Study on the photosynthetic growth characters in Cimicifuga dahurica (Turcz.) Maxim under different supplemental light environments.

Cimicifuga dahurica (C. dahurica) is an important medicinal plant in the northern region of China. The best supplemental light environment helps plant growth, development, and metabolism. In this study, we used two-year-old seedlings as experimental materials. The white light as the control (CK). The different ratios of red (R) and blue (B) combined light were supplemented (T1, 2R: 1B, 255.37 µmol m-2·s-1; T2, 3R: 1B, 279.69 µmol m-2·s-1; T3, 7R: 1B, 211.16 µmol m-2·s-1). The growth characteristics, photosynthetic pigment content, photosynthesis and chlorophyll fluorescence parameters, and primary metabolite content were studied in seedlings. The results showed that: 1) The fresh weight from shoot, root, and total fresh weight were significantly (P < 0.05) increased under T2 and T3 treatment. 2) The contents of chlorophyll a (Chl a), chlorophyll b (Chl b), and total chlorophyll (Chl) were significantly (P < 0.05) increased under T2 treatment, and carotenoid (car) content was reduced. 3) The photochemical quenching (qP), the actual photosynthetic efficiency of PSII (Y(II)), and the photosynthetic electron transfer rate (ETR) from leaves were significantly (P < 0.05) increased under T1 treatment. The Net photosynthetic rate (Pn), stomatal conductance (Gs), intercellular CO2 concentration (Ci), and transpiration rate (Tr) were significantly (P < 0.05) increased under T2 and T3 treatments. 4) A total of 52 primary metabolites were detected in C. dahurica leaves. Compared with CK, 14, 15, and 18 differential metabolites were screened under T1, T2, and T3 treatments. In addition, D-xylose, D-glucose, glycerol, glycolic acid, and succinic acid were significantly (P < 0.05) accumulated under the T2 treatment, which could regulate the TCA cycle metabolism pathway. The correlation analysis suggested that plant growth was promoted by regulating the change of D-mannose content in galactinol metabolism and amino sugar and nucleotide sugar metabolism. In summary, the growth of C. dahurica was improved under T2 treatment.

Rhein promotes TRAIL-induced apoptosis in bladder cancer cells by up-regulating DR5 expression.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) combined with sensitizer is a potential method to reverse TRAIL-resistance in tumor cells. Rhein (RH) is a monomer extracted from Chinese herbs that has been reported to show anti-tumor effects in a variety of tumor cells, but the role of RH in TRAIL-induced anti-tumor effects in bladder cancer cells has not been reported. In this study, we found that the combined treatment of a non-toxic concentration of RH with TRAIL significantly inhibited the proliferation and induced apoptosis in both TRAIL sensitive and resistant bladder cancer cell lines. Furthermore, we found that RH promoted bladder cancer cell apoptosis by up-regulating DR5 expression. Our findings provide potential value in the clinical treatment of bladder cancer.

[Establishment of an ovalbumin-induced bronchial asthma model in mice with intrauterine growth retardation].

OBJECTIVE: To establish and evaluate an ovalbumin (OVA)-induced bronchial asthma model in mice with intrauterine growth retardation (IUGR), and to explore the molecular mechanism of relationship between IUGR and asthma. METHODS: A total of 16 pregnant BALB/c female mice were divided into a low-protein diet group (n=8) and a normal-protein diet group (n=8), which were fed with low-protein (8%) diet and normal-protein (20%) diet respectively. The neonatal mice were weighed 6 hours after birth. Sixteen male neonatal mice with IUGR were randomly chosen from the low-protein diet group and enrolled in the IUGR group, and 16 male neonatal mice from the normal-protein diet group were enrolled in the control group. Blood samples were collected from the mice in both groups for testing of blood glucose. Enzyme-linked immunosorbent assay (ELISA) was used to determine serum insulin level. The mice in the control group were randomized into a control + PBS group and a control + OVA group (n=8 each). The mice in the IUGR group were randomized into an IUGR + PBS group and an IUGR + OVA group (n=8 each). Six-week-old mice in the control + OVA and IUGR + OVA groups were subjected to intraperitoneal injection of 2 mg/mL OVA for sensitization and aerosol inhalation of 1% OVA for challenge. Mice in the control + PBS group and the IUGR + PBS group were treated with an equivalent amount of PBS. ELISA was used to determine serum IgE level in the mice in each group. Bronchoalveolar lavage fluid (BLF) was collected from the mice in each group for cell counting. The lung tissue of the mice in each group was stained with hematoxylin and eosin to observe pathological changes. RESULTS: The body weight at 6 hours after birth was significantly lower for neonatal mice in the low-protein diet group compared with those in the normal-protein diet group (P<0.01). The IUGR group had a significantly lower serum insulin level than the control group (P<0.01). The IUGR + PBS group had a significantly lower IgE level than the control + PBS group (P<0.01). Compared with the control + PBS and IUGR + PBS groups, the control + OVA and IUGR + OVA groups had a significantly increased IgE level, and the IgE level was significantly higher in the IUGR + OVA group than in the control + OVA group (P<0.01). Compared with the control + PBS and IUGR + PBS groups, the control + OVA and IUGR + OVA groups had significantly increased counts of leukocytes, eosinophils, lymphocytes, and macrophages in the BLF (P<0.01). The pulmonary alveoli of OVA-induced IUGR mice showed massive inflammatory cell infiltration and damage of intercellular continuity. Meanwhile, airway epithelial cell proliferation, bronchial wall thickening, bronchial lumen narrowing, and massive inflammatory cell infiltration around the bronchi and the vascular wall were observed. CONCLUSIONS: An OVA-induced bronchial asthma model has been successfully established in the mice with IUGR induced by low-protein diet, which provides a basis for further study of the molecular mechanism of relationship between IUGR and airway inflammation.

[Persistent chest pain for 4 months and progressive lower limb weakness for 2 months in a boy].

A boy, aged 5 years, was admitted due to chest pain for 4 months, right lower limb weakness for 2 months, and weakness of both lower limbs for 10 days. There were no symptoms of defecation/urination disorders or disturbance of consciousness, and the boy had upper motor neuron paralysis in both lower limbs, without cranial nerve involvement or sensory disorder. Spine magnetic resonance imaging revealed tumor in the spinal canal between cervical vertebra 6 and thoracic vertebra 2, which put pressure on the spinal cord. He was transferred to the department of neurosurgery for surgical treatment and fully recovered after tumor resection, and no recurrence was observed after 6 years of follow-up. The pathological diagnosis was clear cell meningioma (WHO grade II). For children with chest pain and dyskinesia, spinal meningioma should be considered.

[Prognosis of bronchopulmonary dysplasia in preterm infants: a follow-up during infancy].

OBJECTIVE: To investigate the physical development, incidence of common respiratory diseases, and motor development during infancy in preterm infants with bronchopulmonary dysplasia (BPD). METHODS: A retrospective analysis was performed on the clinical features and infantile outcomes of preterm infants with BPD who were admitted to the neonatal intensive care unit between January 2012 and December 2015. Preterm infants without BPD were used as controls who were admitted to the neonatal intensive care unit during the same period and had similar gestational age and birth weight. Physical development, number of hospital stays, the incidences of pneumonia and wheezing, and motor development during infancy were compared between the two groups. RESULTS: Compared with the control group, BPD infants had a significantly higher incidence of extrauterine growth retardation at discharge (48% vs 41%; P<0.05); BPD infants were more susceptible to pneumonia, wheezing, eczema and rhinitis; BDP infants also had a significantly higher number of readmissions due to respiratory tract infection (P<0.05). BPD infants had a significantly smaller head circumference than the control group at corrected ages of 3, 6, and 12 months (P<0.05). BPD infants had significantly delayed gross, fine, and overall motor development than the control group at corrected ages of 6 and 9 months (P<0.05). CONCLUSIONS: Infants with BPD are susceptible to extrauterine growth retardation at discharge. Their head circumference growth is relatively slow. They are susceptible to pneumonia and wheezing during infancy. Moreover, they have delayed motor development when compared with those without BPD at corrected ages of 6 and 9 months.

[Asymmetric crying facies and vocal cord paralysis accompanied by congenital heart disease in an infant].

A female infant was admitted to the hospital due to perioral cyanosis two hours after birth. The infant was born at the gestational age of 35 weeks by cesarean section with a birth weight of 2 400 g. Physical examination revealed wry mouth to the left side while crying, small auricles, and high palatal arch; fibrolaryngoscopy suggested bilateral vocal cord paralysis; echocardiography suggested ventricular septal defect; single nucleotide polymorphism testing showed 22q11.21 microdeletion. Therefore, the infant was given a definite diagnosis of asymmetric crying facies syndrome accompanied by 22q11.21 microdeletion. After 8-month follow-up, the infant still had asymmetric crying facies with presence of growth retardation.

[17α-Hydroxylase deficiency with severe hypertension as the initial symptom in a child].

A 14-year-old female (social gender) patient was admitted to the hospital due to severe hypertension for 11 days. The patient had primary amenorrhea. The blood pressure was 146/90 mm Hg. The skin color was slightly black. The development of secondary sexual characteristics was poor. The labia majora could be observed in the vulva. However, the labia minora, clitoris, vagina, and hymen were absent. The levels of renin, cortisol, and sex hormone were low, while the levels of adrenocorticotropic hormone and gonadotropin were high. The levels of blood potassium and aldosterone were both normal. Radiography indicated retardation of bone age. Ultrasound examination revealed that the ovary and uterus were both absent. The patient had bilateral adrenal hyperplasia and cryptorchid testes located in both inguinal canals. The patient had a 46,XY karyotype. Whole genome sequencing revealed two homozygous mutations, c.985T>C and c.987delC, in exon 6 of the CYP17A1 gene of the patient and heterozygous mutations in the same sites of the parents. The patient was diagnosed with congenital adrenal hyperplasia-17α-hydroxylase deficiency. After treatment with hydrocortisone for 2 months, blood pressure returned to normal and the level of adrenocorticotropic hormone was reduced. According to the request of the patient and the parents, hydrocortisone was replaced with estrogen to allow the patient to live as a female. The patient also received surgical excision of cryptorchid testes to prevent gonadal malignancy. It is concluded that in the differential diagnosis of pediatric hypertension, sexual development should be considered and the levels of adrenocorticotropic hormone and cortisol should be evaluated. The rare disease 17α-hydroxylase deficiency should be considered for patients with low-renin hypertension and gonadal dysgenesis.

[Clinical analysis of twin-twin transfusion syndrome complicated by cardiac abnormalities in preterm infants].

OBJECTIVE: To investigate the complications of twin-twin transfusion syndrome (TTTS) in preterm infants and to analyze the clinical conditions and prognosis of cardiac abnormalities in TTTS recipients. METHODS: A retrospective analysis was performed on the clinical data of 17 pairs of preterm infants with TTTS born between June 2009 and December 2012. RESULTS: Compared with the recipients, the donors had significantly lower body weights (1.4±0.6 kg vs 1.9±0.6 kg; P<0.05). With treatment during pregnancy, cardiac complications were found in 14 cases, and brain injuries in 12 cases. The proportion of recipients with cardiac abnormalities (60%) was higher than that of donors (24%). Among 10 recipients who had cardiac complications, cardiac abnormalities mainly included valve thickening, stenosis, or atresia (50%). CONCLUSIONS: Among preterm infants with TTTS, the recipients are more susceptible to complications of valvular heart disease and cardiomyopathy. Fetal echocardiography, evaluation of cardiac function, and treatment should be performed for recipients as early as possible to improve the prognosis.

Effects of endogenous sulfur dioxide on monocrotaline-induced pulmonary hypertension in rats.

AIM: The present study aimed to explore the protective effect of endogenous sulfur dioxide (SO2) in the development of monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats. METHODS: Forty Wistar rats were randomly divided into the MCT group receiving MCT treatment, the MCT+L-aspartate-beta- hydroxamate (HDX) group receiving MCT plus HDX treatment, the MCT+SO2 group receiving MCT plus SO2 donor treatment, and the control group. Mean pulmonary artery pressure (mPAP) and structural changes in pulmonary arteries were evaluated. SO2 content, aspartate aminotransferase activity, and gene expression were measured. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), reduced glutathione (GSH), oxidized glutathione, and malondialdehyde (MDA) levels were assayed. RESULTS: In the MCT-treated rats, mPAP and right ventricle/(left ventricle+septum) increased significantly (P<0.01), pulmonary vascular structural remodeling developed, and SOD, GSHPx, CAT, GSH, and MDA levels of lung homogenates significantly increased (P<0.01) in association with the elevated SO2 content, aspartate aminotransferase activity, and gene expression, compared with the control rats. In the MCT+HDXtreated rats, lung tissues and plasma SO2 content and aspartate aminotransferase activities decreased significantly, whereas the mPAP and pulmonary vascular structural remodeling were markedly aggravated with the decreased SOD, CAT, and GSH levels of lung tissue homogenates compared with the MCT-treated rats (P<0.01). In contrast, with the use of a SO2 donor, the pulmonary vascular structural remodeling was obviously lessened with elevated lung tissue SOD, GSH-Px, and MDA content, and plasma SOD, GSH-Px, and CAT levels. CONCLUSION: Endogenous SO2 might play a protective role in the pathogenesis of MCT-induced PH and promote endogenous antioxidative capacities.

Hydrogen sulfide regulates lung tissue-oxidized glutathione and total antioxidant capacity in hypoxic pulmonary hypertensive rats.

AIM: To investigate the modulatory effect of sodium hydrosulfide on lung tissue-oxidized glutathione and total antioxidant capacity in the development of hypoxic pulmonary hypertension (HPH). METHODS: After 21 d of hypoxia, the mean pulmonary artery pressure was measured by cardiac catheterization. The plasma H2S level and production of H2S in the lung tissues were determined by using a spectrophotometer. The lung homogenates were assayed for total antioxidant capacity (T-AOC), superoxide dismutase (SOD), oxidized glutathione (GSSG), reduced glutathione and malonaldehyde by colorimetry. The mRNA level of SOD was analyzed by real-time PCR, and the SOD expression was detected by Western blotting. RESULTS: In the hypoxia group, the plasma H2S concentration and H2S production in the lung was significantly decreased compared with the control group (187.2+/-13.1 vs 299.6+/-12.4 micromol/L; 0.138+/-0.013 vs 0.289+/-0.036 nmol x mg(-1) x min(-1), P<0.01). The administration of sodium hydrosulfide could reduce the mean pulmonary artery pressure by 31.2% compared with the hypoxia group (P<0.01). Treatment with sodium hydrosulfide decreased GSSG, and the T-AOC level of the lung tissues was enhanced compared with the hypoxia group (P<0.05). There were no significant changes in the lung tissue SOD mRNA level, protein level, and its activity among the 3 groups. CONCLUSION: Oxidative stress occurred in the development of HPH and was accompanied by a decrease in the endogenous production of H2S in the lung tissues. H2S acted as an antioxidant during the oxidative stress of HPH partly as a result of the attenuated GSSG content.

[Effect of hydrogen sulfide on oxidative stress in hypoxic pulmonary hypertension].

OBJECTIVE: To study the modulatory effect of hydrogen sulfide (H(2)S) on oxidative stress in the development of pulmonary hypertension induced by hypoxia. METHODS: Twenty male Wistar rats were randomly divided into control group (n=6), hypoxic group (n=6) and hypoxia+NaHS group (n=8). Hypoxic challenge was performed everyday for 21 days. NaHS solution was injected intra-peritoneally everyday before hypoxic challenge for rats in the hypoxia+NaHS group. After 21 days of hypoxia, the mean pulmonary artery pressure(mPAP) was measured by cardiac catheterization. The weight ratio of right ventricle to left ventricle+septum [RV/(LV+SP)] was also measured. The lung homogenates were assayed for total antioxidant capacity(T-AOC), superoxide dismutase (SOD), oxidized glutathione (GSSG), reduced glutathione (GSH), malondialdehyde(MDA) and hydroxy radical(*OH), and the SOD mRNA levels were assayed by real time polymerase chain reaction. RESULTS: After three weeks of hypoxic disposure, hypoxic hypertension and vascular remodeling developed. Compared with the control group, the mPAP[(23.7+/-2.2) mm Hg vs (16.3+/-3.7) mm Hg,P<0.01] and the weight ratio of RV/(LV+SP) increased (P<0.01), but lung tissue T-AOC was decreased by 21.4% (P<0.01).But GSSG was increased by 68.5% (P<0.01) as compared with those of the control rats. However, compared with those of the hypoxic group, the mPAP in rats of hypoxia+NaHS group was decreased [(16.3+/-2.8) mm Hg vs (23.7 +/-2.2) mm Hg]. Administration of NaHS increased T-AOC by 18.8% (P<0.05) but eliminated GSSG by 23.2% (P<0.05) in rats of hypoxia+NaHS group as compared with the hypoxic group. There were no significant changes in lung tissue SOD mRNA level and its capacity among the three groups. CONCLUSION: Hydrogen sulfide acted as antioxidant during the oxidative stress of hypoxic pulmonary hypertension, and the mechanism was partly through attenuating the content of GSSG.