Objective To investigate the prevalence of vitamin D deficiency in patients in geriatric intensive care unit and the impact of vitamin D deficiency on the prognosis.Methods 213 hospitalized patients admitted into geriatric intensive care unit of Xinhua Hospital,Shanghai from June 2012 to December 2013 were included in the historical cohort study.Serum 25-hydroxyvitamin D [25 (OH)D] was examined in all the subjects.Main laboratory findings,the incidence of multiple organ dysfunction syndrome (MODS),Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score and mortality rate of 30-day kept in hospital were compared among patients with different serum 25-hydroxyvitamin D level.Potential risk factors for mortality were analyzed by multivariate logistic regression analysis.Results 25(OH)D deficiency was identified in 82 patients (38.5％),25(0H)D insufficiency in 90 patients (42.3％),and 25(OH)D sufficiency in 41 patients (19.2％).Compared with 25(0H)D sufficiency group,25(0H)D deficiency group showed the increased levels of APACHE Ⅱ score,plasma lactic acid,C reactive protein (CPR),the incidence of MODS and mortality rate (21.65±-8.89 vs.17.05±8.03,1.89±0.76 mmol/L vs.1.86±1.03 mmol/L,101.08±48.23 mg/L vs.92.48±38.56 mg/L,42.7％ vs.19.5％,30.5％ vs.9.8％,all P＜0.05).Multiple logistic regression analysis suggested that 25 (OH)D deficiency was an independent risk factor for mortality.25(OH)D levels were negatively correlated with length of stay in geriatric intensive care unit (r=0.18,P＜0.05).Conclusions Vitamin D deficiency is highly prevalent among patients admitted into geriatric intensive care unit.Vitamin D deficiency is associated with disease severity and may be an independent risk factor for mortality.

Objective To investigate the expression of peroxisome proliferator-activated rec eptor γ (PPARγ) and glucokinase (GK) induced by Wnt signaling pathway in mice NIT-1 β-cells,and to explore the interaction between PPARγ and Wnt signaling pathways.Methods Recombinant Wnt3a protein was applied to NIT-1 beta-cells to activate Wnt signaling pathway.The expression of PPARγ was determined by real-time PCR and Western blotting.The expression of GK was determined by real time PCR.Results Wnt3a rapidly activated Wnt/β-catenin/TCF signaling pathway,and increased PPARγ and GK mRNA expression by 41.2％ and 65.0％ in NIT-1cells,with PPARγ protein expression increasing by 97.8％ (P＜0.01).These effects were abrogated by Wnt and PIK3 inhibitors,dickkopf 1 and wortmannin treatment (P＜ 0.01).Conclusions PPARγ and GK can be upregulated by Wnt singnaling,and the effects might partially be PI3K-dependent.

Objective To establish whether Wnt-signaling pathway plays a role in mice β-cell function and/or survival in vitro. Methods Mice NIT-1 beta cells were cultured in media with glucose concentration of 33.3 mmol/L and the cytokines interleukin-1β, interferon-γand tumor necrosis factor-α with or without the addition of purified Wnt3a protein in vitro. Subsequently, β-cell apoptosis by Tunnel and flow cytometry, and β-cell proliferation by BrdU were analyzed. Total RNA was extracted to measure gene expressions by real-time PCR.Results Incubations of NIT-1 cells with high glucose and cytokines resulted in an increase in β-cell apoptosis and decrease in β-cell proliferation (P<0.01). In contrast, treatment with Wnt3a protein protected β-cell from glucose and cytokines-induced apoptosis through up-regulating the expressions of above Pitx2、 TCF7L2. Conclusions Wnt-signaling regulates the proliferation of pancreatic β-cell, and protectes β-cell from glucotoxicity and cytokine toxicity with respect to proliferation and apoptosis.

Objective To investigate the relenvant factors of precocious puberty and provide the basis for precaution of high risk group of precocious puberty .Methods A 1:1 case-control study was performed on 50 healthy girls and 50 precocious puberty girls .Results Univariate analysis showed an significant differences in the exposure rates of following five factors between cases and controls:intake of nutritious and health products ,favoring meat and poultry,long time watching television,addiction to TV ads,family economic condition (The Chi-square values are 7.045,9.073,17.478,14.063,12.246 respectively,all P<0.05).The Logisitc regression showed that favoring meat and poultry,long time watching television and addiction to TV ads had significant differences among precocious puber -ty children(The Wald′s Value were 4.846,6.850,5.662 respectively,all P<0.05).Conclusion favoring meat and poultry,long time watching television and addiction to TV play an important roles in precocious puberty .

OBJECTIVE To understand the present situation of hand hygiene execution rate among clinical medical personnel,and discuss a series of scientific,reasonable and practical hand hygiene intervention methods,in order to elevate the hand hygiene execution rate among medical personnel.METHODS Using the self-designed questionoaires in combination with observation on hand hygiene process and investigation of hand hygiene knowledge level among medical personnel in various departments of different levels of hospitals to assess the hand hygiene execution rate.RESULTS The investigation indicated 76.00% medical personnel have had hand hygienic knowledge training,and referred in the stipulation health drafts,the hand hygiene execution rate was 50.00-70.00%.The hand health execution rate before contact with patients was 59.82%,and after contacts with patients was 77.97%;among department the hand hygiene execution rate before contact with patients was highest in the department of pediatrics(82.78%),the lowest was in emergency department(11.11%),after contact with patients the highest was department of infectiong(100.00%),and the larest was in the internal medicine department(39.93%).CONCLUSIONS Medical personnel's hand hygiene consciousness is still weak,with lacked hand hygiene related knowledge,it is necessary to summarize a set of reasonable effective intervention plans to elevate the hand hygiene execution rate,reduce the hospital infection percentage,and lower the patient pain and the economic loss.

This study is to investigate the effects of indirubin on ATP-induced immune responses of macrophages. For this, neutral red dye uptake method was used to test phagocytosis, MTT assay was used for measuring cell death, and reactive oxygen species (ROS) was tested with fluorescent probe DHE. The data showed that extracellular ATP attenuated phagocytosis, induced cell death and increased ROS production, and these effects were restored by pre-treating with indirubin. This result suggested that indirubin blockade the effects of ATP on macrophages, because extracellular ATP-induced effects are dependent on P2 receptors, in particular P2X7 receptors. Furthermore, the effects of indirubin on the activation of P2 receptors were tested, in particular P2X7 receptors. The data showed that indirubin significantly decreased ATP-induced, P2 receptors mediated intracellular Ca2+ concentration ([Ca2+]i) rise and inhibited P2X7 receptor-based ethidium bromide (EB) dye uptake. These results suggested the inhibitory effects of indirubin on the activation of P2X7 receptors, which may underlying the effects on ATP induced ROS production, phagocytosis attenuation and cell death of macrophages.

Objective To investigate the prevalence of hyperuricemia and its relationship with hy-perlipaemia and hyperglycemia in the elderly .Methods We chose the elderly people whose age were over 60 years and who had routine physical examine during August and September in 2009 , the number of them is 1321.Hyperuricemia is defined as the level of serum uric acid (UA) >416 mmol/L.Hyperlipaemia is defined as the level of serum total cholesterol ( TC)≥5.18 mmol/L; triglyceride ( TG)≥1.70 mmol/L;high-density lipoprotein ( HDL) <1.04 mmol/L and low-density lipoprotein ( LDL)≥3.37 mmol/L.Hy-perglycemia is defined as the level of fasting blood glucose ( FBG)≥6.1 mmol/L.Results There were 344 patients with hyperuricemia accounting for 26.04%.With increasing age , the propotion of the patients with hyperuricemia and the mean levels of UA , TC, TG and LDL respectively showed gradually rising ( P<0.05 respectively).The incidence of hyperlipaemia and hyperglycemia was higher in the hyperuricemia group than those in the controls ( P <0.05 respectively ) .Hyperuricemia in the elderly displayed a positive correlation to TC, TG, LDL and FBG( r =0.9954,0.9805,0.9715,0.9682, P <0.05).Conclusion Hyperuricemia , related with hyperlipaemia as well as hyperglycemia , is common in the elderly and should be paid more attention .

Objective To investigate the prevalence of vitamin D deficiency in elderly patients in severe illness and its relationship with severity of disease and prognosis.Methods Totally 325 inpatients admitted to geriatric intensive care unit were included in this study.Serum 25-hydroxyvitamin D [25-(OH)D] was examined.Main laboratory findings,the incidence of multiple organ dysfunction syndrome (MODS),Acute Physiology and Chronic Health Evaluation (APACHE Ⅱ) score and mortality rate of 30-day were compared among patients with different serum 25 (OH) D levels.Potential risk factors for mortality were analyzed by multivariate Logistic regression analysis.Results 25 (OH)D deficiency was identified in 113 (34.77％).Compared to 25(OH) D sufficiency group,25 (OH)D deficiency group has significantly higher plasma lactic acid,APACHE Ⅱ score,the incidence of MODS and mortality rate of 30-day,P ＜0.05.Analysis by multiple logistic regression suggested that 25 (OH) D deficiency was independent risk factor for mortality.Conclusions Vitamin D deficiency is highly prevalent among elderly patients with severe illness,and may be an independent risk factor for mortality.

Objective:To investigate the efficacy and safety of cedilanid in the treatment of severe pneumonia in infants and the value of preventing heart failure.Methods:A total of 80 children with severe pneumonia admitted to Dezhou Maternal and Child Health Hospital from January 2019 to December 2020 were selected and randomly divided into the control group and the observation group, with 40 cases in each group. The control group received comprehensive treatment, while the observation group was treated with cedilanid (0.01 mg/kg, one-time intravenous injection) on the basis of the control group. The efficacy of both groups was observed after 5 d of treatment. The incidence of heart failure, correction time of heart failure, improvement time of symptoms and signs, and length of hospitalization time were compared between the two groups; the inflammatory markers, myocardial markers and arterial blood gas indexes were compared between the two groups before and after the treatment.Results:The total effective rate in the observation group was higher than that in the control group, and the incidence of heart failure in the observation group was lower than that in the control group: 90.0% (36/40) vs. 72.5% (29/40), 32.5%(13/40) vs. 10.0%(4/40), the differences were statistically significant ( χ2 = 4.02, 4.10, P<0.05). The improvement time of symptoms and signs (restlessness elimination, respiratory improvement, heart rate improvement and disappearance of rhonchus in lung) in the observation group were less than those in the control group ( P<0.05). The levels of procalcitonin (PCT) and N-terminal pro-brain natriuretic peptide (NT-ProBNP), myocardial troponin I(cTnI), and creatine kinase isoenzyme (CK-MB) in the observation group after treatment were lower than those in the control group: (6.15 ± 1.03) μg/L vs. (10.85 ± 2.12) μg/L, (112.02 ± 30.09) ng/L vs. (215.39 ± 55.08) ng/L, (0.68 ± 0.17) μg/L vs. (1.12 ± 0.34) μg/L, (19.05 ± 6.11) U/L vs. (28.97 ± 7.82) U/L, P<0.05. The levels of oxygen partial pressure (PaO 2), blood oxygen saturation (SaO 2) and oxygenation index (PaO 2/FiO 2) in the observation group after treatment were higher than those in the control group: (6.15 ± 1.03) μg/L vs. (10.85 ± 2.12) μg/L, (112.02 ± 30.09) ng/L vs. (215.39 ± 55.08) ng/L, (0.68 ± 0.17) μg/L vs. (1.12 ± 0.34) μg/L, (19.05 ± 6.11) U/L vs. (28.97 ± 7.82) U/L, P<0.05. Conclusions:Early application of small dose of cedilanid in infants with severe pneumonia can effectively reduce the occurrence of heart failure, improve the clinical symptoms and blood gas indicators, with significant curative effect, which is worthy of promotion.

Objective To report the clinical features, myopathological changes, and gene mutations in five Chinese patients with mitochondrial diseases caused by POLG gene mutations. Methods Clinical materials of five unrelated patients who were referred to Department of Neurology, Peking University First Hospital from April 2012 to January 2018, carrying POLG gene mutations, were retrospectively analyzed. Muscle/nerve biopsies and targeted second-generation gene sequencing were performed on the patients. Results Among the five patients, three were male and two were female. Two cases were dominant inheritance and three were sporadic or recessive inheritance. The ages of onset were from 15 to 40 years with disease course of one to 26 years. One of them showed atypical SANDO (sensory ataxic neuropathy, dysarthria, and ophthalmoparesis) syndrome accompanied by cardiac preexcitation syndrome. There were two cases with autosomal dominant and one case with recessive progressive external ophthalmoplegia plus syndrome. One case presented with cognitive delay and sensory neuropathy. The pathological changes of mitochondrial myopathy were observed in all four patients with muscle involvement. Sural nerve biopsy in the patient with cognitive delay and sensory ataxia revealed chronic axonal pathological changes. POLG gene mutations were found in all five patients by targeted next generation sequencing, including single heterozygous mutations in two dominant inherited patients (c. 914 G＞A and c. 2864A＞G, respectively), and compound heterozygous POLG gene mutations in the other three sporadic/recessive inherited patients (c. 2591 A＞G/c. 1790 G＞A, c. 924G＞T/c. 3002delG and c. 1613A＞T/c. 1612 G＞T, respectively). There were six novel mutations not reported before, i.e., c.914G＞A(p.S305N), c.924G＞T(p.Q308H), c.1613A＞T(p.E538V), c.1612G＞T(p.E538*), c.1790 G＞A(p.R597Q) and c.3002delG. Conclusions POLG gene mutations can lead to different clinical spectrums. Progressive external ophthalmoplegia, limb weakness and axonal sensory neuropathy are common presentations in this group of patients with POLG gene related mitochondrial neuromuscular diseases. Novel mutations found in this study expand the mutational spectrum of POLG gene.