[Radioanatomic study on the role of Hadad-Bassagasteguy flap in skull base reconstruction in endoscopic endonasal approach].

Objective: To evaluate the value of Hadad-Bassagasteguy flap (HBF) in endoscopic endonasal approaches (EEA) skull base reconstruction by radioanatomic measurements on CT of the skull base of Chinese adults. The following data in terms of anterior skull base defect and reconstruction, sphenoid platform area and middle skull base defect and reconstruction including sphenoid platform and sella area, clivus area defect and reconstruction, and HBF were collected and assessed. Methods: CT image data of 42 Chinese adults were selected to obtain radioanatomic measurement data related to HBF, anterior skull base defect and reconstruction, middle skull base defect and reconstruction, and defect and reconstruction of clivus area. SPSS 26.0 software was used to analyze the data. Results: The radioanatomic measurement data about HBF and skull base of 42 Chinese adults were obtained. The width of the leading edge of HBF [(37.49±2.86) mm] was 6 mm more than the anterior skull base width at the level of the anterior ethmoidal artery [(30.87±8.61) mm], and the width of the trailing edge of HBF [(42.61±3.95) mm] was also 6 mm more than the anterior skull base width at the level of the sphenoethmoidal junction [(26.79±2.79) mm]. The total length of HBF including the pedicle [(79.68±4.96) mm] was 6 mm more than the length of the anterior skull base reconstruction [(54.06±8.67) mm], and the length of HBF without pedicle [(46.27±3.14)] mm was 6 mm more than the length of anterior skull base defect [(30.87±8.61) mm]. The trailing edge width was 6 mm more than the planum sphenoidal width at the level of the optic strut [(30.87±8.61) mm]. The total length of HBF including the pedicle was 6 mm more than the length of the planum sphenoidal, and the sella reconstruction [(64.44±10.25) mm], also was 6 mm more than the length of the planum sphenoidal reconstruction [(73.61±8.28) mm]. The length of HBF without pedicle was 6 mm more than the length of the planum sphenoidal, and the sella defect [(27.88±3.74) mm], also was 6 mm more than the length of the planum sphenoidal defect [(15.50±3.38) mm]. The width of the leading edge of HBF and the width of the trailing edge were both 6 mm more than the width of clivus reconstruction at the level of the foramen lacerum [(21.68±2.30) mm]. The total length of HBF including pedicles was 6 mm more than the clivus reconstruction length [(67.09±5.44) mm], while the length of HBF without pedicles was also 6 mm more than the clivus defect length [(37.19±3.80) mm]. Conclusions: In this study, the radiosanatomic measurements ensured that HBF could provide sufficient tissue flap for the reconstruction of the anterior skull base and sphenoid plateau and extend the reconstruction area to sella and clivus. Preoperative radiosanatomic measurement can be used to predict the size of HBF required for skull base reconstruction, which provides important guidance for flap harvest.

[The clinical study of olfactory dysfunction in IgG4-related disease].

Objective:IgG4-related disease is a newly recognized systemic disease, and its elucidation is progressing. However, little is known about its sinonasal manifestations.The aim of this study was to assess the olfaction of patients with IgG4-related disease.Method:Twenty-two patients with IgG4-related disease underwent the odor stick identification test to measure olfactory function.We analyzed the clinical features, including serum IgG4 levels, involved organs, and sinonasal computed tomography scores to explore the etiology of olfactory dysfunction.Result:Eleven patients with IgG4-related disease were found to have olfactory dysfunction. There were no differences in the clinical features between the olfactory dysfunction group and the normal group.Conclusion:There were no correlation between olfactory function and serum IgG4 level, involved organs or sinonasal computed tomography scores.We found that the prevalence of olfactory dysfunction was high in patients with IgG4-related disease and that it could be reversed.Olfactory dysfunction appears to be a novel important manifestation of IgG4-related disease.

[Tryptase and ECP are related to olfactory dysfunction in allergic rhinitis].

Objective:Olfactory dysfunction is one of the common symptoms in patients with allergic rhinitis(AR),but the underlying mechanisms are not yet known.The purpose of this study was to explore the underlying mechanisms which tryptase and eosinophilic cationic protein(ECP) lead to olfactory dysfunction in patients with AR.Method:We have compared the results between tryptase,ECP,nasal airway resistance and olfactory function of the patients with AR and analyzed the correlations between them.Result:Patients with AR showed impaired olfactory functions compaired to the control group,but there was no differences in the nasal airway resistance between the two groups.Nasal secretion analysis in the patients with AR showed that the level of tryptase and ECP was increased in comparison with the controls.Conclusion:The increase of tryptase and ECP in the olfactory cleft can lead to olfactory dysfunction in patients with AR.

[One case in which papillary thyroid carcinoma and papillary carcinoma occur on the same side].

thyroid carcinoma is a common tumor in the endocrine system. There are four common types of thyroid carcinoma: papillary carcinoma; follicular cancer; medullary carcinoma; undifferentiated carcinoma. Thyroid papillary carcinoma is derived from follicular epithelial cells, which is different from that of medullary thyroid carcinoma. If both occur in the same side of the thyroid gland, this is very rare. In this paper we report a case in which papillary thyroid carcinoma and papillary carcinoma occurr on the same side.

[Analysis of the compliance and effectiveness of the allergen specific immunotherapy in patients with allergic rhinitis].

Objective:To investigate the effectiveness and compliance of the 2 year specific immunotherapy in patients with allergic rhinitis. Method:Two hundred and sixty-two patients of allergic rhinitis were treated with SLIT for 2 years. The symptom questionnaire about effectiveness and compliance were obtained 2 years after SLIT. The patient satisfaction was also investigated. Result:Sixty patients had complete compliance and 202 patients had poor compliance. Of the 142 children, 40 (28%) cases had complete compliance, and of the 118 adult patients, 20 cases (17%) had complete compliance. There was obvious difference between the two (P<0.05). Comparing of before and after treatment, total medication score, total nasal symptom score and every symptom score decreased obviously (P<0.05). Two years after treatment, the total effective rate was 63%,there was significant difference between the children group and the adult group (P<0.05). Conclusion:There are a lot of factors affecting the treatment compliance of sublingual immunotherapy, such as patients, family, health care workers and social support, etc. In the course of treatment, a series of strategies can be adopted to improve the treatment compliance. SLIT is an effective method for the treatment of allergic rhinitis, and the treatment effect of children is better.

Activating protein-1 cooperates with phorbol ester activation signals to increase HIV-1 expression.

OBJECTIVE: To determine whether Jun and Fos, components of the activating protein-1 (AP-1) transcription factor, transactivate HIV-1 proviral expression. DESIGN: The effects of phorbol myristate acetate (PMA) and Jun or Fos transcription factors on HIV-1 expression were investigated using a provirus clone and long terminal repeat (LTR)-reporter gene constructs. The influence of PMA stimulation on AP-1 binding activity was determined with antibodies in gel mobility shift assays. METHODS: Activation of HIV-1 provirus and transcription of HIV-1 LTR sequences in response to cotransfection of Jun or Fos expression plasmids into a permissive colon cancer cell line, SW480, were assessed by p24 core antigen capture and reporter gene assays, respectively. The effect of protein kinase C activation was evaluated by comparing cells grown in the presence or absence of PMA (20 ng/ml). RESULTS: Cotransfection of HIV-1 provirus and expression plasmids for c-Jun or JunB into SW480 cells resulted in increased p24 core antigen and this response was markedly increased following PMA stimulation of cells. c-Fos or JunD alone did not increase p24 production but markedly increased p24 production in PMA-stimulated cells. PMA increased c-Fos and JunD binding activity on an AP-1 binding site within the U5 region of the LTR, as shown in gel mobility shift assays. Functional analysis of this site by transient transfections demonstrated it was required to mediate c-Fos and JunD transactivation of the HIV-1 LTR. CONCLUSIONS: Specific Jun and Fos transcription factors can transactivate the HIV-1 provirus and this response is markedly increased in cooperation with cellular activation signals elicited by PMA. Taken together, the data indicate that AP-1 binding sites downstream of the transcriptional start site in the HIV-1 LTR are capable of binding c-Fos and JunD and may contribute to transactivation of HIV-1 provirus.

U5 region of the human immunodeficiency virus type 1 long terminal repeat contains TRE-like cAMP-responsive elements that bind both AP-1 and CREB/ATF proteins.

Activating protein-1 (AP-1) binding phorbol ester responsive elements (TRE) are located downstream of the transcription initiation site in the U5 region of the human immunodeficiency virus type-1 (HIV-1) long terminal repeat (LTR). These downstream sequence elements, termed DSE, can bind cFos and junD and transmit protein kinase C (PKC) activation signals to the LTR. Further studies suggested the DSE might also bind AP-1-related proteins of the CREB/ATF family. Since enhanced HIV-1 expression is associated with activation of the cAMP-dependent protein kinase A (PKA) signaling pathway, we determined whether binding of CREB/ATF proteins to the DSE mediate cAMP/PKA activation of the HIV-1 LTR. In the present study. DSE binding complexes in nuclear protein extracta from colonic epithelial cells are shown to contain ATF-1, ATF-2, and CREB and transfection of either an ATF-2 or PKA expressing plasmid transactivated the DSE. Cholera toxin (Ctx), a potent activator of the cAMP/PKA pathway. Increased HIV-1 virus production from a latently infected promonocytic cell line, U1. Ctx increased LTR promoter activity and increased the CREB content of DSE binding complexes. Transfection of U1 cells with a series of mutant LTR reporter constructs demonstrated that the Ctx response was in large part mediated by the DSE. The Ctx response was also mediated by a heterologous promoter containing multiple TRE sites. Nuclear protein extracts from a T-cell line infected by HIV-1 contained higher levels of CREB/ATF proteins and manifested increased CREB/ATF binding activity. Collectively, these results indicate the DSE are TRE-like cAMP responsive elements that bind both AP-1 and CREB/ATF permitting induction of the HIV-1 LTR by both PKC and PKA activation signals.

CD exciton chirality method for determination of the absolute configuration of beta-hydroxy-alpha-amino acid derivatives.

The absolute configuration of beta-hydroxy-alpha-amino acids was studied by CD exciton chirality method using 7-diethylaminocoumarin-3-carboxylate as a red-shifted chromophore. The CD spectra of bischromophoric derivatives of (S)-serine and (2S,3R)-threonine methyl esters (2 and 7) were compared with those of acyclic vic-aminoalcohols and diols (3--6 and 8--9). This study indicates that the polar carboxylate group of beta-hydroxy-alpha-amino acids makes them a unique subclass of vic-aminoalcohols. By combining the data of CD and NMR coupling constants, we are able to correlate their preferred conformer B and positive CD to the corresponding absolute configuration.

Insulin-like growth factors and binding proteins in the fetal rat: alterations during maternal starvation and effects in fetal brain cell culture.

Maternal malnutrition adversely affects fetal body and brain growth during late gestation. We utilized a fetal brain cell culture model to examine whether alternations in circulating factors may contribute to reduce brain growth during maternal starvation; we then used specific immunoassay and western blotting techniques, and purified peptides to investigate the potential role that altered levels of insulin-like growth factors (IGFs) and IGF binding proteins (IGFBPs) may play in impaired growth during maternal nutritional restriction. Fetal, body, liver, and brain weight were reduced after 72 hr maternal starvation, and plasma from starved fetuses were less potent than fed fetal plasma in stimulating brain cell growth. Circulating levels of IGF-I were reduced in starved compared to fed fetuses, while levels of IGF-II were similar in both groups. In contrast, [125I]-IGF-I binding assay demonstrated an increase in the availability of plasma IGFBPs following starvation. Western ligand blotting and densitometry indicated that levels of 32 Kd IGFBPs were 2-fold higher in starved compared to fed fetal plasma. Immunoblotting and immunoprecipitation with antiserum against rat IGFBP-1 confirmed that heightened levels of immunoreactive IGFBP-1 accounted for the increase in 32 Kd IGFBPs in starved plasma. Levels of 34 Kd BPs, representing IGFBP-2, were unaffected by starvation. Reconstitution experiments in cell culture showed that IGF-I promoted fetal brain cell growth, and that when they were supplemented with IGF-I, the growth promoting activity of starved fetal plasma was restored to fed levels. These changes were measured using MTT to assess mitochondrial reductase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Retardation of fetal brain cell growth during maternal starvation: circulating factors versus altered cellular response.

Maternal starvation inhibits fetal brain development during late gestation in the rat. To determine whether intrinsic or extrinsic factors might be the principal contributor to altered growth, brain cells from 20 day fetuses were cultured in a 96 well plate with MEM and 10% adult rat serum. Tissue growth was monitored by spectrophotometric measurement of the mitochondrial reduction of a chromagen 3-(4,5 dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide (MTT). After 1, 4 or 6 days incubation, MTT activity in non confluent cultures was shown to be directly related to tissue mass. When fetal brain cell cultures were incubated with 1% and 10% concentrations of adult rat serum, an 11-fold increase in MTT activity paralleled a 15-fold increase in tritiated thymidine incorporation. The impact of maternal starvation on fetal brain cell growth was examined by measuring MTT activity in fetal brain cells from fed and starved mothers. When cultures were incubated for 6 days with graded concentrations of fed adult serum (1.25-10%), the MTT response was slightly but consistently lower in cells from starved when compared with cells from fed mothers. By contrast, a marked difference in MTT activity which was paralleled by a lower DNA content became apparent when fetal rat brain cells were incubated with starved adult serum. Fetal serum and adult male serum were found to support growth equally well, while incubation of fetal brain cells with maternal sera resulted in lower MTT values than with the corresponding fetal sera. When cells were incubated with fetal sera pooled from starved mothers, MTT activity was decreased by 42 to 45%.(ABSTRACT TRUNCATED AT 250 WORDS)

IL-10 cooperates with TNF-alpha to activate HIV-1 from latently and acutely infected cells of monocyte/macrophage lineage.

IL-10 is elevated in HIV-1-infected individuals and has been implicated in disease progression. In this study, we investigated the effects of IL-10 on the activation of HIV-1 from infected monocytes and macrophages. Although IL-10 alone did not induce HIV-1 replication, in the presence of TNF-alpha, IL-10 markedly enhanced virion production from a chronically infected promonocytic cell line (U1) and in acutely infected monocyte-derived macrophages. Neutralizing mAbs to IL-10 and TNF-alpha indicated that both cytokines were essential for the induction and were required to generate a synergistic increase in virus expression. The effects of the two cytokines were distinguishable functionally since pretreatment with TNF-alpha attenuated the cytokine cooperativity, while pretreatment with IL-10 potentiated their cooperativity, suggesting that IL-10 and TNF-alpha play different roles in the activation of virus. Northern blot analysis as well as Ab blocking and cytokine secretion studies indicated that the induction of either endogenous TNF-alpha or IL-10 was not involved in the cooperativity, nor was an up-regulation of TNF-alpha receptors. In combination with TNF-alpha, IL-10 stimulated activating protein-1 (AP-1) and nuclear factor (NF)-kappa B binding activities and cooperated to increase HIV-1 steady-state mRNA levels and enhance long terminal repeat-directed transcription through activation of the NF-kappa B binding sites, suggesting the IL-10 effect occurs at least in part at the transcriptional level. These results indicate that IL-10, in addition to down-regulating the cellular immune response to HIV-1, may also play a role in TNF-alpha-mediated activation of HIV-1 replication in the monocyte/macrophage lineage.