Objective:To develop and evaluate a medical experience assessment scale for debridement and dressing change in chronic wound patients in China, and to provide a reference for improving hospital service quality.Methods:Based on the framework of hospital consumer assessment of healthcare providers and systems survey (HCAHPS) in the United States, a preliminary draft of the scale was formed through a literature review and qualitative interviews with 12 chronic wound patients (7 males and 5 females aged 58.1±12.3 years). Five experts were invited for content validity testing, and 191 chronic wound patients (111 males and 80 females aged 53.5±19.1 years) were selected to evaluate the internal consistency reliability, half reliability, retest reliability, and structural validity of the scale.Results:The Chronic Wound Patient Debridement and Dressing Experience Scale covered 5 dimensions with 30 sub-items and 2 comprehensive evaluation items, including demand response, good and friendly communication, professional trust, optimization of the medical treatment process, and encouragement of patient participation. The scale Cronbach′s α coefficient was 0.967 and ranged from 0.890 to 0.962 for each dimension. The overall retest reliability of the scale was 0.940 and ranged from 0.895 to 0.940 for each dimension. The overall half reliability of the scale was 0.923 and ranged from 0.834 to 0.935 for each dimension. 5 factors were extracted, with a cumulative variance contribution rate of 82.061%.Conclusions:Based on the HCAHPS framework in the United States, the Chronic Wound Debridement and Dressing Experience Scale developed has high reliability and validity, and can be used to evaluate the dressing change experience of patients with chronic wounds. It has clinical practice significance for dressing change in chronic wounds.

Alzheimer's disease(AD) is a common neurodegenerative disease with increasing incidence rate. Up to now,there is no ideal treatment for AD. It has become a public health problem worldwide. Traditional Chinese medicine (TCM) believes that kidney deficiency is the key symptomatic element of deterioration and temporal progression symptoms,accompanied by the AD process. The treatment of tonifying kidneys,supplementing essence and replenishing marrow is the fundamental method for AD in TCM. Clinical studies have shown that kidney-tonifying formula can significantly improve the cognitive function and daily ability of patients with mild and moderate AD and have no obvious adverse reactions. Its mechanism of action may be related to the protection of nerves,reduction of β-amyloid (Aβ) level in the brain,inhibition of inflammatory factors activation and anti-oxidative stress. Besides reviewing the clinical and pharmacological research progress of kidney-tonifying formula for AD,this article also discusses the advantages and shortcomings of kidney-tonifying formula in the prevention and treatment of AD based on TCM theory and modern medical research. The aim of this study is to provide references of kidney nourishing therapy in TCM for the prevention and treatment of neurodegenerative diseases.

Objective:To explore the correlations between serum levels of brain-derived neurotrophic factor(BDNF),interleukin-18(IL-18)and hypersensitivity C-reactive protein(hs-CRP)in patients with acute cerebral infarction and vascular cognitive impairment(VCI),and to provide some clinical ba-ses for early prevention of VCI.Methods:A total of 160 patients with acute cerebral infarction admitted in Department of Neurology of Jincheng People's Hospital from May 2019 to April 2020 were enrolled in this study and were devided into three groups according to whether or not combined with cognitive impair-ment,including no cognitive impairment group(NCI,57 cases),vascular cognitive impairment no de-mentia group(VCIND,56 cases)and vascular dementia group(VaD,47 cases).The cognitive function of all the patients were evaluated by Montreal cognitive assessment(MoCA).The National Institute of Health stroke scale(NIHSS)was used to assess the degree of neurological deficit(mild-,moderate-,se-vere-neurologic deficit group).The infarct size was calculated by Pullicino's method(small-,middle-,large-infarct group).The levels of serum BDNF and IL-18 were measured by enzyme-linked immunosor-bent assay(ELISA),and serum levels of hs-CRP were measured by immunoturbidimetry during the acute phase(0-7 d),recovery period(15-30 d)and 6 months after cerebral infarction.The effects of varying degrees of neurological deficits and different size of infarction on BDNF,IL-18 and hs-CRP were observed.The levels of serum BDNF,IL-18 and hs-CRP in the patients of the three groups with acute,convalescent and six-month cerebral infarction were compared,and their correlations with VCI were ana-lyzed.Results:Serum BDNF level and MoCA scores in mild-neurologic deficit group and small-infarct group were significantly higher than those in moderate-and severe-deficit group,middle-and large-infarct group,respectively(P＜0.05).Their levels of IL-18 and hs-CRP were significantly lower than those in moderate-and severe-deficit group,middle-and large-infarct group,respectively(P＜0.05).The levels of serum BDNF in NCI group,VCIND group and VaD group during the acute phase,convalescence and 6 months after cerebral infarction were in a significant decline,and the differences during the acute phase and recovery period were statistically significant(P＜0.05).The levels of IL-18 and hs-CRP during the acute phase,recovery period and 6 months after cerebral infarction showed a significant increasing trend with significance(P＜0.05).Correlation analysis revealed that the levels of BDNF was positively correlated with MoCA scores but negatively correlated with the severity of cognitive impairment while the expression levels of IL-18 and hs-CRP were negatively correlated with MoCA scores but positively correlated with the severity of cognitive impairment.Conclusion:Serum BDNF,IL-18 and hs-CRP are involved in the patho-logical process of occurrence and development of VCI in the patients with acute cerebral infarction.BDNF has a protective effect on VCI while IL-18 and hs-CRP cause severe cognitive impairment.The levels of se-rum BDNF、IL-18 and hs-CRP in the patients with acute ischemic cerebral infarction are closely related to the severity of cognitive impairment and can be used as biomarkers of early diagnosis of VCI.

CUDC-101, an effective and multi-target inhibitor of epidermal growth factor receptor (EGFR), histone deacetylase (HDAC), and human epidermal growth factor receptor 2 (HER2), has been reported to inhibit many kinds of cancers, such as acute promyelocytic leukemia and non-Hodgkin's lymphoma. However, no studies have yet investigated whether CUDC-101 is effective against myeloma. Herein, we proved that CUDC-101 effectively inhibits the proliferation of multiple myeloma (MM) cell lines and induces cell apoptosis in a time- and dose-dependent manner. Moreover, CUDC-101 markedly blocked the signaling pathway of EGFR/phosphoinositide-3-kinase (PI3K) and HDAC, and regulated the cell cycle G2/M arrest. Moreover, we revealed through in vivo experiment that CUDC-101 is a potent anti-myeloma drug. Bortezomib is one of the important drugs in MM treatment, and we investigated whether CUDC-101 has a synergistic or additive effect with bortezomib. The results showed that this drug combination had a synergistic anti-myeloma effect by inducing G2/M phase blockade. Collectively, our findings revealed that CUDC-101 could act on its own or in conjunction with bortezomib, which provides insights into exploring new strategies for MM treatment.
Humans ; Antineoplastic Agents/therapeutic use* ; Apoptosis ; Bortezomib/pharmacology* ; Cell Line, Tumor ; Cell Proliferation ; ErbB Receptors/antagonists & inhibitors* ; G2 Phase Cell Cycle Checkpoints ; Histone Deacetylase Inhibitors/pharmacology* ; Histone Deacetylases/metabolism* ; M Cells ; Multiple Myeloma/drug therapy*

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling exert essential regulatory function in microbial-and onco-immunology through the induction of cytokines, primarily type I interferons. Recently, the aberrant and deranged signaling of the cGAS-STING axis is closely implicated in multiple sterile inflammatory diseases, including heart failure, myocardial infarction, cardiac hypertrophy, nonalcoholic fatty liver diseases, aortic aneurysm and dissection, obesity, etc. This is because of the massive loads of damage-associated molecular patterns (mitochondrial DNA, DNA in extracellular vesicles) liberated from recurrent injury to metabolic cellular organelles and tissues, which are sensed by the pathway. Also, the cGAS-STING pathway crosstalk with essential intracellular homeostasis processes like apoptosis, autophagy, and regulate cellular metabolism. Targeting derailed STING signaling has become necessary for chronic inflammatory diseases. Meanwhile, excessive type I interferons signaling impact on cardiovascular and metabolic health remain entirely elusive. In this review, we summarize the intimate connection between the cGAS-STING pathway and cardiovascular and metabolic disorders. We also discuss some potential small molecule inhibitors for the pathway. This review provides insight to stimulate interest in and support future research into understanding this signaling axis in cardiovascular and metabolic tissues and diseases.

Objective: To assess the effects of acute exposure to electronic cigarette ( e-cigarette ) on leukocyte and total protein levels in bronchoalveolar lavage fluid ( BALF ) and pulmonary surfactant protein expression in a mouse model, so as to provide insights into the elucidation of the mechanism underlying the damages to the respiratory system caused by e-cigarette. Methods: Twenty-one C57BL/6N female mice were randomly divided into the blank control group, the solvent control group and the nicotine group. Mice in the solvent control group and the nicotine group were exposed to the solvent aerosol or e-cigarette aerosol containing 25 mg/mL nicotine for 3 hours daily, while mice in the blank control group were bred in clean air. Following 3-day exposure, mouse BALF and lung specimens were collected. The cell morphology was observed using microscopy following Wright-Giemsa staining and the leukocyte count was estimated in BALF, while the total protein expression was quantified using bicinchoninic acid ( BCA ) assay. In addition, the mRNA expression of pulmonary surfactant protein genes was detected in mouse lung specimens using quantitative real-time PCR ( qPCR ) assay. Results: All mice in three groups grew well without obvious abnormality or death seen. Wright-Giemsa staining showed a higher number of mononuclear macrophages in mouse BALF in the nicotine group than in the blank control group and the solvent control group. The leukocyte counts were ( 2.00±0.77 )×107, ( 1.79±0.99 )×107 and ( 4.00±1.35 )×107 cells/L ( F=9.199, P=0.002 ), and the total protein levels were ( 0.16±0.03 ), ( 0.12±0.02 ) and ( 0.16±0.04 ) mg/mL in mouse BALF in the blank control group, solvent control group and nicotine group ( F=3.610, P=0.048 ), and the relative mRNA expression of pulmonary surfactant protein B (SP-B) and SP-D was 1.00±0.14, 0.82±0.12 and 0.74±0.07 ( F=5.491, P=0.028 ), and 1.00±0.06, 0.90±0.02 and 0.71±0.15 in mouse lung specimens, respectively ( F=10.460, P=0.005 ). The leukocyte count was significantly higher in the nicotine group than in the blank control group and solvent control group (P=0.007, 0.003), and the total protein content was higher in the nicotine group than in the solvent control group ( P=0.060 ), while the relative SP-B mRNA expression was lower in the nicotine group than in the blank control group ( P=0.025 ), and the relative SP-D mRNA expression was lower in the nicotine group than in the blank control group and solvent control group ( P=0.004, 0.041 ). Conclusion Acute exposure to e-cigarette results in elevated intrapulmonary inflammatory responses, pulmonary capillary barrier impairment and reduced pulmonary surfactant protein expression.

To report the clinical, imaging, and pathological feature of a rare case of central precocious puberty with primary pigmented nodular adrenocortical disease(PPNAD), and to conduct a retrospective analysis of PPNAD with relevant literatures. The pubic hair was found in the child for more than one year. Physical examination showed Cushing′s syndrome. ACTH in blood decreased, cortisol rhythm was disordered, 24-hour urine free cortisol increased and the paradoxical increase of urine free cortisol after high dose dexamethasone suppression test. Adrenal enhancement computed tomography(CT)showed multiple small nodular shadows in bilateral adrenal glands. Gonadotropin releasing hormone(GnRH)stimulation test supported central precocious puberty and GnRH analogue was used to control the sexual development. PPNAD was supported by pathology result. The symptoms of Cushing′s syndrome were relieved partially after left adrenalectomy.

Objective: To apply DNA barcoding to identifying the rodents in Zhejiang Province. Methods : Rodents were captured from Jiashan,Longyou,Yunhe and Ninghai counties in Zhejiang Province. The DNA was extracted from ears of rodent samples,and was amplified and sequenced with mitochondrial cytochrome C oxidase subunit I（COI）genes. The obtained sequences were compared with the related sequences in GenBank,and neighbour-joining evolutionary tree was constructed. Then the results by DNA barcoding and by morphological identification were compared. Results : A total of 22 COI gene samples were amplified. The evolutionary tree constructed by 18 samples was consistent with the morphological identification results and 4 samples were different：Suncus murinus should be Crocidura lasiura,infant rats of Rattus losea and Rattus tanezumi was re-identified as Rattus rattus,infant rats of Microtus fortis（sample number：NH-1）needs further identification. Conclusion DNA barcoding can effectively correct the errors of morphological identification,thus combining the two methods could improve the accuracy of rodent identification.

Objective To study the protective effect of polyene phosphatidylcholine on hepatic injury induced by oxaliplatin and 5?fluorouracil. Methods A subcutaneous tumor model was established by transplanting colocarcinoma HCT116 cells into 30 nude mice,which were random?ized into three groups. The polyene phosphatidylcholine group was injected with polyene phosphatidylcholine(85 mg · kg-1 · d-1)and 5?fluorouracil (20 mg·kg-1·d-1)for 7 days,and then injected with oxaliplatin(6 mg·kg-1·d-1)for 1 day. The hepatic injury group was injected with 5?fluoroura?cil(20 mg·kg-1·d-1)for 7 days and oxaliplatin(6 mg·kg-1·d-1)for 1 day. The tumor?bearing blank group was injected with normal saline. Hepat?ic injury was observed with ultrathin pathological sections. Liver homogenates were prepared to detect superoxide dismutase(SOD)and catalase (CAT)activity. Results In the hepatic injury group,pathological sections revealed dissolved cellular cytoplasm,mitochondrial membrane dam?age,cell membrane edema,and fuzzy,sinusoidal cell expansion . There were no obvious hepatic injuries observed in the polyene phosphatidylcho?line group. The expression of SOD and CAT were lower in the hepatic injury and polyene phosphatidylcholine groups compared to the tumor?bear?ing blank group(P<0.05). The expression of SOD and CAT were higher in the polyene phosphatidylcholine group compared to the hepatic injury group(P<0.05). Conclusion Polyene phosphatidylcholine has a protective effect on hepatic injury induced by oxaliplatin and 5?fluorouracil, which may be related to its effect on membrane repair and inhibition of oxidative stress.

Objective To explore the effect of maintenance of interval time on catheter blockage and infection for intravenous infusion port patients during the off-treatment time. Methods A total of 100 patients with implanted ports, who drew blood well every time, bolus fluently and had informed consent, were divided into experimental group and control group by random number table method on average. The maintenance carried once in the control group every 4 weeks, while it happened in the experimental group every 12 weeks. We compared the catheter blockage and infection between two groups. Results There had no catheter completely block,Ⅲ grade catheter block and infection in the two groups during the 72 weeks, but Ⅰand Ⅱ grade blockage happened. In the experimental group, there was 3 patients having I grade catheter block, and that of the control group was 2 with no statistically significant difference between two groups (χ2 =0. 211,P>0. 05). In the experimental group, there was 1 patients hadⅡgrade catheter block, and that of the control group was 2 with no statistically significant difference between two groups (χ2 =0. 344,P >0. 05). Conclusions The intravenous infusion port patients had no correlation between the length of maintenance and blockage with infection. The maintenance carried once every 4 weeks is easily accepted for patients.