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Mechanical properties and behaviors of bamboo joined by different connections were considered in this work. Makino bamboo (Phyllostachys makinoi) culms from Taiwan were used as the connection material to explore the form of cross-lap joints. Since the cross-lap joint is a common joint in bamboo structures, the mechanical properties of tension, slip, and rotation were evaluated for three types of joints: lashing joint, iron wire joint, and steel bracket joint, under different load conditions. The results showed that the ultimate load of bamboo culms under lateral partial compression has a positive correlation with the number of bamboo nodes and the relative distance to the base-section of the bamboo culms. The mid-sections and end-sections have similar uniaxial compressions in the transverse orientation. According to results of tensile testing, the tensile stiffness of the three joint types is as follows in descending order: iron wire joint, lashing joint, and steel bracket joint, with the reverse order for ultimate load testing. In terms of slip testing, the withstanding of ultimate loads and increases in slip stiffness can be attributed to bamboo nodes that assist in creating slip stiffness in lashing joint. However, ultimately, steel bracket joints hold the highest slip stiffness. Our findings for rotation stiffness value show the following tendency: steel bracket joint > lashing joint > iron wire joint.

Beyond their traditional role in timber production, plantation forests are increasingly recognized for their therapeutic potential. Forest management practices allow for modifications to meet diverse demands, making it crucial to understand the association between stand density and human responses. This knowledge is essential for forest therapy practitioners and landscape designers aiming to maximize the therapeutic effects of these landscapes. This article delves into the effects of viewing forest plantations on health responses, exploring whether different planting densities influence human physiological and psychological reactions. To investigate this, we conducted a between-subject, pretest-posttest field experiment in three plantation forests with varying stand densities (high, medium, and low), using a parking area as a control. Our findings revealed that viewing plantation forests led to both physiological and psychological relaxation effects. Notably, medium-density plantation forests with a 3-meter spacing between trees, demonstrated a more significant relaxation effect on reducing heart rate compared to high and low-density plantations with spacing of 1 m and 5 m, respectively. High-density plantation forests were more effective in reducing total mood disturbance and specific negative mood states, including fatigue-inertia, depression-dejection, and tension-anxiety. Interestingly, regardless of stand density, restorative components were similar among the four experimental settings (high, medium, low, and control). These findings have practical implications for designing restorative environments and leveraging the therapeutic potential of plantation forests.

Seasonal effects on subclinical cardiovascular functions (CVFs) are an important emerging health issue for people living in urban environment. The objectives of this study were to demonstrate the effects of seasonal variations of temperature, relative humidity, and PM2.5 air pollution on CVFs. A total of 86 office workers in Taipei City were recruited, their arterial pressure waveform was recorded by cuff sphygmomanometer using an oscillometric blood pressure (BP) device for CVFs assessment. Results of paried t-test with Bonferroni correction showed significantly increased systolic and diastolic BP (SBP, DBP), central end-systolic and diastolic BP (cSBP, cDBP) and systemic vascular resistance, but decreased heart rate (HR), stroke volume (SV), cardio output (CO), and cardiac index in winter compared with other seasons. After controlling for related confounding factors, SBP, DBP, cSBP, cDBP, LV dp/dt max, and brachial-ankle pulse wave velocity (baPWV) were negatively associated with, and SV was positively associated with seasonal temperature changes. Seasonal changes of air pollution in terms of PM2.5 were significantly positively associated with DBP and cDBP, as well as negatively associated with HR and CO. Seasonal changes of relative humidity were significantly negatively associated with DBP, and cDBP, as well as positively associated with HR, CO, and baPWV. This study provides evidence of greater susceptibility to cardiovascular events in winter compared with other seasons, with ambient temperature, relative humidity, and PM2.5 as the major factors of seasonal variation of CVFs.

Abstract Taiwania (Taiwania cryptomerioides) is a valuable raw material in the wood products industry in Taiwan. An empirical study of the physiological and psychological effects of smelling Taiwania contributes to an understanding of the properties of interior wood that could potentially promote the use of wood materials in a healthy living environment. Prior studies have indicated that pre-knowledge of odors can cause cognitive bias and different responses in subjects. Designed to disclose the therapeutic effects of Taiwania’s scent and its extension to environmental health promotions, this study aimed to (1) investigate its effects on human health responses by stimulating olfaction, and (2) explore the role of cognitive bias in exposure to the scent of Taiwania. The results showed Taiwania’s volatiles had a relaxation effect in reducing the heart rates of participants. Some negative mood states, such as confusion, fatigue, and depression were suppressed. Regarding sensory perceptions, participants reported Taiwania’s scent induced greater affective scores of stimulation, excitement, firmness, distinctiveness, activity, and denseness, but a lower feeling of pleasantness. There were significant effects of positive cognitive bias on reducing the anger-hostility feeling of participants, but no effects on physiological responses. Moreover, the positive information bias alleviated the unpleasantness toward the smell.

Parkinson's disease (PD) is a neurodegenerative disorder featuring progressive loss of midbrain dopaminergic (DA) neurons that leads to motor symptoms. The etiology and pathogenesis of PD are not clear. We found that expression of COUP-TFII, an orphan nuclear receptor, in DA neurons is upregulated in PD patients through the analysis of public datasets. We show here that through epigenetic regulation, COUP-TFII contributes to oxidative stress, suggesting that COUP-TFII may play a role in PD pathogenesis. Elevated COUP-TFII expression specifically in DA neurons evokes DA neuronal loss in mice and accelerates the progression of phenotypes in a PD mouse model, MitoPark. Compared to control mice, those with elevated COUP-TFII expression displayed reduced cristae in mitochondria and enhanced cellular electron-dense vacuoles in the substantia nigra pars compacta. Mechanistically, we found that overexpression of COUP-TFII disturbs mitochondrial pathways, resulting in mitochondrial dysfunction. In particular, there is repressed expression of genes encoding cytosolic aldehyde dehydrogenases, which could enhance oxidative stress and interfere with mitochondrial function via 3,4-dihydroxyphenylacetaldehyde (DOPAL) buildup in DA neurons. Importantly, under-expression of COUP-TFII in DA neurons slowed the deterioration in motor functions of MitoPark mice. Taken together, our results suggest that COUP-TFII may be an important contributor to PD development and a potential therapeutic target.

Abstract Background There are estimated 180–220 species of Tuber described in the world, but the diversity of the genus in Taiwan is poorly known, with only two species recorded, i.e., Tuber formosanum and T. furfuraceum. During our survey of hypogenous fungi in Taiwan, a whitish truffle belongs to Puberulum clade was collected from roots of Keteleeria fortunei var. cyclolepis in central Taiwan and appeared to differ from the two recorded species. Results The whitish truffle is herein described as a new species Tuber elevatireticulatum, which is distinguished from closely resembled Asian whitish truffles species like Tuber thailandicum, T. panzhihuanense, T. latisporum and T. sinopuberulum by the association with Keteleeria host, small light brown ascocarps with a dark brown gleba, dark brownish and elliptical ascospores ornamented with a prominently raised alveolate reticulum. Molecular phylogenetic analyses of both ITS and LSU loci clearly supports T. elevatireticulatum as a new species without any significant incongruence. Conclusions The whitish truffle is herein described as a new species T. elevatireticulatum based on the evidence from morphology and DNA sequences. T. elevatireticulatum is the first scientific record of whitish truffle in Taiwan.

Various surgical techniques for canalicular laceration reconstruction have been described in previous study. But there are still two difficult points which may take time in the operation even with the assistance of magnification. We present a simple and effective way to achieve the bicanalicular nasal intubation for the single canalicular laceration. From Jan 2005 to Dec 2015, 20 patients (21 eyes) with upper or lower canalicular laceration were treated with the Crawford lacrimal intubation set by this stitch guide method. We used the eye pigtail probe and the steel probe of the intubation set to dispose a 4-0 Nylon suture as a guide to pull down the silicone tube to the nostril. The functional and anatomic success rates in the 20 eyes are 90% (18/20) and 85% (17/20) respectively. The average time for bicanalicular nasal intubation by this method is 6.87 ± 1.83 min. The result of stitch guide technique to achieve bicanalicular nasal intubation in single canalicular laceration reconstruction is almost the same as the traditional method. Our anatomic and functional success rates are 85% and 90% respectively which are comparable to the previous studies. But this new method takes less time to complete the intubation with little variation. The magnification with microscopy could be omitted and no new instrument is needed. The stitch guide technique for bicanalicular nasal intubation with Crawford intubation system is a reliable and easy way to perform in single canalicular laceration reconstruction. Keywords: Stitch guide, Bicanalicular nasal intubation, Canalicular laceration, Crawford

Abstract Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) has been shown to inhibit myogenesis and skeletal muscle metabolism in vitro. However, its precise role and in vivo function in muscle development has yet to be clearly defined. COUP-TFII protein expression level is high in undifferentiated progenitors and gradually declines during differentiation, raising an important question of whether downregulation of COUP-TFII expression is required for proper muscle cell differentiation. In this study, we generated a mouse model ectopically expressing COUP-TFII in myogenic precursors to maintain COUP-TFII activity during myogenesis and found that elevated COUP-TFII activity resulted in inefficient skeletal muscle development. Using in vitro cell culture and in vivo mouse models, we showed that COUP-TFII hinders myogenic development by repressing myoblast fusion. Mechanistically, the inefficient muscle cell fusion correlates well with the transcriptional repression of Npnt, Itgb1D and Cav3, genes important for cell-cell fusion. We further demonstrated that COUP-TFII also reduces the activation of focal adhesion kinase (FAK), an integrin downstream regulator which is essential for fusion process. Collectively, our studies highlight the importance of down-regulation of COUP-TFII signaling to allow for the induction of factors crucial for myoblast fusion.

The orphan nuclear receptor COUP-TFII is highly expressed in metastatic prostate cancers and its overexpression accelerates prostate tumour progression in mouse models. Here, the author show that that loss of miR-101 and miR-27a in prostate cancer cells can lead to COUP-TFII expression which in turn directly regulates FOXM1 and CENPFfavouring prostate cancer metastasis.

The highly reactive nature of biogenic volatile organic compounds (BVOCs) impacts the biosphere by acting as a precursor of ozone and aerosols that influence air quality and climate. Here, we assess the influence of BVOCs and their oxidation products on ozone formation and to submicron secondary organic aerosol (SOA) mass in a subtropical forest. A high-resolution proton-transfer-reaction time-of-flight mass spectrometer (PTR-ToF-MS) was employed for the continuous measurement of VOCs. Isoprene, monoterpene, and sesquiterpene mixing ratios in the forest were 0.23, 0.22, and 0.03 ppb, respectively. The total ozone formation potential (OFP) of the terpenes was 12.8 μg m−3, which accounted for only 5.6% of the total OFP. Particle phase bound oxidation products were characterized using a thermal-desorption PTR-ToF-MS. Mass spectra analysis revealed the presence pinonaldehyde, pinonic, norpinonic, and pinic acid in both gas and particle phase. The overall daytime (nighttime) mixing ratio of the oxidized BVOCs in gas phases was 0.062(0.023) ppbv. On the other hand, the mean fraction of the four monoterpene oxidation products in condensed phase was estimated at 42%. Overall, the results of this study evidenced quantitatively the contribution of BVOCs to the total reactivity and SOA mass in the subtropical forest.

Ever since we developed mitochondria to generate ATP, eukaryotes required intimate mito-nuclear communication. In addition, since reactive oxygen species are a cost of mitochondrial oxidative phosphorylation, this demands safeguards as protection from these harmful byproducts. Here we identified a critical transcriptional integrator which eukaryotes share to orchestrate both nutrient-induced mitochondrial energy metabolism and stress-induced nuclear responses, thereby maintaining carbon-nitrogen balance, and preserving life span and reproductive capacity. Inhibition of nutrient-induced expression of CAPER arrests nutrient-dependent cell proliferation and ATP generation and induces autophagy-mediated vacuolization. Nutrient signaling to CAPER induces mitochondrial transcription and glucose-dependent mitochondrial respiration via coactivation of nuclear receptor ERR-α-mediated Gabpa transcription. CAPER is also a coactivator for NF-κB that directly regulates c-Myc to coordinate nuclear transcriptome responses to mitochondrial stress. Finally, CAPER is responsible for anaplerotic carbon flux into TCA cycles from glycolysis, amino acids and fatty acids in order to maintain cellular energy metabolism to counter mitochondrial stress. Collectively, our studies reveal CAPER as an evolutionarily conserved 'master' regulatory mechanism by which eukaryotic cells control vital homeostasis for both ATP and antioxidants via CAPER-dependent coordinated control of nuclear and mitochondrial transcriptomic programs and their metabolisms. These CAPER dependent bioenergetic programs are highly conserved, as we demonstrated that they are essential to preserving life span and reproductive capacity in human cells-and even in C. elegans.

Chronic endoplasmic reticulum (ER) stress results in toxicity that contributes to multiple human disorders. We report a stress resolution pathway initiated by the nuclear receptor LRH-1 that is independent of known unfolded protein response (UPR) pathways. Like mice lacking primary UPR components, hepatic Lrh-1-null mice cannot resolve ER stress, despite a functional UPR. In response to ER stress, LRH-1 induces expression of the kinase Plk3, which phosphorylates and activates the transcription factor ATF2. Plk3-null mice also cannot resolve ER stress, and restoring Plk3 expression in Lrh-1-null cells rescues ER stress resolution. Reduced or heightened ATF2 activity also sensitizes or desensitizes cells to ER stress, respectively. LRH-1 agonist treatment increases ER stress resistance and decreases cell death. We conclude that LRH-1 initiates a novel pathway of ER stress resolution that is independent of the UPR, yet equivalently required. Targeting LRH-1 may be beneficial in human disorders associated with chronic ER stress.

Assessment of health effects of a forest environment is an important emerging area of public health and environmental sciences.To demonstrate the long-term health effects of living in a forest environment on subclinical cardiovascular diseases (CVDs) and health-related quality of life (HRQOL) compared with that in an urban environment.This study included the detailed health examination and questionnaire assessment of 107 forest staff members (FSM) and 114 urban staff members (USM) to investigate the long-term health effects of a forest environment. Air quality monitoring between the forest and urban environments was compared. In addition, work-related factors and HRQOL were evaluated.Levels of total cholesterol, low-density lipoprotein cholesterol, and fasting glucose in the USM group were significantly higher than those in the FSM group. Furthermore, a significantly higher intima-media thickness of the internal carotid artery was found in the USM group compared with that in the FSM group. Concentrations of air pollutants, such as NO, NO2, NOx, SO2, CO, PM2.5, and PM10 in the forest environment were significantly lower compared with those in the outdoor urban environment. Working hours were longer in the FSM group; however, the work stress evaluation as assessed by the job content questionnaire revealed no significant differences between FSM and USM. HRQOL evaluated by the World Health Organization Quality of Life-BREF questionnaire showed FSM had better HRQOL scores in the physical health domain.This study provides evidence of the potential beneficial effects of forest environments on CVDs and HRQOL.

As pleiotropic coregulators, members of the p160/steroid receptor coactivator (SRC) family control a broad spectrum of transcriptional responses that underpin a diverse array of physiological and pathophysiological processes. Because of their potent coregulator properties, strict controls on SRC expression levels are required to maintain normal tissue functionality. Accordingly, an unwarranted increase in the cellular levels of SRC members has been causally linked to the initiation and/or progression of a number of clinical disorders. Although knockout mouse models have underscored the critical non-redundant roles for each SRC member in vivo, there are surprisingly few mouse models that have been engineered to overexpress SRCs. This deficiency is significant since SRC involvement in many of these disorders is based on unscheduled increases in the levels (rather than the absence) of SRC expression. To address this deficiency, we used recent mouse technology that allows for the targeted expression of human SRC-2 in cells which express the progesterone receptor. Through cre-loxP recombination driven by the endogenous progesterone receptor promoter, a marked elevation in expression levels of human SRC-2 was achieved in endometrial cells that are positive for the progesterone receptor. As a result of this increase in coregulator expression, female mice are severely subfertile due to a dysfunctional uterus, which exhibits a hypersensitivity to estrogen exposure. Our findings strongly support the proposal from clinical observations that increased levels of SRC-2 are causal for a number of endometrial disorders which compromise fertility. Future studies will use this mouse model to decipher the molecular mechanisms that underpin the endometrial defect. We believe such mechanistic insight may provide new molecular descriptors for diagnosis, prognosis, and/or therapy in the clinical management of female infertility.

The chicken ovalbumin upstream promoter-transcription factors (COUP-TFI and II) make up the most conserved subfamily of nuclear receptors that play key roles in angiogenesis, neuronal development, organogenesis, cell fate determination, and metabolic homeostasis. Although the biological functions of COUP-TFs have been studied extensively, little is known of their structural features or aspects of ligand regulation. Here we report the ligand-free 1.48 A crystal structure of the human COUP-TFII ligand-binding domain. The structure reveals an autorepressed conformation of the receptor, where helix alpha10 is bent into the ligand-binding pocket and the activation function-2 helix is folded into the cofactor binding site, thus preventing the recruitment of coactivators. In contrast, in multiple cell lines, COUP-TFII exhibits constitutive transcriptional activity, which can be further potentiated by nuclear receptor coactivators. Mutations designed to disrupt cofactor binding, dimerization, and ligand binding, substantially reduce the COUP-TFII transcriptional activity. Importantly, retinoid acids are able to promote COUP-TFII to recruit coactivators and activate a COUP-TF reporter construct. Although the concentration needed is higher than the physiological levels of retinoic acids, these findings demonstrate that COUP-TFII is a ligand-regulated nuclear receptor, in which ligands activate the receptor by releasing it from the autorepressed conformation.

Chicken Ovalbumin Upstream Promoter-Transcription Factor II (COUP-TFII; also known as NR2F2), is an orphan nuclear receptor of the steroid/thyroid hormone receptor superfamily. COUP-TFII-null mice die during the early embryonic development due to angiogenesis and cardiovascular defects. To circumvent the early embryonic lethality and investigate the physiological function of COUP-TFII, we knocked out COUP-TFII gene in a time-specific manner by using a tamoxifen inducible Cre recombinase. The ablation of COUP-TFII during pre-pubertal stages of male development results in infertility, hypogonadism and spermatogenetic arrest. Homozygous adult male mutants are defective in testosterone synthesis, and administration of testosterone could largely rescue the mutant defects. Notably, the rescued results also provide the evidence that the major function of adult Leydig cell is to synthesize testosterone. Further phenotypic analysis reveals that Leydig cell differentiation is arrested at the progenitor cell stage in the testes of null mice. The failure of testosterone to resumption of Leydig cell maturation in the null mice indicates that COUP-TFII itself is essential for this process. In addition, we identify that COUP-TFII plays roles in progenitor Leydig cell formation and early testis organogenesis, as demonstrated by the ablation of COUP-TFII at E18.5. On the other hand, when COUP-TFII is deleted in the adult stage after Leydig cells are well differentiated, there are no obvious defects in reproduction and Leydig cell function. Taken together, these results indicate that COUP-TFII plays a major role in differentiation, but not the maintenance of Leydig cells.

Progesterone and estrogen are critical regulators of uterine receptivity. To facilitate uterine remodeling for embryo attachment, estrogen activity in the uterine epithelia is attenuated by progesterone; however, the molecular mechanism by which this occurs is poorly defined. COUP-TFII (chicken ovalbumin upstream promoter transcription factor II; also known as NR2F2), a member of the nuclear receptor superfamily, is highly expressed in the uterine stroma and its expression is regulated by the progesterone-Indian hedgehog-Patched signaling axis that emanates from the epithelium. To further assess COUP-TFII uterine function, a conditional COUP-TFII knockout mouse was generated. This mutant mouse is infertile due to implantation failure, in which both embryo attachment and uterine decidualization are impaired. Using this animal model, we have identified a novel genetic pathway in which BMP2 lies downstream of COUP-TFII. Epithelial progesterone-induced Indian hedgehog regulates stromal COUP-TFII, which in turn controls BMP2 to allow decidualization to manifest in vivo. Interestingly, enhanced epithelial estrogen activity, which impedes maturation of the receptive uterus, was clearly observed in the absence of stromal-derived COUP-TFII. This finding is consistent with the notion that progesterone exerts its control of implantation through uterine epithelial-stromal cross-talk and reveals that stromal-derived COUP-TFII is an essential mediator of this complex cross-communication pathway. This finding also provides a new signaling paradigm for steroid hormone regulation in female reproductive biology, with attendant implications for furthering our understanding of the molecular mechanisms that underlie dysregulation of hormonal signaling in such human reproductive disorders as endometriosis and endometrial cancer.