Influence of LncRNA UCA1 on glucose metabolism in rats with diabetic nephropathy through PI3K-Akt signaling pathway.

OBJECTIVE: The aim of this study was to investigate the influence of long non-coding ribonucleic acid (lncRNA) urothelial carcinoma associated 1 (UCA1) on glucose metabolism in rats with diabetic nephropathy (DN), and to explore its regulatory mechanism. MATERIALS AND METHODS: A total of 30 healthy Sprague-Dawley (SD) rats were selected in this study. All rats were randomly divided into three groups, including the control group, the model group, and the lncRNA UCA1 inhibitor group. The rat model of DN was successfully established via intraperitoneal injection of streptozotocin (STZ). The pathological changes in kidney tissues were detected via hematoxylin-eosin (HE) staining. The levels of blood urea nitrogen (BUN), serum creatinine (Scr), and urinary protein (UP) were detected using the biochemical method. Meanwhile, the content of serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) was detected via enzyme-linked immunosorbent assay (ELISA). In addition, the messenger RNA (mRNA) and protein levels of phosphatidylinositol 3-hydroxy kinase (PI3K) and protein kinase B (Akt) in kidney tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. RESULTS: The model group showed severe pathological damage to the kidney, compared with the control group. Meanwhile, the levels of BUN, Scr and UP, and the content of serum TNF-α and IL-6 increased significantly in the model group. The mRNA and the protein levels of PI3K and Akt in kidney tissues of the model group were significantly up-regulated as well. LncRNA UCA1 inhibitor group exhibited relieved pathological damage to the kidney, compared with the model group. The levels of BUN, Scr and UP, and the content of serum TNF-α and IL-6 remarkably decreased in UCA1 inhibitor group. Furthermore, the mRNA and the protein levels of PI3K and Akt in kidney tissues of UCA1 inhibitor groups were significantly down-regulated. CONCLUSIONS: LncRNA UCA1 can relieve the pathological damage to the kidney, improve renal function, and alleviate inflammatory response in DN rats. The underlying mechanism may be related to the inhibition of the PI3K-Akt signaling pathway.

Exogenous abscisic acid increases antioxidant enzymes and related gene expression in pepper (Capsicum annuum) leaves subjected to chilling stress.

To elucidate how physiological and biochemical mechanisms of chilling stress are regulated by abscisic acid (ABA) pretreatment, pepper variety (cv. 'P70') seedlings were pretreated with 0.57 mM ABA for 72 h and then subjected to chilling stress at 10°/6°C (day/night). Chilling stress caused severe necrotic lesions on the leaves and increased malondialdehyde and H(2)O(2) levels. Activities of monodehydroascorbate reductase (DHAR), dehydroascorbate reductase, glutathione reductase, guaiacol peroxidase, ascorbate peroxidase, ascorbate, and glutathione increased due to chilling stress during the 72 h, while superoxide dismutase and catalase activities decreased during 24 h, suggesting that chilling stress activates the AsA-GSH cycle under catalase deactivation in pepper leaves. ABA pretreatment induced significant increases in the above-mentioned enzyme activities and progressive decreases in ascorbate and glutathione levels. On the other hand, ABA-pretreated seedlings under chilling stress increased superoxide dismutase and guaiacol peroxidase activities and lowered concentrations of other antioxidants compared with untreated chilling-stressed plants. These seedlings showed concomitant decreases in foliage damage symptoms, and levels of malondialdehyde and H(2)O(2). Induction of Mn-SOD and POD was observed in chilling-stressed plants treated with ABA. The expression of DHAR1 and DHAR2 was altered by chilling stress, but it was higher in the presence than in the absence of ABA at 24 h. Overall, the results indicate that exogenous application of ABA increases tolerance of plants to chilling-induced oxidative damage, mainly by enhancing superoxide dismutase and guaiacol peroxidase activities and related gene expression.

Isolation and expression of GA 2-oxidase2 in tomato.

GA 2-oxidases, a key enzyme involves GA biosynthesis, catalyze the degradation of active C(19)-Gibberellins (GAs) through 2-hydroxylation yields inactive GA product. Searching public tomato database, the putative GA2ox2 sequences were assembled. We isolated a full-length GA2ox2 cDNA with primers designed from the assembled sequence. This gene was designed as SlGA2ox2 (GenBank accession No. EF017805). The full-length GA2ox2 gene contained a complete open reading frame (ORF) of 1203 bp, which encoded 322 amino acid residues. Amino acid sequence homology analysis of SlGA2ox2 showed an 88% identity with NtGA2ox2 in tobacco. And alignments of SlGA2ox2 with other known GA2ox from Arabidopsis, Pea, Adzuki Bean, Winter Squash etc indicate low similarity of 47-70%. Semi-quantitative RT-PCR analysis showed a specific expression profile of SlGA2ox2 in different tissues, which mainly expressed in flowers and traces were detected in roots, stems, leaves and immature fruits.

[Clinical application of distal base sural island flap].

OBJECTIVE: To sum up the experience of clinical application of distal base sural island flap. METHODS: From January 1997 to April 1999, the posterior island flap of leg pedicled with sural nerve and its nutrient vessels was applied to repair heel or dorsum of foot in 6 cases, chronic ulcer of heel in 2 cases, chronic osteomyelitis in 2 cases, scar contracture of bone defect accompanying fistulation in 1 case. The range of flap was 5 cm x 8 cm to 8 cm x 12 cm. RESULTS: All the flaps survived completely without vascular crisis. All the wounds healed by first intention. Followed up 3 to 12 months, no ulcer, osteomyelitis, fistulation were recurrence, and the sensation of flap was recovered slightly. CONCLUSION: The flap do not damage critical blood vessels and nerves, the donating region is hidden. The manual of operation is simple and blood supply of flap is sufficient. It can repair the defect of soft tissue on heel and dorsum with high survival rate.

Mutation analysis of the 6-pyruvoyl-tetrahydropterin synthase gene in Chinese hyperphenylalaninemia caused by tetrahydrobiopterin synthesis deficiency.

Hyperphenylalaninemia (HPA) may be caused by deficiency of phenylalanine hydroxylase or tetrahydrobiopterin (BH4), the essential cofactor for the aromatic amino acid hydroxylases. 6-Pyruvoyl-tetrahydropterin synthase (PTPS) deficiency is a major cause of BH4 deficient HPA. In this study, seven single base mutations at nucleotides 73 (C>G), 155 (A>G), 166 (G>A), 209 (T>A), 259 (C>T), 286 (G>A), and 317 (C>T) on PTPS cDNA were detected in Chinese PTPS-deficient HPA by polymerase chain reaction and solid phase DNA sequencing. These nucleotide alterations result in R25G, N52S, V56M, V70D, P87S, D96N, and T106M amino acid substitutions, respectively. The R25G, V56M, V70D, and T106M were novel mutations found in PTPS gene. By analysis of 38 PTPS mutant alleles from 19 unrelated Chinese PTPS-deficient HPA families, the allele frequency of these mutations in Chinese PTPS-deficient HPA were determined to be approximately 5.3% (R25G), 34.2% (N52S), 7.9% (V56M), 2.6% (V70D), 36.8% (P87S), 7.9% (D96N), and 2.6% (T106M), respectively. Two common mutations, N52S and P87S, were found to account for 71% of the Chinese PTPS mutant alleles. The N52S mutation accounts for 48% of the southern Chinese PTPS mutation, but only one (9%) of the northern Chinese PTPS mutant allele was found to be N52S, which suggested that the N52S mutation might be southern Chinese. Clinically, the V56M mutation was found to associate with the mild form of PTPS deficiency. However, the R25G, N52S, P87S, and D96N were found mainly in the patients with severe clinical symptom. Using polymerase chain reaction-based mutation analysis, a fetus at risk of PTPS deficiency was diagnosed prenatally to be a carrier of N52S mutation.

Lack of seasonality in the month of onset of childhood IDDM (0.7-15 years) in Shanghai, China.

A cohort of 136 children from Shanghai with insulin dependent diabetes mellitus (IDDM) (0.7-15 years) were analyzed for the month of onset of disease and month of birth. In contradistinction to populations with a medium or high incidence of IDDM, no seasonality was registered in the month of onset. On the other hand there was a significant (p < 0.026) seasonality in the month of birth (peak November to January), but which differed in pattern to that observed in populations with medium or high incidence. Our findings support the hypothesis that the initiation of IDDM is due to a viral infection and that one cause for the low incidence of childhood IDDM in certain populations is immunization against infectious pathogens in their early life.

Historical total and respirable silica dust exposure levels in mines and pottery factories in China.

Historical exposure estimates of total dust and respirable silica were made in a recent nested case-referent study of lung cancer among mine and pottery workers in China. Exposure to total dust and respirable silica was assessed in 20 mines and 9 pottery factories. The average total dust concentration was 7.26 mg center dot m-3, with a range from 17.68 mg center dot m-3 in the 1950s to 3.85 mg center dot m-3 in the 1980s, while the average respirable silica dust was 1.22 mg center dot m-3, with a range from 3.89 mg center dot m-3 in the 1950s to 0.43 mg center dot m-3 in the 1980s. The highest respirable silica dust occurred in the underground mining operations (1.43 mg center dot m-3), particularly for manual drillers (9.03 mg center dot m-3). Among all facility types, tungsten mines had the highest respirable silica dust exposure (1.75 mg center dot m-3), while the lowest exposure occurred in copper-iron mines (0.32 mg center dot m-3).

Indirect validation of a retrospective method of exposure assessment used in a nested case-control study of lung cancer and silica exposure.

Validations of retrospective methods of assessment used in occupational epidemiological studies have rarely been published. This study is an indirect validation of a quantitative retrospective assessment of exposure to silica used in a nested case-control study of lung cancer among workers at 29 metal mines and pottery factories in China. Indices of cumulative total dust and cumulative respirable dust were calculated by merging work histories with the historical exposure profile for each subject. To validate indirectly the methods of exposure assessment used in the study of lung cancer, trends for exposure response relation between the two indices of exposure to silica and risk of silicosis were evaluated with 376 patients with silicosis from the study population as the cases, and 1262 controls without silicosis for comparison. Age adjusted odds ratios (ORs) as a measure of risk of silicosis showed striking trends with both indices of exposure to silica. For cumulative respirable dust, the OR (95% confidence interval) rose from 7.6 (5.1-11.4) for low exposure to 20.0 (13.2-30.6) for medium exposure, and to 51.7 (31.0-86.8) for high exposure. The strength of the association between exposure to silica and risk of silicosis suggests that the retrospective assessment of exposure used in the case-control study of lung cancer would accurately reflect an exposure response relation between silica and lung cancer, if it existed.

Estimating historical exposure to silica among mine and pottery workers in the People's Republic of China.

A quantitative retrospective exposure assessment method was developed for use in a nested case-control study of lung cancer among mine and pottery workers exposed to silica dust in the People's Republic of China. Exposure assessment was carried out in 20 mines (10 tungsten, 6 iron/copper, and 4 tin) and nine pottery factories. A job title dictionary was developed and used in both the collection of historical exposure information and work histories of 1,668 (316 cases and 1,352 controls) study subjects. Several data abstraction forms were developed to collect historical and current exposure information and employees' work histories, starting in 1950. A retrospective exposure matrix was developed on the basis of facility/job title/calendar year combinations using available historical exposure information and current exposure profiles. Information on the amount of respirable, thoracic, and free silica content in total dust was used in estimating exposure to silica. Starting in 1950, 6,805 historical estimates had been carried out for 14 calendar-year periods. We estimated the average total dust concentration to be 9 mg/M3, with a range from 28 mg/M3 in earlier years to 3 mg/M3 in recent years. Several exposure indices [such as cumulative dust, average dust, cumulative respirable (< 5 mu in particle size) and thoracic (< 10 mu in particle size) silica dust, average respirable and thoracic silica dust, exposure-weighted duration, and the highest/longest exposure] were calculated for individuals by merging work history and historical exposure matrix for each study subject. We developed these various measures of exposure to allow investigators to compare and contrast different indices of historical exposure to silica.

A comparative study of growth hormone (GH) and GH-releasing hormone(1-29)-NH2 for stimulation of growth in children with GH deficiency.

In this study, 60 patients with proven growth hormone deficiency (GHD) of hypothalamic origin were randomized into three equal groups, and received growth hormone-releasing hormone(1-29)-NH2 (GHRH(1-29)-NH2), 30 or 60 micrograms/kg/day, or growth hormone (GH), 0.1 IU/kg/day, for 6 months. There were no significant differences in growth between the two groups given GHRH(1-29)-NH2, but growth in the GH group was significantly better than in the other two groups (p < 0.01). Mean height velocities at 6 months were 9.2, 9.3 and 14.6 cm/year for the three groups, respectively. Plasma GHRH concentrations increased steadily over the 6-month treatment period, with higher levels in the group on the higher dose. During GHRH(1-29)-NH2 treatment, serum concentrations of insulin-like growth factor I rose initially, but then fell to values similar to those before treatment. No GH antibodies were detected, but all 20 patients on high-dose GHRH(1-29)-NH2 and 19 of 20 patients on low-dose GHRH(1-29)-NH2 developed GHRH antibodies. These had almost disappeared by 9 months after stopping treatment. There was no correlation between antibody titres and increase in height. No serious side-effects were seen, but three patients receiving GHRH(1-29)-NH2 reported mild irritation at the injection site. These results from the continuous infusion of GHRH(1-29)-NH2 over 6 months suggest that this treatment, or the related use of a depot preparation, is unlikely to be as effective as GH for the promotion of growth in GHD.

Treatment of growth hormone deficient patients with recombinant somatropin for 1 year: results of a Chinese multicentre trial.

Fifty-nine patients with idiopathic growth hormone deficiency were included in a Chinese multicentre trial of recombinant somatropin, 0.5-0.7 IU/kg/week s.c. given in six or seven divided doses. The height velocity increased from 2.8 +/- 1.0 cm/year to 13.1 +/- 2.5 cm/year during 1 year of treatment, and typical catch-up growth was observed. The increase in height SDS for chronological age was significant, but the increase in height SDS for bone age was not statistically significant. No adverse reactions to the treatment were recorded. Recombinant somatropin was shown to be very effective and safe during the first year of therapy in patients with growth hormone deficiency.

Methylmalonic and propionic acidemias: lipid profiles of normal and affected human skin fibroblasts incubated with [1-14C]propionate.

Normal human skin fibroblasts and those from methylmalonic acidemia and propionic acidemia patients were grown in culture. Following incubation with [1-14C]propionate, the major lipid classes in the cells were separated by thin layer chromatography and isolated fractions analyzed by radio gas chromatography for the presence of odd-numbered long-chain fatty acids; the pattern of even-numbered long-chain fatty acids was obtained also. Normal fibroblasts incorporated a small percentage of propionate into odd-numbered fatty acids which were present in all lipids studied. The abnormal cells incorporated a larger amount while maintaining the characteristic ratios of odd-numbered fatty acids found in the normal line. Most of the radioactivity was associated with phospholipids which are the predominant constituents of cell membranes. A characteristic C15/C17 ratio was found for different phospholipids and the triglyceride fraction; pentadecanoic acid was the principal odd-numbered fatty acid utilized in the assembly of complex lipids. Compared to even-numbered long-chain fatty acids the absolute amount of odd-numbered fatty acids was low (1-2%), even in affected cells. An unusual polar lipid fraction was isolated in the course of the study. In the normal cell it contained several unlabeled eicosanoids which were missing from the same fraction of both affected cell lines.