Modified Trisection Technique: One-Trip Explantation for Foldable Intraocular Lens.

PURPOSE: We present a new technique that allows an intraocular lens to be explanted through the small incisions used in modern cataract surgery. METHODS AND RESULTS: The intraocular lens optic is cut into three connected pieces at the 1-mm-wide end with scissors. Then, with the stabilizing counterforce provided by a pair of vitreoretinal forceps through a paracentesis, the middle piece is removed first, followed by the two side pieces connected with haptics flipped over at the connected part. These two parts overlap each other when passing through the incision, eventually resulting in the explantation of the intraocular lens, as an intact piece. CONCLUSION: We believe this method provides a simple and effective way to remove intraocular lens through very small incisions, which could also reduce complications and hasten patient's recovery.

Mesenchymal stem cells alleviate AQP-4-dependent glymphatic dysfunction and improve brain distribution of antisense oligonucleotides in BACHD mice.

Huntington's disease (HD) is a neurodegenerative disorder caused by a mutation in the huntingtin (HTT) gene that results in the production of neurotoxic mutant HTT (mHTT) protein. Suppressing HTT production with antisense oligonucleotides (ASOs) is a promising treatment strategy for HD; however, the difficulty of delivering ASOs to deep brain structures is a major barrier for its clinical application. The glymphatic system of astrocytes involving aquaporin 4 (AQP-4) controls the entry of macromolecules from the cerebrospinal fluid into the brain. Mesenchymal stem cells (MSCs) target astrocytes to inhibit neuroinflammation. Here we examined the glymphatic distribution of ASO in the brain and the therapeutic potential of combining intravenously injection of mesenchymal stem cells (IV-MSC) and ASOs for the treatment of HD. Our results show that Cy3-labeled ASOs entered the brain parenchyma via the perivascular space following cisternal injection, but the brain distribution was significantly lower in AQP-4-/- as compared with wild-type mice. Downregulation of the AQP-4 M23 isoform was accompanied by decreased brain levels of ASOs in BACHD mice as well as an increase in astrogliosis and phosphorylation of nuclear factor κB (NF-κB) p65. IV-MSC treatment restored AQP-4 M23 expression, attenuated astrogliosis, and decreased NF-κB p65 phosphorylation; it also increased the brain distribution of ASOs and enhanced the suppression of mHTT in BACHD mice. These results suggest that modulating glymphatic activity using IV-MSC is a novel strategy for improving the potency of ASO in the treatment of HD.

Omega-3 polyunsaturated fatty acids promote amyloid-ß clearance from the brain through mediating the function of the glymphatic system.

Impairment of amyloid-ß (Aß) clearance leads to Aß accumulation in the brain during the development of Alzheimer's disease (AD). Strategies that can restore or improve the clearance function hold great promise in delaying or preventing the onset of AD. Here, we show that n-3 polyunsaturated fatty acids (PUFAs), by use of fat-1 transgenic mice and oral administration of fish oil, significantly promote interstitial Aß clearance from the brain and resist Aß injury. Such beneficial effects were abolished in Aqp4-knockout mice, suggesting that the AQP4-dependent glymphatic system is actively involved in the promoting the effects of n-3 PUFAs on the clearance of extracellular Aß. Imaging on clarified brain tissues clearly displayed that n-3 PUFAs markedly inhibit the activation of astrocytes and protect the AQP4 polarization in the affected brain region after Aß injection. The results of the present study prove a novel mechanism by which n-3 PUFAs exert protective roles in reducing Aß accumulation via mediating the glymphatic system function.-Ren, H., Luo, C., Feng, Y., Yao, X., Shi, Z., Liang, F., Kang, J. X., Wan, J.-B., Pei, Z., Su, H. Omega-3 polyunsaturated fatty acids promote amyloid-ß clearance from the brain through mediating the function of the glymphatic system.

Rifampicin attenuates experimental autoimmune encephalomyelitis by inhibiting pathogenic Th17 cells responses.

Rifampicin, a broad-spectrum antibiotic, has neuroprotective, immunosuppressive, and anti-inflammatory properties. However, the effect of rifampicin on autoimmune disorders of the nervous system is not clear. In this study, we investigated whether rifampicin was beneficial to myelin oligodendrocyte glycoprotein peptide (MOG33-35 )-induced female C57BL/6 experimental autoimmune encephalomyelitis (EAE) mice, the well-established animal model of multiple sclerosis. Rifampicin treatment (daily from the first day after EAE immunization) remarkably attenuated clinical signs and loss of body weight, which are associated with suppression of inflammatory infiltration and demyelination in spinal cords of EAE mice. Furthermore, rifampicin dramatically reduced the disruption of blood-brain barrier integrity, down-regulated serum concentration of IL-6 and IL-17A, inhibited pathological Th17 cell differentiation, and modulated the expression of p-STAT3 and p-p65. These results suggest that rifampicin is effective for attenuating the clinical severity of EAE mice, which may be related to its inhibitive ability in differentiation of Th17 cell and secretion of its key effector molecule IL-17A via regulation of excessive activation of the key signaling molecules of JAK/STAT pathway. Our findings may be helpful for developing therapeutic and preventive strategies for multiple sclerosis.

Exploring the mechanism of bioactive components of Prunella vulgaris L. in treating hepatocellular carcinoma based on network pharmacology.

In traditional Chinese Medicine, Prunella vulgaris L. (PVL) is potentially effective in the treatment of some human malignancies including hepatocellular carcinoma (HCC). However, the detailed mechanism of action remains unclear. The purpose of this study was to decipher the constitutes of the bioactive ingredients of PVL, and its mechanism against HCC using network pharmacology and in vitro experiments. The bioactive components of PVL were obtained by Traditional Chinese Medicine System Pharmacology Database and Analysis platform database, and the targets of bioactive components of PVL was investigated by Swiss Target Prediction database. HCC related targets were obtained from GEO database, GeneCards database and DisGeNET database, and the gene ontology function annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were conducted for annotating the biological function of gene targets. A protein-protein interaction network was constructed using STRING database. Molecular docking of key bioactive ingredients was performed using AutoDock Vina. Cell proliferation and apoptosis were detected by cell counting kit-8 and flow cytometry, respectively. The expression level of the target genes of PI3K/Akt pathway were detected by qPCR. In the present work, 11 bioactive components of PVL were screened out, which acted on 177 potential targets. In addition, 13,517 genes were strongly associated with HCC pathogenesis, of which 158 targets are overlapped with PVL's targets. KEGG results identified 39 signaling pathways closely associated with the 158 targets. Molecular docking showed that the main bioactive components of PVL, kaempferol, morin, quercetin, luteolin, and spinasterol, had good binding activity with the core proteins in cancer biology such as AKT1, EGFR, SRC, ESR1, and PPARG. In vitro assays showed that quercetin, one of the main components of PVL extracts effectively inhibited HCC cell proliferation, and promoted apoptosis, which may be associated with PI3K/AKT signaling pathway. In summary, PVL may regulate HCC progression by regulating core targets such as AKT1, EGFR, SRC, ESR1, and PPARG, and acting on PI3K-Akt signaling pathway.

Isoniazid improves cognitive performance, clears Aß plaques, and protects dendritic synapses in APP/PS1 transgenic mice.

Background and objective: Alzheimer's disease (AD) is characterized by amyloid ß (Aß) aggregation and neuroinflammation. This study aimed to investigate the therapeutic effect of isoniazid (INH) against AD. Methods: The APP/PS1 transgenic mouse model of AD was adopted. The APP/PS1 mice received oral INH (45 mg/kg/d) for 14 days. The cognitive capability was assessed by the Morris Water Maze test. Amyloid plaques and Aß levels were determined by immunohistochemistry and ELISA assay. The dendritic spines were analyzed by DiOlistic labeling. Immunofluorescence staining was used to observe the microglia and astrocytes. Results: The Morris Water Maze test suggested that INH administration can effectively attenuate the reference memory deficit and improve the working memory of the APP/PS1 mice compared to the untreated mice (all p < 0.001). INH significantly decreased the Aß plaques in the hippocampus and cortex and reduced the levels of Aß1-40 and Aß1-42 in the brain homogenates, cerebrospinal fluid, and serum (all p < 0.001). INH also inhibited enzyme activities of ß-site amyloid precursor protein cleaving enzyme 1 (BACE1, p < 0.05) and monoamine oxidase B (Mao-b, p < 0.01). INH significantly increased the protrusion density in the hippocampus (p < 0.01). Immunofluorescence staining revealed that INH significantly reduced the number of activated microglia and astrocytes around the Aß plaques (both p < 0.01). Conclusion: Isoniazid administration effectively improved cognitive performance, cleared Aß plaques, protected dendritic synapses, and reduced innate immune cells around the Aß plaques, suggesting that INH could be a potential drug for AD treatment.

Application of delayed extubation for the free-flap reconstruction of oral and maxillofacial defects in patient with oral diseases.

Tracheostomy and delayed extubation (DE) are two methods for managing patients' airways postoperatively after oral and maxillofacial free flap transplantation. We aimed to determine the safety of both the tracheostomy and DE by conducting a retrospective study in patients undergoing oral and maxillofacial free-flap transfer from September, 2017 to September, 2022. The primary outcome was incidence of postoperative complication. Secondary outcome was measured as factors leading to perioperative performance of airway management. Ninety-five of 148 patients received delayed extubation perioperatively. In comparison to the tracheostomy group, the DE group had fewer overall postoperative complications (p = 0.028). During the postoperative period, fewer patients from the DE group required a return to the operating room, in comparison to those from the tracheostomy group (p = 0.045). The duration of surgery (p = 0.006), time in ICU (p = 0.015), duration of artificial nutrition (p < 0.001), duration of hospitalization (p < 0.001) in the DE group were all significantly shorter when compared with the tracheostomy group. In conclusion, when used in appropriate cases of oral and maxillofacial free flap transplantation patients, delayed extubation can be a safe and effective alternative to tracheostomy.

Feasibility of Imaging-Based Quantitative Hepatic Function Assessment: Gd-EOB-DTPA-Enhanced Liver MR Imaging Combined with T1 Mapping.

OBJECTIVE: to investigate the feasibility of gadoxetic acid (Gd-EOB-DTPA) enhanced MRI combined with T1 mapping in quantitative hepatic function assessment. METHODS: this study retrospectively enrolled 94 patients with Gd-EOB-DTPA enhanced MRI combined with T1 mapping, divided into group A (grade A, n=73), group B (grade B, n=14) and group C (grade C, n=7) based on Child-Pugh classification. Liver T1 relaxation times on plain scan (T1P) and hepatocellular phase (T1E) were measured. Decrease in T1 (T1D) and the percentage of decrease in T1 (T1D%) were calculated as follows: T1D=T1P-T1E, T1D%= T1D/T1P×100%. The relationship between T1P, T1E, T1D, T1D% and liver function classification was analyzed. RESULTS: T1P, T1D, and T1D% in group A were significantly higher than those of group B and C. T1E in group A was lower than those of group B and C. T1D% was significantly different between group B and C. There was no significant difference in T1P, T1E, T1D between groups B and C. T1E was positively correlated with liver function levels, T1P and T1D had a negative correlation with liver function levels. T1P, T1E, T1D, T1D% were significantly different between cirrhotic and non-cirrhotic groups. T1D% of less than 70% suggests liver dysfunction. CONCLUSION: Gd-EOB-DTPA enhanced liver MRI combined with T1 mapping is feasible for quantitative assessment of hepatic function.

Normative value of hyperopia reserve and myopic shift in Chinese children and adolescents aged 3-16 years.

BACKGROUND: This research aims to generate normative values of hyperopia reserve and refractive progression as effective tools to estimate the risk of myopia. METHODS: A 1-year follow-up study was conducted among Chinese children and adolescents aged 3-16 years selected from schools and kinder gardens using cluster sampling. All participants underwent examinations including visual acuity, axial length and cycloplegic autorefraction (1% cyclopentolate). Percentiles of spherical equivalent (SE) were calculated using Lambda-Mu-Sigma (LMS) method. Age-specific refractive progression and hyperopia reserve were determined by backward calculation. RESULTS: Of 3118 participants, 1702 (54.6%) were boys with a mean baseline age of 7.30 years. The 50th percentile of SE estimated by LMS decreased from 1.04 D at 3 years to -2.04 D at 16 years in boys, while from 1.29 D to -2.81 D in girls. The 1-year refractive progression of myopes (0.81 D) was greater than that of non-myopes (0.51 D). The normative value of hyperopia reserve was 2.64 (range: 2.40 D-2.88 D) at 3 years and -0.35 (range: -0.50 to -0.17) D at 16 years, with the maximum progression of 0.35 D at the age of 6 years. CONCLUSION: Age-specific normative values of hyperopia reserve and yearly myopic shift in children and adolescents aged 3-16 years were provided, helping identify and monitor myopia and giving prevention in advance.

Associations between dysbiosis gut microbiota and changes of neurotransmitters and short-chain fatty acids in valproic acid model rats.

Introduction: The microbiota-gut-brain axis plays an important role in the pathophysiology of autism spectrum disorder, but its specific mechanisms remain unclear. This study aimed to explore the associations of changes in neurotransmitters and short-chain fatty acids with alterations in gut microbiota in valproic acid model rats. Methods: The autism model rats were established by prenatal exposure to valproic acid (VPA). The Morris water maze test, open field test, and three-chamber test were conducted to assess the behaviors of rats. 16S rRNA gene sequences extracted from fecal samples were used to assess the gut microbial composition. Gas and liquid chromatography-mass spectroscopy was used to identify short-chain fatty acids in fecal samples and neurotransmitters in the prefrontal cortex (PFC). Results: The results showed that 28 bacterial taxa between valproic acid model rats and control rats were identified, and the most differential bacterial taxa in valproic acid model rats and control rats belonged to metagenomic species and Lactobacillus intestinalis. Acetic acid, butyric acid, valeric acid, isobutyric acid, and isovaleric acid were significantly decreased in the valproic acid model rats compared to those in control rats. Five neurotransmitters (threonine, kynurenine, tryptophan, 5-hydroxyindoleacetic acid, denoted as 5-HIAA, and betaine aldehyde chloride, denoted as BAC) were significantly decreased, whereas betaine was increased in the prefrontal cortex of valproic acid model rats compared to control rats. A variety of neurotransmitters (≥4) were correlated with Pseudomonas, Collisella, and Streptococcus at the genus level, and they were also related to the decrease of short-chain fatty acids. Discussion: According to this study, we can preliminarily infer that gut microbiota or their metabolic productions (such as SCFAs) may influence central neurotransmitter metabolism through related pathways of the gut-brain axis. These results provide microbial and short-chain fatty acid (SCFA) frameworks for understanding the role of the microbiota-gut-brain axis in autism spectrum disorder and shed new light on autism spectrum disorder treatment.

Efficacy of repetitive transcranial magnetic stimulation on chronic migraine: A meta-analysis.

Introduction: Migraine is a neurovascular disorder that affects the quality of life of more than 1 billion people worldwide. Repetitive transcranial magnetic stimulation (rTMS) is a neuromodulation tool that uses pulsed magnetic fields to modulate the cerebral cortex. This meta-analysis ascertained the therapeutic or preventive effect of rTMS on chronic migraine. Methods: We performed a database search of PubMed, Web of Science, Embase, and the Cochrane Library from January 2004 to December 2021. Eligible studies included randomized controlled studies of the analgesic effects of rTMS in patients with chronic migraine. Results: Eight studies were included. Random effects analysis showed an effect size of -1.13 [95% confidence interval (CI): -1.69 to -0.58] on the frequency of migraine attacks, indicating that rTMS was more effective for decreasing migraine attacks than the sham rTMS. Conclusions: The meta-analysis revealed that rTMS is an effective approach for reducing migraine attack when the dorsolateral prefrontal cortex was stimulated. However, rTMS may not be suggested as a method to reduce the pain level. Systematic review registration: http://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42021228344.

ß-Patchoulene represses hypoxia-induced proliferation and epithelial-mesenchymal transition of liver cancer cells.

Hepatocellular carcinoma (HCC) is a malignant tumor originating from liver epithelial cells with a high clinical mortality rate. ß-Patchoulene (ß-PAE) is a compound extracted from patchouli, which has analgesic, anti-inflammatory and antioxidant effects. This research aims to probe the impacts of ß-PAE on hypoxia-induced HCC cell proliferation and epithelial-mesenchymal transition (EMT). Firstly, hypoxic injury models were constructed in HCC Huh-7 and MHCC97 cells, and the hypoxic injury cell models were then treated with different concentrations of ß-PAE. The cell viability, proliferation, migration, invasion and apoptosis were checked by the cell counting kit-8 (CCK-8) assay, colony formation assay, Transwell assay, flow cytometry and terminal deoxyribonucleotide transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay. The expression of Survivin protein, EMT markers and the NF-κB/HIF-1α pathway was gauged by Western blot (WB) or cellular immunofluorescence or reverse transcription-polymerase chain reaction (RT-PCR). The in-vivo experiment was conducted to confirm the anti-tumor role of ß-PAE. As a result, ß-PAE abated hypoxia-induced HCC cell growth, proliferation, migration, invasion and EMT and facilitated apoptosis in vitro and in vivo dose-dependently. Further mechanism studies displayed that ß-PAE inactivated the NF-κB/HIF-1α pathway, and HIF-1α activation significantly reversed the ß-PAE-mediated tumor inhibition. ß-PAE repressed the proliferation and EMT of hypoxia-induced HCC cells by choking the NF-κB/HIF-1α pathway, suggesting that ß-PAE was a potential drug for HCC treatment.

Early stage transplantation of bone marrow cells markedly ameliorates copper metabolism and restores liver function in a mouse model of Wilson disease.

BACKGROUND: Recent studies have demonstrated that normal bone marrow (BM) cells transplantation can correct liver injury in a mouse model of Wilson disease (WD). However, it still remains unknown when BM cells transplantation should be administered. The aim of this study was to investigate the potential impact of normal BM cells transplantation at different stages of WD to correct liver injury in toxic milk (tx) mice. METHODS: Recipient tx mice were sublethally irradiated (5 Gy) prior to transplantation. The congenic wild-type (DL) BM cells labeled with CM-DiI were transplanted via caudal vein injection into tx mice at the early (2 months of age) or late stage (5 months of age) of WD. The same volume of saline or tx BM cells were injected as controls. The DL donor cell population, copper concentration, serum ceruloplasmin oxidase activity and aspartate aminotransferase (AST) levels in the various groups were evaluated at 1, 4, 8 and 12 weeks post-transplant, respectively. RESULTS: The DL BM cells population was observed from 1 to 12 weeks and peaked by the 4th week in the recipient liver after transplantation. DL BM cells transplantation during the early stage significantly corrected copper accumulation, AST across the observed time points and serum ceruloplasmin oxidase activity through 8 to 12 weeks in tx mice compared with those treated with saline or tx BM cells (all P < 0.05). In contrast, BM cells transplantation during the late stage only corrected AST levels from 4 to 12 weeks post-transplant and copper accumulation at 12 weeks post-transplant (all P < 0.05). No significant difference was found between the saline and tx BM cells transplantation groups across the observed time points (P > 0.05). CONCLUSIONS: Early stage transplantation of normal BM cells is better than late stage transplantation in correcting liver function and copper metabolism in a mouse model of WD.

Mycobacteria infection in incomplete transverse myelitis is refractory to steroids: a pilot study.

Incomplete transverse myelitis (ITM) of unknown origin is associated with high rates of morbidity and mortality. This prospective, open-label study was undertaken to determine whether antituberculous treatment (ATT) might help patients with ITM whose condition continues to deteriorate despite receiving IV methylprednisolone treatment. The study consisted of 67 patients with steroid-refractory ITM in whom Mycobacterium tuberculosis (MTB) was suspected clinically and in whom other known causes of myelopathy were excluded. The study occurred from January 2003 to June 2010. Patients underwent trial chemotherapy with ATT. Efficacy was assessed by the American Spinal Injury Association (ASIA) scoring system, the Barthel Index (BI) and the Hauser Ambulation Index (AI) at baseline, 12 months, and 24 months, using magnetic resonance imaging (MRI). Of the 67 patients enrolled, 51 were assessed and 16 withdrew. At 24 months, 49 patients experienced benefits as indicated by significantly increased ASIA and BI scores. The Hauser AI index also improved with markedly decreased abnormal signals in spinal cord MRI over time. The results from this prospective study provide beneficial clinical and MRI data on the efficacy of ATT in ITM patients and suggests mycobacteria may be an important and neglected cause of myelitis.

LncRNA DARS-AS1 aggravates the growth and metastasis of hepatocellular carcinoma via regulating the miR-3200-5p-Cytoskeleton associated protein 2 (CKAP2) axis.

Accumulating signs have found that long noncoding RNAs (lncRNAs) contribute to hepatocellular carcinoma (HCC). Here, we probed the effect and mechanism of lncRNA DARS-AS1 in HCC. The profiles of DARS-AS1 and Cytoskeleton associated protein 2 (CKAP2) in 50 HCC tissues and non-tumor tissues were examined by real-time quantitative polymerase chain reaction (RT-qPCR). DARS-AS1 and CKAP2 overexpression and/or knockdown cell models were established. The proliferation, apoptosis, invasion and epithelial-mesenchymal transition (EMT) were determined. CKAP2, and focal adhesion kinase (FAK)-extracellular signal-regulated kinase (ERK) was tested by Western blot (WB). The relationship between DARS-AS1 and CKAP2 was predicted by Bioinformatics, and the dual-luciferase reporter assay was applied to verify the targeting association between miR-3200-5p and DARS-AS1 and CKAP2. DARS-AS1 was overexpressed in HCC tissues (vs. that in non-tumor tissues) and was closely correlated with the patients' tumor stage. DARS-AS1 facilitated HCC cell proliferation and hampered apoptosis. HCC cell migration and EMT were enhanced by DARS-AS1. DARS-AS1 up-regulated CKAP2, which aggravated HCC. Further investigation illustrated that either DARS-AS1 or CKAP2 activated FAK-ERK pathway, and miR-3200-5p was competitively restrained by DARS-AS1. miR-3200-5p exerted tumor-suppressive effects in HCC and inactivated CKAP2 and FAK-ERK pathway. All in all, this study corroborates that DARS-AS1 facilitates HCC proliferation and metastasis by regulating miR-3200-5p-mediated CKAP2, which provides a potential target for HCC diagnosis and treatment.Abbreviations: CCK-8: cell counting kit-8; CKAP2: Cytoskeleton associated protein 2; cDNA:complementary DNA; DAPI: 4',6-diamidino-2-phenylindole; DARS-AS1: DARS1 antisense RNA 1; DEPC: diethyl pyrocarbonate; DMEM-F12: Dulbecco's minimal essential medium/Ham's-F12; EMT: epithelial-mesenchymal transition; ERK: extracellular signal-regulated kinase; FAK: focal adhesion kinase; FBS: fetal bovine serum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HCC: hepatocellular carcinoma; HE: hematoxylin-eosin; IHC: Immunohistochemistry; LIHC: Liver hepatocellular carcinoma; lncRNAs: long noncoding RNAs; MIAT: lncRNA myocardial infarction-related transcripts; MT: Mutant; NC: negative control; PBS: phosphate-buffered saline; PMSF: Phenylmethylsulfonyl fluoride; PVDF: polyvinylidene difluoride; RT: room temperature; RT-qPCR: real-time quantitative polymerase chain reaction; SDS-PAGE: sodium dodecyl sulfate-polyacrylamide gel electrophoresis; SPF: specific pathogen-free; TMAP: tumor-associated microtubule-associated protein; TUNEL: TdT-mediated dUTP nick end labeling; V: volume; WT: wild type.

Cloning and characterization of a sucrose synthase-encoding gene from muskmelon.

A full-length cDNA clone encoding sucrose synthase (SS; EC 2.4.1.13) was isolated from muskmelon (Cucumis melo L.) by RT-PCR and RACE. The clone, designated as CmSS1, contains 2,585 nucleotides with an open reading frame of 2,412 nucleotides. The deduced 804 amino acid sequence showed high identities with other plant sucrose synthase. Real time PCR analysis indicated that CmSS1 expression differed among root, stem, leaf, flower and fruit tissues. The analysis during fruit development indicated that CmSS1 mRNA showed its maximum level at 5 days after pollination (DAP) and decreased gradually during fruit development until its minimum level in mature fruit. The sucrose content was very low in fruit before 20 DAP but increased dramatically between 20 and 30 DAP during fruit development. However, SS activities in both direction of sucrose synthesis and sucrose cleavage were very low and changed little during fruit development, suggesting that SS may play little role in determining sucrose accumulation during muskmelon fruit.

[Study of copper metabolism and liver damage in TX Mice-an animal model for liver disease].

OBJECTIVE: To provide right time points in selection of right aged animals and the normal physiological data of TX mice. METHODS: 7-12 months old TX and DL mice were studied, each group contained 3 female and 3 male mice of TX or DL mice. The concentration of copper in the serum, dry tissues (liver, brain and kidney), together with copper biochemistry indexes were measured. The liver histopathology was observed under light microscopy and electron microscope. RESULTS: Transaminase increased significantly only in 10 and 11-month- old (AST(TX10) = 218.3 U/L, AST(TX11) = 197.5 U/L, AST(DL10) = 171.5 U/L, AST(DL11) = 165.0 U/L, P(10) less than 0.001, P(11) = 0.022), but the copper concentration of liver, brain and kidney was significantly increased during 7-12 month old (the average concentration of copper, Liver(TX) = (750.0 +/- 85.5) mg/kg, Brain(TX) = (39.7 +/- 2.2)mg/kg, Kidney(TX) = (29.8 +/- 5.0) mg/kg, Liver(DL) = (11.6 +/- 1.5) mg/kg, Brain(DL) = (16.8 +/- 0.9) mg/kg, Kidney(DL) = (14.2 +/- 1.0) mg/kg, t = 21.16, 23.60, 7.47, for all these organs P less than 0.05). CONCLUSION: TX mice is a suitable model of liver disease with natural recovery, so selecting animal model of suitable time point is very important.

Prediction of phonon-mediated superconductivity in hole-doped black phosphorus.

We study the conventional electron-phonon mediated superconducting properties of hole-doped black phosphorus by density functional calculations and get quite a large electron-phonon coupling (EPC) constant λ ~ 1.0 with transition temperature T C ~ 10 K, which is comparable to MgB2 when holes are doped into the degenerate and nearly flat energy bands around the Fermi level. We predict that the softening of low-frequency [Formula: see text] optical mode and its phonon displacement, which breaks the lattice nonsymmorphic symmetry of gliding plane and lifts the band double degeneracy, lead to a large EPC. These factors are favorable for BCS superconductivity.

[Clinical manifestations and molecular genetics of spinal bulbar muscular atrophy: report of 5 cases].

OBJECTIVE: To study the clinical and molecular genetic characteristics of spinal bulbar muscular atrophy (SBMA). METHODS: The clinical data, including case history, physical examination, biochemical analyses of blood, EMG, and muscle biopsy, of 5 Chinese patients with SBMA, all males, aged 29 - 58, with the onset age of 36 (17 - 49), were collected the information of in 5 cases. Four patients underwent PCR to examine the number of copies of CAG repeat region in androgen receptor (AR) gene. RESULTS: The clinical characteristics of the 5 patients included atrophy of lingualis, dysarthria, weakness and waste of the limbs, especially in the hands, and elevated creatine kinase (CK), fasting glucose, testosterone, and progesterone in the blood. EMG showed denervation motor potentials in all cases. The muscle biopsy in one case showed neurogenic atrophy. The number of (CAG) n repeat in AR gene was 50 - 62 in the, remarkably from that of 13 normal controls (19 - 20) without overlapping. CONCLUSION: SBMA affects the middle age males, shows a slowly progressing muscular atrophy in spinal and bulbar muscles. The different number of (CAG) n repeat of AR gene between the SBMA patients and the normal controls may be an important identification to differentiate SBMA from other motor neuron diseases.

The Prevalence of Ocular Allergy and Comorbidities in Chinese School Children in Shanghai.

OBJECTIVE: To investigate the prevalence and features of ocular allergy (OA) and comorbidities among school children in Shanghai, China. METHODS: This was a population-based cross-sectional study. Each participant completed an ISAAC-based questionnaire. The prevalence of OA symptoms, allergic rhinitis (AR) asthma, atopic dermatitis (AD), and sensitization to mites, pollen, and food was analyzed. RESULTS: A total of 724 and 942 completed questionnaires from the 7-9-year-old (young group) and the 12-14-year-old (teen group) groups were analyzed, respectively. The overall prevalence of OA symptoms was 28%. However, more young students (10.6%) reported mild to severe daily life interference caused by OA than the teens (5.7%). The young group had higher prevalence of diagnosed allergic conjunctivitis (10.2%). The overall prevalence of AR symptom, diagnosed asthma, and diagnosed AD was 40.4%, 11.6%, and 16.7%, respectively. Young children had higher prevalence of diagnosed AR and AD than the teens. There were gender associated differences in the prevalence of AR and asthma among young children, but not among the teens. The comorbidities associated with OA was also analyzed. Sensitization to mites, food, and pollen was associated with higher prevalence of allergic conditions. CONCLUSIONS: OA together with other allergic conditions affected a significant number of children in Shanghai.