The rise of baobab trees in Madagascar.

The baobab trees (genus Adansonia) have attracted tremendous attention because of their striking shape and distinctive relationships with fauna1. These spectacular trees have also influenced human culture, inspiring innumerable arts, folklore and traditions. Here we sequenced genomes of all eight extant baobab species and argue that Madagascar should be considered the centre of origin for the extant lineages, a key issue in their evolutionary history2,3. Integrated genomic and ecological analyses revealed the reticulate evolution of baobabs, which eventually led to the species diversity seen today. Past population dynamics of Malagasy baobabs may have been influenced by both interspecific competition and the geological history of the island, especially changes in local sea levels. We propose that further attention should be paid to the conservation status of Malagasy baobabs, especially of Adansonia suarezensis and Adansonia grandidieri, and that intensive monitoring of populations of Adansonia za is required, given its propensity for negatively impacting the critically endangered Adansonia perrieri.

Homozygous pathogenic variants in ACTL9 cause fertilization failure and male infertility in humans and mice.

Total fertilization failure (TFF) can occur during in vitro fertilization (IVF) treatments, even following intracytoplasmic sperm injection (ICSI). Various male or female factors could contribute to TFF. Increasing evidence suggested that genetic variations in PLCZ1, which encodes 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase zeta-1 (PLCζ), is involved in oocyte activation and is a key male factor in TFF. In the present study, we explored the genetic variants in male individuals that led to TFF. A total of 54 couples with TFF or poor fertilization (fertilization rate < 20%) were screened, and 21 couples were determined to have a male infertility factor by the mouse oocyte activation test. Whole-exome sequencing of these 21 male individuals identified three homozygous pathogenic variants in ACTL9 (actin like 9) in three individuals. ACTL9 variations led to abnormal ultrastructure of the perinuclear theca (PT), and PLCζ was absent in the head and present in the neck of the mutant sperm, which contributed to failed normal calcium oscillations in oocytes and subsequent TFF. The key roles of ACTL9 in the PT structure and TFF after ICSI were further confirmed in an Actl9-mutated mouse model. Furthermore, assisted oocyte activation by calcium ionophore exposure successfully overcame TFF and achieved live births in a couple with an ACTL9 variant. These findings identified the role of ACTL9 in the PT structure and the correct localization of PLCζ. The results also provide a genetic marker and a therapeutic option for individuals who have undergone ICSI without successful fertilization.

HES1 deficiency impairs development of human intestinal mesenchyme by suppressing WNT5A expression.

Serious intestinal side-effects that target the NOTCH-HES1 pathway in human cancer differentiation therapy make it necessary to understand the pathway at the human organ level. Herein, we endogenously introduced HES1-/- mutations into human embryonic stem cells (hESCs) and differentiated them into human intestinal organoids (HIO). The HES1-/- hESCs retained ES cell properties and showed gene expression patterns similar to those of wild-type hESCs when they differentiated into definitive endoderm and hindgut. During the formation of the HES1-/- lumen we noted an impaired development of mesenchymal cells in addition to the increased differentiation of secretory epithelium. RNA-Seq revealed that inhibited development of the mesenchymal cells may have been due to a downregulation of WNT5A signaling. Overexpression of HES1 and silencing of WNT5A in the intestinal fibroblast cell line CCD-18Co indicated that HES1 was involved in the activation of WNT5A-induced fibroblast growth and migration, suggesting the likelihood of the Notch pathway in epithelial-mesenchymal crosstalk. Our results facilitated the identification of more precise underlying molecular mechanisms displaying distinct roles in HES1 signaling in stromal and epithelial development in human intestinal mucosa.

Low-dose telomerase is required for the expansion and migration of placental mesenchymal stem cells.

Telomerase is activated in pluripotent stem cells and the majority of tumors and is postulated to be necessary for the acquisition of self-renewal and long-term proliferation. Placental mesenchymal stem cells (PMSCs) are very promising in regenerative medicine owing to their great capacity for self-renewal and differentiation potential. Although telomerase activity in the placenta is naturally low, it remains unclear whether telomerase activity is required for the properties of PMSCs. We herein isolated and identified a PMSC line carrying compound heterozygote variations in hTERT (DC-PMSCs) that lost telomerase activity, showed a typical surface phenotype of MSCs, and was able to differentiate into multiple cell lineages. DC-PMSCs showed accelerated telomere erosion, advanced senescence, and diminished migratory and invasive capabilities. RNA-seq identified 361 differentially expressed genes between DC-PMSCs and control groups, most of which were enriched in extracellular matrix, ECM, and related pathways. Knockdown of telomerase subunit genes in PMSCs confirmed the phenotype and attenuated the expression of extracellular matrix components and matrix metalloproteases. Our results suggest that low telomerase activity is not essential for the properties of MSCs, but that it is required for community maintenance and for the migration of PMSCs.

Identification of a heterozygous variant of ZP2 as a novel cause of empty follicle syndrome in humans and mice.

STUDY QUESTION: Is a recurrent heterozygous mutation in ZP2, c.1925G>A (p.R642Q), associated with the Empty follicle syndrome (EFS)? SUMMARY ANSWER: ZP2, c.1925G>A (p.R642Q), led to female infertility related to EFS in humans and mice and resulted in ZP2 accumulation in the cytoplasm of oocytes. WHAT IS KNOWN ALREADY: EFS is a complex disease defined as a complete failure of oocyte retrieval after ovarian stimulation and after repeated aspirations and flushing of mature ovarian follicles. Furin-mediated cleavage is a post-translational modification (PTM) involved in various physiological processes, but the clear role of PTM mediated by furin cleavage of ZP2 protein on female fertility needs to be further explored. PTM is required for proteins to function in physiological conditions, and its perturbation has been linked to a growing number of human pathologies. Zona pellucida (ZP) proteins, which are important for oocyte development, are regulated post-translationally by well-characterized glycosylation events, as well as by furin-mediated cleavage. However, knowledge of the relevance of the consensus furin cleavage site of ZP proteins in female reproduction remains lacking. STUDY DESIGN, SIZE, DURATION: This was a basic medical research project to assess the pathogenicity of a heterozygous mutation in the ZP2 gene in EFS. PARTICIPANTS/MATERIALS, SETTING, METHODS: We studied 3 families with EFS and a control group 2213 women with proven fertility. Whole-exome sequencing detected a heterozygous mutation in the ZP2 gene in all EFS patients. The mouse strain Zp2Arg635Gln/+ (ZP2R642Q) was generated by CRISPR-Cas9-mediated genome editing. RNA-sequencing was applied to investigate transcriptional changes in the ovaries of heterozygous ZP2R642Q knock-in (KI) mice compared to WT mice. MAIN RESULTS AND THE ROLE OF CHANCE: We found a heterozygous mutation of ZP2, c.1925G>A (p.R642Q), in unrelated females with EFS, which was inherited in an autosomal-dominant manner. We used CRISPR-Cas9 to generate a mouse model encoding the orthologous variant of ZP2R642Q detected in humans, and the female ZP2R642Q KI mice recapitulated the human EFS phenotype. We further found the decreased expression of key genes involved in oocyte maturation in ZP2R642Q KI mice compared to WT mice by RNA-sequencing analysis. LARGE SCALE DATA: N/A. LIMITATIONS, REASONS FOR CAUTION: Only three families affected by EFS with the mutation were available because of its rare incidence. Although we have found different expressions of the several indispensable genes related to oocyte development between WT mice and ZP2R642Q KI mice through RNA-sequencing analysis, the specific regulatory mechanisms of the oocyte apoptosis in ZP2R642Q KI mice need to be studied further. WIDER IMPLICATIONS OF THE FINDINGS: These results are expected to open new avenues for researchers in the exploration of potential therapeutic strategies in treating EFS. STUDY FUNDING/COMPETING INTEREST(S): This project is funded by the National Key Research and Development Program of China (2018YFC1002804, 2017YFC1001500 and 2016YFC1000200). All authors declared no competing interests. TRIAL REGISTRATION NUMBER: N/A.

To roll or not to roll: nyctinastic behavior in young leaves of sacred lotus, Nelumbo nucifera.

Foliar nyctinasty refers to the daily rhythm in leaf orientation that occurs in evolutionarily diverse taxa. Traditionally, two mechanisms have been identified for the sleep movement of leaves, namely pulvinar and non-pulvinar. Here, we report upon some novel aspects of the nyctinastic behavior of leaves of the sacred lotus (Nelumbo nucifera Gaertn., Nelumbonaceae). We discovered that expanding leaves underwent daily oscillations in leaf orientation with a more vertical position at night, which is similar to many nyctinastic species. Additionally, however, the immature leaves were observed to exhibit a second type of nyctinasty that involved nocturnal rolling of leaf blades, which has not previously been reported. These two distinct mechanisms acted synergistically to make the young leaves more compact at night during a brief period (6 days) of leaf ontogenesis, during which petiole and blade showed substantial growth. We propose that the nyctinastic behavior of immature N. nucifera leaves is an adaptation that facilitates leaf growth at night by reducing mechanical interference with other leaves and plants.

Expanding the genetic and phenotypic spectrum of the subcortical maternal complex genes in recurrent preimplantation embryonic arrest.

The subcortical maternal complex (SCMC) is an oocyte-to-embryo-specific maternal functional module. Some variants of SCMC genes that contribute to preimplantation embryonic arrest have been identified. However, more novel variants should be identified to broaden the genetic and phenotypic spectrum of SCMC genes and establish their roles in embryonic development. We identified 13 novel variants in the SCMC genes, TLE6, NLRP5, NLRP2, and PADI6, from 10 of a total of 50 infertile females with recurrent preimplantation embryonic arrest. Six variants in TLE6 were found in five patients with embryonic arrest, accompanied by direct cleavage and severe fragmentation at the cleavage stage. Three patients carried NLRP5 variants, and one patient each who carried NLRP2 and PADI6 variants had subsequent poor or failed fertilization and cleavage arrest with a relatively lower ratio of severely fragmented embryos. Our findings expand the genetic and phenotypic spectrum of SCMC genes associated with human embryogenesis and might help lay the foundation for the genetic diagnosis of female infertility.

Novel homozygous variations in PLCZ1 lead to poor or failed fertilization characterized by abnormal localization patterns of PLCζ in sperm.

Total fertilization failure (TFF), which is the failure of fertilization in all oocytes, occurs in 1%-3% of intracytoplasmic sperm injection (ICSI) cycles. However, the sperm-related factors that cause fertilization failure in humans are still largely unknown. Here, we identified three novel homozygous variations in the PLCZ1 gene in a recessive inheritance pattern in three consanguineous families, which all located in a key catalytic domain, and predicted to modify its secondary structure and thus impair its hydrolytic activity. Moreover, immunofluorescent staining revealed that PLCζ in mutant sperm exhibited abnormal localization patterns. ICSI-AOA resulted in an increased rate of normal fertilization compared with previous ICSI cycles (75.0% vs 2.2%, P < .001). In summary, we identified three novel homozygous variations in PLCZ1 that led to poor or failed fertilization that could be overcame by ICSI-AOA.

New biallelic mutations in PADI6 cause recurrent preimplantation embryonic arrest characterized by direct cleavage.

PURPOSE: To investigate the pathogenesis of the recurrent preimplantation embryonic arrest characterized by direct cleavage. METHODS: Two affected individuals underwent time-lapse imaging to observe the cleavage behaviors in their final ICSI attempts. In addition, both patients were subjected to whole-exome sequencing. After the identification of possible causative genes, molecular modeling analyses were used to evaluate the possible effects of candidate mutations on protein secondary structure. RESULTS: All the bipronucleated (2PN) zygotes from both individuals presented multiple abnormal cleavage behaviors, particularly direct cleavage (DC) and subsequent cleavage arrest. Mutation analysis identified one new frameshift mutation c.1521dupC (p.S508Qfs*5) and two missense mutations c.A1117C and c.C1708T (p.T373P and p.R570C, respectively) of the PADI6 gene, which were in the protein-arginine deiminase (PAD) domain and highly conserved. CONCLUSION: This study expands the mutation spectrum of PADI6 and is the first to propose that the preimplantation embryonic arrest with concomitant abnormal cleavage behaviors, especially DC, maybe associated with PADI6 mutations.

ZP2 pathogenic variants cause in vitro fertilization failure and female infertility.

PURPOSE: The oocyte-borne genetic causes leading to fertilization failure are largely unknown. We aimed to identify novel human pathogenic variants (PV) and genes causing fertilization failure. METHODS: We performed exome sequencing for a consanguineous family with a recessive inheritance pattern of female infertility characterized by oocytes with a thin zona pellucida (ZP) and fertilization failure in routine in vitro fertilization. Subsequent PV screening of ZP2 was performed in additional eight unrelated infertile women whose oocytes exhibited abnormal ZP and similar fertilization failure. Expression of ZP proteins was assessed in mutant oocytes by immunostaining, and functional studies of the wild-type and mutant proteins were carried out in CHO-K1 cells. RESULTS: Two homozygous s PV (c.1695-2A>G, and c.1691_1694dup (p.C566Wfs*5), respectively) of ZP2 were identified in the affected women from two unrelated consanguineous families. All oocytes carrying PV were surrounded by a thin ZP that was defective for sperm-binding. Immunostaining indicated a lack of ZP2 protein in the thin ZP. Studies in CHO cells showed that both PV resulted in a truncated ZP2 protein, which might be intracellularly sequestered and prematurely interacted with other ZP proteins. CONCLUSION: We identified loss-of-function PV of ZP2 causing a structurally abnormal and dysfunctional ZP, resulting in fertilization failure and female infertility.

ZP1 mutations are associated with empty follicle syndrome: evidence for the existence of an intact oocyte and a zona pellucida in follicles up to the early antral stage. A case report.

Empty follicle syndrome (EFS) is the complete failure to retrieve oocytes after ovarian stimulation. Although LHCGR and ZP3 were identified as causative genes, it is still unclear what happens to these patients' oocytes, and the pathogenesis of EFS remains obscure. Here, we identified six novel ZP1 mutations associated with EFS and female infertility that was inherited recessively in five unrelated families. Studies in CHO-K1 cells showed that these mutations resulted in either degradation or truncation of ZP1 protein. Immunohistochemistry using ovarian serial sections demonstrated that all preantral follicles had normal architecture, but with a thin ZP, lacking ZP1, surrounding the growing oocytes. The antral follicles were also defective in normal cumulus-oocyte complex organisation, leading us to speculate that the lack of ZP1 might lead to oocyte degeneration or increased fragility of the oocyte during follicular puncture, ultimately resulting in EFS. To our knowledge, this is the first study that presents morphological evidence showing normal preantral folliculogenesis with abnormal ZP assembly in EFS patients. Our data provides a better understanding of the biological functions of ZP1 in human ZP assembly and folliculogenesis and gives new insights into the pathogenesis of EFS and possible therapeutic developments.

Novel inactivating mutations in the FSH receptor cause premature ovarian insufficiency with resistant ovary syndrome.

RESEARCH QUESTION: What is the genetic aetiology of three resistant ovary syndrome (ROS) pedigrees from 13 Chinese Han families with non-syndromic premature ovarian insufficiency (POI). DESIGN: The proband in each family was subjected to whole-exome sequencing. Bioinformatic and in-vitro functional analyses were performed for the functional characterization of the FSHR mutations. RESULTS: Four novel mutations, two homozygous mutations (c.419delA, c.1510C>T), and a compound heterozygous mutation (c.44G>A and deletion of exons 1 and 2) of FSHR were identified in the three non-syndromic POI-with-ROS families. Bioinformatic analysis predicted that the three novel point mutations in FSHR are deleterious and associated with POI in the three families, which was confirmed by in-vitro functional analysis, in which FSH-induced adenosine 3',5'-cyclic monophosphate production was abolished for all receptors. CONCLUSIONS: The three novel point mutations in FSHR were all functional inactivating mutations, and were the genetic aetiology of the three non-syndromic POI-with-ROS families. The first FSHR frameshift mutation is reported here, and the first missense mutation in the signal peptide-encoding region of FSHR to be associated with POI. Women affected by ROS should consider undergoing mutation screening for FSHR.

Resource reallocation patterns within Sagittaria trifolia inflorescences following differential pollination.

PREMISE OF THE STUDY: Understanding resource allocation to reproduction, a key factor in life history tradeoffs, has long intrigued plant ecologists. Despite the recognized importance of understanding the movement of resources among flowers following variable pollination, the patterns of resource reallocation to plant reproductive organs have not been thoroughly addressed. In this study, we aimed to empirically explore how resources redistribute within inflorescences in response to differential pollination intensities. METHODS: Using a common herb, Sagittaria trifolia, we conducted supplemental and controlled pollination for single, some, or all flowers in simple and complex inflorescences, and compared their resulting fruiting probabilities, seed production, and average seed masses. KEY RESULTS: Pollen supplementation of a single flower significantly increased its fruiting probability; however, the same manipulation of an inflorescence did not increase its overall reproduction. Single pollen-supplemented flowers had a higher percentage fruit set than inflorescences receiving supplemental pollination. In complex inflorescences, supplemental pollination had no effect on the reproductive success of flowers on the lateral or main branches. CONCLUSIONS: We provided evidence of resource reallocation from controlled to pollen-supplemented flowers in simple inflorescences; however, resources were unlikely to be reallocated between the main and lateral branches in the complex inflorescences, suggesting that flowering branches represent integrated physiological units in S. trifolia. The results also demonstrated that single-flower supplemental pollination would exaggerate pollen limitation and lead to a biased understanding of a plant's reproductive status.

Transcriptional activation of human CDCA8 gene regulated by transcription factor NF-Y in embryonic stem cells and cancer cells.

The cell division cycle associated 8 (CDCA8) gene plays an important role in mitosis. Overexpression of CDCA8 was reported in some human cancers and is required for cancer growth and progression. We found CDCA8 expression was also high in human ES cells (hESCs) but dropped significantly upon hESC differentiation. However, the regulation of CDCA8 expression has not yet been studied. Here, we characterized the CDCA8 promoter and identified its cis-elements and transcription factors. Three transcription start sites were identified. Reporter gene assays revealed that the CDCA8 promoter was activated in hESCs and cancer cell lines. The promoter drove the reporter expression specifically to pluripotent cells during early mouse embryo development and to tumor tissues in tumor-bearing mice. These results indicate that CDCA8 is transcriptionally activated in hESCs and cancer cells. Mechanistically, two key activation elements, bound by transcription factor NF-Y and CREB1, respectively, were identified in the CDCA8 basic promoter by mutation analyses and electrophoretic motility shift assays. NF-Y binding is positively correlated with promoter activities in different cell types. Interestingly, the NF-YA subunit, binding to the promoter, is primarily a short isoform in hESCs and a long isoform in cancer cells, indicating a different activation mechanism of the CDCA8 transcription between hESCs and cancer cells. Finally, enhanced CDCA8 promoter activities by NF-Y overexpression and reduced CDCA8 transcription by NF-Y knockdown further verified that NF-Y is a positive regulator of CDCA8 transcription. Our study unearths the molecular mechanisms underlying the activation of CDCA8 expression in hESCs and cancer cells, which provides a better understanding of its biological functions.

Abnormalities in centrosome number in human embryos and embryonic stem cells.

Chromosomal abnormalities are common in human embryos. Previous studies have suggested links between centrosome number and chromosome abnormalities, but information regarding abnormalities in centrosome number in human embryos is limited. We analyzed abnormalities in centrosome number in human embryos and embryonic stem cells (hESCs). Following normal fertilization, supernumerary centrosomes were present at rates of 7.3% in two-pronucleus (2PN)-stage zygotes and 6.5% in first-cleavage zygotes. Supernumerary centrosomes were also detected in 24.4% of blastomeres from 60% of embryos derived from 2PN zygotes. Conversely, in mono- (1PN) and tri-pronucleus (3PN) zygotes, the frequency of abnormal centrosome number increased substantially at first cleavage. Rates in blastomeres of Day-3 embryos, however, were about the same between embryos derived from 1PN and 2PN zygotes, whereas abnormalities in centrosome number were higher in those from 3PN zygotes. By comparison, the rate of abnormal centrosome numbers in hESCs was 1.5-11.2%. Thus, abnormalities in centrosome number existed in human zygotes and cleaved embryos-especially those resulting from aberrant fertilization-but the frequency of such abnormalities was lower in hESCs derived from these embryos. These findings identify a source of the chromosomal instability in human embryos and hESCs, and highlight new safety issues for human assisted reproductive technology. Mol. Reprod. Dev. 83: 392-404, 2016. © 2016 Wiley Periodicals, Inc.

The mean and variability of a floral trait have opposing effects on fitness traits.

BACKGROUND AND AIMS: Floral traits are essential for ensuring successful pollination and reproduction in flowering plants. In particular, style and anther positions are key for pollination accuracy and efficiency. Variation in these traits among individuals has been well studied, but less is known about variation within flowers and plants and its effect on pollination and reproductive success. METHODS: Style deflexion is responsible for herkogamy and important for pollen deposition in Passiflora incarnata. The degree of deflexion may vary among stigmas within flowers as well as among flowers. We measured the variability of style deflexion at both the flower and the plant level. The fitness consequences of the mean and variation of style deflexion were then evaluated under natural pollination by determining their relationship to pollen deposition, seed production and average seed weight using structural equation modelling. In addition, the relationship between style deflexion and self-pollen deposition was estimated in a greenhouse experiment. KEY RESULTS: We found greater variation in style deflexion within flowers and plants than among plants. Variation of style deflexion at the flower and plant level was positively correlated, suggesting that variability in style deflexion may be a distinct trait in P. incarnata. Lower deflexion and reduced variation in that deflexion increased pollen deposition, which in turn increased seed number. However, lower styles also increased self-pollen deposition. In contrast, higher deflexion and greater variability of that deflexion increased variation in pollen deposition, which resulted in heavier seeds. CONCLUSIONS: Variability of style deflexion and therefore stigma placement, independent from the mean, appears to be a property of individual P. incarnata plants. The mean and variability of style deflexion in P. incarnata affected seed number and seed weight in contrasting ways, through the quantity and potentially quality of pollen deposition. This antagonistic selection via different fitness components may maintain diverse style phenotypes.

Regional fibrocartilage variations in human anterior cruciate ligament tibial insertion: a histological three-dimensional reconstruction.

PURPOSE: We studied anterior cruciate ligament (ACL) tibial insertion architecture in humans and investigated regional differences that could suggest unequal force transmission from ligament to bone. MATERIALS AND METHODS: ACL tibial insertions were processed histologically. With Photoshop software, digital images taken from the histological slides were collaged, contour lines were drawn, and different gray values were filled based on the structure. The data were exported to Amira software for three-dimensional reconstruction. RESULTS: The uncalcified fibrocartilage (UF) layer was divided into three regions: lateral, medial and posterior according to the architecture. The UF zone was significantly thicker laterally than medially or posteriorly (p < 0.05). Similarly, the calcified fibrocartilage (CF) thickness was significantly greater in the lateral part of the enthesis compared to the medial and posterior parts (p < 0.05). CONCLUSIONS: The UF quantity (more UF laterally) corresponding to the CF quantity (more CF laterally) at the ACL tibial insertion provides further evidence suggesting that the load transferred from the ACL to the tibia was greater laterally than medially and posteriorly.

Construction of finite element model and stress analysis of anterior cruciate ligament tibial insertion.

OBJECTIVE: The aim of the present study was to develop a more realistic finite element (FE) model of the human anterior cruciate ligament (ACL) tibial insertion and to analyze the stress distribution in the ACL internal fibers under load. METHODS: The ACL tibial insertions were processed histologically. With Photoshop software, digital images taken from the histological slides were collaged, contour lines were drawn, and different gray values were filled based on the structure. The data were exported to Amira software and saved as ".hmascii" file. This document was imported into HyperMesh software. The solid mesh model generated using HyperMesh software was imported into Abaqus software. The material properties were introduced, boundary conditions were set, and load was added to carry out the FE analysis. RESULTS: The stress distribution of the ACL internal fibers was uneven. The lowest stress could be observed in the ACL lateral fibers under tensile and shear load. CONCLUSION: The establishment of ACL tibial insertion FE model and mechanical analysis could reveal the stress distribution in the ACL internal fibers under load. There was greater load carrying capacity in the ACL lateral fibers which could sustain greater tensile and shear forces.

Successive stamen movement in Saxifraga candelabrum is responsive to weather and pollinator visits.

BACKGROUND: Successive stamen movement is a complex plant behavior involving successive uplift of stamens and pollen release, which plays a role in reducing sexual interference, increasing pollen deposition and promoting pollen export. Although reported from several taxa, studies on whether the movement can be influenced by abiotic and biotic factors are scarce. METHODS: In this study, we here for the first time described a pattern of successive stamen movement in Saxifraga candelabrum (Saxifragaceae). We then compared the rates of stamen movement in S. candelabrum under different weather and varying pollinator visits. Pollen packaging and presentation schedule of S. candelabrum were also investigated. RESULTS: The results showed that the number of stamens bent per day in sunny days was significantly higher than overcast and rain. Flowers that receive more pollinator visits (control treatment) had significantly higher number of stamen movement than those that received fewer (removal treatment) and none (bagging treatment). Throughout the staminate phase of a flower, there was a progressive increase in both pollen quantity of individual stamens and pollen presentation during each day. CONCLUSION: Our research demonstrates that successive stamen movement in S. candelabrum was accelerated by favorable weather and increased pollinator visits, which may promote pollen export. Moreover, incremental pollen packaging is likely an adaptation to seasonal regularity in variations of sex ratio resulting from protandry.

Evaluation of a concise fall risk stratification among older adults with cataracts in day surgery settings: A historically controlled study.

AIM: This study aimed to evaluate the use of a concise fall risk stratification in assessing and predicting falls compared with the Morse Falls Scale among older adults with cataracts in day surgery settings. METHODS: A historically controlled study conducted from July 2020 to June 2022 was used in a municipal ophthalmic hospital in China. The concise fall risk stratification which directly graded fall risk by multifactorial judgment was used during the intervention period, while the Morse Falls Scale which graded fall risk by scale scores was used during the control period. The fall risk levels, fall assessment time, fall rates, fall-related injuries, predictive validity, and patient satisfaction with day surgery care were extracted. Propensity score matching was performed to balance baselines. RESULTS: After matching, 4132 patients were included in the final analysis. Compared with the control group, the intervention group had significantly higher assessment results for fall risk level, a significantly shorter (by 48.15%) fall assessment time, and higher patient satisfaction. There were no differences in fall rates and fall-related injuries. Compared with the Morse Falls Scale, the concise fall risk stratification had higher sensitivity and negative predictive validity, and lower specificity and positive predictive validity, while the area under curve did not differ significantly. CONCLUSION: The use of the concise fall risk stratification reduced fall assessment time, improved patient satisfaction, and is unlikely to impact falls with an overall predictive performance comparable to that of the Morse Falls Scale for older cataract adults in day surgery settings.