Effects of drinking water temperature in winter on growth performance, water consumption, surface temperature, and intestinal development of geese from 21 to 49 days of age.

This research aimed to investigate the effects of drinking water temperatures on growth performance, water consumption, surface temperature, organ indices, blood parameters, and intestinal development of geese, and determine the optimal drinking water temperature for 21 to 49-d geese. A total of 192 twenty-one-day male Yuzhou white geese were allocated randomly to 4 groups with 8 replicate pens per group according to the drinking water temperature (drinking water temperature [7℃-12℃] at ambient temperature [TC], 18℃ [T1], 27℃ [T2], and 36℃ [T3], respectively). The results showed that increasing drinking water temperature did not significantly improve the BW, ADG, and ADFI of geese (P > 0.05), whereas drinking warm water of 36℃ for geese had a trend to increase FCR (0.05 < P < 0.1). Geese in group T2 drank the most water per day on average, whereas geese in group TC drank the least (P < 0.001). Geese in groups T1, T2, and T3 had higher eyes temperatures than group TC (P < 0.001). No significant differences were found on the organ indices and blood biochemical parameters (P > 0.05). Geese from group T1 had higher crypt depth and muscularis thickness of duodenum (P < 0.05), and lower ratio of villus height to crypt depth than other groups (P < 0.001). Geese from group T1 had higher activities of trypsin in duodenum and jejuna and amylase in jejuna at 49 d than other groups (P < 0.01). Overall, these data indicate drinking water at 18℃ can increase water consumption and eyes temperature, and improve the activity of digestive enzymes and promote intestinal development. Under our experimental conditions, we recommend that the optimal drinking water temperature for geese from 21 to 49 d of age is 18°C.

Effects of citric acid supplementation on growth performance, intestinal morphology and microbiota, and blood parameters of geese from 1 to 28 days of age.

This study was conducted to investigate the effects of citric acid (CA) supplementation on growth performance, intestinal morphology, intestinal microbiota, and blood parameters of geese from 1 to 28 d of age and evaluate the optimum additional level of citric acid. A total of 180 one-day-old male goslings were randomly allotted to 5 treatment groups of 36 birds with 6 replications. The control group was fed a basal diet, and the other groups were fed the basal diet supplemented with 0.25, 0.50, 1.00, and 2.00% of citric acid, respectively. The results showed that goslings fed the diet supplemented with 1.00% CA had higher final body weight (FBW) and average daily gain (ADG) than other groups (P < 0.05). The CA supplementation at 0.25 to 1.00% improved the morphology of duodenum or jejunum (P < 0.05). The jejunal content pH value was significantly reduced with the addition of CA compared with the control group (P < 0.05). As citric acid levels increased, the IgA concentrations in plasma increased and then decreased, and the goslings fed 1.00% CA supplementation had the highest IgA concentrations (P < 0.05). The supplementation of 1.00% and 2.00% CA in diet significantly reduced the malondialdehyde (MDA) concentration in plasma (P < 0.05). No significant difference was found on some indices related to liver function in plasma (P > 0.05), while creatinine significantly increased by the 2.00% CA supplementation (P < 0.05). Besides, the higher Coliform level in cecal content and worse intestinal morphology were observed when CA supplementation was up to 2.00%. Hence, the dietary CA supplementation (especially 1.00%) in goslings improves the growth performance, intestinal morphology, immunity and antioxidant, while excessive CA addition may cause negative effects. According to the quadratic polynomial model, the addition of CA in diet for obtaining maximum average daily feed intake (ADFI) should be 1.09% (10.9 g/kg diet) for goslings from 1 to 28 d of age.

Effects of ambient temperature on growth performance, blood parameter, and fat deposition of geese from 14 to 28 days of age.

An experiment was conducted to investigate the effects of ambient temperature on the growth performance, blood parameter, and fat deposition in geese from 14 to 28 d of age in order to establish their optimal temperature requirements. A total of 150 14-day-old geese were allocated randomly to 5 environmentally controlled chambers with ambient temperature set at 18, 21, 24, 27, and 30°C from 14 to 28 d of age, respectively. As ambient temperature increased from 18 to 30°C, the feed intake decreased linearly (P < 0.05) and was accompanied by linearly or quadratically (P < 0.05) decreasing 28-day-old body weight, weight gain, and feed/gain. The upper critical level of ambient temperature from 14 to 28 d of age for 28-day-old body weight and weight gain were 25.83 and 26.17°C, respectively. There were no differences in plasma biochemical parameters or plasma hormones between geese fed at ambient temperature regimen at 18, 21, 24, 27, and 30°C. The abdominal fat weight and abdominal fat rate decreased linearly (P ≤ 0.05) with higher ambient temperature, but the ambient temperature had no effect on subcutaneous fat thickness or intermuscular fat width. It was concluded that the upper critical temperature of the ambient temperature for geese from 14 to 28 d of age was 26.17°C and high ambient temperature could lead to growth depression.

[Resection and free flap repair of recurrent maxillofacial and paranasal sinus skull base malignant tumor: report of 9 cases].

Objective: To investigate the treatment method and effect of surgical resection and free flap repair of recurrent malignant tumors of maxillofacial paranasal sinus and skull base. Methods: The clinical data of 9 patients with recurrent maxillofacial paranasal sinus and skull base malignant tumors who underwent surgical resection and free flap repair in the Department of Otorhinolaryngology Head and Neck Surgery of Shandong Provincial Hospital from August 2009 to May 2019 were analyzed retrospectively, including 5 males and 4 females, aged 32-69 years. There were 4 cases of squamous cell carcinoma, 3 cases of adenoid cystic carcinoma, 1 case of myoepithelial carcinoma and 1 case of malignant fibrous histiocytoma. All patients were repaired with anterolateral femoral flap. The treatment process and postoperative effect were analyzed by descriptive statistics. Results: All patients were followed up from 16 months to 6 years. There were 6 cases of recurrence after operation, including 1 case of local recurrence and 5 cases of skull base and craniocerebral recurrence. The median tumor free survival time of recurrent patients was 35 months. Conclusion: Surgical resection and free flap repair can effectively prolong the life of patients with recurrent maxillofacial paranasal sinus and skull base malignant tumors.

The histone deacetylase inhibitor chidamide induces intermittent viraemia in HIV-infected patients on suppressive antiretroviral therapy.

OBJECTIVES: To evaluate the safety and efficacy of chidamide to reverse HIV-1 latency in vivo and to compare the effects of four clinically tested histone deacetylase (HDAC) inhibitors on non-histone proteins in vitro. METHODS: Participants received chidamide orally at 10 mg twice weekly for 4 weeks while maintaining baseline antiretroviral therapy. The primary outcome was plasma viral rebound during chidamide dosing and the secondary outcomes were safety, pharmacokinetic and pharmacodynamic profiles, changes in cell-associated HIV-1 RNA and HIV-1 DNA, and immune parameters. Western blotting was used to compare the in vitro effects of the four HDAC inhibitors on HSP90, NF-κB and AP-1. RESULTS: Seven aviraemic participants completed eight oral doses of chidamide, and only grade 1 adverse events were observed. Cyclic increases in histone acetylation were also detected. All participants showed robust and repeated plasma viral rebound (peak viraemia 147-3850 copies/mL), as well as increased cell-associated HIV-1 RNA, during chidamide treatment. Furthermore, we identified an enhanced HIV-1-specific cellular immune response and a modest 37.7% (95% CI: 12.7-62.8%, P = 0.028) reduction in cell-associated HIV-1 DNA. Compared with the other three HDAC inhibitors, chidamide had minimal cytotoxicity in vitro at clinically relevant concentrations and showed mechanistically superior effects on non-histone proteins, including HSP90, NF-κB and AP-1. CONCLUSIONS: Chidamide safely and vigorously disrupts HIV-1 latency in vivo, which makes it a promising latency-reversing agent.

[The correlation studies between ambulatory blood pressure and OSA in non-hypertensive patients].

Objective:To discuss the changes and rules of nighttime blood pressure in obstructive sleep apnea(OSA) patients without hypertension.Method:Eighty-nine non-hypertensive patients whose office blood pressure was lower than 130/85 mmHg and diagnose with OSA by PSG in sleep monitoring room were choose as the research group.Forty non-hypertensive and polyp of vocal cord or vocal nodules patients whose office blood pressure was lower than 130/85 mmHg and diagnose with non-OSA by PSG were choose as matched group.All the patients were in treatment in our hospital from December 2017 to June 2018. All the patients got PSG,and the same time got the ambulatory blood pressure monitoring based on pulse transit time all night.Compared the mean value of systolic blood pressure,the mean value of diastolic blood pressure.Higher than 12 mmHg blood pressure rise index,the mean rise in blood pressure. The highest increase in blood pressure, maximum systolic pressure between the study group and the marched group all night.Result:The difference of all the test index between the study group and the marched group was significant(P<0.05).In OSA patients.The difference of all the test index between the severe OSA group and the mild OSA group or the moderate OSA group was significant(P<0.05).In severe OSA group.The difference between the fluctuation of blood pressure caused by respiratory events and spontaneous blood pressure fluctuation was significant(P=0.004).The difference of the mean value of diastolic blood pressure(P=0.032) blood pressure rise index(P=0.037) the mean rise in blood pressure(P=0.045) between age 55 or older patients and under 55years old patients.Conclusion:Ambulatory blood pressure monitoring synchronizatied in PSG contribute to the early diagnosis and prevention of hypertension in OSA patients.

NtBRC1 suppresses axillary branching in tobacco after decapitation.

Axillary branching is controlled by a very complex mechanism involving various endogenous and environmental factors. Previous studies have shown that Tb1/BRC1 is the point of integration in the network of molecular mechanisms regulating axillary branching in plants. In this study, we cloned the Tb1/BRC1 ortholog, NtBRC1, from Nicotiana tabacum and functionally analyzed its role in the control of axillary branching in tobacco. Overexpression of NtBRC1 resulted in significant retardation of axillary branching, and downregulation of this gene resulted in significant acceleration of axillary branching after decapitation. This indicates a negative role for this gene in the regulation of axillary branching. In-line with previous reports, NtBRC1 was found to be expressed predominantly in axillary buds. Additionally, as expected, expression was decreased 8 h following decapitation, which further confirms its role in the suppression of axillary branching. Furthermore, the expression of NtBRC1 was significantly downregulated by cytokinin, but was not affected by GR24, a synthetic strigolactone. Based on the data collected in the present study, we demonstrate that NtBRC1 negatively regulates axillary branching in tobacco after decapitation and functions downstream of the cytokinin signaling pathway inside axillary buds.

Tobacco serine/threonine protein kinase gene NrSTK enhances black shank resistance.

A serine/threonine protein kinase gene (NrSTK) was cloned from Nicotiana repanda based on the sequence of a previously isolated resistance gene analog (RGA). Expression of RGA was induced by challenge with the pathogen black shank. The NrSTK gene was predicted to encode a protein kinase that contained an ATP binding site at residues 41-69 and a serine/threonine protein kinase activation sequence spanning the region 161-173. Overexpression of NrSTK in the susceptible tobacco variety Honghuadajinyuan significantly enhanced resistance to black shank, indicating that NrSTK plays a role in incompatibility reactions between tobacco and the pathogen. Characterization of NrSTK will help elucidate the molecular mechanisms involved in black shank resistance in N. repanda.

Multiple pathologies are common in Alzheimer patients in clinical trials.

OBJECTIVE: To determine the frequency of multiple pathology [Alzheimer Disease (AD) plus Vascular Dementia and/or Dementia with Lewy Bodies] in patients enrolled in clinical trials of AD therapy, and to compare the cognitive and functional assessments between patients with pure AD and AD with multiple pathology. METHODS: We conducted a retrospective analysis of patients with a clinical diagnosis of AD who were enrolled in AD therapy clinical trials and subsequently received an autopsy for confirmation of their diagnosis from 2000 to 2009. Performance on cognitive screening tests, namely Modified Mini Mental state (3MS) exam, Mini Mental state Exam (MMSE) and Functional Rating Scale (FRS) were compared between patients with pure AD and multiple pathology. RESULTS: Autopsy reports were available for 16/47 (34%) of deceased patients. Of these 16 patients, 5 (31%) had pure AD pathology, 10 (63%) had AD with other pathology, and 1 (6%) had non-AD pathology. Compared to patients with pure AD, patients with AD mixed with other pathology had poorer baseline FRS in problem-solving (p<0.01) and community affairs (p<0.02). CONCLUSION: While the strict enrollment criteria for clinical trials identified the presence of AD pathology in the majority of cases (15/16), multiple pathology was more common than pure AD in our series of autopsied patients. Premortem biomarkers that can distinguish between pure AD and AD with multiple pathology will be beneficial in future clinical trials and dementia patient management.

Regulation of GADD153 induced by mechanical stress in cardiomyocytes.

BACKGROUND: Growth arrest and DNA damage-inducible gene 153 (GADD153), an apoptosis regulated gene, increased during endoplasmic reticulum stress. However, the expression of GADD153 in cardiomyocytes under mechanical stress is little known. We aimed to investigate the regulation mechanism of GADD153 expression and apoptosis induced by mechanical stress in cardiomyocytes. MATERIALS AND METHODS: Aorta-caval shunt was performed in adult Sprague-Dawley rats to induce volume overload. Rat neonatal cardiomyocytes grown on a flexible membrane base were stretched by vacuum to 20% of maximum elongation, at 60 cycles min(-1). RESULTS: The increased ventricular dimension measured using echocardiography in the shunt group (n = 8) was reversed to normal by treatment with chaperon 4-phenylbutyric acid (PBA) (n = 8) at 500 mg kg(-1) day(-1) orally for 3 days. GADD153 protein and mRNA were up-regulated in the shunt group when compared with sham group (n = 8). Treatment with PBA reversed the protein of GADD153 to the baseline values. The TUNEL assay showed that PBA reduced the apoptosis induced by volume overload. Cyclic stretch significantly increased GADD153 protein and mRNA expression after 14 h of stretch. Addition of c-jun N-terminal kinase (JNK) inhibitor SP600125, JNK small interfering RNA and tumour necrosis factor-alpha (TNF-alpha) antibody 30 min before stretch, reduced the induction of GADD153 protein. Stretch increased, while GADD153-Mut plasmid, SP600125 and TNF-alpha antibody abolished the GADD153 promoter activity induced by stretch. GADD153 mediated apoptosis induced by stretch was reversed by GADD153 siRNA, GADD153-Mut plasmid and PBA. CONCLUSIONS: Mechanical stress enhanced apoptosis and GADD153 expression in cardiomyocytes. Treatment with PBA reversed both GADD153 expression and apoptosis induced by mechanical stress in cardiomyocytes.

Myostatin expression in ventricular myocardium in a rat model of volume-overload heart failure.

BACKGROUND: Mechanical stress increases myocardial myostatin expression. However, the expression of myostatin in chronic heart failure resulting from volume-overload and after treatment with beta-blockers is little known. The authors hypothesize that myostatin plays a role in the failing myocardium because of volume-overload. MATERIALS AND METHODS: Aorto-caval shunt was created over a 4-week period in adult Sprague-Dawley rats to induce volume-overload heart failure. RESULTS: Heart weight and body weight ratio significantly increased after shunting. The left ventricular end-diastolic dimension also significantly increased. Treatment with carvedilol in the shunt group reversed the increase in heart weight and ventricular dimension to the baseline values. Myocardial and skeletal myostatin proteins were up-regulated in the shunt group. The mRNA of myocardial myostatin also increased in the shunt group. Treatment with carvedilol reversed both protein and mRNA of myocardial myostatin to the baseline values. Treatment with N-acetylcysteine and doxazosin partially decreased myostatin mRNA and protein expression as compared with the shunt group. Carvedilol normalized the increased immunohistochemical labelling of myocardial myostatin in the shunt group. CONCLUSION: Myocardial myostatin mRNA and protein expression were up-regulated in the rat model of volume-overload heart failure. Treatment with carvedilol is associated with a limitation of increased myostatin expression in the failing ventricular myocardium.

Combined cord blood stem cells and gene therapy enhances angiogenesis and improves cardiac performance in mouse after acute myocardial infarction.

BACKGROUND: Gene and stem cell therapies hold promise for the treatment of ischaemic cardiovascular disease. However, combined stem cell and angiogenic growth factor gene therapy for acute ischaemic myocardium has not been previously reported. This study hypothesized that combined stem cell and gene therapy would not only augment new vessels formation but also improve myocardial function in acute ischaemic myocardium. METHODS: Human angiopoietin-1 (Ang1) cDNA and VEGF(165) cDNA were ligated into AAV vector. The purified CD34(+) cells were obtained from human umbilical cord blood samples. Cord blood CD34(+) cells were transduced with AAV vector encoding either the human Ang1 (AAV-Ang1) or VEGF(165) (AAV-VEGF) cDNA alone, or both (AAV-Ang1 plus VEGF). Immediately after ligation of the left anterior descending coronary artery in male SCID mice, culture-expanded CD34(+) cells transduced with AAV-Ang1, AAV-VEGF or AAV-Ang1 plus VEGF were injected intramyocardially at the left anterior free wall. RESULTS: Western blot showed that Ang1 and VEGF protein expressions were enhanced in the CD34(+)cells transduced with AAV-Ang1 and AAV-VEGF, respectively. Infarct size significantly decreased and capillary density significantly increased after treatment with CD34(+)/AAV-Ang1 plus VEGF when compared with treatment by CD34(+) only. Combined therapy with CD34(+) and AAV-Ang1, CD34(+) and AAV-VEGF, CD34(+) and AAV-Ang1 plus VEGF, all showed significantly higher cardiac performance in echocardiography than the therapy with CD34(+) alone 4 weeks after myocardial infarction. CONCLUSIONS: Combined therapy with human umbilical cord blood CD34(+) cells and both Ang1 and VEGF genes reduced infarct size, attenuated the progression of cardiac dysfunction and increased capillary density in acute myocardial infarction in mice.

External biliary drainage plus bile acid feeding is not equal to internal drainage in preserving the cellular immunity following prolonged obstructive jaundice.

This study investigates the importance of intestinal bile flow in cellular immunity. Sprague-Dawley rats undergoing bile duct ligation (BDL) and sham ceiliotomy (Sham) for 14 and 21 days were investigated. Experimental animals following BDL were further divided into an external drainage (ED) group, an ED group with rat chow mixed with 2:2:1 cholic acid, chenodeoxycholic acid, and deoxycholic acid (ED + BF), and an internal drainage (ID) group. Fourteen days later, they were killed and analyzed for spleen lymphocytic [3H] thymidine uptake (LHU) under mitogen stimulation with phytohemagglutinin, blood biochemistry, hemogram, and liver pathology. In the 14-day BDL experiment, LHU and serum albumin level were decreased in the BDL group (P < 0.05). After drainage, they were not significantly different among sham, ED, ED + BF, and ID groups. In the 21-day BDL experiment, the red cell volume was decreased (P < 0.05). After drainage, the ED, ED + BF, and ID groups still had a significantly lower LHU than the sham group (P < 0.05). However, the ID group had higher LHU than the ED and ED + BF groups (P < 0.05). The ED + BF group had a slightly higher LHU than the ED group but not statistically significant. Liver pathology returned to normal after drainage in the 14-day BDL model. In contrast, the 21-day BDL group had prominent periportal necrosis and developed periportal fibrosis after drainage. The present study reveals the duration of BDL determines the severity of hepatic damage. In the 14-day BDL groups, all kinds of drainage completely reverse the impaired liver function and cellular immunity. In the 21-day BDL group, 14-day drainage is inadequate for recovery because irreversible pathological changes are found. The reversal of cellular immunity in ID is better and faster, because it provides a better hepatic functional, nutritional, and hematological recovery besides the presence of primarily secreted bile acids.

Treatment of rheumatoid arthritis with total lymphoid irradiation: long-term survival.

OBJECTIVE: Total lymphoid irradiation (TLI) has been used to treat rheumatoid arthritis (RA) since the 1970s. This study reviews long-term (15-20-year) mortality outcomes of patients treated with TLI for RA at Stanford University Medical Center and compares these outcomes with those in patients treated with disease-modifying antirheumatic drugs (DMARDs). METHODS: Fifty-three patients with RA were treated with full-dose TLI at Stanford University Medical Center. All had failed previous therapy with gold salts and penicillamine. One hundred six control patients were selected from the Arthritis, Rheumatism, and Aging Medical Information Systems database and were matched with the patients for age, sex, disease duration, and mean Health Assessment Questionnaire (HAQ) score. Survival was analyzed using Kaplan-Meier methods and Cox proportional hazards regression. RESULTS: No significant difference in age and sex was found between TLI-treated patients and controls. TLI-treated patients had more education (mean 13.4 years versus 11.8 years; P = 0.016) and received more DMARDs prior to TLI (mean 2.1 versus 1.3; P = 0.0001). TLI-treated patients had lower mean HAQ scores at the time of TLI (2.0 versus 2.4; P = 0.0002). TLI had no significant overall effect on survival in treated patients compared with controls (P = 0.62). The survival curves appeared to cross over at approximately 11 years of followup, with better early survival in the TLI group and better late survival in the control group. There was a total of 25 deaths in the TLI group. There were 45 deaths in the control group, with causes of death available for 20 patients. There were 3 patients with lymphoma and 2 with myelodysplastic syndrome in the TLI group, and none in the control group. The most common cause of death in both groups was infection. CONCLUSION: TLI had no significant effect on overall survival, with trends toward higher early mortality in controls and trends toward higher late mortality in TLI-treated patients. Overall, there was no difference in mortality, but it appears that there may have been more lymphoproliferative malignancies in the TLI cohort. We would recommend that TLI be used cautiously for patients with refractory RA in whom the benefits outweigh the risks.

Angiotensin II receptor antagonist blocks the expression of connexin43 induced by cyclical mechanical stretch in cultured neonatal rat cardiac myocytes.

Mechanical forces have profound effects on cardiomyocytes. To test whether angiotensin II is a potential mediator of stretch-induced effects on gap junctions, we used the angiotensin II (AT1) receptor antagonist, losartan, to investigate the cyclical stretch-induced expression of connexin43 (Cx43), the major cardiac muscle gap junction channel protein. Cultured neonatal rat cardiomyocytes grown on a flexible membrane base were stretched by vacuum to 20% of maximum elongation, at 60 cycles/min. The levels of Cx43 protein began to increase as early as 2 h after stretch was applied, reached a maximum of six-fold over the control by 24 h and remained at this level another 24 h (i.e. up to 48 h after stretch was applied). These increases of Cx43 protein at 24 h were largely (73%) and completely (100%) attenuated (P<0.001) by the addition (30 min before stretch) of 10 n M and 100 n M losartan, respectively. Similarly, the Cx43 mRNA levels in stretched cardiomyocytes rose 89% (P<0.01) above control (non-stretched cells) mRNA levels. This increase also was blocked by losartan. Cyclical stretch increased (and losartan decreased) the immunohistochemical labeling of Cx43 and significantly increased release of angiotensin II into the culture media from 7.5+/-0.6 ng/ml to 23.8+/-1.0 ng/ml (P<0.01) after a 1 h stretch. These findings indicate that cyclical mechanical stretch augments angiotensin II production and Cx43 gene expression in cultured cardiomyocytes, partially through mediation of the AT1 receptors, and suggests interaction between the cardiomyocyte local rennin-angiotensin system and Cx43 in response to stretch.

Cyclical mechanical stretching increases the expression of vascular endothelial growth factor in rat vascular smooth muscle cells.

BACKGROUND AND PURPOSE: Mechanical forces have profound effects on vascular smooth muscle cells (VSMCs). The mechanism by which mechanical stimuli regulate vascular endothelial growth factor (VEGF) expression and regulation has yet to be elucidated. We investigated the effect of cyclical mechanical stretching on regulation of the VEGF gene in VSMCs. MATERIALS AND METHODS: Cultured rat VSMCs grown on a flexible membrane base were stretched by applying a vacuum at 60 cycles/minute. VEGF concentration in the cultured media was determined by enzyme-linked immunoassay. VEGF gene expression was determined by Western blot and Northern blot. The location of VEGF in the VSMC was studied immunohistochemically. Chimeric constructs of the VEGF promoter were deleted and the promoter activity was determined by luciferase activity. RESULTS: VEGF concentration increased by 21 to 32% as early as 10 minutes after stretching and remained at this level for up to 12 hours. The concentration of VEGF reached a maximum of 2.8-fold over that in control cells by 2 hours after stretching and declined slightly thereafter. The amount of VEGF mRNA in stretched cells increased as early as 1 hour after stretching, reached a maximum of 3.2-fold over the amount in control cells by 2 hours, and remained at this level for up to 6 hours after stretching. Immunohistochemical study confirmed increased VEGF expression in VSMCs after stretching. Stretched cells transfected with a Sac-Nhe fragment showed only 46% of the luciferase activity of unstretched control cells. However, stretched cells transfected with chimeric plasmids containing a Spe-Nhe fragment showed 2.8-fold luciferase activity over that in control cells. CONCLUSIONS: Cyclical mechanical stretching upregulates expression of the VEGF gene in VSMCs at the transcription level. The VEGF 5'-flanking region contains a negative stretch-response element located in the 0.4-kb Sac-Pst fragment and a positive stretch-response element located in the 0.6-kb Spe-Sac fragment.

Superior mesenteric arteriovenous fistula associated with portal obstruction.

Superior mesenteric arteriovenous fistula is rarely encountered. Unrecognized in early stage, it can cause hazardous sequelae of portal hypertension. Herein we report a rare case of portal obstruction associated with an aneurysmal dilatation of the superior mesenteric vein, which was caused by a superior mesenteric arteriovenous fistula. The patient was a 74-year-old woman admitted for continuous hemetemesis, presenting with a palpable abdominal mass. The computed tomogram revealed a 6.5 cm superior mesenteric venous aneurysm and thrombotic portal venous obstruction. On account of impending shock, an emergent portal venous thrombectomy and portocaval shunt was carried out. Superior mesenteric arterial angiography performed 4 months later confirmed the diagnosis. Being without symptoms, the patient was clinically followed and remained in stable condition for 3 and a half years. The clinical presentation of a mesenteric arteriovenous fistula varies, with occasional gastrointestinal tract hemorrhage. When complicated with portal obstruction, the condition can be disastrous. We believe that creation of a porto-systemic shunt with resection of the arterio-venous fistula is the proper treatment. This patient is now under close observation.

Priority-setting for nursing research in the Republic of China.

The question of how public funds for research should be allocated has led to participatory priority-setting in prosperous democracies like Taiwan, Republic of China. Useful criteria for research priorities are scientific merit, social benefit and feasibility. Taking a health needs approach and using these criteria, nearly 200 nurses from service and education in a national forum participated in describing research priorities. Through the group method of idea-writing, for clinical nursing, of high priority were assessing quality, care of the elderly, and preventing infectious disease. For nursing education, research addressing advanced role preparation and bridging nursing education and practice were priorities. For nursing management, research of highest priority pertained to economic evaluation, personnel administration, and effectiveness. These suggestions from the deliberation of a committed group of nurses can help shape future national decisions about research funding and training.

Effects of norepinephrine on apoptosis in rat neonatal cardiomyocytes.

BACKGROUND AND PURPOSE: Norepinephrine (NE) is elevated in heart failure and can induce apoptosis in adult cardiac myocytes. However, it is not known whether NE can induce apoptosis in neonatal cardiac myocytes. This study examined the ability of NE to stimulate apoptosis in rat neonatal cardiac myocytes in vitro. METHODS: Neonatal rat cardiac myocytes were exposed to NE alone, NE + propranolol, or NE + prazosin for 24 hours. Apoptosis was assayed by DNA laddering with agarose gel electrophoresis and immunofluorescent terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Reverse transcription polymerase chain reaction was used to evaluate the expression of Mcl-1. Creatine kinase activity in the cultured medium was used as a measure of the toxicity of NE on myocytes. RESULTS: NE increased DNA laddering on agarose gel electrophoresis and increased the number of apoptotic cells in a dose-dependent manner. No increase in apoptosis was found in response to NE doses between 1 and 50 mumol/L. NE at concentrations of 100 to 400 mumol/L increased apoptosis from 10% to 31% of cells. The ability of NE to stimulate apoptosis in rat neonatal cardiac myocytes was completely blocked by propranolol, but not prazosin. NE treatment at high concentrations sharply reduced the level of Mcl-1 mRNA, coincident with the increase in the number of apoptotic cells. Creatine kinase activity in the cultured medium was similar among the controls and NE-treated myocytes. CONCLUSIONS: Our results showed that NE at high concentrations stimulated apoptosis in rat neonatal cardiac myocytes in vitro. Apoptosis induced by NE was associated with down-regulation of Mcl-1. However, NE at the same concentration was not toxic to rat neonatal cardiac myocytes.