ABSTRACT
During the consumption of alkanes, Alcanivorax borkumensis will form a biofilm around an oil droplet, but the role this plays during degradation remains unclear. We identified a shift in biofilm morphology that depends on adaptation to oil consumption: Longer exposure leads to the appearance of dendritic biofilms optimized for oil consumption effected through tubulation of the interface. In situ microfluidic tracking enabled us to correlate tubulation to localized defects in the interfacial cell ordering. We demonstrate control over droplet deformation by using confinement to position defects, inducing dimpling in the droplets. We developed a model that elucidates biofilm morphology, linking tubulation to decreased interfacial tension and increased cell hydrophobicity.
Subject(s)
Alcanivoraceae , Alkanes , Biofilms , Petroleum , Alcanivoraceae/metabolism , Alkanes/metabolism , Petroleum/metabolism , Biodegradation, EnvironmentalABSTRACT
OBJECTIVE: Hysterectomy is the second most common surgery performed mainly for benign uterine pathologies in females. The association between hysterectomy and the subsequent risk of hypertension remains controversial. This study investigated the risk of developing hypertension in women who had a hysterectomy. DESIGN: Population-based retrospective cohort study. SETTING: We used the Taiwan National Health Insurance Research Database with claims data of 1 million randomly selected insured individuals. POPULATION: Women with and without hysterectomy and bilateral salpingo-oophorectomy, aged 30-49 years, were identified in 2000-2013 from the insurance data. METHODS: From the claims data, we identified 6674 women with hysterectomy without hypertension at the time of the surgery. The comparison cohort were 26 696 women randomly selected from women without hysterectomy and hypertension, matched by age and the year hysterectomy was performed. Adjusted hazard ratio (aHR) of hypertension was estimated after controlling for comorbidities. MAIN OUTCOME MEASURE: Prediction for hypertension following hysterectomy for benign disease. RESULTS: Both cohorts had a median age of 43.9 years. After a median follow up of 6.4 years, the incident hypertension was higher in the hysterectomy cohort than in the comparison cohort, with an adjusted hazard ratio (aHR) of 1.35 [95% confidence interval (CI) 1.27-1.44]. The incidence increased with age, with a higher aHR in hysterectomised women aged 40-49 years (aHR 1.37, 95% CI 1.06-1.83) than in those aged 30-39 years (aHR 1.22, 95% CI 1.02-1.46). CONCLUSION: Findings in this study suggest that women with hysterectomy are more likely to be diagnosed with hypertension in the follow-up period. TWEETABLE ABSTRACT: Women with hysterectomy before 50 years of age are at an increased risk of developing subsequent hypertension. PLAIN LANGUAGE SUMMARY: Hysterectomy is one of the most common surgeries for women with benign uterine disease. Hysterectomy may lead to a sudden decline in the production of sex hormone (estrogen and progesterone), which is responsible for vessel wall endothelial dysfunction leading to hardening of arteries and subsequent hypertension. However, the association between hysterectomy and risk of hypertension remains controversial. This study investigated whether premenopausal women have an elevated risk of hypertension after hysterectomy. This study employed the Taiwan National Health Insurance Research Database to identify 6674 women 30-49 years old who had a hysterectomy between 2000 and 2013, and a comparison group of 26 696 women who did not have a hysterectomy matched by age. Women in both the groups had no hypertension at baseline (recruiting date or within 1 year after recruiting date). By the end of 2013, we found that 1196 (17.9%) and 3613 (13.5%) women had developed hypertension in the hysterectomy and the comparison groups, respectively. The hypertension incidence was 1.4-fold greater in the hysterectomy group than in the control group (27.8 versus 20.2/1000 person-years).
Subject(s)
Hypertension/epidemiology , Hysterectomy/statistics & numerical data , Adult , Age Factors , Case-Control Studies , Female , Humans , Incidence , Middle Aged , Retrospective Studies , Risk Factors , Taiwan/epidemiologyABSTRACT
BACKGROUND: With the continuous improvement of liver transplantation technology, the survival rate of liver transplantation has been improved, but recurrent or de novo malignancy remains one of the major factors affecting the long-term survival of liver transplant recipients. CASE REPORT: A 45-year-old Chinese man had a plastic biliary stent placed on account of biliary anastomotic stenosis after 3 years of piggyback liver transplantation. He came to our hospital because of recurrent fever and jaundice for 2 weeks, and his carcinoembryonic antigen-199 had increased. The patient's duodenal papillary was cauliflower-like at endoscopic retrograde cholangiopancreatography to replace the biliary stent. He was initially suspected of having duodenal papillary carcinoma after liver transplantation. However, the pathology from endoscopic retrograde cholangiopancreatography and endoscopic ultrasound-guided biopsy showed inflammation. While awaiting the result of biopsy, his CA-199 decreased significantly after anti-infection and symptomatic treatment. The patient was diagnosed with biliary anastomotic stenosis and duodenal papillitis. He was discharged uneventfully; to date, there is no evidence of malignant tumor. CONCLUSIONS: We report this case to provide helpful information to clinicians about the management of the duodenal papilla cauliflower-like neoplasm after liver transplantation, which should be considered as inflammatory first. Perhaps our view can avoid the risk of bringing an excessive medical treatment and unnecessary economic burden to patients and their families.
Subject(s)
Ampulla of Vater , Bile Ducts/surgery , Common Bile Duct Neoplasms/etiology , Liver Transplantation/adverse effects , Postoperative Complications/etiology , Anastomosis, Surgical/adverse effects , Cholangiopancreatography, Endoscopic Retrograde , Cholestasis/etiology , Humans , Male , Middle Aged , Stents/adverse effects , Transplant RecipientsABSTRACT
Expanding real-name HIV test is the basis of the real-time reporting system in China, and it plays an important role for the progress. In year of 2003, there were 45 092 cases of HIV positives reported cumulatively, which accounted for only 5.4% of the estimated population of HIV positives. Since implementation of real-name HIV test and establishment, real-time reporting system, up to year 2005, the total of reported HIV positives was 577 000, which took up 67.9% of the estimated HIV positives. Also among reported cases, 387 000 cases have received the anti-retroviral treatment. Normalization of HIV prevention and control will pave the way to medical insurance for HIV positives. It is a goal that all the people have medical insurance in China, and the normalization is an ideal working condition, and real-name HIV test is a measure for it. The both are very closely connected and improving each anther.
Subject(s)
AIDS Serodiagnosis , Acquired Immunodeficiency Syndrome/prevention & control , HIV Infections/prevention & control , Acquired Immunodeficiency Syndrome/diagnosis , China , Communicable Diseases , HIV Infections/diagnosis , Humans , Sentinel SurveillanceABSTRACT
Doxorubicin (Dox) could trigger a large amount of apoptotic cells in the myocardium, which leads to dilated cardiomyopathy and heart failure. S-propargyl-cysteine (SPRC), a producing agent of endogenous hydrogen sulfide (H2S), possesses cardioprotective efficacy. However, the specific effect and mechanism of SPRC in Dox-induced cardiotoxicity remain elusive. Given gp130 with its main downstream signaling molecule, signal transducer and activator of transcription 3 (STAT3), is involved in cardiac myocyte survival and growth; the present study was performed to elucidate whether SPRC counteracts Dox-induced cardiotoxicity, and if so, whether the gp130/STAT3 pathway is involved in this cardioprotective activity. SPRC stimulated the activation of STAT3 via gp130-mediated transduction tunnel in vitro and in vivo. In Dox-stimulated cardiotoxicity, SPRC enhanced cell viability, restored expression of gp130/STAT3-regulated downstream genes, inhibited apoptosis and oxidative stress, and antagonized mitochondrial dysfunction and intracellular Ca(2+) overload. Intriguingly, blockade of gp130/STAT3 signaling abrogated all these beneficial capacities of SPRC. Our findings present the first piece of evidence for the therapeutic properties of SPRC in alleviating Dox cardiotoxicity, which could be attributed to the activation of gp130-mediated STAT3 signaling. This will offer a novel molecular basis and therapeutic strategy of H2S donor for the treatment of heart failure.
Subject(s)
Cardiotoxicity/metabolism , Cardiotoxicity/prevention & control , Cysteine/analogs & derivatives , Cytokine Receptor gp130/metabolism , Doxorubicin/adverse effects , Hydrogen Sulfide/pharmacology , STAT3 Transcription Factor/metabolism , Animals , Calcium/metabolism , Cardiotoxicity/pathology , Cell Nucleus/drug effects , Cell Nucleus/metabolism , Cysteine/pharmacology , Male , Mice, Inbred C57BL , Mitochondria/drug effects , Mitochondria/metabolism , Models, Biological , Myocytes, Cardiac/drug effects , Myocytes, Cardiac/metabolism , Phosphorylation/drug effects , Protein Transport/drug effects , Rats , Reactive Oxygen Species/metabolism , Signal Transduction/drug effectsABSTRACT
Glioblastoma multiforme (GBM) is the most common and aggressive brain tumour. The neoplasms are difficult to resect entirely because of their highly infiltration property and leading to the tumour edge is unclear. Gliadel wafer has been used as an intracerebral drug delivery system to eliminate the residual tumour. However, because of its local low concentration and short diffusion distance, patient survival improves non-significantly. Axl is an essential regulator in cancer metastasis and patient survival. In this study, we developed a controlled-release polyanhydride polymer loading a novel small molecule, n-butylidenephthalide (BP), which is not only increasing local drug concentration and extending its diffusion distance but also reducing tumour invasion, mediated by reducing Axl expression. First, we determined that BP inhibited the expression of Axl in a dose- and time-dependent manner and reduced the migratory and invasive capabilities of GBM cells. In addition, BP downregulated matrix metalloproteinase activity, which is involved in cancer cell invasion. Furthermore, we demonstrated that BP regulated Axl via the extracellular signal-regulated kinases pathway. Epithelial-to-mesenchymal transition (EMT) is related to epithelial cells in the invasive migratory mesenchymal cells that underlie cancer progression; we demonstrated that BP reduced the expression of EMT-related genes. Furthermore, we used the overexpression of Axl in GBM cells to prove that Axl is a crucial target in the inhibition of GBM EMT, migration and invasion. In an in vivo study, we demonstrated that BP inhibited tumour growth and suppressed Axl expression in a dose-dependent manner according to a subcutaneous tumour model. Most importantly, in an intracranial tumour model with BP wafer in situ treatment, we demonstrated that the BP wafer not only significantly increased the survival rate but also decreased Axl expression, and inhibited tumour invasion. These results contribute to the development of a BP wafer for a novel therapeutic strategy for treating GBM invasion and increasing survival in clinical subjects.
Subject(s)
Glioblastoma/drug therapy , Glioblastoma/genetics , Phthalic Anhydrides/administration & dosage , Proto-Oncogene Proteins/biosynthesis , Receptor Protein-Tyrosine Kinases/biosynthesis , Animals , Cell Line, Tumor , Cell Movement/drug effects , Drug Delivery Systems , Epithelial-Mesenchymal Transition/drug effects , Gene Expression Regulation, Neoplastic/drug effects , Glioblastoma/pathology , Humans , Mice , Neoplasm Invasiveness/genetics , Neoplasm Metastasis , Phthalic Anhydrides/chemistry , Polymers/administration & dosage , Polymers/chemistry , Proto-Oncogene Proteins/genetics , Receptor Protein-Tyrosine Kinases/genetics , Xenograft Model Antitumor Assays , Axl Receptor Tyrosine KinaseABSTRACT
We have used high-resolution neutron spectroscopy experiments to determine the complete spin wave spectrum of the heavy-fermion antiferromagnet CeRhIn5. The spin wave dispersion can be quantitatively reproduced with a simple frustrated J1-J2 model that also naturally explains the magnetic spin-spiral ground state of CeRhIn5 and yields a dominant in-plane nearest-neighbor magnetic exchange constant J0=0.74(3) meV. Our results pave the way to a quantitative understanding of the rich low-temperature phase diagram of the prominent CeTIn5 (T=Co, Rh, Ir) class of heavy-fermion materials.
ABSTRACT
Traumatic brain injury (TBI), often called the signature wound of Iraq and Afghanistan wars, is characterized by a progressive histopathology and long-lasting behavioral deficits. Treatment options for TBI are limited and patients are usually relegated to rehabilitation therapy and a handful of experimental treatments. Stem cell-based therapies offer alternative treatment regimens for TBI, and have been intended to target the delayed therapeutic window post-TBI, in order to promote "neuroregeneration," in lieu of "neuroprotection" which can be accomplished during acute TBI phase. However, these interventions may require adjunctive pharmacological treatments especially when aging is considered as a comorbidity factor for post-TBI health outcomes. Here, we put forward the concept that a combination therapy of human umbilical cord blood cell (hUCB) and granulocyte-colony stimulating factor (G-CSF) attenuates neuroinflammation in TBI, in view of the safety and efficacy profiles of hUCB and G-CSF, their respective mechanisms of action, and efficacy of hUCB+G-CSF combination therapy in TBI animal models. Further investigations on the neuroinflammatory pathway as a key pathological hallmark in acute and chronic TBI and also as a major therapeutic target of hUCB+G-CSF are warranted in order to optimize the translation of this combination therapy in the clinic.
Subject(s)
Aging/physiology , Brain Injuries/drug therapy , Granulocyte Colony-Stimulating Factor/therapeutic use , Inflammation/drug therapy , Stem Cells , Animals , Comorbidity , Humans , Inflammation/epidemiologyABSTRACT
BACKGROUND: To this date, only a small number of studies have described the long-term use of BTX in Hemifacial spasm. AIM: To assess the prognosis and long-term effectiveness of Botulinum toxin A (BTXA) in the treatment of unilateral spasms of the eyelid. PATIENTS AND METHODS: From September 1998 to January 2006, 245 consecutive cases of unilateral spasms of the eyelid were included in this retrospective study. Among them, 143 patients (BTXA group) underwent BTXA injection treatment, and 102 patients did not receive any intervention (control group). BTXA injections were made subcutaneously around the eye with the dose of 2.5U other than the temporal canthus of 5U. Follow-up was performed for 1-7 years after the last injection. RESULTS: In BTXA treatment group, the complete remission rate was 78.3% (112/143), recurrence rate was 21.7% (31/143) and the incidence of hemifacial spasm (HFS) was 18.9% (27/143); complete remission rate for patients with disease duration less than 3 months was 96.6% (86/89); for patients with a 3-6 months disease history, complete remission rate was 75.8% (25/33), and patients having the disease course exceeding 6 months had a complete remission rate of 4.8% (1/21). In the control group, the complete remission rate was 12.7% (13/102), and the prevalence of HFS was 71.6% (73/102); 16.7% (9/56) of patients with the disease duration less than 3 months were remitted, but the complete remission rate was 12.9% (4/31) for patients with a 3-6 months disease history. None was in remission when the disease history exceeded 6 months. CONCLUSIONS: BTXA treatment can improve the complete remission rate and prevent further progression of unilateral spasms of the eyelid into HFS, especially in early stage.
Subject(s)
Blepharospasm/drug therapy , Botulinum Toxins, Type A/administration & dosage , Hemifacial Spasm/drug therapy , Neuromuscular Agents/administration & dosage , Adult , Female , Follow-Up Studies , Humans , Injections, Subcutaneous , Male , Middle Aged , Remission Induction , Retrospective Studies , Time Factors , Treatment OutcomeABSTRACT
A full-length cDNA, designated as the Populus tomentosa disease resistance-like 01 (PtDrl01) gene, was isolated from triploid white poplar [(Populus tomentosa × P. bolleana) × P. tomentosa]. The protein thought to be produced by the PtDrl01 gene contains a nuclear localisation sequence (NLS), a toll/interleukin-1 receptor (TIR) homologue region, a nucleotide binding site (NBS) and a leucine-rich repeat (LRR) domain. The protein also exhibits a considerable degree of homology to N-like resistance proteins. Real-time quantitative RT-PCR analysis revealed that expression of the PtDrl01 gene in triploid white poplar leaves could be induced by two defence signalling molecules: methyl jasmonate (MeJA) and salicylic acid (SA). Over-expression of the PtDrl01 gene in transgenic tobacco induced enhanced resistance to tobacco mosaic virus (TMV). Long-term resistance from the PtDrl01 gene to TMV infection was also observed in transgenic tobacco plants. Additionally, over-expression of the PtDrl01 gene resulted in transcriptional changes in genes expressing pathogenesis-related proteins in transgenic tobacco under non-stress conditions. These data strongly suggest that the PtDrl01 gene is involved in plant defence responses to pathogen infection.
Subject(s)
Nicotiana/metabolism , Nicotiana/virology , Plant Proteins/metabolism , Populus/metabolism , Tobacco Mosaic Virus/physiology , Amino Acid Sequence , Conserved Sequence , Gene Expression Regulation, Plant , Molecular Sequence Data , Plant Proteins/chemistry , Plant Proteins/genetics , Sequence Alignment , Nicotiana/chemistry , Nicotiana/genetics , TriploidyABSTRACT
OBJECTIVE: To observe the long-term effect of laser occlusion of the posterior semicircular canal for benign paroxysmal positional vertigo. METHOD: Case report and review of the relevant world literature. RESULTS: We treated a patient with refractory benign paroxysmal positional vertigo using laser occlusion of the posterior semicircular canal, and achieved satisfactory results. Three months after the operation, the patient was able to lead a normal life. There was no recurrence over five years of follow up. CONCLUSION: To our knowledge, this is the first report in the world literature of a patient with refractory benign paroxysmal positional vertigo being treated with laser occlusion of the posterior semicircular canal. This method had long-term effectiveness, and may be one of the most effective methods of treating patients with refractory benign paroxysmal positional vertigo.
Subject(s)
Laser Therapy/methods , Semicircular Canals/surgery , Vertigo/surgery , Female , Follow-Up Studies , Humans , Middle Aged , Treatment OutcomeABSTRACT
Spinosad (spinosyns A and D) is a mixture of secondary metabolites produced by Saccharopolyspora spinosa. It is used in agriculture as a potent insect control agent with exceptional safety to non-target organisms. In this study, we applied genome shuffling of S. spinosa to achieve a rapid improvement of spinosad production. Ten strains with subtle improvements in spinosad production were obtained from the populations generated by the mutation with nitrosoguanidine and ultraviolet irradiation, and then they were subjected for recursive protoplast fusion. After four rounds of genome shuffling, a high yielding strain, designated as S. spinosa 4-7, was successfully isolated. Its production reached 547 mg/L, which was increased by 200.55% and 436.27% in comparison with that of the highest parent strain and the original strain, respectively. The subculture experiments indicated that the high producer of S. spinosa 4-7 was stable. Spinosad fermentation experiments by S. spinosa 4-7 were carried out in a 5-L fermentor, and its production of spinosad reached 428 mg/L after 168 h of fermentation.
Subject(s)
Genome, Bacterial/physiology , Macrolides/metabolism , Saccharopolyspora/genetics , Saccharopolyspora/metabolism , Drug Combinations , Genetic Engineering/methods , Genome, Bacterial/geneticsABSTRACT
With Monte Carlo simulations, we study the dynamic relaxation at perfect and imperfect surfaces of the three-dimensional Ising model with an ordered initial state. The time evolution of the surface magnetization, the line magnetization of the defect line, and the corresponding susceptibilities and second cumulants is carefully examined. Universal dynamic scaling forms including a dynamic crossover scaling form are identified at the ordinary, special, and surface phase transitions. The critical exponents beta1 of the surface magnetization and beta2 of the line magnetization are extracted. The impact of the defect line on the universality classes is investigated.
ABSTRACT
The majority of cloned plant disease resistance genes (R genes) encode a nucleotide binding site (NBS) and a leucine-rich repeat (LRR) domain. In this study, to better understand the R genes in white poplar, 59 resistance gene analogues (RGAs) were identified from a triploid white poplar [(Populus tomentosa x Populus bolleana) x P. tomentosa], based on conserved NBS regions. The 59 RGAs were phylogenetically classified into 10 subfamilies, and 54 RGAs with open-reading frames (ORFs) were further grouped into two classes, toll and interleukin-1 receptor (TIR) and non-TIR. BLAST searches with reference to the genomic sequence of Populus trichocarpa found 96 highly homologous regions distributed in 37 loci, suggesting the abundance and divergence of NBS-encoding genes in the triploid poplar genome. Within subfamilies 1-3, the average non-synonymous/synonymous substitution (omega) rates were < 1, indicating purifying selection on these RGAs, but some sites were clearly under diversifying selection with omega > 1. Many intergenic exchanges were also detected among these RGAs, indicating a probable role in homogenising NBS domains. Quantitative real-time PCR analysis revealed dramatic variations in the transcript level of 18 RGAs in the mature leaves, bark and roots of the triploid poplar, and identified two RGAs that had significantly higher level of transcripts in bark, four RGAs in mature leaves, and 14 in the above-ground portion of poplars, suggesting their probable roles in resistance against diseases attacking the organs. Our results shed light on genetic resources of poplar resistance and will be useful for further resistance gene isolation and exploitation.
Subject(s)
Genes, Plant , Nucleotides/metabolism , Polyploidy , Populus/genetics , Amino Acid Sequence , Gene Expression Profiling , Molecular Sequence Data , Phylogeny , Polymerase Chain Reaction , Polymorphism, Genetic , Populus/immunology , Populus/metabolism , Sequence Alignment , Sequence Analysis, DNAABSTRACT
We describe here a novel HLA-DRB1* allele, DRB1*0331, observed from a Taiwanese bone marrow donor using DNA sequence-based typing (SBT) method. The 'new' allele differs from DRB1*0306 and DRB1*0325 by one nucleotide at positions 196 and 227, respectively. Nucleotide mutations caused amino acid substitutions from N to Y at codon 37 and from F to Y at codon 47, as compared with amino acid sequence encoded by the DRB1*030101 allele. The donor was first typed as DRB1*0403/0406/0439/0441/0446/0451/0452 (NMDP code DRB1*04XX) and DRB1*0304/0323/0325 (NMDP code DRB1*03APDA) by sequence-specific oligonucleotide (SSO) typing kit. Subsequent typing of the donor by high-resolution sequence-specific primer (SSP) protocol indicated DRB1*0403 and DRB1*0306. The anomalous result of DRB1*03 was resolved by SBT and recognized as DRB1*0331. We concluded that SSP or SSO alone may mistype a precedent unrecognized allele and that two different typing techniques or SBT may have to be employed to safe guard true HLA typing when rare alleles are encountered at the first time.
Subject(s)
Bone Marrow/immunology , HLA-DR Antigens/genetics , Alleles , Base Sequence , Bone Marrow Transplantation , HLA-DRB1 Chains , Humans , Molecular Sequence Data , Sequence Analysis, DNA , Taiwan , Tissue DonorsABSTRACT
BACKGROUND AND PURPOSE: Actions of glutamate and serotonin on their respective receptors in the dorsal facial area (DFA) of the medulla are known to regulate common carotid arterial (CCA) blood flow in cats. Less is known about acetylcholine action on its nicotinic receptor (nAChR) subtypes in the DFA for regulation of CCA blood flow and this aspect was investigated. EXPERIMENTAL APPROACH: Nicotinic and muscarinic agonists and antagonists were microinjected into the DFA through a three-barrel tubing in anesthetized cats. RESULTS: CCA blood flow was dose-dependently increased by nicotine (a non-selective nAChR agonist) and choline (a selective alpha7-nAChR agonist). These effects of nicotine were attenuated by alpha-bungarotoxin (an alpha7-nAChR antagonist), methyllycaconitine (an alpha7-nAChR antagonist), mecamylamine (a relatively selective alpha3beta4-nAChR antagonist) and dihydro-beta-erythroidine (a relatively selective alpha4beta2-nAChR antagonist). The choline-induced flow increase was attenuated by alpha-bungarotoxin and mecamylamine, but not by dihydro-beta-erythroidine. Muscarinic agonists (muscarine and methacholine) and antagonist (atropine) affected neither the basal nor the nicotine-induced increase in the CCA blood flow. CONCLUSIONS AND IMPLICATIONS: Functional alpha7, alpha4beta2, and alpha3beta4 subunits of the nAChR appear to be present on the DFA neurons. Activations of these receptors increase the CCA blood flow. The present findings do not preclude the presence of other nAChRs subunits. Muscarinic receptors, if any, on the DFA are not involved in regulation of the CCA blood flow. Various subtypes of nAChRs in the DFA may mediate regulation of the CCA and cerebral blood flows.
Subject(s)
Carotid Artery, Common/metabolism , Medulla Oblongata/blood supply , Receptors, Nicotinic/physiology , Animals , Cats , Choline/physiology , Dose-Response Relationship, Drug , Female , Male , Nicotine/pharmacology , Nicotinic Agonists/pharmacology , Regional Blood Flow/drug effects , Regional Blood Flow/physiologyABSTRACT
We perform molecular dynamics and Monte Carlo simulations of two-dimensional melting with dipole-dipole interactions. Both static and dynamic behaviors are examined. In the isotropic liquid phase, the bond orientational correlation length xi 6 and susceptibility chi 6 are measured, and the data are fitted to the theoretical ansatz. An algebraic decay is detected for both spatial and temporal bond orientational correlation functions in an intermediate temperature regime, and it provides an explicit evidence for the existence of the hexatic phase. From the finite-size scaling analysis of the global bond orientational order parameter, the disclination unbinding temperature Ti is estimated. In addition, from dynamic Monte Carlo simulations of the positional order parameter, we extract the critical exponents at the dislocation unbinding temperature Tm. All the results are in agreement with those from experiments and support the Kosterlitz-Thouless-Halperin-Nelson-Young (KTHNY) theory.
ABSTRACT
Stem cell therapies are an important strategy for the treatment of stroke. Bone marrow-derived stem cells (BMSCs) may promote structural and functional repair in several organs via stem cell plasticity. The tissue damage could stimulate the stem cells migration, and they track into the site of damage and then undergo differentiation. The plasticity functions of BMSCs in an injuries tissue are dependent on the specific signals present in the local environment of the damaged tissue. Recent studies have also identified the specific molecular signals, such as SDF-1/CXCR4, required for the interaction of BMSCs and damaged host tissues. This review summarizes the current understanding of how BMSCs reach and function in cerebral ischemic tissues.
Subject(s)
Brain Ischemia/therapy , Stem Cell Transplantation , Stroke/therapy , Animals , Chemokines, CXC/physiology , Chemotaxis , Granulocyte Colony-Stimulating Factor/physiology , Humans , Receptors, CXCR4/physiologyABSTRACT
Recent studies suggest that inflammation may play an important role in the pathogenesis of Parkinson's disease (PD). Because the C(-260) --> T polymorphism in the promoter of the CD14 monocyte receptor gene (pCD14) could affect the predisposition to the inflammatory response, we conducted a case-control study to investigate a possible genetic susceptibility of the pCD14 polymorphism in patients with PD. This study included 200 sporadic PD patients and 200 controls, matched by sex and case-control pairs for age at onset in the case. All observed genotype frequencies were in Hardy-Weinberg equilibrium. Results revealed that the CD14-T allele of the pCD14 polymorphism in the female PD patients existed statistically significant difference from that of the female controls (OR = 1.262, P = 0.038), but not for male. Female individuals with homozygote CD14-TT genotype were significantly increased risk of PD by 1.28 time (P = 0.027). Furthermore, a logistic regression analysis confirmed that the homozygote CD14-TT genotype was an independent risk factor for PD (OR = 1.576, P = 0.030). In conclusion, results of this study indicate the pCD14 polymorphism to be a genetic risk factor for PD in females.
Subject(s)
Lipopolysaccharide Receptors/genetics , Monocytes/metabolism , Parkinson Disease/epidemiology , Parkinson Disease/genetics , Aged , DNA/genetics , Ethnicity , Female , Gene Frequency , Humans , Logistic Models , Male , Middle Aged , Polymorphism, Genetic/genetics , Reverse Transcriptase Polymerase Chain Reaction , Risk , Sex CharacteristicsABSTRACT
Cellular prion protein (PrP(C)) expression can be regulated by heat-shock stress, and we designed the present study to determine whether hypoglycemia could affect PrP(C) expression. RT-PCR and Western blotting were used to measure the expression of PrP(C) and heat-shock protein (Hsp70) in mouse neuroblastoma (N18) cells cultured 3 hr to 3 days in media deprived of 97.5% (L) or 75% (M) of its glucose. Hypoglycemia caused a concomitant time-dependent and glucose dose-dependent increase in PrP(C) and Hsp70. In addition, hypoglycemia also increased phosphorylated c-Jun N-terminal kinase (JNK) protein levels in a time-dependent manner. The upregulation of PrP(C) and Hsp70 under hypoglycemic conditions was disrupted by the specific JNK inhibitor SP600125. It was also found from in vitro studies that hypoglycemic conditions induced higher levels of PrP(C) promoter activity in PrP(C) promoters containing a heat-shock element (HSE) than in PrP(C) promoters lacking HSE. We propose that hypoglycemia-increased PrP(C) expression might be due to JNK phosphorylation of a heat-shock transcriptional factor, which then interacts with HSE in the promoter of PrP(C).