Marine anoxia linked to abrupt global warming during Earth’s penultimate icehouse

Piecing together the history of carbon (C) perturbation events throughout Earth’s history has provided key insights into how the Earth system responds to abrupt warming. Previous studies, however, focused on short-term warming events that were superimposed on longer-term greenhouse climate states. Here, we present an integrated proxy (C and uranium [U] isotopes and paleo CO₂) and multicomponent modeling approach to investigate an abrupt C perturbation and global warming event (∼304 Ma) that occurred during a paleo-glacial state. We report pronounced negative C and U isotopic excursions coincident with a doubling of atmospheric CO₂ partial pressure and a biodiversity nadir. The isotopic excursions can be linked to an injection of ∼9,000 Gt of organic matter–derived C over ∼300 kyr and to near 20% of areal extent of seafloor anoxia. Earth system modeling indicates that widespread anoxic conditions can be linked to enhanced thermocline stratification and increased nutrient fluxes during this global warming within an icehouse.

Observations and climate models indicate that the dissolved oxygen inventory of the modern ocean is decreasing, with temperature-driven decline in oxygen solubility being a key driver (1). A decline in ocean dissolved oxygen, expressed as an expanded oxygen minimum zone (OMZ), will negatively impact marine ecosystems, leading to significant loss of biodiversity in the ocean (2). This is of significant concern for the world’s largest fisheries situated in the most productive areas of global oceans, as these regions are particularly susceptible to ocean deoxygenation (3, 4). Substantial uncertainty in estimating the extent of deoxygenation over the upcoming millennia, however, drives the current focus on understanding past episodes of ocean deoxygenation.Empirical constraints on the magnitude of ocean deoxygenation during climate perturbations come predominantly from the Quaternary glacial–interglacial transitions (5, 6) or early Cenozoic rapid warming events, in particular the Paleocene–Eocene Thermal Maximum (PETM) event (7, 8). The temporal scales of warming and deoxygenation of these events differ by an order of magnitude (10⁴ vs. 10⁵ y). Constraints on ocean circulation and biogeochemical cycles across warming events in the Quaternary are more robust than in Earth’s deep past (5, 9). On the other hand, Quaternary partial pressure of CO₂ (pCO₂) and temperature shifts were gradual and the overall perturbations small in magnitude (10) relative to predicted changes for the next millennia or two. Although changes in pCO₂ during the early Cenozoic warming events (foremost, the PETM) were larger in magnitude and more rapid than carbon (C) perturbations of Quaternary glacial–interglacial transitions (11, 12), they occurred under a background greenhouse climate state characterized by high baseline atmospheric pCO₂ (∼1,000 ppm). Other periods of pre-Cenozoic C perturbations (13, 14), such as the Cretaceous and Jurassic (Toarcian) ocean anoxic events (OAEs) (15, 16), and the end-Triassic (17) and the end-Permian mass extinction events (18), also occurred during background greenhouse climates (19, 20). These greenhouse OAEs have provided constraints on and insights into how to model climate change and marine redox evolution. To date, the degree of deoxygenation and spread of anoxic conditions with warming in a glacial state is relatively unexplored.Here, we provide a perspective on global warming–induced ocean deoxygenation by documenting a 10⁵-y C-perturbation event associated with widespread oceanic anoxia, superimposed on the late Paleozoic glacial climate state. This past icehouse (with main episode between ∼340 and 290 Ma) existed under atmospheric CO₂ levels comparable to that of the past few million years (21) and was a period of dynamic and widespread glaciation in the Southern Hemisphere (Gondwana). As such, it provides unique constraints on deoxygenation with warming under a background glacial state, albeit with different paleogeographic boundary and marine and ecosystem conditions compared with those of the younger greenhouse periods of C perturbation.     

Consumption of Ultra-Processed Foods Is Inversely Associated with Adherence to the Mediterranean Diet: A Cross-Sectional Study

Information on the consumption of ultra-processed foods (UPF) in relation to an adherence to the Mediterranean diet (MD) is limited. Our aim was to assess UPF consumption in a group of Italian adults and to evaluate the relationship with the MD adherence. A total of 670 participants (median age: 30 years) were included in the analysis. The consumption of UPF was assessed through the NOVA Food Frequency Questionnaire (NFFQ). Adherence to the MD was assessed through the Medi-Lite score. The percentage of UPF in the diet was 16.4% corresponding to 299 g of UPF per day. These amounts were significantly (p < 0.05) higher in men than in women and came mainly from ready-to-eat meals or pre-packaged bread, bread alternatives, pizza, frozen potato chips (24.5% of total UPF intake), pre-packaged biscuits and sweets (20.7%), soft drinks (15.8%), and dairy products such as flavored yogurt (12%). As to the MD adherence, a significant inverse association between the Medi-Lite score and the percentage of UPF in the diet (R = −0.35; p < 0.001) was observed. Participants with a low adherence to the MD had a significantly higher contribution of UPF in the diet (22.2%) compared to those with a moderate (16.2%) and high (12.6%) adherence. In terms of individual UPF, the largest difference between low and high MD adherents was observed for pre-packaged biscuits and sweets, soft and energy drinks, sausages and other reconstituted meat products, and pre-packaged bread and bread alternatives. These results suggest that public health strategies are needed to implement more effective actions to promote healthy eating habits in the population.     

Effect of Intermittent Fasting on Reproductive Hormone Levels in Females and Males: A Review of Human Trials

Intermittent fasting is a popular diet for weight loss, but concerns have been raised regarding the effects of fasting on the reproductive health of women and men. Accordingly, we conducted this literature review to clarify the effects of fasting on reproductive hormone levels in humans. Our results suggest that intermittent fasting decreases androgen markers (i.e., testosterone and the free androgen index (FAI)) while increasing sex hormone-binding globulin (SHBG) levels in premenopausal females with obesity. This effect was more likely to occur when food consumption was confined to earlier in the day (eating all food before 4 pm). In contrast, fasting did not have any effect on estrogen, gonadotropins, or prolactin levels in women. As for men, intermittent fasting reduced testosterone levels in lean, physically active, young males, but it did not affect SHBG concentrations. Interestingly, muscle mass and muscular strength were not negatively affected by these reductions in testosterone. In interpreting these findings, it is important to note that very few studies have been conducted on this topic. Thus, it is difficult to draw solid conclusions at present. From the limited data presented here, it is possible that intermittent fasting may decrease androgen markers in both genders. If this is the case, these results would have varied health implications. On the one hand, fasting may prove to be a valuable tool for treating hyperandrogenism in females with polycystic ovarian syndrome (PCOS) by improving menstruation and fertility. On the other hand, fasting may be shown to decrease androgens among males, which could negatively affect metabolic health and libido. More research is warranted to confirm these preliminary findings.     

Expanding the phenotype of the recurrent truncating eIF2γ pathogenic variant p.(Ile465Serfs*4) identified in two brothers with MEHMO syndrome

We describe two brothers with a recurrent truncating EIF2S3 variant and MEHMO (Mental retardation, Epileptic seizures, Hypogonadism and ‐genitalism, Microcephaly, Obesity). Both had the previously described facial dysmorphic features, microcephaly, developmental impairment, hypoglycemia, hypothyreosis, diabetes mellitus, epilepsy, hypertonus, obesity, and micropenis. Additionally, we describe hypothermia and reduced umbilical blood flow.     

Oxidative Stress and Left Ventricular Performance in Patients with Different Glycometabolic Phenotypes

The aim of the present study was to evaluate the possible correlation between oxidative stress and subclinical myocardial damage, assessed with speckle tracking echocardiography (STE), in normal glucose tolerance (NGT) patients with one-hour plasma glucose values ≥ 155 mg/dL (NGT ≥ 155), comparing them to NGT < 155 subjects, impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) newly diagnosed patients. We enrolled 100 Caucasian patients. All subjects underwent OGTT. The serum values of oxidative stress markers (8-isoprostane and Nox-2) were assessed with an ELISA test. Echocardiographic recordings were performed using an E-95 Pro ultrasound system. We observed significant differences, among the four groups, for fasting plasma glucose (p < 0.0001), one-hour postload (p < 0.0001), and two-hour postload plasma glucose (p < 0.0001). As compared with NGT < 155, NGT ≥ 155 exhibited significantly worse insulin sensitivity and higher values of hs-CRP. No significant differences were observed between NGT ≥ 155 and IGT patients. There was a significant increase in 8-isoprostane (p < 0.0001) and Nox-2 (p < 0.0001), from the first to fourth group, indicating an increase in oxidative stress with the worsening of the metabolic status. Serum levels of 8-isoprostane and Nox-2 were significantly increased in NGT ≥ 155 compared to the NGT < 155 group, but similar to IGT. The global longitudinal strain (GLS) appeared progressively lower proceeding from the NGT < 155 to T2DM group (p < 0.0001). For similar values of left ventricular ejection fraction (LVEF), NGT ≥ 155 exhibited reduced GLS compared to NGT < 155 (p = 0.001), but similar to IGT patients. Our study demonstrated that NGT ≥ 155 subjects exhibit early functional impairment of myocardial contractile fibres, these alterations are correlated with increased oxidative stress.     

Pseudomyxoma peritonei involving the canal of Nuck: The added value of magnetic resonance imaging for detection and presurgical planning

The canal of Nuck is an abnormal patent pouch of the parietal peritoneum caused by the incomplete obliteration of the processus vaginalis in females. The most common disorders of the canal of Nuck are: hernia, hydrocele and endometriosis. Pseudomyxoma Peritonei (PMP) is a clinical condition characterized by the accumulation of mucinous material on the surfaces and in the recesses of the peritoneal cavity, resulting from the perforation of an appendiceal mucinous neoplasm. We report the case of a young woman with a clinical history of chronic pelvic pain and infertility who was referred to our center after being diagnosed with appendiceal mucinous neoplasm and PMP. MRI staging examination revealed the right canal of Nuck filled with mucinous material, which was confirmed at surgery. The involvement of canal of Nuck is extremely rare in PMP. MRI provides a sensitive imaging modality for appropriate preoperative planning of PMP and helps surgeons identify uncommon disease sites such such as the canal of Nuck in women, which, if missed, may prevent complete cytoreductive surgery.     

Toxic Effects and Tumor Promotion Activity of Marine Phytoplankton Toxins: A Review

Phytoplankton are photosynthetic microorganisms in aquatic environments that produce many bioactive substances. However, some of them are toxic to aquatic organisms via filter-feeding and are even poisonous to humans through the food chain. Human poisoning from these substances and their serious long-term consequences have resulted in several health threats, including cancer, skin disorders, and other diseases, which have been frequently documented. Seafood poisoning disorders triggered by phytoplankton toxins include paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), amnesic shellfish poisoning (ASP), diarrheic shellfish poisoning (DSP), ciguatera fish poisoning (CFP), and azaspiracid shellfish poisoning (AZP). Accordingly, identifying harmful shellfish poisoning and toxin-producing species and their detrimental effects is urgently required. Although the harmful effects of these toxins are well documented, their possible modes of action are insufficiently understood in terms of clinical symptoms. In this review, we summarize the current state of knowledge regarding phytoplankton toxins and their detrimental consequences, including tumor-promoting activity. The structure, source, and clinical symptoms caused by these toxins, as well as their molecular mechanisms of action on voltage-gated ion channels, are briefly discussed. Moreover, the possible stress-associated reactive oxygen species (ROS)-related modes of action are summarized. Finally, we describe the toxic effects of phytoplankton toxins and discuss future research in the field of stress-associated ROS-related toxicity. Moreover, these toxins can also be used in different pharmacological prospects and can be established as a potent pharmacophore in the near future.     

Clinical significance of molecular subtypes of gastrointestinal tract adenocarcinoma

Adenocarcinomas of the gastrointestinal tract (esophagus, stomach, and colon) represent a heterogeneous group of diseases with distinct etiology, clinical features, treatment approaches, and prognosis. Studies are ongoing to isolate molecular genetic subtypes, perform complete biological characterization of the tumor, determine prognostic groups, and find predictive markers to the effectiveness of therapy. Separate molecular genetic classifications were created for esophageal adenocarcinoma [The Cancer Genome Atlas (TCGA)], stomach cancer (TCGA, Asian Cancer Research Group), and colon cancer (Colorectal Cancer Subtyping Consortium). In 2018, isolation of TCGA molecular genetic subtypes for adenocarcinomas of the gastrointestinal tract (esophagus, stomach, and colon) highlighted the need for further studies and clinical validation of subtyping of gastrointestinal adenocarcinomas. However, this approach has limitations. The aim of our work was to critically analyze integration of molecular genetic subtyping of gastrointestinal adenocarcinomas in clinical practice.