Prevalence and Risk Factors Underlying Occupational Stress and Depression Among Clinical Nurses in Secondary and Tertiary Hospitals of China During COVID-19 Setting.

Aim: This study was designed to develop an effective measurement tool for occupational stress among medical staff and to identify the underlying risk factors among clinical nurses in China under depression during and after COVID-19. Methods: In the first stage, an occupational stress scale was developed for medical staff based on qualitative and quantitative methods. The dimensions of the scale were based on childhood stress and seven other parameters of working stress. In the second stage, a provincial survey was conducted among clinical nurses in Hainan. The structure of Medical Staff Occupational Stress Scale was tested in secondary and tertiary hospitals. The socio-demographic information, occupational stress (measured using the developed scale), and current depression symptoms (assessed with the nine-item Patient Health Questionnaire) were evaluated. The risk factors for occupational stress-induced depression were tested using multivariate logistic regression. Results: The Medical Staff Occupational Stress Scale consisted of 42 items under eight dimensions with strong reliability and validity. Almost 80% of the clinical nurses reported obvious symptoms of depression. Based on multivariate logistical regression analysis, the significant risk factors for depression in nurses at secondary hospitals and tertiary hospitals were childhood stress, teaching stress, relationship with patient stress, and administration stress. Conclusion: The Medical Staff Occupational Stress Scale utilized in nursing population is based on strong psychometric features. Childhood stress contributes to occupational stress in nurses. The selection of nurses for clinical work may require evaluation of past history for childhood stress to prevent occupational depression. Teaching stress, relationship with patient stress and administration stress play significant roles in the prevention of depression among clinical nurses.

Takotsubo cardiomyopathy misdiagnosed as acute myocardial infarction under the Chest Pain Center model: A case report.

BACKGROUND: With the spread and establishment of the Chest Pain Center in China, adhering to the idea that "time is myocardial cell and time is life", many hospitals have set up a standardized process that ensures that patients with acute myocardial infarction (AMI) who meet emergency percutaneous coronary intervention (PCI) guidelines are sent directly to the DSA room by the prehospital emergency doctor, saving the time spent on queuing, registration, payment, re-examination by the emergency doctor, and obtaining consent for surgery after arriving at the hospital. Takotsubo cardiomyopathy is an acute disease that is triggered by intense emotional or physical stress and must be promptly differentiated from AMI for its appropriate management. CASE SUMMARY: A 52-year-old female patient was taken directly to the catheterization room to perform PCI due to 4 h of continuous thoracalgia and elevation of the ST segment in the V3-V5 lead, without being transferred to the emergency department according to the Chest Pain Center model. Loading doses of aspirin, clopidogrel and statins were administered and informed consent for PCI was signed in the ambulance. On first look, the patient looked nervous in the DSA room. Coronary angiography showed no obvious stenosis. Left ventricular angiography showed that the contraction of the left ventricular apex was weakened, and the systolic period was ballooning out, showing a typical "octopus trap" change. The patient was diagnosed with Takotsubo cardiomyopathy. Five days later, the patient had no symptoms of thoracalgia, and the serological indicators returned to normal. She was discharged with a prescription of medication. CONCLUSION: Under the Chest Pain Center model for the treatment of patients with chest pain showing ST segment elevation, despite the urgency of time, Takotsubo cardiomyopathy must be promptly differentiated from AMI for its appropriate management.

Acute coronary artery stent thrombosis caused by a spasm: A case report.

BACKGROUND: Acute stent thrombosis (AST) is a serious complication of percutaneous coronary intervention (PCI). The causes of AST include the use of stents of inappropriate diameters, multiple overlapping stents, or excessively long stents; incomplete stent expansion; poor stent adhesion; incomplete coverage of dissection; formation of thrombosis or intramural hematomas; vascular injury secondary to intraoperative mechanical manipulation; insufficient dose administration of postoperative antiplatelet medications; and resistance to antiplatelet drugs. Cases of AST secondary to coronary artery spasms are rare, with only a few reports in the literature. CASE SUMMARY: A 55-year-old man was admitted to the hospital with a chief complaint of back pain for 2 d. He was diagnosed with coronary heart disease and acute myocardial infarction (AMI) based on electrocardiography results and creatinine kinase myocardial band, troponin I, and troponin T levels. A 2.5 mm × 33.0 mm drug-eluting stent was inserted into the occluded portion of the right coronary artery. Aspirin, clopidogrel, and atorvastatin were started. Six days later, the patient developed AST after taking a bath in the morning. Repeat coronary angiography showed occlusion of the proximal stent, and intravascular ultrasound showed severe coronary artery spasms. The patient's AST was thought to be caused by coronary artery spasms and treated with percutaneous transluminal coronary angioplasty. Postoperatively, he was administered diltiazem to inhibit coronary artery spasms and prevent future episodes of AST. He survived and reported no discomfort at the 2-mo follow-up after the operation and initiation of drug treatment. CONCLUSION: Coronary spasms can cause both AMI and AST. For patients who exhibit coronary spasms during PCI, diltiazem administration could reduce spasms and prevent future AST.

Gastrointestinal discomforts and dietary intake in Chinese urban elders: A cross-sectional study in eight cities of China.

BACKGROUND: Gastrointestinal (GI) discomforts are common in the elderly population; however, whether such discomforts are associated with dietary intake has not been studied. AIM: To evaluate GI discomforts in Chinese urban elders and the associated factors. METHODS: The gastrointestinal symptom rating scale (GSRS) was used to identify GI discomforts in 688 elders from eight cities of China. The semi-quantitative food frequency questionnaire and one time of 24 h dietary recall were used to access the food intake, identify dietary pattern, and calculate the nutrients intake. RESULTS: About 83% of studied elders experienced at least one of GI discomforts in the past 6 mo; dyspepsia was the most commonly reported (66.7%), followed by reflux (44.8%), abdominal pain (35.9%), constipation (35.8%), and diarrhea (34.7%). Female gender, lower education level, and lower family income were associated with a higher GSRS score. Participants who were diagnosed with a GI-related disease had a higher score of constipation, but a lower score of reflux. Chronic diseases were positively associated with certain GI discomforts. Three dietary patterns were identified by the method of principal component analysis, which were characterized as high intake of salt and tea; more frequent intake of tubers, fruits, aquatic products, and soybeans; and high intake of cereal, vegetables, and meat, respectively. However, no associations between dietary patterns and GSRS score were found. The elders with a higher GSRS score had significantly lower intake of bean products. The elders whose GSRS score was ≥ 21 and 18-20 decreased their bean production intake by 7.2 (0.3, 14.3) g/d and 14.3 (1.2, 27.3) g/d, respectively, compared with those who had a GSRS score ≤ 17. There were no differences in other food categories, calories, or nutrients intake among elders with different GSRS scores. CONCLUSION: GI discomforts are common in Chinese urban elders. GI discomforts might be associated with the choice of food.

[A clinical analysis of electrical status epilepticus during sleep in children and a follow-up study of methylprednisolone pulse therapy].

OBJECTIVE: To study the clinical features of electrical status epilepticus during sleep (ESES) in children, as well as the clinical effect of methylprednisolone pulse therapy in children with ESES. METHODS: A retrospective analysis was performed using the clinical data of 78 children with ESES. Among these children, 56 children who had had the failure of antiepileptic drugs were treated with methylprednisolone pulse therapy at a dose of 15-20 mg/(kg·d) for three courses. Each course of treatment was 3 days, followed by oral prednisone [1-2 mg/(kg·d)] for 3 days. The role of methylprednisolone pulse therapy in eliminating ESES, controlling clinical seizures, and improving intelligence and behaviors was analyzed. RESULTS: The mean age of onset of epilepsy in 78 children was 6.8±2.4 years, and the mean age for the first occurrence of ESES was 7.6±2.5 years. Compared with normal children, children with ESES had delayed intelligence development and higher scores of some behavior problems. Methylprednisolone pulse therapy had an overall response rate of 73% (41/56) on clinical seizures, and the overall response rate on electroencephalography (EEG)/spike-wave index was 70% (39/56) after treatment. There were significant improvements in verbal intelligence quotient, performance intelligence quotient and full intelligence quotient, and significant reductions in the scores of learning problems, impulse-hyperactivity and hyperactivity index after treatment (P<0.05). The overall recurrence rate after 1-year follow-up was 29% (11/38). CONCLUSIONS: ESES often presents around school age and impairs children's intelligence and behaviors. Methylprednisolone pulse therapy has a marked efficiency in reducing clinical seizures and EEG discharges in children with ESES and can improve intelligence and behavior development, but the recurrence rate remains high.

[Effects of rosuvastatin in homocysteine induced mouse vascular smooth muscle cell dedifferentiation and endoplasmic reticulum stress and its mechanisms].

OBJECTIVE: To investigate the effect of rosuvastatin on homocysteine (Hcy) induced mousevascular smooth muscle cells(VSMCs) dedifferentiation and endoplasmic reticulum stress(ERS). METHODS: VSMCs were co-cultured with Hcy and different concentration of rosuvastatin (0.1, 1.0 and 10 µmol/L). Cytoskeleton remodeling, VSMCs phenotype markers (smooth muscle actin-α, calponin and osteopontin) and ERS marker mRNAs (Herpud1, XBP1s and GRP78) were detected at predicted time. Tunicamycin was used to induce, respectively 4-phenylbutyrate(4-PBA) inhibition, ERS in VSMCs and cellular migration, proliferation and expression of phenotype proteins were analyzed. Mammalian target of rapamycin(mTOR)-P70S6 kinase (P70S6K) signaling agonist phosphatidic acid and inhibitor rapamycin were used in Rsv treated VSMCs. And then mTOR signaling and ERS associated mRNAs were detected. RESULTS: Compared with Hcy group, Hcy+ Rsv group (1.0 and 10 µmol/L) showed enhanced α-SMA and calponin expression (P<0.01), suppressed ERS mRNA levels (P<0.01) and promoted polarity of cytoskeleton. Compared with Hcy group, Hcy+Rsv group and Hcy+4-PBA group showed suppressed proliferation, migration and enhanced contractile protein expression (P<0.01); while tunicamycin could reverse the effect of Rsv on Hcy treated cells. Furthermore, alleviated mTOR-P70S6K phosphorylation and ERS (P<0.01)were observed in Hcy+Rsv group and Hcy+rapamycin group, compared with Hcy group; while phosphatidic acid inhibited the effect of Rsv on mTOR signaling activation and ERS mRNA levels (P<0.01). CONCLUSIONS: Rosuvastatin could inhibit Hcy induced VSMCs dedifferentiation via suppressing ERS, which might be regulated by mTOR-P70S6K signaling.

[Effects of yellow wine polyphenols on cardiomyocyte apoptosis in diabetic cardiomyopathy rats].

OBJECTIVE: To investigate the effects of yellow wine polyphenols on the apoptosis of cardiomyocytes in diabetic cardiomyopathy rats. METHODS: Thirty SD rats were randomly divided into control group (Control), diabetic cardiomyopathy group (DCM) and diabetic cardiomyopathy treated with yellow wine polyphenols group (DCM+YWP). A single intraperitoneal injection of 65 mg/kg streptozotocin (STZ) was utilized to establish a rat model of DCM. The rats in control group were treated with citrate buffer at the same dose of a single intraperitoneal injection. DCM+YWP group were treated with 18 mg/kg Yellow wine polyphenols by ig after modeling. After treated for 12 weeks, the general condition of rats were observed. The cardiac structure and function of the rats were observed by Doppler echocardiography. The ultrastructure of myocardium were observed using electron microscopy. The inflammation index of myocardial tissue was detected by enzyme-linked immunosorbent assay (ELISA). The oxidative stress in myocardial tissues was assessed by oxidative stress detection kits. The expressions of Bax, Bcl-2 and Caspase-3 (cleaved) in myocardial were detected by Western blot. RESULTS: Compared with DCM group, the blood glucose levels and body weight of rats in the DCM+YWP group were not changed significantly. Echocardiography showed that left ventricular end-diastolic diameter, left ventricular end-systolic diameter were decreased (P<0.05), while fractional shortening and E/A ratio and Ea/Aa ratio were elevated (P<0.05). The levels of tumor factor-α(TNF-α), interleukin 1ß(IL-1ß) and interleukin 6(IL-6) in myocardium were decreased (P<0.05). The levels of oxidative stress malondiadehyde(MDA) were decreased and Superoxide dismutase(SOD), glutathione peroxidase(GSH-Px) were increased in myocardial tissue (P<0.05). The expression levels of Bax and Caspase-3 (cleaved) protein in myocardium were decreased (P<0.05), and the expression of Bcl-2 protein was increased (P<0.05). CONCLUSIONS: Yellow wine polyphenols can improve the diabetic cardiomyopathy rat cardiac function, attenuates inflammation and oxidative stress in diabetic rats, inhibit the apoptosis of cardiomyocytes in diabetic cardiomyopathy.

Autophagy prevents autophagic cell death in Tetrahymena in response to oxidative stress.

Autophagy is a major cellular pathway used to degrade long-lived proteins or organelles that may be damaged due to increased reactive oxygen species (ROS) generated by cellular stress. Autophagy typically enhances cell survival, but it may also act to promote cell death under certain conditions. The mechanism underlying this paradox, however, remains unclear. We showed that Tetrahymena cells exerted increased membrane-bound vacuoles characteristic of autophagy followed by autophagic cell death (referred to as cell death with autophagy) after exposure to hydrogen peroxide. Inhibition of autophagy by chloroquine or 3-methyladenine significantly augmented autophagic cell death induced by hydrogen peroxide. Blockage of the mitochondrial electron transport chain or starvation triggered activation of autophagy followed by cell death by inducing the production of ROS due to the loss of mitochondrial membrane potential. This indicated a regulatory role of mitochondrial ROS in programming autophagy and autophagic cell death in Tetrahymena. Importantly, suppression of autophagy enhanced autophagic cell death in Tetrahymena in response to elevated ROS production from starvation, and this was reversed by antioxidants. Therefore, our results suggest that autophagy was activated upon oxidative stress to prevent the initiation of autophagic cell death in Tetrahymena until the accumulation of ROS passed the point of no return, leading to delayed cell death in Tetrahymena.

[Exploring the active ingredient of Chinese yellow wine which could inhibit the Hcy induced proliferation and migration of vascular smooth muscle cells].

OBJECTIVE: To explore the active ingredients in the Chinese yellow wine could inhibit the proliferation and migration of rat vascular smooth muscle cells induced by homocysteine (Hcy). METHODS: The primary culture and identification of rat vascular smooth muscle cells (VSMCs) was conducted, and the VSMCs in passage 4-7 were used in the following experiments. The VSMCs were divided into 7 groups: control, Hcy (1 mmol/L), Hcy + oligosaccharide, Hcy + polypeptides, Hcy + polyphenols, Hcy + alcohol, Hcy + Chinese yellow wine and were given the corresponding treatment. The proliferation of VSMCs was determined by MTT. Transwell chambers and would healing were employed to test the migratory ability of VSMCs. Wester blot and gelatin zymography were used to investigate the expressions and activities of metal matrix proteinase 2/9 (MMP-2/9) and tissue inhibitor of metalloproteinase 2 (TIMP-2) in VSMCs of each group. RESULTS: Compared with control group, the proliferation, migration and the expression and activity of MMP-2/9 of VSMCs were significantly increased in the VSMCs of Hcy group (P < 0.01). Compared with Hcy group, the proliferation, migration and the expression and activity of MMP-2/9 of VSMCs were significantly decreases in the VSMCs of polypeptides group, polyphenols group and Chinese yellow wine group. However, the expression of TIMP-2 among each group had no significant difference. CONCLUSION: Polypeptides and polyphenols in the Chinese yellow wine could inhibit the proliferation and migration of VSMCs induced by Hcy.

Novel rhodamine derivate as high selective detection lead sensor.

A novel rhodamine based sensor 1 has been synthesized and characterized by NMR, FT-IR and mass. The binding properties of sensor 1 were investigated in the presence of various metal ions by UV-Vis spectroscopy and fluorescence spectroscopy. Sensor 1 showed colorimetric and high emission intensity enhancement in the presence of Pb(2+) in chloroform-THF (7:3).

A Selective Fluorescent Sensor for Hg(2+).

A novel rhodamine based fluorescent chemosensor RQP was prepared and characterized by (1)HNMR, (13)CNMR and HR-MS. The properties of RQP were studied through UV-Vis spectroscopy and fluorescence spectroscopy. RQP showed highly selectivity toward Hg(2+) over other metal ions, including Ag(+), Cd(2+), Cu(2+), Na(+), Mg(2+), Ni(2+), Pb(2+), Fe(3+), and Zn(2+) in aqueous solutions. The recognition process is reversible and confirmed by EDTA experiment.

Report on childhood obesity in China (10): association of sleep duration with obesity.

OBJECTIVES: To explore the association of sleep duration with obesity among children in urban areas of China. METHODS: A total of 6 576 children (3 293 boys and 3 283 girls) aged 7-11 years were randomly selected from 36 primary schools in 6 metropolitan cities in China. A 7-day Physical Activity Recall was used to assess the sleep duration and physical activity level. The height, weight, waist circumference (WC) and percentage of body fat (%BF, as determined by bioelectrical impedance analysis technique) were measured by following the standardized operation procedures. The information on demography, lifestyle and eating habits was collected with a self-administered questionnaire from participants and their parents. RESULTS: The average sleep duration per night in the children was 9.7 h with the decreasing trends along with the increase of age (P < 0.05). The sleep duration was negatively associated with body mass index (BMI) and WC in both boys and girls after adjustment for confounders (beta value -0.23 and -0.82 for boys, -0.24 and -0.91 for girls, respectively, P < 0.01). However, no significant association of sleep duration with %BF was found. Children who slept less than 9.0 h per night had a higher risk for overweight and obesity (OR = 1.29, 95% CI: 1.01, 1.64) and abdominal obesity (OR=1.38, 95% CI: 1.04, 1.83) as compared with those who slept for 10.0-10.9 h. CONCLUSIONS: Short sleep duration is associated with obesity. It is important to ensure adequate sleep duration of children and foster their healthy lifestyle at an early stage of life.

The role of glutathione S-transferase M1 and T1 gene polymorphisms and fruit and vegetable consumption in antioxidant parameters in healthy subjects.

The correlation of glutathione S-transferase (GST) M1/T1 genetic polymorphisms with oxidative stress-related chronic diseases was proved recently. The aim of the present study was to investigate the association of GSTM1/T1 genetic polymorphisms with antioxidant biomarkers and consumption of fruits and vegetables (F&V) in healthy subjects. In this study, for conducting a 3 d dietary survey, 190 healthy adults were recruited. After DNA extraction, a multiple PCR method was used for GSTM1/T1 genotyping. A spectrophotometer method was applied for the determination of plasma total antioxidant capacity (T-AOC), vitamin C level and erythrocyte GST enzyme activity. A general linear model was used to compare the mean values of antioxidant parameters for different GSTM1/T1 genotypes and consumption of F&V. Polymorphisms of GSTM1/T1 had no effects on plasma T-AOC and vitamin C levels. Deletion of the GSTM1 gene decreased the erythrocyte GST activity. There was correlation between plasma T-AOC and consumption of F&V in the GSTM1⁻ or GSTT1⁺ subjects. A similar pattern was evident for erythrocyte GST activity in the GSTM1⁻ subjects. No association was found among consumption of F&V and GSTM1/T1 genotypes and plasma vitamin C level. Different consumption of F&V had no impact on plasma T-AOC and vitamin C levels in the GSTM1⁻/GSTT1⁺ or GSTM1⁻/GSTT1⁻ subjects. The erythrocyte GST activity was more sensitive to consumption of F&V in the individuals with the GSTM1⁻/GSTT1⁺ genotype. Association was found among GSTM1/T1 genotypes, antioxidant parameters and consumption of F&V. Large-scale and multiple ethnic studies are needed to further evaluate the relationship.

[Risk factors on anemia among rural elderly women aged 50-75 y in Xinning county, Anhui province, China].

OBJECTIVE: To study the risk factors on anemia among elderly women in rural areas of Xiuning county, Anhui province, China. METHODS: Xiuning county was selected as working field and elderly women aged 50-75 y were selected as subjects. Finger hemoglobin (Hb) was measured and basic health survey was face-to-face interviewed. 220 elderly women with anemia entered into the case group; and matched by age, another 220 women with normal Hb concentration entered the control group. Survey on diet, questionnaire regarding health and lifestyle and related blood indexes were studied and tested. RESULTS: When comparing the data from both case and control groups, weight was (49.4 +/- 7.3) kg vs. (52.5 +/- 8.4) kg (t = 3.97, P < 0.01), waist circumference was (75.8 +/- 7.8) cm vs. (79.1 +/- 9.3) cm (t = 3.85, P < 0.01), BMI was (21.8 +/- 2.6) kg/m2 vs. (22.9 +/- 3.2) kg/m2 (t = 3.775, P < 0.01), respectively. The total protein was (76.4 +/- 5.0) g/L vs. (78.4 +/- 5.6)g/L (t = 3.83, P < 0.01), albumin was (45.7 +/- 3.1) g/L vs. (47.3 +/- 2.9)g/L (t = 5.24, P < 0.01), serum iron was ( 10.3 +/- 4.1) micromol/L vs. (12.7 +/- 4.6) micromol/L (t = 5.48, P < 0.01), and saturation of transferrin was (19.0 +/- 7.6)% vs. (23.1 +/- 9.1) % (t = 4.90, P < 0.01), respectively. Results from multifactor conditioned logistic regression analysis showed that the odd ratios (OR) for anemia with staple food, BMI and vitamin A were 1.54, 1.89, 1.69, and the OR for anemia with BMI, staple food, animal food, carbohydrate and vitamin A were 2.0, 1.6, 1.6, 1.4, 1.6, with their confidence intervals (CI) as 1.3-2.9, 1.1-2.3, 1.0-2.3, 1.0-2.1, 1.1-2.4, respectively. CONCLUSION: The quality of diet, health status and related blood indexes on anemia among elderly women were lower than that in control group. Lower BMI, less staple food and animal food, less carbohydrate and vitamin A intake appeared to be risk factors of anemia.

[Study on the distribution of prevalence of hypercholesterolemia and borderline high cholesterol in Chinese adults].

OBJECTIVE: To study the distribution of prevalence on hypercholesterolemia and borderline high cholesterol of Chinese residents aged 20 years and above. METHODS: To detect the total fasting plasma cholesterol in 48 299 subjects among 20 year-olds and above. RESULTS: Within a certain age range, the prevalence of both hypercholesterolemia and borderline high cholesterol increased with age, but there was a decreasing trend after 60-years of age in some regions. The prevalence of hypercholesterolemia increased to 12.53% in over 70 year-olds group from 1.36% in urban 20-year-olds, and increased to 5.15% from 60-year-olds group comparing to 0.98% of the 20-year-old group in rural areas. When comparing to the 20-year-old age group, the prevalence of borderline high cholesterol of the 70 age group in urban and rural increased by 4.4 and 4.2 times, respectively. The prevalence of hypercholesterolemia in each age group in urban were higher than that of in rural areas. In Rural I, it was higher than that of in Rural II , Rural III and Rural IV. The prevalence rates of both hypercholesterolemia and borderline high cholesterol of the males in the less than 50 year-olds group were higher than that in females, which was quite different from the group older than 50 years of age. As to borderline high cholesterol, similar result was also noticed. CONCLUSION: Within a certain age range, there was a trend that the prevalence of both hypercholesterolemia and borderline high cholesterol increased with age and related to regions which were classified by economic status. A distinct difference between males and females also existed.

Quantification of prion gene expression in brain and peripheral organs of golden hamster by real-time RT-PCR.

Determination of tissue-specific expression of cellular prion protein (PrPc) is essential for understanding its poorly explained role in organisms. Herein we report on quantification of PrP mRNA in golden hamsters, a popular experimental model for studying mechanisms of transmissible spongiform encephalopathies (TSE), by real-time RT-PCR. Total RNA was isolated from four different regions of the brain and six peripheral organs of eight golden hamsters. PrP mRNA copy numbers were determined using absolute standard curve method with real-time quantitative PCR instrument. It was found that high mRNA levels were present in all four regions of the brain examined, including obex, neocortex, cerebellum, and thalamus. In peripheral organs examined, inguinal lymph node showed high level of the expression similar to that in overall brain; spleen, heart, liver, and lung showed moderate levels of the expression; and kidney showed the lowest expression. Our result is consistent with the potential involvement of different organs in prion diseases and offers essential data for further study of TSE mechanism in this animal model.

[Relationship between maternal DHA intake and DHA status and development of fetus and infant].

The important physiological function of docosahexaenoic acid (DHA) is being the focus of nutriology fields. The DHA status of pregnant and lactation women, who are the main nutrition provider for fetus and infants, had an important effect on DHA nutrition and development of their fetus and infants. The infants whose mother had a supplement of DHA during pregnancy and lactation have higher blood DHA level and better development results of body, visual acuity and intelligence. This paper reviewed the recent international research data on the relationship between maternal DHA intake and DHA status and development of fetus and infant.

Altered expression of the prion gene in rat astrocyte and neuron cultures treated with prion peptide 106-126.

Neuronal degeneration and astrogliosis are hallmarks of prion disease. Synthetic prion protein (PrP) peptide 106-126 (PrP106-126) can induce death of neurons and proliferation of astrocytes in vitro and this neurotoxic effect depends on the expression of cellular PrP (PrPC) and is hence believed to be PrP(C) -mediated. To further elucidate the involvement of PrPC in PrP106-126-induced neurotoxicity, we determined the expression of PrP mRNA in primary culture of rat cortical neuron cells, cerebellar granule cells, and astrocytes following treatment with 50 microM of PrP106-126 scrambled PrP106-126 by quantitative real-time RT-PCR. As shown by MTT test, PrP106-126 induced significant death of neuron cells and marked proliferation of astrocytes after 10 days of treatment. Under the same treatment regimens, the level of PrP gene expression was significantly down-regulated in cortical neuron cell cultures and cerebellar granule cell cultures and was up-regulated in astrocyte cultures. The altered PrP gene expression occurred as early as 3 days after the treatment. After 10 days of treatment, while the cultured cortical neurons underwent further apoptosis, their expression of PrP gene started to recover gradually. These findings indicate that PrP 106-126 regulates transcription of the PrP gene and this activity is associated with its neurotoxicity in primary rat neuronal cultures.