A Coral Damage Index and its Application to Diving Sites in the Egyptian Red Sea

A coral damage index (CDI) is provided, to screen sites to obtain a perspective on the extent and severity of physical damage to coral. Sites are listed as “hot spots” if in any transect the percent of broken coral colonies (BCC) is greater than or equal to 4% or if the percent cover of coral rubble (CR) is greater than or equal to 3%. To demonstrate its utility, the CDI is applied to a real-life management situation off Hurghada and Safaga, Egypt in the Red Sea. The extent of coral damage covered all four diving sites. Forty percent of all the transects were “hot spots” that required management action. Thirty-one percent of the 16 “hot spot” transects were identified by both broken coral and rubble criteria, 25% by only broken coral criterion and 44% by only coral rubble criterion of the CDI, suggesting that past breakage was responsible for most of the observed damage. Sixty-three percent of the “hot spot” transects were at 4 m depth versus 37% at 8 m depth, suggesting that most of the damage was caused by anchors dragging across the reef in shallow water. The severity of coral damage, reflected by CR, was the greatest at Small Giftun in transect 5 at 4 m depth (333% above the CDI). EI Fanous experienced the most severe degree of broken coral damage (325% above the CDI) at 8 m depth along transect 2. Estimates of the number of dives per year show diving carrying capacities for El Fanous, Gotta Abu Ramada, Ras Abu Soma and Small Giftun being exceeded by large amounts. The CDI can be used globally to; gauge the severity and extent of damage, focus managers on areas that need mooring buoys and associated dive site management programs, and provide a starting point from which to focus more detailed coral reef assessments and restoration programs

A Quantitative Ecological Assessment of Diving Sites in the Egyptian Red Sea During a Period of Severe Anchor Damage: A Baseline for Restoration and Sustainable Tourism Management

This paper assesses damage to diving sites off Hurghada and Safaga, Egypt, and examines management responses and options. Data were obtained using the line-intercept-transect method. Using general field observations, a control site comparison and a historical comparison, it was found that the four diving sites studied suffered varying degrees of physical damage and needed management attention. Some transect locations had experienced severe physical damage while others had escaped damage. The most obvious difference between the control site and the four damaged sites (at both 4 and 8 m depths) was the consistently high percentage cover of hard coral (especially Acropora coral) and low percentage cover of soft corals among all transects at the Giftun Canal control site. Total algae percentages were also consistently higher at impacted transect sites versus the control site. From a historical perspective, at the Small Giftun site from 1987 to 1996, percentage hard coral cover decreased by 43% and algal cover increased over fourfold. If the diving tourism industry is to sustain itself in the Egyptian Red Sea, every management effort must be made to minimise controllable sources of stress on the coral reef system. Dive site management programme options, based on peer-reviewed carrying capacity research and stakeholder involvement, are reviewed

Disciplinary Action Against UK Health Professionals for Sexual Misconduct: A Matter of Reputational Damage or Public Safety?

© 2021 Federation of State Medical Boards. All Rights Reserved.The regulation of health care professionals in the United Kingdom (UK) falls under the authority of one of nine General Councils, each of which has a statutory duty to ensure the fitness to practice of a subdivision of these professionals. Among the matters that may call fitness to practice into question are deviations from published standards of behavior, which include the maintenance of appropriate sexual boundaries by practitioners. The aim of this article is to examine how the common fitness-to-practice process utilized by General Councils deals with registered health care professionals who have exceeded these boundaries.Deductive thematic analysis was carried out on cases involving academic misconduct among registrants of the General Medical Council, General Dental Council, General Pharmaceutical Council, and Nursing and Midwifery Council, using themes derived from each council’s standards for registrants and guidance for disciplinary panel members.While each of these four cases involved some form of sexually motivated misconduct, the facts in each case were significantly different; however, not only was the outcome the same, but the rationale was similar in each instance. While the protection of the health, safety and well-being of the public may be considered in cases involving sexual misconduct, the need to maintain public and professional confidence in their respective professions is sufficient grounds alone to end the careers of health professionals who engage in sexual misconduct.Peer reviewedFinal Published versio

High sensitivity M-protein detection in a case of light-chain cardiac amyloidosis without evidence of plasma cell dyscrasia

https://www.ncbi.nlm.nih.gov/pubmed/3057510

Mast cells promote small bowel cancer in a tumor stage-specific and cytokine-dependent manner

Mast cells (MCs) are tissue resident sentinels that mature and orchestrate inflammation in response to infection and allergy. While they are also frequently observed in tumors, the contribution of MCs to carcinogenesis remains unclear. Here, we show that sequential oncogenic events in gut epithelia expand different types of MCs in a temporal-, spatial-, and cytokine-dependent manner. The first wave of MCs expands focally in benign adenomatous polyps, which have elevated levels of IL-10, IL-13, and IL-33, and are rich in type-2 innate lymphoid cells (ILC2s). These vanguard MCs adhere to the transformed epithelial cells and express murine mast cell protease 2 (mMCP2; a typical mucosal MC protease) and, to a lesser extent, the connective tissue mast cell (CTMC) protease mMCP6. Persistence of MCs is strictly dependent on T cell-derived IL-10, and their loss in the absence of IL-10–expressing T cells markedly delays small bowel (SB) polyposis. MCs expand profusely in polyposis-prone mice when T cells overexpress IL-10. The frequency of polyp-associated MCs is unaltered in response to broad-spectrum antibiotics, arguing against a microbial component driving their recruitment. Intriguingly, when polyps become invasive, a second wave of mMCP5+/mMCP6+ CTMCs expands in the tumor stroma and at invasive tumor borders. Ablation of mMCP6 expression attenuates polyposis, but invasive properties of the remaining lesions remain intact. Our findings argue for a multistep process in SB carcinogenesis in which distinct MC subsets, and their elaborated proteases, guide disease progression

Mast cells promote small bowel cancer in a tumor stage-specific and cytokine-dependent manner

Mast cells (MCs) are tissue resident sentinels that mature and orchestrate inflammation in response to infection and allergy. While they are also frequently observed in tumors, the contribution of MCs to carcinogenesis remains unclear. Here, we show that sequential oncogenic events in gut epithelia expand different types of MCs in a temporal-, spatial-, and cytokine-dependent manner. The first wave of MCs expands focally in benign adenomatous polyps, which have elevated levels of IL-10, IL-13, and IL-33, and are rich in type-2 innate lymphoid cells (ILC2s). These vanguard MCs adhere to the transformed epithelial cells and express murine mast cell protease 2 (mMCP2; a typical mucosal MC protease) and, to a lesser extent, the connective tissue mast cell (CTMC) protease mMCP6. Persistence of MCs is strictly dependent on T cell-derived IL-10, and their loss in the absence of IL-10–expressing T cells markedly delays small bowel (SB) polyposis. MCs expand profusely in polyposis-prone mice when T cells overexpress IL-10. The frequency of polyp-associated MCs is unaltered in response to broad-spectrum antibiotics, arguing against a microbial component driving their recruitment. Intriguingly, when polyps become invasive, a second wave of mMCP5+/mMCP6+ CTMCs expands in the tumor stroma and at invasive tumor borders. Ablation of mMCP6 expression attenuates polyposis, but invasive properties of the remaining lesions remain intact. Our findings argue for a multistep process in SB carcinogenesis in which distinct MC subsets, and their elaborated proteases, guide disease progression