Since 2014, Stony Coral Tissue Loss Disease (SCTLD) has led to mass mortality of the majority of hard coral species on the Florida Reef Tract. Following the successful treatment of SCTLD lesions on laboratory corals using water dosed with antibiotics, two topical pastes were developed as vehicles to directly apply antibiotic treatments to wild corals. These pastes were tested as placebos and with additions of amoxicillin on active SCTLD lesions on multiple coral species. The effectiveness of the pastes without antibiotics (placebo treatments) was less than 10%, no different from untreated controls. Adding amoxicillin to both pastes significantly increased effectiveness to 70% and 84%. Effectiveness with this method was seen across five different coral species, with success rates of the more effective paste ranging from 67% (Colpophyllia natans) to 90% (Orbicella faveolata and Montastraea cavernosa). Topical antibiotic application is a viable and effective tool for halting disease lesions on corals affected by SCTLD.

Since 2014, Stony Coral Tissue Loss Disease (SCTLD) has led to mass mortality of the majority of hard coral species on the Florida Reef Tract. Following the successful treatment of SCTLD lesions on laboratory corals using water dosed with antibiotics, two topical pastes were developed as vehicles to directly apply antibiotic treatments to wild corals. These pastes were tested as placebos and with additions of amoxicillin on active SCTLD lesions on multiple coral species. The effectiveness of the pastes without antibiotics (placebo treatments) was less than 10%, no different from untreated controls. Adding amoxicillin to both pastes significantly increased effectiveness to 70% and 84%. Effectiveness with this method was seen across five different coral species, with success rates of the more effective paste ranging from 67% (Colpophyllia natans) to 90% (Orbicella faveolata and Montastraea cavernosa). Topical antibiotic application is a viable and effective tool for halting disease lesions on corals affected by SCTLD.

Surgical exploration of eight chronically afflicted haemophilic knee joints in patients aged 6 to 31 years, has revealed a pattern of progressive arthropathy.Significant synovial changes occurred very early. Cellular overgrowth produced thickening, convolution and increased vascularity. Haemosiderin was deposited heavily in all cell layers. Fibrosis ultimately contracted the synovium.Chronic inflammation produced epiphyseal overgrowth. Initially, articular cartilage changes resembled chondromalacia, but fissuring soon occurred and ultimately cartilage was totally lost over central weight-bearing areas and in the intercondylar region. Anomalies of matrix, chondrocyte aggregation and death, and subchondral round cell infiltration were features. Haemosiderin staining was sparse, occurring only in some chondrocytes and infiltrating cells.Biochemical analysis of articular cartilage biopsies revealed a severe depletion of glycosaminoglycans. There was no biochemical evidence of a reaction of repair.Articular cartilage damage occurred mainly between the ages of 6 and 10 years. This evidence suggests that early surgical synovectomy may arrest the process that produces progressive joint destruction.

A number of polymerase chain reaction (PCR) inhibitors have been identified from biological and environmental samples. By and large, such substances are treated as random nuisances and contaminants with alternate functions; their inhibitory effects on DNA replication being a coincidental property of their molecular structure. Here, we demonstrate the presence of a localized PCR inhibitor in the foregut of the porcelain crab Petrolisthes rufescens (Anomura: Porcellanidae) from the Red Sea. The inhibitor precluded amplification of 28s, 16s and 18s gene sequences effectively but lost activity at 10-2 dilutions from initial concentration. Heat treatment was ineffective in arresting inhibition and spectrophotometric techniques suggested that the inhibitor was not a melanin-type compound. The compound was not detected from midgut, hindgut, or gills of the crab. Activity of the inhibitor was precluded when samples were treated with suspensions from the midgut, suggesting that enzymatic degradation of the inhibitor likely happens at that part of the gut. As many microbial pathogens invade their hosts via ingestion, we suggest the presence of the localized inhibitor could carry a defensive or immunological role for P. rufescens. The identity of the inhibitory molecule remains unknown.

A number of polymerase chain reaction (PCR) inhibitors have been identified from biological and environmental samples. By and large, such substances are treated as random nuisances and contaminants with alternate functions; their inhibitory effects on DNA replication being a coincidental property of their molecular structure. Here, we demonstrate the presence of a localized PCR inhibitor in the foregut of the porcelain crab Petrolisthes rufescens (Anomura: Porcellanidae) from the Red Sea. The inhibitor precluded amplification of 28s, 16s and 18s gene sequences effectively but lost activity at 10-2 dilutions from initial concentration. Heat treatment was ineffective in arresting inhibition and spectrophotometric techniques suggested that the inhibitor was not a melanin-type compound. The compound was not detected from midgut, hindgut, or gills of the crab. Activity of the inhibitor was precluded when samples were treated with suspensions from the midgut, suggesting that enzymatic degradation of the inhibitor likely happens at that part of the gut. As many microbial pathogens invade their hosts via ingestion, we suggest the presence of the localized inhibitor could carry a defensive or immunological role for P. rufescens. The identity of the inhibitory molecule remains unknown.