CAD/CAM design and 3D printing of a personalised rapid palatal expander for maxillary transverse deficiency.

Bone -borne ra pid ma xilla ry expansion appliances can achieve skeletal expansion while avoiding the undesirable dental side effec ts caused by a conventional rapid palatal expansion appliance. Typically, t hese (bone-bo rne appliances) included prefabricated devices, which can have limitations such as inadequate palatal adaptation leading to anch orage los s. In addit ion, a s bone thickness is not accounted for, prefabricated expanders cannot ensure the primary stability of the mini-implants. These disadvantages can be overcom e by customisation. This repor t aims to describe the digital design and three-dimensional printing workflow for constructing a personali sed M iniscrewassisted rapid palatal expansion (pMARPE) and present a case depicting its application in a 27-year-old female with 5.0 mm t ransverse discrepancy b etween the maxilla and the mandible. The result demonstrated that the pMARPE could be manufactured without the need for conventional impre s sion or laborator y p rocedures and effec tively e xpanded the palate of an ad ult pat ient with maxillar y transverse deficiency.

Skeletal and dentoalveolar modifications in adults with different sagittal facial patterns after personalized miniscrew-assisted rapid palatal expansion: A prospective cone-beam computed tomography study.

INTRODUCTION: This study aimed to compare the skeletal and dental modifications in adults with different sagittal facial patterns by a personalized miniscrew-assisted rapid palatal expander (pMARPE). METHODS: Forty subjects (aged 18-28 years; 15 females and 25 males) with maxillary transverse deficiency were assigned to 1 of 3 groups (Class I, II, and III relationship) on the basis of their sagittal facial patterns. Each patient was treated with an individually customized expander. A similar expansion protocol was used for all patients. Cone-beam computed tomography scans were obtained before and after expansion. One-way analysis of variance was used to analyze differences among 3 groups in skeletal, dentoalveolar, and periodontal changes (P <0.05). RESULTS: The success rates of expansion were higher in patients with a Class I or II relationship than those with a Class III relationship. Patients with a Class I or II relationship had greater changes in the anterior nasal spine and maxillary basal bone widths. A more parallel sutural opening in the anteroposterior direction was seen in those with a Class II relationship. The tipping of the maxillary first molar increased, and the buccal alveolar bone thickness decreased in all groups after expansion, especially in patients with a Class III relationship. CONCLUSIONS: The pMARPE effectively split the midpalatal suture among adults. However, midpalatal suture expansion was more difficult, and there were more dentoalveolar side effects and fewer orthopedic effects in patients with a Class III relationship than in those with Class I or II relationships.

LncRNA HOXA-AS3 promotes gastric cancer progression by regulating miR-29a-3p/LTßR and activating NF-κB signaling.

BACKGROUND: Gastric cancer (GC) is among the most common and deadliest cancers globally. Many long non-coding RNAs (lncRNAs) are key regulators of GC pathogenesis. This study aimed to define the role of HOXA-AS3 in this oncogenic context. METHODS: Levels of HOXA-AS3 expression in GC were quantified via qPCR. The effects of HOXA-AS3 knockdown on GC cells function were evaluated in vitro using colony formation assays, wound healing assays and transwell assays. Subcutaneous xenograft and tail vein injection tumor model systems were generated in nude mice to assess the effects of this lncRNA in vivo. The localization of HOXA-AS3 within cells was confirmed by subcellular fractionation, and predicted microRNA (miRNA) targets of this lncRNA and its ability to modulate downstream NF-κB signaling in GC cells were evaluated via luciferase-reporter assays, immunofluorescent staining, and western blotting. RESULTS: GC cells and tissues exhibited significant HOXA-AS3 upregulation (P < 0.05), and the levels of this lncRNA were found to be correlated with tumor size, lymph node status, invasion depth, and Helicobacter pylori infection status. Knocking down HOXA-AS3 disrupted GC cell proliferation, migration, and invasion in vitro and tumor metastasis in vivo. At a mechanistic level, we found that HOXA-AS3 was able to sequester miR-29a-3p, thereby regulating the expression of LTßR and modulating NF-κB signaling in GC. CONCLUSION: HOXA-AS3/miR-29a-3p/LTßR/NF-κB regulatory axis contributes to the progression of GC, thereby offering novel target for the prognosis and treatment of GC.

Expression of Fatty Acid-Binding Protein-3 in Gastrointestinal Stromal Tumors and Its Significance for Prognosis.

BACKGROUND: FABP3 is a member of the fatty acid-binding protein (FABP) family, whose role in various cancers has been reported in the past. However, little is known about the role that FABP3 plays in gastrointestinal stromal tumors (GISTs). METHODS: FABP3 expression was analyzed in 119 patients with GISTs using immunohistochemistry and tissue microarrays to interrogate the relationship between expression and prognosis. Kaplan-Meier analysis was used to calculate patient survival rates using complete follow-up data and to evaluate the potential prognostic value of FABP3 using Cox regression analysis. RESULTS: FABP3-positive signals were detected as brown particles located in the cytoplasm using immunohistochemistry. Among the 119 tissue samples, we observed high FABP3 expression in 64 and low or negative expression in 55. Immunohistochemical analyses suggested that FABP3 expression was significantly correlated with tumor size (P = 0.006), mitotic index (P = 0.016), gross classification (P = 0.048), and AFIP-Miettinen risk classification (P = 0.007). Multiple logistic regression analysis showed that the expression of FABP3 was significantly associated with tumor size (P = 0.021). Kaplan-Meier survival curves showed that patients with GISTs with low expression of FABP3 and classified with a very low to moderate AFIP-Miettinen risk had better prognosis. Multivariate analysis further showed that high expression of FABP3 (P = 0.017) was significantly associated with poor 5-year overall survival. CONCLUSIONS: High FABP3 expression has a prognostic value for patients with GISTs.

Hypertension-associated mitochondrial DNA 4401A>G mutation caused the aberrant processing of tRNAMet, all 8 tRNAs and ND6 mRNA in the light-strand transcript.

Mitochondrial tRNA processing defects were associated with human diseases but their pathophysiology remains elusively. The hypertension-associated m.4401A>G mutation resided at a spacer between mitochondrial tRNAMet and tRNAGln genes. An in vitro processing experiment revealed that the m.4401A>G mutation caused 59% and 69% decreases in the 5' end processing efficiency of tRNAGln and tRNAMet precursors, catalyzed by RNase P, respectively. Using human umbilical vein endothelial cells-derived cybrids, we demonstrated that the m.4401A>G mutation caused the decreases of all 8 tRNAs and ND6 and increases of longer and uncleaved precursors from the Light-strand transcript. Conversely, the m.4401A>G mutation yielded the reduced levels of tRNAMet level but did not change the levels of other 13 tRNAs, 12 mRNAs including ND1, 12S rRNA and 16S rRNA from the Heavy-strand transcript. These implicated the asymmetrical processing mechanisms of H-strand and L-strand polycistronic transcripts. The tRNA processing defects play the determined roles in the impairing mitochondrial translation, respiratory deficiency, diminishing membrane potential, increasing production of reactive oxygen species and altering autophagy. Furthermore, the m.4401A>G mutation altered the angiogenesis, evidenced by aberrant wound regeneration and weaken tube formation in mutant cybrids. Our findings provide new insights into the pathophysiology of hypertension arising from mitochondrial tRNA processing defects.

SOX9-activated PXN-AS1 promotes the tumorigenesis of glioblastoma by EZH2-mediated methylation of DKK1.

Increasing evidence has validated the essential regulation of long non-coding RNAs (lncRNAs) in the biological process of tumours. LncRNA PXN-AS1 has been discovered to be as a tumour suppressor in pancreatic cancer; however, its function and mechanism remain greatly unknown in glioblastoma (GBM). Our present study indicated that PXN-AS1 was highly expressed in GBM tissues and cells. Besides, the knock-down of PXN-AS1 was closely associated with the inhibitory proliferation and inducing apoptosis of GBM cells. PXN-AS1 inhibition was also found to restrain GBM tumour growth. Importantly, SOX9 functioned as a transcription factor and activated PXN-AS1 expression, and overexpressed PXN-AS1 rescued the inhibitory role of down-regulated SOX9 in GBM cell growth. Subsequently, it was discovered that PXN-AS1 activated Wnt/ß-catenin pathway. DKK1 was widely known as an inhibitor gene of Wnt/ß-catenin pathway, and its expression was negatively associated with PXN-AS1 and SOX9. Interestingly, we found that PXN-AS1 could recruit EZH2 to mediate the H3K27me3 level of DKK1 promoter. Restoration experiments manifested that DKK1 knock-down counteracted PXN-AS1 depletion-mediated repression in GBM cell growth. All facts pointed out that PXN-AS1 might be of importance in exploring the therapeutic strategies of GBM.

SNHG16/miR-605-3p/TRAF6/NF-κB feedback loop regulates hepatocellular carcinoma metastasis.

The mechanism by which miR-605-3p regulates hepatocellular carcinoma (HCC) metastasis has not been clarified. In this study, we found that miR-605-3p was down-regulated in HCC and that low miR-605-3p expression was associated with tumour thrombus and tumour satellites. HCC patients with low miR-605-3p expression showed shorter overall survival and disease-free survival after surgery. Overexpression of miR-605-3p inhibited epithelial-mesenchymal transition and metastasis of HCC through NF-κB signalling by directly inhibiting expression of TRAF6, while silencing of miR-605-3p had the opposite effect. We also found that SNHG16 directly bound to miR-605-3p as a competing endogenous RNA. Mechanistically, high expression of SNHG16 promoted binding to miR-605-3p and inhibited its activity, which led to up-regulation of TRAF6 and sustained activation of the NF-κB pathway, which in turn promoted epithelial-mesenchymal transition and metastasis of HCC. TRAF6 increased SNHG16 promoter activity by activating NF-κB, thereby promoting the transcriptional expression of SNHG16 and forming a positive feedback loop that aggravated HCC malignancy. Our findings reveal a mechanism for the sustained activation of the SNHG16/miR-605-3p/TRAF6/NF-κB feedback loop in HCC and provide a potential target for a new HCC treatment strategy.

HAX-1 promotes the migration and invasion of hepatocellular carcinoma cells through the induction of epithelial-mesenchymal transition via the NF-κB pathway.

The expression of HS-1-associated protein X-1 (HAX-1) plays a major role in the development of hepatocellular carcinoma (HCC). However, the function of HAX-1 in HCC metastasis is unclear. Quantitative real-time PCR and western blotting were used to examine HAX-1 expression in HCC cell lines with different metastatic potential, and in tumor tissues with or without intrahepatic metastasis. HCC tissue arrays (n = 144) were used to assess correlations between clinicopathological parameters and HAX-1 expression. We also examined the effect of HAX-1 on promoting HCC cell metastasis in vivo and in vitro. The results showed that the expression levels of HAX-1 were higher in metastatic HCC cell lines than in non-metastatic HCC cell lines. HAX-1 was also significantly upregulated in primary HCC tissues with intrahepatic metastasis compared with those without intrahepatic metastasis. HCC in patients with high HAX-1 expression is more likely to metastasize. HAX-1 expression was associated with malignant progression and poor prognosis, and HAX1 silencing inhibited HCC cell migration and invasion in vitro and decreased HCC cell lung metastasis in vivo, whereas HAX-1 overexpression had the inverse effect. Moreover, HAX-1 increased HCC cell metastasis by promoting the epithelial-mesenchymal transition (EMT) process. Finally, we revealed that HAX-1 modulated EMT in HCC cells by increasing NF-κB/p65 nuclear translocation. In conclusion, HAX-1 promotes HCC metastasis by EMT through activating the NF-κB pathway, suggesting that HAX-1 could be a potential therapeutic target for HCC treatment.

Rafoxanide promotes apoptosis and autophagy of gastric cancer cells by suppressing PI3K /Akt/mTOR pathway.

Rafoxanide is commonly used as anti-helminthic medicine in veterinary medicine, a main compound of salicylanilide. Previous studies have reported that rafoxanide, as an inhibitor of BRAF V600E mutant protein, inhibits the growth of colorectal cancer, multiple myeloma, and skin cancer. However, its therapeutic effect on gastric cancer (GC) and the potential mechanism has not been investigated. Here, we have found that rafoxanide inhibited the proliferation of GC cells in vitro, arrested the cell cycle in the G0/G1 phase, and promoted apoptosis and autophagy in GC cells. Treatment with specific autophagy inhibitor 3-methyladenine drastically inhibited the apoptotic cell death effect by suppressing the switch from autophagy to apoptosis. Mechanistically, we found that rafoxanide inhibited the growth of GC cells in vitro by inhibiting the activity of the PI3K/Akt/mTOR signaling pathway. This process induced autophagy, which essentially resulted in the apoptosis of GC cells. Results from subcutaneous implanted tumor models in nude mice also indicated that rafoxanide inhibited the growth of GC cells in vivo. Taken together, our findings revealed that rafoxanide inhibited the growth of GC cells both in vitro and vivo, indicating a potential drug candidate for the treatment of GC.

Anthropometric Research of Metric Characters in Zygomatic Complex Region.

OBJECTIVES: To get and analyze the metric data of zygomatic region for the plasty of zygoma. MATERIALS AND METHODS: A total of 108 dry skulls in Chinese Han population were randomly collected and measured. The metrical data were divided into 4 parts, including the relative position of contour height of zygomatic bone, the relative prominence of zygomatic bone, the relative prominence of zygomatic arch, and the angle of the zygomatic bone and arch. RESULTS: The measurements in the 4 parts showed significantly difference between male and female (P < 0.05). For relative position of contour height of zygomatic bone group, the data of male is significantly bigger than female (P < 0.05). For relative prominence of zygomatic bone/zygomatic arch group, zygoma/zygomatic arch of male significantly protruded more than female (P < 0.05). CONCLUSION: The location of male zygoma is more protruding than female. The female zygoma is squarer than male and marginal process is helpful in zygomatic plasty. CLINICAL RELEVANCE: These studies show and analyze the metric data of zygomatic region in Chinese Han population for the plasty of zygoma. These different characters between males and females could be helpful in zygomatic plasty of Chinese Han population based on this research.

High-level expression of PRSS3 correlates with metastasis and poor prognosis in patients with gastric cancer.

BACKGROUND AND OBJECTIVES: Serine protease-3 (PRSS3) is a known contributor to the genesis and development of malignant tumors, although its role in gastric cancer (GC) is still unclear. METHODS: PRSS3 expression in GC tissue samples and its relationship with clinicopathological features were analyzed. Effects of GC cellular responses to the introduction of small interfering RNA (siRNA)-mediated and short hairpin RNA (shRNA)-mediated interference with tumor PRSS3 expression were also assessed. RESULTS: PRSS3 was significantly upregulated in GC tissues, and PRSS3 protein levels were higher in tumors that developed metastases soon after the surgery compared with those that remained metastasis-free. High expression of PRSS3 was associated with tumor N staging and independently predictive of postoperative prognosis in patients with GC. The V1 variant of PRSS3 was primarily detected in GC tissue and cell lines, the others (V2-V4) being scarcely detectable. Methylation and demethylation drugs had no impact on expression levels of any PRSS3 transcriptional variant. The downregulated PRSS3 expression suppressed GC cell growth, migration, and invasion in vitro and in vivo. CONCLUSIONS: PRSS3 appears to act as an oncogene of GC. High PRSS3 expression portends postoperative metastasis, serving as an effective biomarker of poor therapeutic outcomes.

Short DNA Hairpins Compromise Recombinant Adeno-Associated Virus Genome Homogeneity.

Short hairpin (sh)RNAs delivered by recombinant adeno-associated viruses (rAAVs) are valuable tools to study gene function in vivo and a promising gene therapy platform. Our data show that incorporation of shRNA transgenes into rAAV constructs reduces vector yield and produces a population of truncated and defective genomes. We demonstrate that sequences with hairpins or hairpin-like structures drive the generation of truncated AAV genomes through a polymerase redirection mechanism during viral genome replication. Our findings reveal the importance of genomic secondary structure when optimizing viral vector designs. We also discovered that shDNAs could be adapted to act as surrogate mutant inverted terminal repeats (mTRs), sequences that were previously thought to be required for functional self-complementary AAV vectors. The use of shDNAs as artificial mTRs opens the door to engineering a new generation of AAV vectors with improved potency, genetic stability, and safety for both preclinical studies and human gene therapy.

Land Cover Classification with GF-3 Polarimetric Synthetic Aperture Radar Data by Random Forest Classifier and Fast Super-Pixel Segmentation.

Chinese Gaofen-3 (GF-3), a vital satellite for high-resolution earth observation, was the first C-band polarimetric synthetic aperture radar (SAR) launched in China with a resolution of up to one meter. Polarimetric SAR can obtain the complete physical scattering mechanisms of targets, thereby having the potential to differentiate objects. In this paper, several classification methods are briefly summarized and the types of features that should be chosen during classification are discussed. A pre-classification step is introduced to reduce the workload of precise labeling. The Random Forest classifier, which performs well for many other classification tasks, is used for the initial land cover classification. Then, based on a polarimetric constant false-alarm rate (CFAR) edge detector, a fast super-pixel generation method for polarimetric SAR image is proposed, which does not require the adjustment of parameters in advance. Following that, majority vote is conducted on the initial classification result based on the super-pixels, so that the classification result can be optimized to better meet the mapping requirements. The experimental results based on GF-3 polarimetric SAR data verify the effectiveness of proposed procedure and demonstrate that GF-3 data has excellent performance in land cover classification.

Different effects of neuropeptide Y on proliferation of vascular smooth muscle cells via regulation of Geminin.

The proliferation-promoting effect of neuropeptide Y (NPY) always functions in low-serum-cultured vascular smooth muscle cells (VSMCs), and the phenotypic switch of VSMCs is regulated by concentrations of serum. Whether the property of the NPY proliferative effect in VSMCs relies on phenotype of VSMCs is unclear. We aimed to explore the role of NPY on proliferation of different VSMC phenotypes in the pathogenesis of atherosclerosis. By stimulating A10 cells with 200 nM NPY in 0.5 or 10% serum, 3H-thymidine and 5-ethynyl-2'-deoxyuridine (EdU) and CCK8 measurements were used to detect VSMC proliferation. RT-PCR and Flow cytometry were performed to detect the factors involved in different properties of the NPY proliferative effect in VSMCs. Instead of facilitating proliferation, NPY had no significant effect on the growth of VSMCs when cultured in 10% serum (VSMCs stayed at synthetic states). The underlying mechanism may be involved in down-regulation of Y1 receptor (P < 0.05 vs. Vehicle) and up-regulation of Geminin (P < 0.05 vs. Vehicle) in 10% serum-cultured VSMCs co-incubated with 200 nM NPY. Besides, modulation of Geminin was effectively blocked by the Y1 receptor antagonist. The stimulation of NPY on proliferation of VSMCs could be a double-edged sword in the development of atherosclerosis and thus provides new knowledge for therapy of atherosclerosis.

The value of serum RASSF10 hypermethylation as a diagnostic and prognostic tool for gastric cancer.

The tumor-suppressing role of Ras-association domain family 10 (RASSF10) has been described in several types of cancers. Here, we evaluated the potential use of the hypermethylation status of the RASSF10 promoter in serum as a new diagnostic and prognostic tool in gastric cancer (GC). We used bisulfite sequencing polymerase chain reaction to examine RASSF10 methylation levels in serum and/or tumor samples from 82 GC, 45 chronic atrophic gastritis (CAG), and 50 healthy control patients. In the serum of GC patients, the median level of RASSF10 methylation was higher at 47.84 % than those in the serum of CAG and healthy control patients at 11.89 and 11.35 %, respectively. The median level of RASSF10 methylation in GC tumor tissue was similarly high at 62.70 %. Furthermore, RASSF10 methylation levels were highly correlated between paired serum and tumor samples from GC patients. We performed receiver-operating characteristic curve analyses to verify that serum RASSF10 methylation levels could effectively distinguish GC from control patients. Moreover, multivariate analyses showed that high serum RASSF10 methylation levels in GC patients were associated with large tumors, lymph node metastasis, and high carcinoembryonic antigen (CEA) levels. Survival analyses showed that GC patients with high serum RASSF10 methylation levels had shorter overall and disease-free survival after D2 lymphadenectomy than those with low levels. High serum RASSF10 methylation levels were also an independent predictor of tumor recurrence and GC patient survival. In conclusion, serum RASSF10 promoter methylation levels can serve as a valuable indicator for the diagnosis and prognosis of GC in the clinic.

Low expression of fibulin-1 correlates with unfavorable prognosis in gastric cancer.

The tumor-suppressing role of fibulin-1 has been described in several types of cancers. However, the expression and role of fibulin-1 in the development and progression of gastric cancer (GC) remain largely unknown. In this study, RT-PCR and immunochemistry were used to detect the fibulin-1 expression in GC samples. We have found that the fibulin-1 protein and mRNA levels were downregulated in GC. When investigating the correlation between fibulin-1 expression and clinicopathological characteristics, we have found that low fibulin-1 protein expression was associated with poor tumor differentiation and advanced N stage. Low fibulin-1 protein expression was also an independent prognostic factor for patient survival. To clarify the reason of fibulin-1 downregulation in GC, the mRNA expression and methylation status of fibulin-1 were examined in GC fresh tissue samples (n = 36). We found that the transcriptional expression of fibulin-1 was negatively associated with fibulin-1 promoter hypermethylation, and fibulin-1 hypermethylation was associated with Helicobacter pylori infection. Finally, the effects of fibulin-1 overexpression on cell proliferation and apoptosis were examined. We have found that fibulin-1 overexpression suppressed the growth of GC both in vitro and in vivo and induced apoptosis by increasing cleaved caspase-3 expression. In conclusion, fibulin-1 acts as a tumor suppressor gene, is frequently hypermethylated in GC, and can potentially serve as a useful biomarker for patient prognosis.

PDGFR-ß-activated ACK1-AKT signaling promotes glioma tumorigenesis.

Aberrant PDGF-PDGFR signaling and its effects on downstream effectors have been implicated in glioma development. A crucial AKT regulator, ACK1 (TNK2) has been shown to be a downstream mediator of PDGF signaling; however, the exact underlying mechanisms in gliomas remain elusive. Here, we report that in glioma cells, PDGFR-ß activation enhanced the interaction between ACK1 and AKT, resulting in AKT activation. PDGF treatment consistently promoted the formation of complexes containing PDGFR-ß and ACK1. Mutational analysis suggested that Y635 of ACK1 is a PDGFR-ß phosphorylation site and that the ACK1 Y635F mutant abrogated the sequential activation of AKT. Moreover, PDK1 interacted with ACK1 during PDGF stimulation, which is required for the binding of ACK1 to PDGFR-ß. Further mutational analysis showed that T325 of ACK1 was crucial for the ACK1 and PDK1 interaction. ACK1 Y635F or T325A mutants abolished PDGFR-ß-induced AKT activation, the subsequent nuclear translocation of ß-catenin and the expression of cyclin D1. Glioma cell cycle progression, proliferation and tumorigenesis were accordingly blocked by ACK1 Y635F or T325A. In glioblastoma multiforme samples from 51 patients, increased ACK1 tyrosine phosphorylation correlated with upregulated PDGFR-ß activity and AKT activation. Taken together, our data demonstrate that ACK1 plays a pivotal role in PDGF-PDGFR-induced AKT signaling in glioma tumorigenesis. This knowledge contributes to our understanding of glioma progression and may facilitate the identification of novel therapeutic targets for future glioma treatment.

Acute Effects of Haloperidol, Amisulpride, and Quetiapine on Bone Turnover Markers in Patients With Schizophrenia.

OBJECTIVE: This prospective study sought to compare the acute effects of haloperidol, amisulpride, and quetiapine on serum markers of bone formation and resorption in relatively young patients with minimal previous exposure to antipsychotic drugs. METHODS: Patients included in the study were randomly assigned to receive haloperidol, amisulpride, or quetiapine monotherapy in an open-label manner. Serum osteocalcin (OC, a marker of bone formation), C-terminal peptide of type I collagen (CTX, a marker of bone resorption), prolactin (PRL), estradiol, and testosterone were measured in 70 patients at baseline and after 4 weeks of antipsychotic treatment. RESULTS: A repeated-measures analysis of variance revealed a significant difference in CTX levels and in the OC to CTX ratio between treatment groups (F = 4.481, P < 0.05; F = 8.114, P < 0.01). After 4 weeks of treatment, only the amisulpride group had significantly increased CTX levels and decreased OC/CTX. In addition, an obvious increase in PRL level and a reduction of sex hormone secretion after amisulpride treatment were found. No significant changes in bone turnover were observed in the haloperidol or quetiapine groups. Notably, a positive correlation between the CTX change to the change in PRL after treatment (r = 0.255, P < 0.05) was observed. CONCLUSIONS: The PRL-raising antipsychotic drug amisulpride influenced bone turnover balance very early in the course of treatment, which may require long-term monitoring of bone metabolism. Bone resorption marker changes induced by acute antipsychotic drug treatment are likely related to increased PRL levels.

Effectiveness of Lactobacillus reuteri in infantile colic and colicky induced maternal depression: a prospective single blind randomized trial.

Infant colic, excessive crying of unknown cause, is a major burden to families and effects about 10-30 % of infants. Despite decades of research, the exact cause and treatment of infant colic has remained elusive. The use of Lactobacillus reuteri (DSM 17938) in infant colic is somewhat controversial and hence, we designed this study to evaluate its efficacy in infantile colic. We recruited predominantly or exclusively breastfed infants, aged less than 4 months in a placebo controlled observational randomized study. Participants' were assigned to receive L. reuteri at a dose 10(8) colony forming units (n = 21) and placebo (n = 21). Placebo was an identical formulation without live micro-organisms. Treatment was given to subjects for 21 days and they were followed for 4 weeks. Treatment success (primary outcome), daily reduction in crying time, parent satisfaction and reduction in maternal depression (secondary outcomes) were assessed at the end of study period. Treatment success was observed in all infants (100 %) of the probiotic group while it was seen in 15.7 % of the placebo group. Mean daily crying time was more significantly reduced to 32.1 ± 8.3 min/day (P < 0.01) from 200.9 ± 6.3 min/day in the probiotic group as compared to the placebo group (120.6 ± 20.0 min/day). Moreover, throughout the study period, parent's satisfaction and improvement in maternal depression (Edinburgh postnatal depression scale) was also significantly higher in the probiotic group. In our study population, reduction in crying time was significant (P < 0.01) even during first week of initiation of therapy. We conclude that L. reuteri (DSM 17938) reduces daily crying time and maternal depression during infantile colic. We suggest L. reuteri may be a safe and efficacious option for reducing infant colic.

Analysis of poly-ß-hydroxyalkonates (PHA) during the enhanced biological phosphorus removal process using FTIR spectroscopy.

Enhanced biological phosphorus removal (EBPR) is the main phosphorus removal technique for wastewater treatment. During the anaerobic-aerobic alternative process, the activated sludge experienced the anaerobic storage of polyhydroxy-ß-alkonates (PHA) and aerobic degradation, corresponding the infrared peak intensity of sludge at 1 740 cm(-1) increased in the aerobic phase and declined in the anaerobic phase. Compared with PHA standard, this peak was indentified to attribute the carbonyl of PHA. The overlapping peaks of PHA, protein I and II bands were separated using Gaussian peak fitting method. The infrared peak area ratios of PHA versus protein I had a good relationship with the PHA contents measured by gas chromatography, and the correlation coefficient was 0.873. Thus, the ratio of the peak area of PHA versus protein I can be considered as the indicator of the PHA content in the sludge. The infrared spectra of 1 480-1 780 cm(-1) was selected, normalized and transferred to the absorption data. Combined with the chromatography analysis of PHA content in the sludge sample, a model between the Fourier-transform infrared spectroscopy (ETIR) spectra of the sludge and PHA content was established, which could be used for the prediction of the PHA content in the unknown sample. The PHA content in the sludge sample could be acquired by the infrared spectra of the sludge sample and the established model, and the values fitted well with the results obtained from chromatograph. The results would provide a novel analysis method for the rapid characterization and quantitative determination of the intracellular PHA content in the activated sludge.