Hong Kong is an impact crater: Proof from the geomorphological and geological evidence

Hong Kong is a city in southern China. The urban districts of Hong Kong, Kowloon, and Victoria Harbour are situated within Hong Kong. Hong Kong is surrounded by mountains with a diameter of 11 km. Three million people live inside the basin. The round structure of the mountains in Hong Kong has been describd as a granite dome that is deeply eroded (batholith). The circularity of the mountains, the existence of a central hill, the inner slope of the mountains being greater than the outer slope, the presence of deep layer rock inside the basin, and the depth-to-diameter ratio were studied. All this evidence shows that the Hong Kong structure satisfies the geomorphological requirement of an impact crater. Some shock metamorphic phenomena of the rocks in Hong Kong such as planar features, microspherilitic silica glass (lechaterlierite), fused margins of rock fragments, concussion fractures, impact glass in which some schlierens are consistent with pyroxene spiculites, etc., were first discovered in Oct. 1990. In Hong Kong Island, an impact melt sheet was observed from the Victoria Peak to the southern shore. Quenching fractures of quartz in Kowloon fine-grained granite was also discovered. In our work, the K-Ar age (83.34 + 1.26 m.y.) of the impact melt rock, which is younger in comparison to the K-Ar age (117 m.y.) in Hong Kong and Kowloon granite, was measured, and the phenomena indicate that after the granite body formed, there was another geologic event. Maybe it is the Hong Kong cratering event

ATM Regulates Insulin-Like Growth Factor 1-Secretory Clusterin (IGF-1-sCLU) Expression that Protects Cells against Senescence

Downstream factors that regulate the decision between senescence and cell death have not been elucidated. Cells undergo senescence through three pathways, replicative senescence (RS), stress-induced premature senescence (SIPS) and oncogene-induced senescence. Recent studies suggest that the ataxia telangiectasia mutant (ATM) kinase is not only a key protein mediating cellular responses to DNA damage, but also regulates cellular senescence induced by telomere end exposure (in RS) or persistent DNA damage (in SIPS). Here, we show that expression of secretory clusterin (sCLU), a known pro-survival extracellular chaperone, is transcriptionally up-regulated during both RS and SIPS, but not in oncogene-induced senescence, consistent with a DNA damage-inducible mechanism. We demonstrate that ATM plays an important role in insulin-like growth factor 1 (IGF-1) expression, that in turn, regulates downstream sCLU induction during senescence. Loss of ATM activity, either by genomic mutation (ATM-deficient fibroblasts from an ataxia telangiectasia patient) or by administration of a chemical inhibitor (AAI, an inhibitor of ATM and ATR), blocks IGF-1-sCLU expression in senescent cells. Downstream, sCLU induction during senescence is mediated by IGF-1R/MAPK/Egr-1 signaling, identical to its induction after DNA damage. In contrast, administration of an IGF-1 inhibitor caused apoptosis of senescent cells. Thus, IGF-1 signaling is required for survival, whereas sCLU appears to protect cells from premature senescence, as IMR-90 cells with sCLU knockdown undergo senescence faster than control cells. Thus, the ATM-IGF-1-sCLU pathway protects cells from lethality and suspends senescence

Homer1a Attenuates Endoplasmic Reticulum Stress-Induced Mitochondrial Stress After Ischemic Reperfusion Injury by Inhibiting the PERK Pathway

Homer1a is the short form of a scaffold protein that plays a protective role in many forms of stress. However, the role of Homer1a in cerebral ischemia/reperfusion (I/R) injury and its potential mechanism is still unknown. In this study, we found that Homer1a was upregulated by oxygen and glucose deprivation (OGD) and that overexpression of Homer1a alleviated OGD-induced lactate dehydrogenase (LDH) release and cell death in cultured cortical neurons. After OGD treatment, the overexpression of Homer1a preserved mitochondrial function, as evidenced by less cytochrome c release, less reactive oxygen species (ROS) production, less ATP and mitochondrial membrane potential (MMP) loss, less caspase-9 activation, and inhibition of endoplasmic reticulum (ER) stress confirmed by the decreased expression of phosphate-PKR-like ER Kinase (p-PERK)/PERK and phosphate- inositol-requiring enzyme 1 (p-IRE1)/IRE1 and immunofluorescence (IF) staining. In addition, mitochondrial protection of Homer1a was blocked by the ER stress activator Tunicamycin (TM) with a re-escalated ROS level, increasing ATP and MMP loss. Furthermore, Homer1a overexpression-induced mitochondrial stress attenuation was significantly reversed by activating the PERK pathway with TM and p-IRE1 inhibitor 3,5-dibromosalicylaldehyde (DBSA), as evidenced by increased cytochrome c release, increased ATP loss and a higher ROS level. However, activating the IRE1 pathway with TM and p-PERK inhibitor GSK2656157 showed little change in cytochrome c release and exhibited a moderate upgrade of ATP loss and ROS production in neurons. In summary, these findings demonstrated that Homer1a protects against OGD-induced injury by preserving mitochondrial function through inhibiting the PERK pathway. Our finding may reveal a promising target of protecting neurons from cerebral I/R injury

Incidence of Stress-Induced Hyperglycemia in Acute Ischemic Stroke: A Systematic Review and Meta-Analysis

The aim of this study was to systematically evaluate the incidence of stress-induced hyperglycemia (SIH) in acute ischemic stroke (AIS). Studies that reported SIH incidence in AIS and examined risk factors for SIH and non-SIH patients were systematically searched in PubMed, Embase, Cochrane Library, and Web of Science from the inception of each database to December 2021. Article screening and data extraction were performed by two independent reviewers according to the inclusion and exclusion criteria. The quality of the included studies was assessed using the Newcastle–Ottawa Scale (NOS), and meta-analysis was performed using Stata. A total of 13 studies involving 4552 patients (977 in the SIH group and 3575 in the non-SIH group) were included. Meta-analysis showed that the incidence of SIH was 24% (95% CI: 21–27%) in the total population, 33% (14–52%) in North America, 25% (20–29%) in Europe, and 21% (12–29%) in Asia. Subgroup analysis by year of publication revealed that the pooled incidence of SIH was 27% (22–32%) in studies published before 2010 and 19% (14–24%) in those published after 2010. SIH is relatively common in AIS and poses a serious public health problem. Therefore, more emphasis should be placed on the prevention and control of SIH in AIS

Low dose IR-induced IGF-1-sCLU expression: a p53-repressed expression cascade that interferes with TGFß1 signaling to confer survival

To better understand tissue responses after low IR doses, we generated a reporter system using human clusterin promoter fused to firefly luciferase (hCLUp-Luc). Secretory clusterin (sCLU), an extra-cellular molecular chaperone, induced by low doses of cytotoxic agents, clears cell debris promoting survival. Low dose IR (>2 cGy) exposure induced hCLUp-Luc activity with peak levels at 96 h, consistent with endogenous sCLU levels. As doses increased (>1 Gy), sCLU induction amplitudes increased and time to peak response decreased. sCLU expression was stimulated by IGF-1, but suppressed by p53. Responses in transgenic hCLUp-Luc reporter mice after low IR doses showed that specific tissues (i.e., colon, spleen, mammary, thymus, bone marrow) of female mice induced hCLUp-Luc activity more than male mice after whole body >10 cGy. Tissue-specific, non-linear dose- and time-responses of hCLUp-Luc and endogenous sCLU levels were noted. Colon maintained homeostatic balance after 10 cGy. Bone marrow responded with delayed, but prolonged and elevated expression. Intraperitoneal administration of the α-TGFß1 (1D11) antibody, but not a control antibody (13C4), immediately following IR exposure abrogated CLU induction responses. Induction in vivo also correlated with Smad signaling via activated TGFß1 after IR. Mechanistically, media with elevated sCLU levels suppressed signaling, blocked apoptosis and increased survival of TGFß1-exposed tumor or normal cells. Thus, sCLU is a TGF-ß1-induced pro-survival, potential bystander factor expressed in certain exposed tissues that, in turn, abrogates TGFß1 signaling and may promote wound healing and likely contributes to a pro-tumor growth microenvironment

A High-Performance Base-Metal Approach for the Oxidative Esterification of 5-Hydroxymethylfurfural

Exploring high-performance base-metal approaches for the sustainable production of chemicals from biomass is presently attracting immense interest and is truly important to promote their industrialized application. Herein, CoOx-N/C and alpha-MnO2 were combined as a base-metal catalyst that can achieve high yields of furan-2,5-dimethylcarboxylate (FDMC, 95.6%) for the catalytic oxidative esterification of 5-hydroxymethylfurfural (HMF) without basic additive. The reaction proceeds through fast conversion of HMF to diformylfuran (DFF) with alpha-MnO2 and subsequent transformation of DFF to FDMC by CoOx-N/C. Quantitative X-ray photoelectron spectroscopy (XPS) analysis and density functional theory (DFT) calculations indicated that the pyridinic-N present in doped carbon could behave as a Lewis base to promote the abstraction of hydrogen for the oxidative esterification reaction. Consequently, CoOx-N/C is a high performance catalyst for the synthesis of FDMC from DFF in a neutral medium

Additional file 2: of Effect of L-arginine and sildenafil citrate on intrauterine growth restriction fetuses: a meta-analysis

Quality of enrolled RCTs [8–16]. (DOC 40 kb

Additional file 1: of Effect of L-arginine and sildenafil citrate on intrauterine growth restriction fetuses: a meta-analysis

Identification process for eligible studies. (DOC 35 kb