gene assay, we found that CREB further activated ABCG2 via binding to the promoter of ABCG2 to induce transcription. Taken together, our study demonstrated that empagliflozin treatment played an essential role in attenuating HUA by upregulation of ABCG2 via AMPK/AKT/CREB signaling pathway.

Calcium Dobesilate Restores Autophagy by Inhibiting the VEGF/PI3K/AKT/mTOR Signaling Pathway.

Objective: Calcium dobesilate (CaD), an effective drug for the treatment of diabetic microvascular complications, especially diabetic retinopathy, is widely used in the clinic. Interestingly, several studies have indicated that CaD is therapeutic for diabetic kidney disease (DKD). Recently, evidence has indicated that altered vascular endothelial growth factor (VEGF) expression and decreased autophagy are the main pathological mechanisms of proteinuria. Thus, this study was conducted to explore the effect of CaD on restoring autophagy in DKD and the possible signaling pathway between VEGF and autophagy. Methods: Obese mice with spontaneous diabetes (KK-Ay) and high-fat diet- and streptozotocin-induced diabetic mice (HFD/STZ) were used in this study. Biochemical staining, western blotting, and immunohistochemistry were conducted to determine the angioprotective effect of CaD and the underlying mechanism between autophagy and VEGF/VEGFR. Results: Our results showed that CaD was capable of reducing albuminuria and restoring renal histological changes in KK-Ay and HFD/STZ-induced diabetic mice. CaD restored autophagy by decreasing the protein expression of LC3 II, Atg5, and beclin 1 and increasing the expression of P62. Moreover, CaD reduced the activation of the autophagy-related PI3K/AKT/mTOR pathway possibly via decreasing VEGF and downregulating VEGF receptor 2. Conclusion: Overall, CaD, as a novel potential therapeutic drug for DKD, plays a key role in protecting renal function and restoring autophagy by blocking VEGF/VEGFR2 and inhibiting the PI3K/AKT/mTOR signaling pathway.

Empagliflozin prevents cardiomyopathy via sGC-cGMP-PKG pathway in type 2 diabetes mice.

Cardiovascular complications contribute to the major mortality and morbidity in type 2 diabetes. Diabetic cardiomyopathy (DCM) is increasingly recognized as an important cause of heart failure. EMPA-REG OUTCOME trial has reported that empagliflozin, the sodium-glucose cotransporter 2 inhibitor, exerts cardiovascular benefits on diabetic population. However, the mechanism by which empagliflozin alleviates DCM still remains unclear. In the current study, we investigated the cardiac protective effects of empagliflozin on spontaneous type 2 diabetic db/db mice and its potential mechanism. Eight weeks of empagliflozin treatment (10 mg/kg/day) decreased body weight and blood glucose level, and increased urinary glucose excretion (UGE) in diabetic mice. Echocardiography revealed that both systolic and diastolic functions of db/db mice were also obviously improved by empagliflozin. Furthermore, empagliflozin-treated diabetic mice presented with amelioration of cardiac hypertrophy and fibrosis. In addition, diabetic hearts exhibited the deterioration of oxidative stress, apoptosis and pyroptosis, while these effects were significantly counteracted after empagliflozin treatment. Moreover, empagliflozin rescued diabetes-induced suppression of sGC (soluble guanylate cyclase enzyme)-cGMP (cyclic guanosine monophosphate)-PKG (cGMP-dependent protein kinase) pathway. However, when sGC-ß expression of hearts was inhibited by transvascular delivery of small interfering RNA, cardiac dysfunction was aggravated and the advantages of empagliflozin were reversed through inhibiting sGC-cGMP-PKG pathway. Collectively, these findings indicate that empagliflozin improves cardiac function involving the inhibition of oxidative stress-induced injury via sGC-cGMP-PKG pathway and may be a promising therapeutic option for DCM.

Attitudes and knowledge of undergraduate nursing students about palliative care: An analysis of influencing factors.

BACKGROUND: With the growing aging population, continual increase of the number of the old, and increase of cancer survival rate, palliative care is being considered a global public health issue. As a core force for the sustainable development of the nursing field, undergraduate nursing students' knowledge about and attitudes toward palliative care will directly affect the quality of care for dying patients in the future. OBJECTIVE: To investigate undergraduate nursing students' knowledge about and attitudes toward palliative care and analyze their influencing factors. METHODS: This descriptive and cross-sectional survey was conducted in 2016. A total of 1200 Chinese undergraduate nursing students were randomly selected as the survey subjects using stratified sampling method. The revised palliative care quiz for nursing (PCQN) and a self-designed questionnaire were used to measure students' knowledge and attitudes. RESULTS: The mean score of the revised PCQN was 16.10 ±â€¯5.04. Only a few respondents (19.8%) expressed desire to work in palliative care in the future. The findings show that knowledge and school, grade, gender, birthplace, and religious beliefs have statistically significant impacts (P < 0.01). In addition, logistic regression analysis showed that talking about death and caring for dying family members can have a significant influence on students' attitudes (P < 0.05). CONCLUSION: At present, Chinese undergraduate nursing students' knowledge about palliative care is minimal with the majority holding negative attitudes. Thus, the development of an effective end-of-life care program for nursing students is critical.

Effects of SGLT2 inhibitors on fractures and bone mineral density in type 2 diabetes: An updated meta-analysis.

BACKGROUND: The aim of the study is to update and determine the effects of sodium glucose cotransporter 2 (SGLT2) inhibitor therapy on fracture and bone mineral density (BMD) in patients with type 2 diabetes mellitus (T2DM). METHODS: We identified 27 eligible randomized controlled trials (RCTs) that compared the efficacy and safety of SGLT2 inhibitors to a placebo in 20 895 T2DM participants, with an average duration of 64.22 weeks. The relative risk (RR) of bone fracture and weighted mean difference (WMD) of changes in the BMD from baseline were determined to evaluate the risk of fracture. The degree of heterogeneity was evaluated by the I2 statistic, and publication bias was estimated using a funnel plot and Egger test. RESULTS: The pooled RR was 1.02 (95% CI [0.81, 1.28]) with low heterogeneity, indicating that SGLT2 inhibitor treatment was not correlated with a higher risk of fracture. Additionally, no increased risk was found for patients with different ages, sexes, and levels of HbA1c and some biochemical indicators. Three trials with 1303 patients reported a change in the BMD from baseline. SGLT2 inhibitor treatment did not decrease the BMD at four skeletal sites (lumbar spine, femoral neck, total hip, and distal forearm), and the overall WMD was 0.08 (95% CI [-0.09, 0.26]). No significant publication bias was detected. CONCLUSIONS: No increased risk for bone fracture was detected in patients with T2DM treated with SGLT2 inhibitors in this meta-analysis. SGLT2 inhibitor therapy did not appear to affect bone health, but more long-term detailed data are needed to validate this conclusion.

Pancreatic kallikrein protects against diabetic retinopathy in KK Cg-Ay/J and high-fat diet/streptozotocin-induced mouse models of type 2 diabetes.

AIMS/HYPOTHESIS: Many studies have shown that tissue kallikrein has effects on diabetic vascular complications such as nephropathy, cardiomyopathy and neuropathy, but its effects on diabetic retinopathy are not fully understood. Here, we investigated the retinoprotective role of exogenous pancreatic kallikrein and studied potential mechanisms of action. METHODS: We used KK Cg-Ay/J (KKAy) mice (a mouse model of spontaneous type 2 diabetes) and mice with high-fat diet/streptozotocin (STZ)-induced type 2 diabetes as our models. After the onset of diabetes, both types of mice were injected intraperitoneally with either pancreatic kallikrein (KKAy + pancreatic kallikrein and STZ + pancreatic kallikrein groups) or saline (KKAy + saline and STZ + saline groups) for 12 weeks. C57BL/6J mice were used as non-diabetic controls for both models. We analysed pathological changes in the retina; evaluated the effects of pancreatic kallikrein on retinal oxidative stress, inflammation and apoptosis; and measured the levels of bradykinin and B1 and B2 receptors in both models. RESULTS: In both models, pancreatic kallikrein improved pathological structural features of the retina, increasing the thickness of retinal layers, and attenuated retinal acellular capillary formation and vascular leakage (p < 0.05). Furthermore, pancreatic kallikrein ameliorated retinal oxidative stress, inflammation and apoptosis in both models (p < 0.05). We also found that the levels of bradykinin and B1 and B2 receptors were increased after pancreatic kallikrein in both models (p < 0.05). CONCLUSIONS/INTERPRETATION: Pancreatic kallikrein can protect against diabetic retinopathy by activating B1 and B2 receptors and inhibiting oxidative stress, inflammation and apoptosis. Thus, pancreatic kallikrein may represent a new therapeutic agent for diabetic retinopathy.

Air Embolism during Upper Endoscopy: A Case Report.

Air embolism is a rare complication of upper endoscopy and potentially causes life-threatening events. A 67-year-old man with a history of surgery of cardiac carcinoma and pancreatic neuroendocrine tumor underwent painless upper endoscopy because of tarry stools. During the procedure, air embolism developed, which caused decreased pulse oxygen saturation and delayed sedation recovery. He recovered with some weakness of the left upper limb in the intensive care unit without hyperbaric oxygen therapy. The etiology, clinical manifestations, and treatments of air embolism are discussed based on the literature reports. Although air embolism is uncommon in endoscopic examinations, the patients' outcomes could be improved if clinicians are alert to this potential complication, and promptly start proper diagnostic and therapeutic measures.

Different effects of oxycodone and remifentanil in patients undergoing ultrasound-guided percutaneous radiofrequency ablation of hepatic cancer: a randomized trial.

BACKGROUND: Percutaneous radiofrequency ablation (RFA) is a recently introduced alternative technique for the treatment of hepatic cancer. Anesthesia is required for RFA of hepatic cancer to achieve patient comfort and immobilization during this painful procedure. The purpose of this study was to investigate the analgesic efficacy and evaluate the safety of a single intravenous injection of oxycodone hydrochloride for this procedure. PATIENTS AND METHODS: A total of 120 American Society of Anesthesiologists class I-II grade patients for elective ultrasound-guided percutaneous RFA were enrolled in this randomized controlled trial. Patients were randomized (1:1) to receive either a single intravenous injection of oxycodone (group O) or continuous infusion of remifentanil (group R). Both groups received the continuous infusion of dexmedetomidine for sedation. Visual analog scale (VAS), rescue analgesic, and side effects were checked during the periprocedural period. In addition, patient and oncologist satisfaction on a scale of 1-5 were determined. RESULTS: VAS score in group O was significantly lower than in group R at 1, 2, and 3 hours after RFA, and patients in group O required analgesics significantly later and less doses in the first 24 hours after RFA. The occurrence of unwanted body movements was significantly lower in group O. We found no complications including allergic reaction, excessive sedation, and chest wall rigidity in all patients. The patient satisfaction score was significantly higher in group O than that in group R. CONCLUSION: Ultrasound-guided percutaneous RFA for hepatic cancer can be completed both with continuous infusion of remifentanil or a single intravenous injection of oxycodone. However, oxycodone hydrochloride provides better patient experience with higher satisfactory score and less unwanted body movements, relieves post-procedural pain better, and is not associated with an increase in adverse effects.

SGLT2 inhibition with empagliflozin attenuates myocardial oxidative stress and fibrosis in diabetic mice heart.

BACKGROUND: Hyperglycaemia associated with myocardial oxidative stress and fibrosis is the main cause of diabetic cardiomyopathy. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor has recently been reported to improve glycaemic control in patients with type 2 diabetes in an insulin-independent manner. The aim of this study was to investigate the effect of empagliflozin on myocardium injury and the potential mechanism in type 2 diabetic KK-Ay mice. METHODS: Thirty diabetic KK-Ay mice were administered empagliflozin (10 mg/kg/day) by oral gavage daily for 8 weeks. After 8 weeks, heart structure and function were evaluated by echocardiography. Oxidants and antioxidants were measured and cardiac fibrosis was analysed using immunohistochemistry, Masson's trichrome stain and Western blot. RESULTS: Results showed that empagliflozin improved diabetic myocardial structure and function, decreased myocardial oxidative stress and ameliorated myocardial fibrosis. Further study indicated that empagliflozin suppressed oxidative stress and fibrosis through inhibition of the transforming growth factor ß/Smad pathway and activation of Nrf2/ARE signaling. CONCLUSIONS: Glycaemic control with empagliflozin significantly ameliorated myocardial oxidative stress injury and cardiac fibrosis in diabetic mice. Taken together, these results indicate that the empagliflozin is a promising agent for the prevention and treatment of diabetic cardiomyopathy.

Triptolide Attenuates Renal Tubular Epithelial-mesenchymal Transition Via the MiR-188-5p-mediated PI3K/AKT Pathway in Diabetic Kidney Disease.

Triptolide possesses the trait of renal protection. Epithelial-mesenchymal transition (EMT) is closely linked to the pathogenesis of diabetic kidney disease (DKD). MicroRNAs have recently emerged as critical regulators of DKD. However, it is poorly understood whether triptolide alleviates renal EMT by regulating microRNAs in DKD. In this study, we found that triptolide decreased albuminuria, improved the renal structure and reduced renal EMT in rats with DKD. Furthermore, activation of the PI3K/AKT signaling pathway was increased in diabetic rats, which was partly reversed by triptolide. Triptolide also alleviated glucose-induced EMT in HK-2 cells in vitro. PI3K/AKT signaling pathway activation was reduced after triptolide treatment. Moreover, triptolide decreased the increase in miR-188-5p expression stimulated by high glucose levels in HK-2 cells. miR-188-5p inhibited PTEN expression by directly interacting with the PTEN 3'-untranslated region. Additionally, downregulation of miR-188-5p, which imitates the effects of triptolide, attenuated the activation of the PI3K/AKT pathway and HG-induced EMT, whereas miR-188-5p overexpression reversed the effects of triptolide on the PI3K/AKT pathway and EMT. In conclusion, we demonstrated that triptolide ameliorates renal EMT via the PI3K/AKT signaling pathway through the interaction between miR-188-5p and PTEN, indicating that miR-188-5p may be a therapeutic target of triptolide in DKD.

Saxagliptin regulates M1/M2 macrophage polarization via CaMKKß/AMPK pathway to attenuate NAFLD.

Non-alcoholic fatty liver disease (NAFLD), a hepatic manifestation of metabolic disease, is an important complication of diabetes mellitus (DM). Inflammation plays a crucial role in the development and progression of NAFLD. Moreover, the pathological formation of NAFLD is closely related to accumulation and polarization of hepatic macrophages. Saxagliptin, a newly antidiabetic agent, can suppress hepatic inflammation reportedly. However, underlying mechanisms remain poorly explored. In this study, we showed saxagliptin alleviated lipid accumulation and attenuated liver inflammation with downregulation of inflammation factors in diabetic rats. Moreover, saxagliptin could reduce the phenotype of M1 macrophage iNOS and increase the phenotype of M2 macrophage CD206. We also found saxagliptin increased CaMKKß/AMPK activation. In vitro, human THP-1 monocytes were differentiated into M1/M2 macrophages by LPS/IL-4. We clarified saxagliptin's anti-inflammatory effect by reducing NF-κB, TNF-α expression and promoting M2 macrophage polarization. Furthermore, we demonstrated CaMKKß-dependent AMPK activation was involved in macrophage polarization. In conclude, our results detected saxagliptin could attenuated inflammation through regulation of M1/M2 macrophage polarization and might be via CaMKKß/AMPK pathway.

[XCT790 inhibits rat vascular smooth muscle cells proliferation through down-regulating the expression of estrogen-related receptor alpha].

Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays an important role in several pathological processes of cardiovascular diseases. In this study, the effects of XCT790, a potent and selective inverse agonist of estrogen-related receptor alpha (ERRalpha), on rat VSMCs proliferation and related signal pathways were investigated. The proliferative activity of VSMCs was determined by CCK-8 assay. The mRNA levels of ERRalpha, PGC-1alpha, OPN and MCAD were assayed by RT-PCR. The protein levels of ERRalpha, ERK2 and p-ERK1/2 were evaluated by Western blotting. ELISA was used to assess the protein expression of VEGF. The results showed that XCT790 (5-20 micromol x L(-1)) inhibited rat VSMCs proliferation, and the expression of ERRalpha and its target genes, as well as p-ERK1/2, were also inhibited. XCT790 inhibited VSMCs proliferation in a dose-dependent manner at the dose range from 5 to 20 micromol x L(-1) and in a time-dependent manner at the dose range from 10 to 20 micromol x L(-1). These findings demonstrate that XCT790 inhibits rat VSMCs proliferation by down-regulating the gene level of ERRalpha and thus inhibiting the ERK signal pathway, suggesting that ERRalpha may be a novel potential target for therapeutic approaches to inhibit VSMCs proliferation, which plays an important role in several cardiovascular diseases.