In glaucoma, lowered intraocular pressure (IOP) confers neuroprotection. Elevated IOP characterizes glaucoma and arises from impaired aqueous humor (AH) outflow. Increased resistance in the trabecular meshwork (TM), a filter-like structure essential to regulate AH outflow, may result in the impaired outflow. Flow through the 360° circumference of TM structures may be non-uniform, divided into high and low flow regions, termed as segmental. After flowing through the TM, AH enters Schlemm’s canal (SC), which expresses both blood and lymphatic markers; AH then passes into collector channel entrances (CCE) along the SC external well. From the CCE, AH enters a deep scleral plexus (DSP) of vessels that typically run parallel to SC. From the DSP, intrascleral collector vessels run radially to the scleral surface to connect with AH containing vessels called aqueous veins to discharge AH to blood-containing episcleral veins. However, the molecular mechanisms that maintain homeostatic properties of endothelial cells along the pathways are not well understood. How these molecular events change during aging and in glaucoma pathology remain unresolved. In this review, we propose mechanistic possibilities to explain the continuum of AH outflow control, which originates at the TM and extends through collector channels to the episcleral veins.

The ischemic state of the myocardium of the isolated working rat heart after induction of normothermic ischemic cardiac arrest was assessed by the interrelationship among changes in myocardial ultrastructure, mitochondrial oxidative phosphorylation, and tissue high energy phosphate contents. At all time intervals (10-40 minutes) studied, the ultrastructural changes were more severe in the subendocardium than in the subepicardium. After 25-40 minutes of normothermic ischemic cardiac arrest, the mitochondrial oxygen uptake (state 3) became increasingly depressed, particularly in mitochondria isolated from the subendocardium. Mitochondrial oxidative function, as measured in vitro, did not correlate well with mitochondrial ultrastructural damage. In addition, the effects of coronary reperfusion on the ability of the ischemic heart to recover in terms of ultrastructure, mechanical, and metabolic function were evaluated. Hearts subjected to 10-40 minutes of normothermic ischemic cardiac arrest showed almost complete ultrastructural recovery of the subepicardium upon reperfusion; regression of ultrastructural changes occurred to a lesser extent in the subendocardium. Reperfusion for 30 minutes did not alleviate the depression in mitochondrial oxidative function, while tissue ATP levels did not return to control, preischemic levels. After 20 minutes of normothermic ischemic cardiac arrest, the mechanical performance of the working heart during reperfusion was significantly depressed, compared with pre-ischemic control values. Normal ultrastructure of the subendocardium always accompanied mechanical recovery, while improvement of mitochondrial oxidative function was not essential.

A new species of Heydrichia (Sporolithales), Heydrichia cerasina sp. nov., is described, found only on pebbles in the low intertidal zone along a 10 km stretch of the South African south coast from Cape Agulhas to Struisbaai. The species is characterized by the following suite of features that distinguish it from the other two species of Heydrichia found in South Africa: (1) unusual cherry-red colour when freshly collected; (2) uniformly warty growth form; (3) relatively thin crust (up to 1400 mm thick); (4) tetra/bisporangial sori comprised of mostly single sporangial chambers; and (5) unbranched spermatangial structures distributed on the floor, walls, and roof of the mature male conceptacle. The species appears to be most closely related to Heydrichia homalopasta from Australia. This study has affirmed that the distribution of spermatangial structures within male chambers is a feature that cannot be used to separate Heydrichia from Sporolithon, the only other genus in Sporolithales, although features of thallus construction and tetra/bisporangia continue to distinguish the genera. A key to the southern African species from the order Sporolithales is provided.

DNA sequence data from a 296 base pair variable region of the plastid encoded rbcL gene was obtained from 19th century type material of Spongites decipiens and of Lithophyllum tumidum (¼Pseudolithophyllum neofarlowii) and matched to field-collected material, confirming the application of these specific epithets in the northeast Pacific. Phylogenetic analyses of separate and concatenated rbcL and psbA gene sequences show that both species belong in Spongites. Based on DNA sequences, the distribution of S. decipiens is confirmed from Haida Gwaii, British Columbia, Canada, south to its type locality at San Pedro, Los Angeles County, California, whereas, Spongites tumidum is distributed from near Sitka, Alaska, to Monterey County, California. Sequence data from S. decipiens and South African specimens called Spongites yendoi confirm anatomical studies that these two species are distinct but that a previously undescribed, cryptic species, Spongites agulhensis, also is present in South Africa. Anatomically and morphologically S. agulhensis is very similar to both northeast Pacific S. decipiens and South African S. yendoi, differing from the former by a single anatomical character and from the latter by two anatomical characters. Anatomy, ecology and distributions are useful in separating the South African species of Spongites, as well as the northeast Pacific species. Sequence divergence values align with biogeographic patterns and not with anatomical similarities for these Spongites species. We question the practice of placing into synonymy geographically widely separated non-geniculate coralline algal species based solely on anatomical features that likely have resulted from convergent evolution.

BackgroundThere is a marked paucity of data concerning AKI in Sub-Saharan Africa, where there is a substantial burden of trauma and HIV.MethodsProspective data was collected on all patients admitted to a multi-disciplinary ICU in South Africa during 2017. Development of AKI (before or during ICU admission) was recorded and renal recovery 90 days after ICU discharge was determined.ResultsOf 849 admissions, the mean age was 42.5 years and mean SAPS 3 score was 48.1. Comorbidities included hypertension (30.5%), HIV (32.6%), diabetes (13.3%), CKD (7.8%) and active tuberculosis (6.2%). The most common reason for admission was trauma (26%). AKI developed in 497 (58.5%). Male gender, illness severity, length of stay, vasopressor drugs and sepsis were independently associated with AKI. AKI was associated with a higher in-hospital mortality rate of 31.8% vs 7.23% in those without AKI. Age, active tuberculosis, higher SAPS 3 score, mechanical ventilation, vasopressor support and sepsis were associated with an increased adjusted odds ratio for death. HIV was not independently associated with AKI or hospital mortality. CKD developed in 14 of 110 (12.7%) patients with stage 3 AKI; none were dialysis-dependent.ConclusionsIn this large prospective multidisciplinary ICU cohort of younger patients, AKI was common, often associated with trauma in addition to traditional risk factors and was associated with good functional renal recovery at 90 days in most survivors. Although the HIV prevalence was high and associated with higher mortality, this was related to the severity of illness and not to HIV status per se.

We have previously demonstrated that tumor necrosis factor alpha (TNFalpha), a cytokine known to be induced by ischemia, independently promotes preconditioning in part via ceramide generation. As reactive oxygen species (ROS) signaling is evoked by ischemic preconditioning, by TNFalpha and by ceramide we reasoned that ceramide-induced preconditioning is ROS-mediated. Fibroblastic L-cells were subjected to 8 hours simulated ischemia and were preconditioned by pretreatment with cell permeable c2 ceramide (1 microM) with or without the antioxidant N-mercaptopropionyl glycine (MPG; 1 mM). Pretreatment with ceramide reduced lactate dehydrogenase release at the end of the simulated ischemia but this cytoprotective effect was lost in the presence of MPG. Concurrent temporal ROS generation was measured using confocal microscopy on cells stained with dichlorofluorescein diacetate (DCF-DA). Ceramide increased ROS production after 30 minutes and this induction was decreased by MPG. Incubation of ceramide with cyclooxygenase-2 inhibitor, NS 398 (10 microM), or with a mitochondrial respiratory chain inhibitor, rotenone (10 microM) reduced the cytoprotective effect of ceramide in parallel with a partial diminution in ROS generation. In contrast, inhibition of other ROS-producing systems including nitric oxide synthase, xanthine oxidase, or NADPH oxidase failed to modulate ceramide-induced cytoprotection. Collectively, these data demonstrate that ceramide induces a cell survival program through ROS signaling activated, in part, via cyclooxygenase and the mitochondrial respiratory chain.

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