Interaction of smoking and aging on emphysema and small airways disease in asymptomatic healthy men by CT-based parametric response mapping analysis.

AIM: To explore whether small airway disease and emphysema were affected by the interaction between smoking and aging on chest computed tomography (CT) images of asymptomatic healthy men analysed using a quantitative imaging tool parametric response mapping (PRM). MATERIALS AND METHODS: In this retrospective study, 95 asymptomatic healthy men underwent biphasic chest CT. The PRM classifies lung as a percentage of normal (PRMNormal%), functional small airway disease (PRMfSAD%), and emphysema (PRMEmph%). The patients were divided into groups based on their age and smoking status. Multiple linear regression analysis was applied to explore the factors influencing lung injury. Simple effects analysis was performed to explore the interaction between different age groups and smoking status. RESULTS: The interaction between aging and smoking significantly affected PRMfSAD% and PRMEmph% (p<0.001). The age range 60-69 and smoking were associated with increased PRMfSAD% and PRMEmph% (p<0.05). Futher stratification into different age subgroups showed that smoking was associated with increased PRMfSAD% and PRMEmph% in the 50-59 year age group. Besides, smoking in the 50-59 and 60-69 years group was associated with decreased PRMNormal%, while smoking in the 60-69 years group did not significantly influence the prevalence of PRMfSAD% and PRMEmph% (p>0.05). CONCLUSIONS: PRM reveals the interplay between smoking and aging in the development of lung injury in asymptomatic healthy men. Aging and smoking are important factors of emphysema and small airway disease in the 50-69 years group. In the 60-69 years group, aging poses a greater risk of lung injury compared to smoking.

[Analysis of discordance between HbA1c and FPG criteria for dysglycemia screening in physical examination individuals].

The general data, blood routine, liver and kidney function, glucose metabolism and lipid metabolism of 11 922 participants who underwent physical examination at the Health Management Center of the Second Xiangya Hospital of Central South University from January 2019 to December 2019 were collected. Clinical characteristics and independent factors of patients with discordance between HbA1c and FPG were evaluated and analyzed. The prevalence of HbA1c-defined diabetes and prediabetes (respectively 8.13%, 34.79%) were significantly higher than that in FPG-defined diabetes and prediabetes (respectively 4.70%, 8.97%) (χ²=2 635.940;P<0.001). The prevalence of inconsistence between HbA1c and FPG was 35.65% and increased with increasing age. This inconsistence mainly occurred in population with HbA1c:5.7%-6.0% and FPG<5.6 mmol/L, followed by population with HbA1c:6.1%-6.4% and FPG<5.6 mmol/L. The risk factors of inconsistency included advanced age, overweight or obesity, hypoalbuminemia, dyslipidemia and hyperuricemia. Among these special participants, compared with participants under 45 years old, participants with over 45 years of age (OR=3.525, 95%CI: 3.216-3.863, P<0.001) were more likely to have inconsistence between HbA1c and FPG; and overweight participants (OR=1.474, 95%CI: 1.341-1.620, P<0.001) or obese participants (OR=1.856, 95%CI: 1.633-2.110, P<0.001) are prone to have the inconsistence than those with normal weight.

[Assessment of the burden of clonorchiasis and its temporal changes in China].

OBJECTIVE: To assess the burden of clonorchiasis and identify its temporal and spatial changes in China, thus to provide insights into the control and prevention of the diseases. METHODS: The disability-adjusted life years (DALYs) was employed as the primary indicator for the disease burden. The prevalence data of Clonorchis sinensis infection were obtainted from the three national surveys on important human parasitic diseases in China, conducting during the period from 1988 to 1922, from 2001 to 2004 and from 2014 to 2016, respectively, and the demographic data from National Bureau of Statistics of China. DALYs of clonorchiasis were calculated and the temporal changes were analyzed at both national and provincial levels, using the disability weight (DW) obtained from a community study in China. Sensitivity analysis was carried out to compare the resulted DALYs of China calculated under the method adopted in this study and that calculated with other commonly used methods. RESULTS: The national burden of clonorchiasis was 489174.04 [95% confidence interval (CI): (391648.87, 597509.87)] DALYs in China in 2016, indicating 0.36 [95% CI: (0.28, 0.43)] DALYs per 1 000 populations. The regions with a high burden of clonorchiasis were concentrated in southern China and northeastern China, and the provinces with the three highest burdens of clonorchiasis included Guangxi Zhuang Autonomous Region, Guangdong Province and Heilongjiang Province, which accounted for 91.18% of total burdens of clonorchiasis in China. During the periods of the three national surveys on important human parasitic diseases in China, the national burden of clonorchiasis was found to show a tendency of first rise and then decrease in China; however, the burden of clonorchiasis has recently shown a tendency towards a rise in Guangxi Zhuang Autonomous Region, Heilongjiang Province and Jiangxi Province. Sensitivity analysis showed that the calculation of diseases burden with age-stratified prevalence of clonorchiasis was similar to that of our method without age stratification; however, the burden estimates calculated only based on the DW of the severe symptoms were much lower than our estimates. CONCLUSIONS: The burden of clonorchiasis is high in China, with a large regional difference. Recently, the overall burden of clonorchiasis has shown a tendency of decline in China; however, there is a tendency towards a rise in some provinces. Therefore, the control of clonorchiasis requires more adaptations to local circumstances.

Alcohol, coffee and tea intake and the risk of cognitive deficits: a dose-response meta-analysis.

AIMS: Lifestyle interventions are an important and viable approach for preventing cognitive deficits. However, the results of studies on alcohol, coffee and tea consumption in relation to cognitive decline have been divergent, likely due to confounds from dose-response effects. This meta-analysis aimed to find the dose-response relationship between alcohol, coffee or tea consumption and cognitive deficits. METHODS: Prospective cohort studies or nested case-control studies in a cohort investigating the risk factors of cognitive deficits were searched in PubMed, Embase, the Cochrane and Web of Science up to 4th June 2020. Two authors searched the databases and extracted the data independently. We also assessed the quality of the studies with the Newcastle-Ottawa scale. Stata 15.0 software was used to perform model estimation and plot the linear or nonlinear dose-response relationship graphs. RESULTS: The search identified 29 prospective studies from America, Japan, China and some European countries. The dose-response relationships showed that compared to non-drinkers, low consumption (<11 g/day) of alcohol could reduce the risk of cognitive deficits or only dementias, but there was no significant effect of heavier drinking (>11 g/day). Low consumption of coffee reduced the risk of any cognitive deficit (<2.8 cups/day) or dementia (<2.3 cups/day). Green tea consumption was a significant protective factor for cognitive health (relative risk, 0.94; 95% confidence intervals, 0.92-0.97), with one cup of tea per day brings a 6% reduction in risk of cognitive deficits. CONCLUSIONS: Light consumption of alcohol (<11 g/day) and coffee (<2.8 cups/day) was associated with reduced risk of cognitive deficits. Cognitive benefits of green tea consumption increased with the daily consumption.

Local infiltration analgesia in primary total knee arthroplasty.

INTRODUCTION: Postoperative pain in total knee arthroplasty (TKA) can hinder rehabilitation and cause morbidity. Local infiltration analgesia (LIA), comprising an anaesthetic drug, non-steroidal anti-inflammatory drug, and adrenaline, has been introduced to reduce pain and systemic side-effects. This study evaluated the efficacy of LIA in TKA with respect to morphine consumption and postoperative pain score. METHODS: This single-centre retrospective cohort study recruited patients with knee osteoarthritis who were scheduled for primary TKA during the period from January 2017 to December 2017. Patients with chronic inflammatory joint disease, contra-indications for LIA, or dementia were excluded. Patients in the LIA group were administered single-dose LIA intra-operatively, while those in the control group were not. Primary outcomes were postoperative pain score, morphine demand, and morphine consumption; secondary outcomes were range of motion, quadriceps power, and postoperative length of stay. RESULTS: In total, 136 patients were recruited (68 per group). Total postoperative morphine demand and consumption, as well as pain scores from postoperative day (POD) 1 to POD 4, were lower in the LIA group than in the control group. The range of motion from POD 1 to POD 4 and quadriceps power on POD 1 were higher in the LIA group than in the control group. Quadriceps power from POD 2 to POD 4 and postoperative length of stay were not significantly different between groups. CONCLUSIONS: Intra-operative single-dose LIA can effectively reduce postoperative pain, morphine demand, and morphine consumption. Therefore, the use of LIA is recommended during TKA.

Trismus, xerostomia and nutrition status in nasopharyngeal carcinoma survivors treated with radiation.

The aims of the study were to: (1) examine levels of trismus, xerostomia and nutritional status; (2) compare levels of trismus, xerostomia and nutritional status in patients with nasopharyngeal carcinoma (NPC) receiving different types of radiation modalities; and (3) identify factors related to NPC survivors' risk status for malnutrition and existing malnutrition. A cross-sectional study with consecutive sampling was conducted. NPC survivors were recruited from otolaryngology/oncology outpatient clinics in a medical centre in Northern Taiwan. Study measures included (1) Mandibular Function Impairment Questionnaire, (2) Xerostomia Questionnaire, (3) Mini Nutrition Assessment, (4) Hospital Anxiety and Depression Scale - Depression subscale, and (5) Symptom Severity Scale. A total of 110 subjects were recruited. Those receiving intensity-modulated radiation therapy had less trismus and xerostomia than patients receiving two-dimensional radiation therapy. Patients with female gender, advanced stage, completion of treatments within 1 year, higher levels of depression, more severe trismus and higher symptom severity tended to have malnutrition or were at risk of malnutrition. Trismus and xerostomia are long-term problems in some NPC survivors and may contribute to malnutrition. To better manage a patient's trismus and xerostomia and to enhance nutritional status, clinicians should develop a patient-specific care programme based on careful assessment and targeted measures to improve oral function and insure adequate nutritional intake.

Neuregulin 1 protects against ischemic brain injury via ErbB4 receptors by increasing GABAergic transmission.

Identifying novel neuroprotectants that can halt or even reverse the effects of stroke is of interest to both clinicians and scientists. Neuregulin 1 (NRG1) is an effective neuroprotectant, but its molecular mechanisms are largely unclear. In this study, NRG1 rescued cortical neurons from oxygen-glucose deprivation (OGD) model, but the effect was blocked by neutralizing NRG1 and ErbB4 inhibition. In addition, γ-Aminobutyric acid (GABA) receptor agonists had no synergistic effect with NRG1, and the neuroprotective effect of NRG1 against OGD was partly blocked by GABA receptor antagonists. Importantly, NRG1 neuroprotection against brain ischemia was abolished in the mice with specific deletion of ErbB4 in parvalbumin (PV)-positive interneurons. In summary, NRG1 protects against ischemic brain injury via ErbB4 receptors by enhancing GABAergic transmission.

Efficient optical coupling in AlGaN/GaN quantum well infrared photodetector via quasi-one-dimensional gold grating.

In this letter, a new kind of grating, quasi-one-dimensional gold grating, has been proposed to enhance the optical coupling in AlGaN/GaN quantum well infrared photodetector (QWIP). The electric field distribution, current density and energy flow are analyzed by an algorithm of finite element method (FEM). Significantly enhanced electric field component E(z) perpendicular to multiple quantum wells (MQWs) is explained by introducing the resonant coupling of surface plasmon polariton (SPP) and localized surface plasmon (LSP). The |E(z)|(2) in MQWs reaches 0.85 (V/m(2) when the electric field intensity (|E(0)|(2)) of normal incidence is 1 (V/m(2) at 4.65 µm, showing 2 times and 1.3 times increase compared with that obtained via a one-dimensional gold grating and a two-dimensional gold grating, respectively. The results confirm that the quasi-one-dimensional gold grating provides more plasma excitation source and higher charge density with structure optimization, resulting in a high optical coupling efficiency of 85% in quantum well region.

Double-resonance enhanced intersubband second-order nonlinear optical susceptibilities in GaN/AlGaN step quantum wells.

Second-order nonlinear optical susceptibilities for second harmonic generation (SHG) associated with intersubband transitions in GaN/AlGaN single quantum well and step quantum well have been studied theoretically by solving Schrödinger and Poisson equations self-consistently. The calculated results suggest that due to the very large polarization-induced field in the quantum well, the potential profile becomes asymmetrical, leading to large second-order susceptibilities. A high value about 4 × 10-7 m/V can be obtained in single quantum well structure. Furthermore, by adopting step quantum well structure to increase the asymmetry degree of the potential profile and manipulate the energy levels for double-resonance, a significant enhancement of second-order susceptibility can occur in step quantum well. Specifically, the susceptibility can be as large as 4 × 10-6 m/V with structure optimization, about an order of magnitude greater than that in single quantum well. The results indicate that nonlinear optical elements based on GaN/AlGaN step quantum wells are very promising for SHG in a wide range of wavelengths from telecommunication to mid-infrared, especially effective in longer wavelength.

Prospective cross-sectional study using questionnaire to assess the effect of a different nomenclature for psychiatric illnesses on the perception of these diseases by university students.

OBJECTIVE. To assess the effect of a difference in nomenclature for psychiatric illness on perceptions of university students. DESIGN. Cross-sectional study. SETTING. Three local universities in Hong Kong. PARTICIPANTS. A total of 201 university students (undergraduates or postgraduates) were interviewed with a questionnaire. MAIN OUTCOME MEASURES. Score difference between the new and old nomenclature of each disease for each question of the questionnaire, using a 5-point Likert scale and an integrated score difference for each disease. RESULTS. Of the seven diseases investigated, six yielded a significant yet mild increase in positive perceptions with the new nomenclature. These diseases included schizophrenia (integrated score difference: +0.158, P<0.001), neurasthenia (integrated score difference: +0.117, P<0.001), paranoia (integrated score difference: +0.209, P<0.001), personality disorder (integrated score difference: +0.282, P<0.001), attention deficit hyperactivity disorder (integrated score difference: +0.086, P=0.005), and bipolar disorder (integrated score difference: +0.154, P<0.001). Epilepsy showed a negative perception with its new nomenclature (integrated score difference: -0.119, P<0.001). CONCLUSIONS. The new nomenclature system for psychiatric diseases achieves more positive perceptions among the university students than the old nomenclature. Epilepsy was the exception for which the old nomenclature conferred a more positive perception. Further studies on this topic involving a more general population should be advocated to confirm the improvements in perception with the new naming system for psychiatric diseases.

Tunable optical gap at a fixed lattice constant in group-IV semiconductor alloys.

A direct absorption edge tunable between 0.8 and approximately 1.4 eV is demonstrated in strain-free ternary Ge_{1-x-y}Si_{x}Sn_{y} alloys epitaxially grown on Ge-buffered Si. This decoupling of electronic structure and lattice parameter-unprecedented in group-IV alloys-opens up new possibilities in silicon photonics, particularly in the field of photovoltaics. The compositional dependence of the direct band gap in Ge_{1-x-y}Si_{x}Sn_{y} exhibits a nonmonotonic behavior that is explained in terms of coexisting small and giant bowing parameters in the two-dimensional compositional space.

alpha2a adrenoceptors regulate phosphorylation of microtubule-associated protein-2 in cultured cortical neurons.

Adrenoceptors have been suggested to mediate neuronal development. This study revealed the expression of alpha2A adrenoceptors in the cortical plate of fetal mouse cerebral wall. The effects of alpha2A adrenoceptor on dendrite growth were investigated in primary neuronal cultures. Application of alpha2 adrenoceptor agonists, BHT 933 or UK 14304 for 24 or 72 h resulted in a 1.5-2-fold increase in dendrite lengths. This effect was blocked by alpha2 adrenergic antagonists, RX 821002 or yohimbine, as well as a alpha2A selective antagonist, BRL 44408, but not by alpha2B/alpha2C selective antagonists ARC 239, imiloxan and rauwolscine. Guanfacine, a alpha2A selective agonists, also significantly increased the dendrite lengths in culture. These results suggest that the morphological effect is wholly attributable to alpha2A adrenoceptor activation. We further tested the hypothesis that alpha2A adrenoceptors act through altering the phosphorylation state of microtubule-associated protein 2. The results showed that the phosphorylation of microtubule-associated protein 2 was significantly reduced on both serine and threonine residues by over 40% after 2 h of application of guanfacine and was maintained at this low level for a prolonged time up to 96 h. These findings suggest that alpha2A adrenoceptors regulate the phosphorylation of microtubule-associated protein 2, which in turn mediates dendrite growth of cortical neurons.

D1 dopamine receptor regulation of microtubule-associated protein-2 phosphorylation in developing cerebral cortical neurons.

This study addresses the hypothesis that the previously described capacity of D1 dopamine receptors (D1Rs) to regulate dendritic growth in developing cortical neurons may involve alterations in the phosphorylation state of microtubule-associated protein-2 (MAP2). The changes in phosphorylation of this protein are known to affect its ability to stabilize the dendritic cytoskeleton. The study involved two systems: primary cultures of mouse cortical neurons grown in the presence of the D1R agonists, SKF82958 or A77636, and the cortex of neonatal transgenic mice overexpressing the D1A subtype of D1R. In both models, a decrease in dendritic extension corresponded with an elevation in MAP2 phosphorylation. This phosphorylation occurred on all three amino acid residues examined in this study: serine, threonine, and tyrosine. In cultured cortical neurons, D1R stimulation-induced increase in MAP2 phosphorylation was blocked by the protein kinase A (PKA) inhibitor, H-89, and mimicked by the PKA activator, S(p)-cAMPS. This indicates that D1Rs modulate MAP2 phosphorylation through PKA-associated intracellular signaling pathways. We also observed that the elevations in MAP2 phosphorylation in neuronal cultures in the presence of D1R agonists (or S(p)-cAMPS) were maintained for a prolonged time (up to at least 96 hr). Moreover, MAP2 phosphorylation underwent a substantial increase between 24 and 72 hr of exposure to these drugs. Our findings are consistent with the idea that D1Rs can modulate growth and maintenance of dendrites in developing cortical cells by regulating the phosphorylation of MAP2. In addition, our observations suggest that MAP2 phosphorylation by long-term activation of D1Rs (and PKA) can be divided into two phases: the initial approximately 24-hr-long phase of a relatively weak elevation in phosphorylation and the delayed phase of a much more robust phosphorylation increase taking place during the next approximately 48 hr.

Mechanism of measles virus failure to activate NF-kappaB in neuronal cells.

Lack of IFN-beta and MHC class I expression in measles virus (MV) infected neurons could impair the host antiviral defense mechanism and result in virus escape from recognition by cytotoxic T-cells. Induction of IFN-beta and MHC class I gene expression requires NF-kappaB activation which depends on degradation of IkappaBalpha, an inhibitory protein of NF-kappaB. In earlier studies we demonstrated that in contrast to glial cells, MV was unable to induce IkappaBalpha degradation in neuronal cells. It is unclear whether this failure is due to the presence of a neuron-specific IkappaBalpha isoform or a defect in the MV signaling cascade that leads to IkappaBalpha phosphorylation and degradation. In this study, an IkappaBalpha-wild type (WT) expression vector was transfected into neuronal and glial cells and subsequently exposed to MV. In contrast to glial cells, IkappaBalpha-WT was degraded in neuronal cells in response to TNFalpha but not MV. The findings eliminate the existence of an IkappaBalpha isoform in neuronal cells that is resistant to phosphorylation by MV. Blocking de novo protein synthesis with cyclohexamide had no effect on neuronal IkappaBalpha, indicating that lack of degradation rather than increased synthesis is responsible for IkappaBalpha accumulation in MV-stimulated neuronal cells. To determine if malfunction in the MV receptor CD46 is responsible for failure of IkappaBalpha phosphorylation and degradation, neuronal cells were transfected with a wild type CD46 (CD46-WT) expression vector. MV stimulation of CD46-WT transfected cells failed to induce IkappaBalpha degradation. Collectively these findings indicate that failure of MV to phosphorylate neuronal IkappaBalpha is not due to a presence of an IkappaBalpha isoform or malfunction of the MV receptor, and is more likely to be due to a defect in the signaling pathway that normally leads to IkappaBalpha phosphorylation and degradation.

Origins of accessory small ring marker chromosomes derived from chromosome 1.

Three patients with accessory small ring chromosomes derived from chromosome 1 are presented together with additional clinical details and cytogenetic analyses of a previously reported patient. Cytogenetic analysis was undertaken by FISH using a reverse painting probe generated from one of the patients by microdissection of the r(1) chromosome and with a BAC923C6 which maps to 1p12. Results indicated that patients with r(1) chromosomes consisting of 1q12 heterochromatin and short arm pericentric euchromatin which extends to at least the BAC923C6 were associated with a normal or mild phenotype. Patients with abnormal phenotypes possessed two types of rings. One patient had evidence for contiguous pericentric short arm euchromatin which extended from the centromere to beyond the BAC923C6. Two patients showed molecular cytogenetic results which were compatible with non-contiguous chromosome 1 euchromatin. The diversity of origin of r(1)s will hamper attempts to define phenotype/genotype relationships.

Failure of measles virus to activate nuclear factor-kappa B in neuronal cells: implications on the immune response to viral infections in the central nervous system.

Neurons are postmitotic cells that foster virus persistence. These cells lack the HLA class I molecules required for clearance of infected cells. Previously, we showed that HLA class I is induced by measles virus (MV) on glial cells, which is primarily mediated by IFN-beta. In contrast, MV was unable to induce HLA class I or IFN-beta in neuronal cells. This failure was associated with lack of NF-kappa B binding to the positive regulatory domain II element of the IFN-beta promoter, which is essential for virus-induced IFN-beta gene activity. In this study, we demonstrate that the failure to activate NF-kappa B in neuronal cells is due to the inability of MV to induce phosphorylation and degradation of I kappa B, the inhibitor of NF-kappa B. In contrast, TNF-alpha induced degradation of I kappa B alpha in the neuronal cells, suggesting that failure to induce I kappa B alpha degradation is likely due to a defect in virus-mediated signaling rather than to a defect involving neuronal I kappa B alpha. Like MV, mumps virus and dsRNA failed to induce I kappa B alpha degradation in the neuronal cells, suggesting that this defect may be specific to viruses. Autophosphorylation of the dsRNA-dependent protein kinase, a kinase possibly involved in virus-mediated I kappa B alpha phosphorylation, was intact in both cell types. The failure of virus to induce I kappa B alpha phosphorylation and consequently to activate NF-kappa B in neuronal cells could explain the repression of IFN-beta and class I gene expression in virus-infected cells. These findings provide a potential mechanism for the ability of virus to persist in neurons and to escape immune surveillance.

High resolution characterization of an interstitial deletion of less than 1.9 Mb at 4p16.3 associated with Wolf-Hirschhorn syndrome.

Wolf-Hirschhorn syndrome (WHS) caused by 4p16.3 deletions comprises growth and mental retardation, distinct facial appearance and seizures. This study characterized a subtle interstitial deletion of 4p16.3 in a girl with mild retardation and possessing facial traits characteristic of WHS. The patient had generalized seizures in conjunction with fever at 3 and 5 years of age. Fluorescence in situ hybridization (FISH) with a series of markers in the 4p16.3 region showed that the interstitial deletion in this patient was between the probes D4S96 and D4S182, enabling the size of the deletion to be estimated as less than 1.9 Mb. This is the smallest interstitial deletion of 4p16.3 which has been reported. The patient contributes to a refinement of the phenotypic map of the WHS region in 4p16.3. The critical region for the characteristic facial changes of WHS, failure to thrive and developmental delay is now localized to a region of less than 700 kb. The mental retardation of this patient was mild suggesting that small interstitial deletion may have less severe phenotypic consequences.

Improvement of schizophrenic symptoms and changes in plasma HVA concentrations, plasma anti-D2 and anti-5-HT2 receptor activities with clozapine.

In order to investigate the biological mechanisms underlying the clinical efficacy of clozapine, 200 mg/day of clozapine was added to the drug regimens of 19 patients with chronic, anti-psychotic-resistant schizophrenia, and the plasma homovanillic acid (HVA), clozapine concentrations, anti-dopamine D2 and anti-serotonin 5-HT2 receptor activities were measured. After 28 days, six patients showed an improvement of more than 20% over baseline Brief Psychiatric Rating Scale (BPRS) scores. Mean plasma HVA concentrations and anti-D2 receptor activities did not change significantly in the entire group or in the six patients showing improvement. However, anti-5-HT2 receptor activities increased significantly in all 19 patients. Changes in BPRS scores did not correlate significantly with changes in plasma HVA or with changes in clozapine concentrations, or with anti-D2 and anti-5-HT2 receptor activities.