[Effects of exogenous hydrogen sulfide on pulmonary hypertension in rabbits with endotoxic shock].

Objective: To investigate the effects of exogenous hydrogen sulfide (H2S) on pulmonary vascular reactivity induced by endotoxic shock (ES) in rabbits. Methods: In this experiment, the model of endotoxic shock (ES) was induced by injection of lipopolysaccharides (LPS) to New Zealand big eared white rabbit through jugular vein (8 mg/0.8 ml/kg), the intervention was performed by H2S donor(sodium hydrosulfide, NaHS) which was injected intraperitoneally (28 µmol/kg) 15 min in advance. New Zealand rabbits were randomly divided into 4 groups(n=8):control group, LPS group, LPS+NaHS group and NaHS group. The changes of mean arterial pressure (MAP) and mean pulmonary arterial pressure (MPAP) were detected. The tension of pulmonary artery ring (PARs) was detected byin vitro vascular ring technique. The ultrastructure of pulmonary artery wall and pulmonary artery endothelial cells were observed by light microscope and scanning electron microscope. Results: ①MAP was decreased while MPAP was increased in rabbits after LPS injection, and ES animal model was established successfully. Compared with LPS group, mPAP of rabbit in LPS+NaHS group was decreased significantly (all P＜0.05). ②Compared with normal control group, pulmonary artery of rabbits in LPS group had an increased contractile response to phenylephrine (PE) and a decreased relaxation response to acetylcholine (ACh) (both P＜0.01); Compared with LPS group, pulmonary artery of rabbits in LPS+NaHS group had a decreased contractile response to PE and an increased relaxation response to ACh (both P＜0.05). ③Under light microscope, the structure of vascular endothelial cells was continuous in the normal control group, the elastic fibers were intact in the subcutaneous layer, and the smooth muscle layer was arranged neatly. LPS can shed some of the pulmonary artery endothelial cells, break the subcutaneous elastic fibers, and disorder the smooth muscle layer structure. Compared with LPS group, the injury of pulmonary artery wall in LPS+NaHS group was ameliorated. The morphology of pulmonary artery wall was normal in NaHS group. It is showed that some endothelial cells of pulmonary artery were missing in LPS group by Scanning electron microscopy. The morphology of pulmonary artery endothelial cells in LPS+NaHS group was similar to that in the control group: slightly widened intercellular space was observed, and no cell exfoliation was observed. Conclusion: These results suggest that exogenous H2S can protect pulmonary artery endothelial cells and regulate the reactivity changes of pulmonary artery during ES, which may be one of the mechanisms reducing PAH in ES rabbits.

Xylomexicanins K-N: limonoids from the leaves and twigs of Xylocarpus granatum.

Six new compounds, xylomexicanins K-N (1-4), granasteroid (5) and 5-methoxy-2-pentylbenzofuran-7-ol (6), along with nine known compounds were isolated from the leaves and twigs of Xylocarpus granatum. Among them, 1 was a biogenetic precursor of 1,8,9-phragmalin limonoid, and 4 represent the first example of degraded A-ring limonoid. The structures of them were elucidated on the basis of one- and two-dimensional NMR spectroscopic data (including 1H, 13C-NMR, DEPT, 1H-1H COSY, HSQC, HMBC, and NOESY) and confirmed by high-resolution mass spectrometry.[Formula: see text].

MicroRNA-214 protects L6 skeletal myoblasts against hydrogen peroxide-induced apoptosis.

MicroRNAs (miRNAs) have been reported as key gene regulators, and they control many fundamental biological processes. Previously, we demonstrated that miR-214 had a protective effect against myocardial apoptosis and myocardial fibrosis. In this study, we sought to investigate the expression of miR-214 in L6 skeletal myoblast (SKM), the regulatory effect of miR-214 on hydrogen peroxide (H2O2) induced cell apoptosis and the underlying mechanisms of the antiapoptotic effect. MiR-214 expression was up-regulated by H2O2 in a dose and time-dependent manner in L6 SKMs. To investigate the regulatory effects of miR-214 on L6 SKM, both gain-of-function and loss-of-function approaches were applied. The results showed that miR-214 improved cell survival and inhibited cell apoptosis, and blockage of miR-214 abrogated the protective effect on cell survival and resistance to apoptosis. Phosphatase and tensin homolog (PTEN) was negatively regulated by miR-214, and PTEN inhibitor obviously reversed the effect of miR-214 blockage on enhancing cell apoptosis. In addition, miR-214 up-regulated antiapoptotic protein Bcl-2, down-regulated proapoptotic protein Bax, prevented release of cytochrome c and inhibited caspase-3 activation. In summary, H2O2-induced injury increases miR-214 expression in L6 SKM, and miR-214 contributes to the protection of L6 SKM against apoptosis via lowering PTEN and subsequently inhibiting the mitochondrial-mediated caspase-dependent apoptotic signaling pathway.

Relationship between puberty growth and sexual development of boys / 中国学校卫生

Objective@#To analyze the characteristics of puberty growth of boys and to explore the relationship between puberty growth and sexual development of boys.@*Methods@#Pubertal development of boys from grade 1 to grade 4 in Jiulongpo district of Chongqing was followed up once every six months. The data of height, weight, BMI, the age of first ejaculation and testicular development of boys from baseline to follow-up every 6 months for 5 years were analyzed. Based on peak height velocity (PHV), the average level of PHV and age at peak height velocity(PHA) were analyzed. ANOVA was used to compare the height growth rate of boys in different age groups before and after the first ejaculation. Kendall rank correlation was used to analyze the relationship between different stages of testicular development and BMI.@*Results@#The mean age of PHA was (11.72±1.03) years in adolescent height speed cohort, and the mean age of first ejaculation was (12.45±0.98) years before and after the first ejaculation cohort. There was significant difference in the increment of height before and after one year of the age of first ejaculation (P<0.05), the younger the age of the first ejaculation, the greater increase of height in the following year. The height, weight, BMI of boys aged 11 to 14 years were positively correlated with testicular volume(P<0.05).@*Conclusion@#The height growth of boys reached its peak one year before the first ejaculation, and began to decrease after first ejaculation, and the age of the first ejaculation of boys was negatively correlated with the increment of height in the following year, while the testicular development of boys was positively correlated with height, weight and BMI.

[The interventional effects of saturated hydrogen saline on lung injury in rats with cecal ligation and puncture operation].

OBJECTIVE: To investigate the hypothesis that hydrogen could ameliorate cecal ligation and puncture (CLP)-induced lung injury of rats by inhibiting cystathionine-gamma-lyase/hydrogen sulfide (CSE/H2S) system. METHODS: A total number of 24 healthy male SD rats weighting 250～300 g were randomly divided into four groups (n=6 in each group): sham operation group(sham group), hydrogen-rich saline control group(H2 group), CLP group and hydrogen-rich saline treatment group(CLP+H2 group). The rats were treated with hydrogen-rich saline or saline 10 min before CLP or sham operation. At 8 h of sham or CLP operation, lung samples were obtained to detect the changes of the CSE/H2S system using biochemical and RT-PCR methods. In order to further confirm the role of H2S during hydrogen improve the lung injury of CLP rats, we also observed the effect of hydrogen-rich saline on the lung injury induced by H2S donor-sodium sodium hydrosulfide (NaHS). Thirty-two healthy male SD rats (250~300 g) were randomly divided into four groups (n=8 in each group): control group, H2S group, H2S+H2 group and H2 group. Saline(10 mg/kg) or NaHS(H2S donor, 56 µmol/kg) was injected intraperitoneally (10 mg/kg) respectively into rats in the control rats or H2S group. For rats in the H2S+H2 and H2 group, hydrogen-rich saline (10 mg/kg) was injected 10 min before saline or NaHS administration. Eight hours after the LPS saline or NaHS administration, lung coefficient, MDA content, and MPO activity were detected. The contents of TNF-α, IL-6 and IL-10 in lung tissue were measured, and the morphological changes of lung tissue were also observed. RESULTS: CSE/H2S system up-regulating were observed in animals exposed to CLP. Hydrogen-rich saline treatment significantly inhibited CSE/H2S system as indicated by significantly reduced H2S production in lung, along with a decreased CSE activity and CSE mRNA expression (all P＜0.05). Importantly, the results showed that lung injury and lung tissue inflammation were observed in animals exposed to NaHS. Hydrogen-rich saline treatment significantly attenuated lung injury as indicated by significantly improved histological changes in lung, significantly reduced index of quantitative assessment (IQA), MDA content and lung coefficient (all P＜0.05). MPO activity in lung tissue was significantly reduced along with decreased productions of TNF-α and IL-6, and an increased production of IL-10 in the presence of hydrogen (all P＜0.05), demonstrating antioxidant and anti-inflammatory effect of hydrogen in NaHS-induced ALI. CONCLUSION: These results indicate that hydrogen-rich saline peritoneal injection improves the lung injury induced by CLP operation. The therapeutic effects of hydrogen-rich saline may be related to suppressing the production of H2S.

Sulfur dioxide reduces lipopolysaccharide-induced acute lung injury in rats.

INTRODUCTION: Recent studies suggested that sulfur dioxide (SO2) can be produced endogenously by pulmonary vessels and attenuate acute lung injury (ALI) with vasorelaxant effects. This study was conducted to determine whether SO2 can inhibit lung inflammation and relax pulmonary arteries via inhibition of the mitogen-activated protein kinase (MAPK) pathway. MATERIAL AND METHODS: Forty-eight adult male Sprague Dawley rats (250~300 g) were randomly divided into six treatment groups: control (n = 8), control + SO2 (n = 8), control + L-aspartic acid-ß-hydroxamate (HDX) (n = 8), LPS (n = 8), LPS + SO2 (n = 8) and LPS + HDX (n = 8). RESULTS: Six hours after LPS treatment, rats exhibited elevated pulmonary artery hypertension (PAH), marked pulmonary structure injury with elevated pulmonary myeloperoxidase (MPO) activity and increased expression of intercellular adhesion molecule 1 (ICAM-1) and CD11b, along with decreased pulmonary SO2 production and reduced pulmonary aspartate aminotransferase (AAT) activity. Pretreatment with SO2 saline solution significantly reduced, while HDX (AAT inhibitor) aggravated, the pathogenesis of LPS-induced ALI. Moreover, SO2 saline solution significantly down-regulated expression of Raf-1, MEK-1 and phosphorylated ERK (p-ERK). It also prevented pulmonary hypertension in association with an up-regulated SO2/AAT pathway. However, HDX advanced pulmonary hypertension and inflammatory responses in the lung were associated with a down-regulated SO2/AAT pathway. CONCLUSIONS: Our results suggest that SO2 markedly relieved inflammatory responses, in association with Raf-1, MEK-1 and p-ERK during ALI induced by LPS. The down-regulation of the SO2/AAT pathway may be involved in the mechanism(s) of LPS-induced lung injury.

Anti-IL-20 monoclonal antibody suppresses hepatocellular carcinoma progression.

Interleukin (IL)-20 is a member of the IL-10 family of cytokines, which has been reported to participate in autoimmune inflammatory diseases. However, the potential role of IL-20 in hepatocellular carcinoma (HCC) progression has not yet been investigated. In the present study, it was observed that IL-20 mRNA and protein levels were markedly increased in the HCC tissues examined via reverse transcription-quantitative polymerase chain reaction and immunohistochemical staining. In addition, IL-20 expression was significantly associated with tumor size, metastasis, TNM stage and poor prognosis in patients with HCC. Mouse recombinant IL-20 (mIL-20) enhanced liver cancer cell proliferation, migration and invasion in vitro, while the anti-IL-20 monoclonal antibody (mAb) attenuated the effect of mIL-20, inhibiting cancer cell migration and invasion in vitro and suppressing cell growth in vitro and in vivo. This was detected by Cell Counting Kit-8, colony formation, Transwell assays and a xenograft tumor nude mouse model. Western blotting revealed that IL-20 promoted HCC progression through inducing transforming growth factor-ß and matrix metalloproteinase 9 expression and enhancing the phosphorylation of Jun N-terminal kinase and signal transducer and activator of transcription 3. The results of the present study indicated that IL-20 promotes HCC development. In addition, anti-IL-20 mAb may attenuate the effect of IL-20 and suppress liver tumorigenesis in vitro and in vivo, indicating that anti-IL-20 mAbs may potentially serve as effective therapeutic agents for HCC.

Complete mitochondrial genome sequence and mutations of the liver cancer model inbred C57BL/6 mice strain.

In the present work, we undertook the complete mitochondrial genome sequencing of an important liver cancer model inbred rat strain for the first time. The total length of the mitogenome was 16,308 bp. It harbored 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes and 1 non-coding control region (D-loop region). The mutation events were also reported.

Role of sulfur dioxide in acute lung injury following limb ischemia/reperfusion in rats.

Sulfur dioxide (SO2) is naturally synthesized by glutamate-oxaloacetate transaminase (GOT) from L-cysteine in mammalian cells. We aim to investigate the role of SO2 in inflammation in acute lung injury (ALI) following limb ischemia/reperfusion (I/R). Male Wistar rats were subjected to limb I/R and were injected with saline, GOT inhibitor hydroxamate (HDX, 0.47 mmol/kg), or the SO2 donor Na2 SO3 /NaHSO3 (0.54 mmol/kg/0.18 mmol/kg). Compared with the sham operation, the plasma SO2 levels were significantly decreased by limb I/R treatment. In addition, SO2 concentration and GOT activity in the lung tissue were also reduced in ALI. The occurrence of ALI following limb I/R can be prevented by Na2 SO3 /NaHSO3 treatment, whereas it can be significantly aggravated by HDX. The plasma IL-1ß, IL-6, and IL-10 levels were consistent with myeloperoxidase activity and inflammation in lung tissue. In conclusion, our data suggest that downregulation of endogenous SO2 production might be involved in pathogenesis of ALI following limb I/R in rats.

[Hydrogen sulfide reduces lipopolysaccharide-induced acute lung injury and inhibits expression of phosphorylated p38 MAPK in rats].

To investigate the influence of hydrogen sulfide (H2S) on p38 MAPK signaling pathway during acute lung injury (ALI) caused by lipopolysaccharide (LPS), the rats were randomly divided into six groups: control group, LPS group, LPS + NaHS group, LPS + PPG (cystathionine-γ-lyase inhibitor) group, NaHS group and PPG group. The rats were sacrificed 6 h after injection and lung tissues were obtained. The structure of lung tissues and the number of polymorphonuclear leucocyte (PMN) was observed under optical microscope; the lung myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were tested; intercellular adhesion molecule-1 (ICAM-1) protein expression changes were detected by immunohistochemical staining; phosphorylated p38 MAPK (p-p38 MAPK) protein expression was detected by Western blotting. The results showed that the lung injury in LPS group was observed, at the same time the MPO activity, the content of MDA, ICAM-1 and p-p38 MAPK protein expressions, the number of PMN were all higher than those in control group (all P < 0.05). Pre-injection of NaHS alleviated the changes induced by LPS, while pre-injection of PPG aggravated those alterations (all P < 0.05). ICAM-1 and p-p38 MAPK protein expressions in lung tissue were positively correlated (r = 0.923, P < 0.01). The results suggest that H2S may reduce LPS-induced ALI through inhibiting the conjugation of p38 MAPK and reducing the expression of ICAM-1.

Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis.

AIM: We speculated that the enhanced apoptosis of polymorphonuclear neutrophil (PMN) might be responsible for the inhibition of PMN infiltration in the lung. This study was designed to investigate the effects of sulfur dioxide (SO(2)) on PMN apoptosis in vivo and in vitro, which may mediate the protective action of SO(2) on pulmonary diseases. METHODS: Acute lung injury (ALI) was induced by intratracheally instillation of lipopolysaccharide (LPS, 100 µg/100 g, in 200 µL saline) in adult male SD rats. SO(2) solution (25 µmol/kg) was administered intraperitoneally 30 min before LPS treatment. The rats were killed 6 h after LPS treatment. Lung tissues were collected for histopathologic study and SO(2) concentration assay. Bronchoalveolar lavage fluid (BALF) was collected for the measurement of PMN apoptosis. For in vitro experiments, rat peripheral blood PMNs were cultured and treated with LPS (30 mg/L) and SO(2) (10, 20 and 30 µmol/L) for 6 h, and apoptosis-related protein expression was detected by Western blotting, and apoptosis rate was measured with flow cytometry. RESULTS: LPS treatment significantly reduced the SO(2) concentrations in the lung tissue and peripheral blood, as compared with the control group. Pretreatment with SO(2) prevented LPS-induced reduction of the SO(2) concentration in the lung tissue and peripheral blood. LPS treatment significantly reduced PMN apoptosis both in vivo and in vitro, which could be prevented by the pretreatment with SO(2). The protein levels of Caspase-3 and Bax was significantly increased, but Bcl-2 was decreased by the pretreatment with SO(2), as compared with LPS administration alone. CONCLUSION: SO(2) plays an important role as the modulator of PMN apoptosis during LPS-induced ALI, which might be one of the mechanisms underlying the protective action of SO(2) on pulmonary diseases.

Berberine ameliorates COX-2 expression in rat small intestinal mucosa partially through PPARγ pathway during acute endotoxemia.

Berberine hydrochloride (BBR), a plant alkaloid, has been used to treat intestinal inflammation or infection for years. Cyclooxygenase-2 (COX-2) is pro-inflammatory mediator and involved in the induction of gut inflammation. The expression of COX-2 in small bowel mucosa was determined and the mechanism by which BBR modulated COX-2 expression was explored in a rat model of endotoxemia induced by lipopolysaccharide (LPS). The results showed that without LPS stimulation COX-2 was constitutively expressed at low levels in control rats. LPS challenge rapidly induced COX-2 gene transcription resulting in high levels of inducible COX-2 expression in endotoxemic rats. BBR pre- and post-treatment had no marked effect on constitutive COX-2 expression but inhibited inducible COX-2 overexpression. LPS challenge increased the expression and phosphorylation of peroxisome proliferator-activated receptor gamma (PPARγ), p38 and activating transcription factor 2 and 3 (ATF2, ATF3), but the effects of LPS were inhibited by BBR treatment. GW9662 did not influence constitutive COX-2 expression but enhanced inducible COX-2 overproduction. Besides, GW9662 abolished the inhibitory effect of BBR on inducible COX-2, p38, ATF2, 3 expression and phosphorylation. Collectively, these results indicated that BBR gavage could attenuate the overexpression of inducible COX-2, not constitutive COX-2, in ileal mucosa during acute endotoxemia in part via activation of PPARγ pathway, which negatively interfered with p38/ATFs cascade.

[Administration of hydrogen sulfide intraperitoneally reverses the hyporesponsiveness of rat pulmonary artery induced by lipopolysaccharide and its relationship with carbon monoxide].

OBJECTIVE: To explore the effect of hydrogen sulfide (H(2)S) on abnormal pulmonary artery reactivity induced by lipopolysaccharide (LPS) and its relationship with carbon monoxide (CO). METHODS: Forty eight rats were divided into four groups randomly according to table of random number: control group (normal saline, NS), LPS group, a donor of H(2)S sodium hydrosulfide (NaHS)+LPS group, and NaHS+NS group (n=12 in each group). Rats were given LPS by intratracheal instillation (0.8 ml/kg). 0.5 ml of NaHS (28 µmol/kg) was injected intraperitoneally 10 minutes before LPS or NS instillation and 2 hours after LPS or NS instillation in NaHS+LPS and NaHS+NS groups. Twelve hours after instillation of LPS, 6 rats from each group were sacrificed. The pulmonary artery rings (PARs) were prepared and the changes in cumulative relaxation response of PARs to NaHS were detected before and after incubation with an inhibitor of heme oxygenase-1 (HO-1) zinc protoporphyrinIX (ZnPPIX) using isolated vascular ring tension detecting technique. Twelve hours after LPS instillation, the remaining 6 rats in each group were sacrificed, and the contents of carboxyhemoglobin (COHb) in efferent pulmonary blood (EPB) and afferent pulmonary blood (APB) were measured, and the difference between the contents of COHb in EPB and that of APB was calculated to represent content of CO from pulmonary circulation. RESULTS: In the present study, compared with control group, after the instillation of LPS the percentage of relaxation response of PARs to NaHS was significantly declined [(75.72±7.22)% vs. (96.40±4.40)%, P<0.01]. After being incubated with ZnPPIX, the decreased relaxation response of PARs to NaHS induced by LPS was further depressed [(62.91±8.22)% vs. (75.72±7.22)%, P<0.01]. Administration of NaHS intraperitoneally reversed the hyporesponsiveness of PARs to NaHS, the percentage of relaxation response of PARs to NaHS was significantly increased [(94.65±8.45)% vs. (75.72±7.22)%, P<0.01]. However ZnPPIX also attenuated the effect [(83.75±9.76)% vs. (94.65±8.45)%, P<0.01]. NO significant changes were observed between NaHS+NS group and control group, also between the results before and after ZnPPIX incubation . Compared with control group, the difference between the contents of COHb in EPB and that of APB increased after instillation of LPS [(3.12±0.48)% vs. (2.12±0.32)%, P<0.05], which further increased after intraperitoneal administration of NaHS [(4.03±0.56)%, P<0.01]. CONCLUSION: The results suggested that intraperitoneal administration of H(2)S could reverse hyporesponsiveness of PARs to H(2)S induced by LPS, and the result might be related to an intensification of HO-1/CO system in pulmonary artery tissue.

[Effect of hydrogen sulfide on rat pulmonary artery reactivity and injury induced by lipopolysaccharide].

OBJECTIVE: To explore the effects of hydrogen sulfide (H2S) on abnormal pulmonary artery reactivity and injury induced by lipopolysaccharide (LPS). METHODS: Seventy-two rats were divided into four groups randomly according to table of random number: control group, LPS group, sodium hydrosulfide (NaHS) as a donor of H2S+LPS group and NaHS+normal saline (NS) group (n=18 in each group). Rats were challenged with 0.8 ml/kg LPS (200 microg/200 microl) by intratracheal instillation. NaHS (28 micromol/kg, 0.5 ml) was injected intraperitoneally 10 minutes before LPS instillation and 2 hours after LPS instillation. Twelve hours later, 6 rats from each group were sacrificed. Blood from carotid artery was collected to detect H2S content in serum. After that, pulmonary artery rings (PARs) were prepared carefully, then the contraction response of PARs to phenylephrine (PE, 10(-6) mol/L) and the endothelium-dependent relaxation response to acetylcholine (ACh, 10(-6) mol/L) were measured using isolated vascular ring tension detecting technique. Six rats from each group were sacrificed for determination of malondialdehyde (MDA) content of pulmonary artery, and the remaining 6 rats from each group were sacrificed for observation of morphological changes in pulmonary artery tissue. RESULTS: Compared with control group, after LPS instillation, the contraction response (g/mg) of PARs to PE increased greatly (0.86+/-0.20 vs. 0.56+/-0.13), the relaxation response to ACh significantly decreased [(65.18+/-7.05)% vs. (84.13+/-8.84)%]. MDA content (mmol/L) in pulmonary artery tissues increased (32.03+/-7.81 vs. 5.82+/-0.92), and H2S (micromol/L) content in serum decreased (175.23+/-27.36 vs. 238.12+/-16.38). Changes of all results were significant (P<0.05 or P<0.01). The pulmonary artery tissue and endothelium were injured. However, these changes were reversed by administration of NaHS intraperitoneally, the contraction response of PARs to PE decreased [(0.61+/-0.17) g/mg], the relaxation response to ACh increased [(82.92+/-9.71)%], MDA content in pulmonary artery tissue decreased [(16.88+/-3.54) mmol/L] and H2S content in serum increased [(242.70+/-38.80) micromol/L]. There was significant difference in all results (P<0.05 or P<0.01). The injury to the tissue induced by LPS were alleviated significantly. There was no statistical difference in above indexes between NaHS+NS group and control group, except for the level of H2S. CONCLUSION: Exogenous H2S could not only reverse abnormal vascular reactivity of PARs induced by LPS but also alleviate the injury to pulmonary artery tissue induced by LPS.

Clinical, cytogenetic, and molecular characterization of a girl with some clinical features of Down syndrome resulting from a pure partial trisomy 21q22.11-qter due to a de novo intrachromosomal duplication.

We report a girl with a de novo pure partial trisomy 21 with some clinical features of Down syndrome. The girl patient presented a flat broad face, brachycephaly, and a flat nasal bridge. She also had upwardly slanted palpebral fissures, epicanthal folds, blepharitis, brushfield spots, and strabismus. Her mouth was wide with downturned corners, prominent lower lip, narrow and furrowed tongue, and short palate. G-banded chromosomal analysis of metaphases in cells from both skin and blood showed a 46,XX karyotype with additional chromosomal material on the distal short arm of one chromosome 21. Parental chromosomes were normal. Molecular analyses with the short-tandem-repeat (STR) marker D21S2039 (interferon-alpha/beta receptor [IFNAR]) (21q22.1) showed a triallelic pattern. Subtelomeric fluorescent in situ hybridization (FISH) analyses, LSI 13 (retinoblastoma 1 [RB1])/LSI 21(21q22.13-q22.2), and whole chromosome painting probes specific for chromosome 21 showed trisomy for the segment 21q22.13-21q22.2 due to a de novo intrachromosomal duplication. A 500K SNP microarray analysis was then performed and revealed a 13-Mb duplication of 21q22.11-qter. This duplicated material had been translocated onto the end of the "p" arm of one of the chromosome 21s. The karyotype was provisionally defined as 46,XX,add(21)(p12).ish der (21)t(21;21)(p12;q22.11)(WCP21q+,PCP21q++,D215259/D21S341/D21S342++)dn. At the age of 4 years and 10 months, a comprehensive psychological examination was performed and the diagnostic criteria for mental retardation were not fulfilled. In comparison with previously published cases of pure partial trisomy 21, this is a rare finding. Additional studies of such rare patients should aid in the study of the pathogenesis of Down syndrome.

[Effect of exogenous hydrogen sulfide on polymorphonuclear neutrophil accumulation in acute lung injury rat induced by lipopolysaccharides and its mechanism].

OBJECTIVE: To study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced polymorphonuclear neutrophil (PMN) accumulation and its mechanism. METHODS: The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS). Adult male Spraguce-Dawley (SD) rats were randomly divided into four groups (n = 8 - 12 per group): Control group (0.5 ml/kg normal saline i.v.), LPS-treated group (1 mg/kg, i.v.), LPS plus NaHS (1 mg/kg i.v. and 28 micromol/kg i.p., respectively) and NaHS group (28 micromol/kg i.p.). Animals were sacrificed at 6 h after agent administration. Morphological changes of lung tissues were observed and polymorphonuclear neutrophil (PMN) number in alveolar septum was tested. The apoptosis of PMN in the bronchoalveolar lavage fluid (BALF) was examined with in situ TdT-mediated dUTP end labeling (TUNEL). Intercellular adhesion factor-1 (ICAM-1) and nuclear factor-kappaB (NF-kappaB) expressions in the lung tissue were analyzed by Western Blot. RESULTS: The results showed that bleeding, edema, PMN accumulation and other pathological signs in the lung tissue emerged after LPS injection. Compared to control rats, the LPS-treated rats had increased PMN number, decreased PMN apoptotic percentages, and increased expressions of ICAM-1 and NF-kappaB. Administration of NaHS into LPS-treated rats reduced the PMN number and expressions of ICAM-1 and NF-kappaB but increased PMN apoptotic percentages. In addition, NaHS alleviated the degree of ALI. There were no significant differences of the above indicators between NaHS-treated rats and control rats. CONCLUSION: NaHS can reduce the PMN accumulation in the lung, and its mechanism is related to down-regulation expression of ICAM-1 and promotion of PMN apoptosis induced by inhibition of NF-kappaB pathway.

[Ameliorative effects of exogenous sulfur dioxide on lipopolysaccharide-induced acute lung injury in rats].

To investigate the influence of sulfur dioxide (SO2) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), we examined the influence of exogenous SO2 on pulmonary tissue inflammatory response. A rat model of ALI induced by intravenous (IV) injection of LPS was developed. Male Sprague-Dawley (SD) rats were divided into four groups randomly: control group, LPS group, LPS plus SO2 group (IV injection of 0.5 mL Na2SO3/NaHSO3 10 min before LPS administration) and SO2 group (only given Na2SO3/NaHSO3). Animals were sacrificed 6 h after agent administration. Lung weight/body weight ratio (LW/BW) was measured and calculated. Morphological changes of lung tissues were observed. The number of polymorphonuclear neutrophil (PMN) in the bronchoalveolar lavage fluid (BALF), intercellular adhesion factor-1 (ICAM-1) expression in the lung tissue and IL-1, IL-6 and IL-10 levels in the serum were tested. The results showed that, compared to control rats, the LPS-treated rats had severe injuries of lung tissues and an increased LW/BW, increased index of quantitative assessment (IQA) score, increased PMN number in the BALF, increased ICAM-1 expression in the lung tissue and increased IL-1, IL-6 and IL-10 levels in the serum 6 h after LPS injection. Administration of the SO2 donor, Na2SO/3NaHSO3, into LPS-treated rats reduced the LW/BW, PMN number and ICAM-1 expression, and alleviated the degree of ALI (measured by the IQA score). In addition, Na2SO3/NaHSO3 decreased IL-1 and IL-6 levels, but increased IL-10 level in the serum. There were no significant differences in the above indexes between SO2-treated rats and control rats. These results suggest that exogenous SO2 could inhibit the pulmonary tissue inflammatory response in rats with LPS-induced ALI.

[Application of fluorescence in situ hybridization in prenatal diagnosis of complex chromosomal abnormalities].

OBJECTIVE: To investigate the application of fluorescence in situ hybridization (FISH) technique in prenatal diagnosis of complex chromosomal abnormalities. METHODS: Eleven prenatal diagnosis cases (8 from amniocentesis and 3 from cord blood) with complex chromosomal abnormalities detected by routine G-banding, were further analyzed by FISH. RESULTS: The FISH technique confirmed the results of balanced chromosome rearrangements detected by G-banding, and clarified the structure of the derivative chromosomes in the 3 amniocentesis samples and the origin of the mark chromosomes in the 2 cord blood samples. CONCLUSION: FISH can be used to diagnose the complex chromosomal abnormalities accurately in prenatal diagnosis, and can provide very useful genetic information for clinical diagnosis and treatment.

[Role of polymorphonuclear neutrophil in exogenous hydrogen sulfide attenuating endotoxin-induced acute lung injury].

The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS) and cultured human peripheral blood polymorphonuclear neutrophil (PMN) were used to study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. Control group, NaHS group, LPS group and LPS + NaHS group were established both in in vivo and in vitro studies. Microvascular permeability, PMN accumulation in lung and apoptosis of PMN were detected. The results showed that: (1) In in vivo study, PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS + NaHS group (P<0.05, P<0.01); (2) In in vitro study, the apoptotic rates of PMN in LPS group and NaHS group were significantly higher than that in control group (P<0.01), while compared with LPS group, LPS + NaHS group showed significantly higher apoptotic rate (P<0.01). These results suggest that NaHS attenuates LPS-induced microvascular permeability and alleviates ALI. PMN apoptosis induced by NaHS is possibly one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.