1B). This could be caused by the use of different reporter genes (nuclear-targeted β-galactosidase

in the previous study vs. cytosolic EGFP in the current study) and the different mechanism by which genes were delivered to neurons. The efficiency of DNA entry into cells is also compromised in the IUE method, as a trade-off in preventing electroporation-induced damage to the embryo. Nevertheless, we found that transfected Purkinje find more cells could efficiently coexpress at least three transgenes (Figs 3 and 4). This situation is quite advantageous for electrophysiological analyses, because recordings from transfected and neighboring non-transfected (control) neurons can be easily compared. In addition, EGFP introduced at E11.5 remained highly expressed 1 month after birth (Fig. 2) and was maintained at least until P90 (data not shown). Immature Purkinje cells originally have a fusiform shape with a few dendrites. Purkinje cells lose these primitive dendrites almost completely VEGFR inhibitor by P3–P4 in rats (Sotelo & Dusart, 2009). As the virus-mediated overexpression of human RORα1 accelerates this process in wild-type and restores it in staggerer cerebellum organotypic slice cultures, RORα1 was proposed to play a crucial role in the regression of primitive dendritic branches (Boukhtouche et al., 2006). In the present study, we showed that the IUE-mediated overexpression of dominant-negative RORα1 in Purkinje cells in vivo could recapitulate the morphological

abnormalities observed in staggerer mice (Fig. 5). These results not only support but also extend the hypothesis that cell-autonomous activities of RORα1 in Purkinje cells are responsible for the process controlling the regression of primitive dendrites in vivo. Notably, because of the limited migration of Purkinje cells in organotypic slice cultures, the migration defect of staggerer Purkinje cells was not analysed previously (Boukhtouche et al., 2006), and it remains unclear whether the regressive phase begins during or after the migration of Purkinje cells to their final domains. We observed that some Purkinje cells expressing dominant-negative RORα1 did not reach the Purkinje cell

layer in vivo, indicating that RORα1 regulates not either only the regression of dendrites but also the migration process of Purkinje cells. It is unclear why the phenotypes of Purkinje cells expressing dominant-negative RORα1 were variable, but small differences in transgene expression levels and/or the developmental stage of the transfected Purkinje cell progenitors could have contributed to the variation. A more robust suppression of RORα1 gene expression by IUE-based RNA interference (Matsuda & Cepko, 2004) will help clarify the role of RORα1 in the early events during Purkinje-cell development. Future studies taking advantage of IUE to enable gene expression from the early postmitotic stage will facilitate studies on the mechanisms of Purkinje cell development and migration.

Their article also described the distribution of flagellar systems in 43 actinobacterial genomes, as well as in four actinomycetes that possessed a flagellin gene (e.g. Nocardioides sp. JS614, Leifsonia xyli, Acidothermus cellulolyticus, and Kineococcus radiotolerans). Analysis Obeticholic Acid solubility dmso of these four actinomycete genomes revealed that there were no genes encoding FlgF (proximal

rod) and FlgG (distal rod), and that the flagellar system may be incomplete (Snyder et al., 2009). However, all species belonging to the genus Kineococcus are motile, and polar flagella have been observed in K. radiotolerans SRS30216 (Phillips et al., 2002). Similarly, several species belonging to the genera Nocardioides and Leifsonia were observed to have motile cells and flagella (Cho et al., 2010; Madhaiyan et al., 2010). Interestingly, whole genome sequence data from A. cellulolyticus 11B revealed the presence NVP-BEZ235 cell line of a flagellar system, even though this actinomycete species was previously reported to be non-motile (Barabote et al., 2009).

In addition, genes for the flagellar system in Salinispora tropica, CNB-440, which belongs to the family Micromonosporaceae, have not yet been identified (Udwary et al., 2007). Taken together, these findings indicate that the distribution and diversity of flagellar genes in actinomycetes is unclear (Snyder et al., 2009). This study therefore sought to characterize the flagellin-encoding gene in Actinoplanes species as a representative of motile actinomycetes. In this article, we amplified, sequenced and analyzed flagellin gene sequences from selected Actinoplanes type strains. In addition, structural predictions were performed using the SWISS-MODEL server

(Schwede et al., 2003), with a template from a known flagellin protein from Salmonella typhimurium (Maki-Yonekura et al., 2010). Finally, phylogenetic analysis based on the N-terminal region of the flagellin gene was conducted and the obtained phylogeny was discussed. DNA from 21 Actinoplanes strains preserved at NITE Biological Resource Center (NBRC) was extracted for amplification and sequencing of the flagellin gene (Table 1). All of the tested strains were grown in YG broth (yeast extract, 10 g L−1; glucose 10 g L−1; pH 7.0) for 7 days at Staurosporine ic50 30 °C. Cells were recovered by centrifugation (1600 g, 10 min) and washed twice with 0.5 M EDTA. Genomic DNA was extracted as described by Saito & Miura (1963) with minor modifications. Isolated DNAs were stored at −20 °C until analysis. To amplify the flagellin gene from Actinoplanes strains, the degenerate PCR primers 5F_Fla (5′-GTC TYC GCA TCA ACC AGA ACA TCG-3′) and 1219R_Fla (5′-GCA CGC CCT GCG RGG MCT GGT TCG CG-3′), corresponding to N- and C-terminal regions of the flagellin gene, respectively, were used. The primers were designed by comparing flagellin gene sequences derived from the genome sequence of Actinoplanes missouriensis NBRC 102363T (AB600179), Nocardioides sp. JS614 (CP000509 REGION: 814334..815251), and K.

, 2005, 2006). For confocal analysis, biofilms were grown under similar conditions for Estrogen antagonist 24 and 72 h, and were treated with either Live/Dead BacLight fluorescent dye (Invitrogen, CA) or concanavalin A lectin conjugated with Alexa Fluor 488 and SYTO 59 (Invitrogen) before optical dissections using an Olympus Fluoview BX61 confocal laser scanning microscope (Olympus). Simulated xyz three-dimensional images were generated using

slidebook 5.0 (Olympus). To measure the extracellular glucose polymers in biofilms, a phenol-sulfuric acid assay was used with known concentrations of glucose as the standards (Mukasa et al., 1985; Kumada et al., 1987; Ausubel et al., 1992; Werning et al., 2008). Briefly, 3-day biofilms

were grown in BMGS on glass slides in 50-mL tubes IDH tumor as described elsewhere (Phan et al., 2000; Wen et al., 2010a, b). Following brief sonication, bacterial cells were removed by centrifugation (4000 g, 4 °C for 15 min). Exopolysaccharide in the supernatant fluid was precipitated with two volumes of ethanol overnight at −20 °C, and was washed twice with 80% ethanol before the OD490 nm was measured (Ausubel et al., 1992; Werning et al., 2008). To evaluate the ability of S. mutans strains to withstand oxidative stress, 3-day biofilms were prepared using glass slides as described above, and hydrogen peroxide challenge assays were carried out as detailed elsewhere (Wen & Burne, 2004, 2006, 2010a, b). For transcriptional profiling, S. mutans strains were grown in 50 mL of BHI broth, and following brief treatment with RNAProtect as suggested by the manufacturer, total RNAs were isolated using hot phenol as described previously (Wen & Burne, 2004; Wen

et al., 2005, 2006, 2010a). To remove all DNA, RNA preps were treated with DNaseI (Ambion Inc.) and retrieved with the RNeasy purification kit (Qiagen Inc.). Array analysis was performed using the whole-genome S. mutans microarrays Amobarbital that were obtained from The J. Craig Venter Institute (JCVI, http://pfgrc.jcvi.org) by following the protocols recommended by JCVI as described elsewhere (Abranches et al., 2006; Wen et al., 2006, 2010a). Array data were normalized with the TIGR Microarray Data Analysis System (http://www.jcvi.org/software) and further analyzed using brb array tools 3.01 (developed by Dr Richard Simon and Amy Peng Lam, National Cancer Institute, MD, http://linus.nci.nih.gov/BRB-ArrayTools.html) as described elsewhere (Abranches et al., 2006; Wen et al., 2006, 2010a). Genes that were differentially expressed by a minimal ratio of 1.5-fold and at a statistical significance level of P<0.001 were then identified. For RealTime-PCR analysis, cDNA was synthesized with 1 μg of total RNA using the iScript cDNA synthesis kit (Bio-Rad) by following the procedures recommended by the manufacturer.

, 1998). The genome size of the bacteriophages (φVh1, φVh2, φVh3, and φVh4) based on PFGE was minimal (0.8–3.2 kb) and was estimated to be 85, 58, 64, and 107 kb, respectively, by PFGE. The genome size of the members of the family Siphoviridae is reported to range from 14.5 kb in Lactococcus prophage bIL311 to 134.4 kb in Bacillus phage SPBc2 (http://www.ncbi.nlm.nih.gov/genomes/GenomesGroup.cgi?taxid=10699). The genome size of the VHS1 Siphoviridae phage of V. harveyi described earlier was approximately 80 kb (Pasharawipas et al., 2005), and six of INCB024360 them described by Shivu and others had genome sizes ranging from 44 to 94 kb as determined by REA

(Shivu et al., 2007). The phylogenetic analysis showed that the four bacteriophages were distinct from one another as revealed by cluster analysis. The clustering pattern based on both REA and PFGE showed distinct genetic nature of φVh3. A marine phage capable of specifically transducing the tryptophan region was described almost three and a half decades back (Keynan et al., 1974). In the present study, all the four bacteriophages were capable of transducing the plasmid DNA between V. harveyi with a transduction frequency ranging from 4.1 × 10−7 to 2 × 10−9 PFU−1. A similar efficiency was reported with indigenous marine phage host isolates in an earlier report (Jiang & Paul, 1998). It has been demonstrated that the vibriophages in the coastal

environment transfer genes from O1 El Tor strain to RG7422 purchase non-O1/O139 through transduction, suggesting the process as one of the mechanisms of pathogenicity evolution among environmental over V. cholerae

(Choi et al., 2010). Possibilities of genetic interaction among the bacteriophage genomes and chromosomal and plasmid-borne DNA of vibrios such as Vibrio parahaemolyticus strains and of genetic transmission among strains through filamentous phages have been suggested (Chang et al., 1998). The use of a wide variety of antibiotics in aquaculture has resulted in the emergence of antibiotic-resistant bacteria in aquaculture environments (Cabello, 2006). The abundant occurrence of bacteria along with their bacteriophages in seawater and aquatic sediments is known to facilitate such a transfer (Fuhrman, 1999). In conclusion, results from this study provide description of three bacteriophages of the family Siphoviridae and one of the family Podoviridae. Literature search shows that the latter group of bacteriophages has not been reported from the shrimp aquaculture ecosystem so far. The significance of the present study is that these bacteriophages were able to bring about generalized transduction and can transfer genetic elements such as antibiotic resistance or pathogenicity traits among V. harveyi and possibly in other vibrio species in the brackishwater aquaculture ecosystem. Authors are thankful to the Indian Council of Agricultural Research, New Delhi for the financial assistance [F.No.

Female patients with Lynch syndrome complicate with endometrial cancer at a high incidence. In the revised 1999 Amsterdam II Criteria (AC II), endometrial cancer was included as a cancer with similar features to colon, small intestine, ureteral and kidney cancers.[13] The prevalence of Lynch syndrome is 0.9–2.7%[14] and approximately 2.3% of cases of endometrial cancer occur due to Lynch syndrome.[15] The lifetime risk of endometrial cancer is 28–60% in women with aberrant genes associated with Lynch

syndrome.[16] hMLH1, hMSH2 and hMSH6 mutations are particularly selleck products important in families of patients with Lynch syndrome. Most mutations occur in hMLH1 and hMSH2, whereas hMHS6 mutations are important in tumorigenesis in patients with endometrial cancer.[17, 18] Kawaguchi et al.[19] proposed a possible new cascade in which hMSH6 mutation is induced by silencing of hMLH1 due to aberrant DNA hypermethylation in endometrial cancer. Westin et al.[20] showed that the incidence of Lynch syndrome was 1.8% in endometrial cancer in total and 9% in endometrial cancer in Selleckchem HKI 272 women aged less than 50 years old, but 29% in cases with lower uterine

segment cancer (LUS) and germ cell mutation of hMSH2. These results suggest a correlation between endometrial cancer of the uterine isthmus and Lynch syndrome. Masuda et al.[21] also found germ cell mutations of hMLH1 in 1.4% of patients with LUS. Based on these findings, Lynch syndrome may be

clinically predictive of the onset site of endometrial cancer. Several gene mutations have emerged as candidates for roles in carcinogenesis of type I and II endometrial cancer (Fig. 2), based on observation of the mutation in endometrial hyperplasia and at least a similar incidence of mutation in endometrial cancer. Different genes are involved in carcinogenesis of the two types of endometrial cancer. Gene mutations found in type I endometrial cancer include those in PTEN, β-catenin and Sulfite dehydrogenase K-ras. PTEN is a tumor suppressor gene on chromosome 10 and has been identified as a disease gene in three autosomal dominant disorders (Cowden disease, Lhermitte-Duclos disease and Bannayan-Zonana syndrome). PTEN inactivation is also found in malignant melanoma, brain tumors, and endometrial, ovarian, thyroid, breast and prostate cancers. PTEN protein induces apoptosis and carcinogenesis occurs in cells with PTEN mutation due to avoidance of apoptosis. PTEN mutations have been detected in 20–33% of cases of atypical endometrial hyperplasia and 33–50% of cases of endometrial cancer;[22-24] thus, PTEN appears to be involved in the early stage of carcinogenesis, which is a pattern that differs from that in late-onset cancer, including rectal cancer.

Serofendic acid did not regulate rCBF at ischemic and reperfusion phase (Table 1). Several physiological parameters (pH, PaO2, PaCO2, and glucose content of arterial blood) influence the degree of cerebral damages induced ischemia-reperfusion. Thus, we investigated the effect of serofendic

acid on physiological parameters Dasatinib nmr 30 min after each of the three administrations. We found no effect of serofendic acid on any physiological parameters in the sham-operated and ischemia-reperfusion-operated groups (Table 2). Next, we administered a single dose of serofendic acid (30 mg/kg) at 30 min before ischemia, just after ischemia, or just before reperfusion in order to determine whether three administrations are necessary to achieve protective effects. No single administration

of serofendic acid showed any protective effect on infarct volume or neurological deficit score (Fig. 4). The major finding of this study is that serofendic acid, administered intravenously, has the protective effect on the injury induced by cerebral ischemia-reperfusion. We have previously reported that intracerebroventricular administration of serofendic acid protects against ischemic injury in tMCAo model rats (Nakamura Selleckchem Seliciclib et al., 2008). However, it was not sufficient for considering about clinical application of serofendic acid because of the poor permeability into brain in case of peripheral administration. In the present study, we showed that intravenous administration of serofendic acid, when administrated three times, reduced infarct volume PtdIns(3,4)P2 and improved neurological function without affecting rCBF or physiological parameters. As shown in Fig.

3, serofendic acid reduced the infarct volume in the cortex but not in striatum, similar to our previous results for intracerebroventricular administration (Nakamura et al., 2008). We previously reported that serofendic acid inhibits caspase-3 activation in vitro (Kume et al., 2006) and several reports showed that inhibition of caspases attenuates apoptosis in the penumbra in tMCAo models (Lei et al., 2004 and Sung et al., 2007). Thus, the inhibition of activation of caspases-3 is suggested to play a central role in the protective effect of serofendic acid in the cortex. We previously reported that serofendic acid affords protection against reactive oxygen species (ROS)-induced oxidative injury (Osakada et al., 2004). Many anti-oxidative substances have been shown to have protective effects against cerebral ischemia-reperfusion injury (Amemiya et al., 2005, Connell et al., 2011 and Shih et al., 2005). Taken together, we can assume that the anti-oxidative properties of serofendic acid contribute its protective effect against cerebral ischemia-reperfusion injury. Based on our previous reports regarding the permeability of serofendic acid into the brain (Terauchi et al.

Sometimes a discrete, tender pain-trigger point is no more than a few centimeters in diameter, but pressure upon it can cause it to be referred over a wider area. Most muscular pain is caused by either exercise or straining but may have been incurred with just routine chores

or even sneezing during sleep. My last patient had a discrete area of tenderness in the lateral rectus muscle and remembered, Silmitasertib chemical structure upon further discussion, perhaps lifting a heavier weight than usual in the gym shortly before this pain began. Clinically he had a small tear in his rectus sheath, although I did not see it on a prior CT scan. Solely on the basis of physical examination, I was able to suspect the diagnosis, reassure him, and discontinue the proton pump inhibitor. I prescribed a nonsteroidal anti-inflammatory drug, which gave him rapid relief, although whether it was the medication or my assurance that was more helpful, I do not know. I do know, however, that he was relieved and satisfied to have found a doctor who was comfortable in touching him and not just relying on the impersonal, albeit sophisticated, diagnostic imaging modalities so readily available today. The author disclosed no financial relationships relevant to this publication. “
“GI stromal tumors

(GISTs) originating from the muscularis propria are challenging to diagnose and treat by endoscopy.1 and 2 Tissue acquisition by EUS guidance is often too scant for immunohistochemical diagnosis and mitotic index calculation.3 and 4 Resection by snaring and submucosal dissection has been reported, but carries click here a high risk of perforation.5, 6, 7 and 8 Tumor ligation

by using bands and loops reduces the risk of perforation,9, 10, 11 and 12 but can be technically difficult in nonpedunculated tumors and may not achieve complete ablation. To address current limitations of endoscopic diagnosis and therapy, we developed the retract-ligate-unroof-biopsy (RLUB) technique for upper GISTs. A novel retract-ligate-unroof-biopsy (RLUB) method enables endoscopic diagnosis and therapy of large (>2 cm) nonpedunculated stromal tumors. Active retraction of a stromal tumor can evert the bowel wall and may enable curative full-thickness ligation leading ifenprodil to tumor ablation. The RLUB technique was performed on consecutive patients with suspected upper GISTs on EUS examination starting in December 2010. All lesions fulfilled the following criteria: (1) broad based, (2) benign appearance on endoscopy (no ulceration or friability) (Fig. 1A), (3) benign appearance on EUS (well circumscribed, homogeneously hypoechoic, no cystic areas or calcifications), (4) originating from the muscularis propria layer on EUS, and (5) larger than 2 cm by maximum cross-section measurement on EUS. All patients were symptomatic and/or had a previous EUS-FNA diagnosis of GIST.

1). REPC express ecto-5′-nucleotidase (CD73) and platelet-derived growth factor receptor β-polypeptide (PDGFRB),[9] and [13] both are also markers of pericytes and EPO-negative interstitial fibroblasts.14Epo expression in tubular epithelial cells appears to be suppressed by GATA transcription factors, in particular GATA-2 and GATA-3, and can be reactivated under normoxic

or hypoxic conditions when the GATA core consensus binding sequence upstream of the Epo transcription start site is mutated. 11 The kidney responds to hypoxia by increasing the number of REPC in an O2-dependent manner and therefore regulates EPO output through adjustments in REPC number. [8] and [11] O2-dependent Epo transcription is controlled by distinct regulatory DNA sequences. These Quizartinib flank the Epo coding sequence on both sides, the kidney-inducibility element CYC202 concentration in the 5′-region and the liver-inducibility element in the 3′-region. [15], [16] and [17] The 3′-hypoxia enhancer region is absolutely required for the hypoxic induction of Epo in the liver, as shown by genetic studies in mice. 18 REPC have been visualized

in BAC transgenic mice through the use of green fluorescent protein (GFP). In this transgenic model the Epo coding sequence was replaced by GFP cDNA, which brings GFP under the control of Epo regulatory elements. 11 GFP expression was found in renal peritubular interstitial cells and in a subpopulation of hepatocytes that were localized around the central vein, supporting the notion that these two cell types represent the major sites of physiologic EPO production under conditions of systemic hypoxia. In the kidney, GFP-positive interstitial cells were unique in their morphologic appearance,

as they displayed dendrite-like processes and expressed neuronal-specific markers, such as microtubule-associated protein 2 (MAP2) and neurofilament protein light polypeptide (NFL), indicating that REPC may be derived from progenitor cells of neuronal origin. This notion is furthermore supported by lineage tracing studies that utilized myelin protein zero (P0)-Cre transgenic mice, which express Cre-recombinase in neural crest-derived cells. 13 In keeping with this observation, Frede and colleagues Sitaxentan established an EPO-producing renal tumor cell line with similar morphologic and molecular characteristics. 19 Although the hypoxic induction of Epo was reported in 4E cells, a mesenchymal cell clone with characteristics of embryonic kidney stromal cells, 20 primary REPC that retain their EPO-producing ability are difficult to culture. The molecular mechanisms underlying this phenomenon are unclear. Transdifferentiation of REPC into myofibroblasts, which are a main source of collagen in fibrotic kidneys, has been proposed as a potential mechanism by which REPC loose their ability to synthesize EPO in CKD ( Fig. 1).

While local muscle resident MSCs are a logical candidate as HO progenitors, other cells have been proposed. Some studies have implicated vascular endothelial cells as a potential source for HO progenitors [8]. Constitutively activated ACVRI in FOP change the morphology of endothelial cells to mesenchymal-like

cells and induce the co-expression of mesenchymal markers in vitro, a process that Obeticholic Acid price resembles the endothelial–mesenchymal transition [8]. Moreover, endothelial marker Tie2 has been histologically observed in heterotopic lesions from patients with FOP. In addition, lineage tracing studies using Tie2-Cre reporter mice indicated that these cells generate approximately half the chondrocytes and osteoblasts found in skeletal muscle lesions [8] and [9]. However, Tie2 is not specific to endothelial cells and is also expressed in a number of non-endothelial cell types, including perivascular cells [10] and [11]. It has also

been shown in vivo that the endothelial fraction of murine Tie2 cells (Tie2+CD31+) does not participate JQ1 in HO whereas the non-endothelial fraction of Tie2 cells (Tie2+CD31−) does [12]. These recently published findings strongly suggest that the Tie2 progenitors observed in HO are not of endothelial origin [7]. Indeed, more than 90% of Tie2+CD31− cells are also PDGFRα+Sca1+, pointing to a mesenchymal rather than an endothelial origin [12], which supports the findings of Leblanc et al., who showed that

a Sca1+CD31− muscle resident stromal cell population contributes to HO [2]. In humans, PDGFRα has been reported to be a specific marker for interstitial mesenchymal progenitors that are distinct from CD56+ myogenic cells and that possess adipogenic and fibrogenic potentials [13]. While human skeletal muscle PDGFRα+ cells display osteogenic potential in vivo [14], the confirmation of their osteogenic activity came from subcutaneous-implanted cell-loaded PLGA-hydroxyapatite blocks, which are not likely representative of the HO environment. In addition, their osteogenic activity was comparable to CD56 myogenic Dipeptidyl peptidase cells [14], suggesting that PDGFRα may not be a marker that is exclusive to osteogenic progenitors. Other human studies have shown that a fraction of skeletal muscle adherent cells can give rise to osteoblasts and that this potential is greatly increased following trauma [15] and [16]. A multipotent myo-endothelial cell population in human skeletal muscle has been characterized based on the presence of myogenic (CD56) and endothelial (CD34, CD144) cell surface markers and the ability to differentiate into mesenchymal lineages [17]. Interestingly, the brown adipogenic potential of these putative HO progenitors has not been investigated, although it has been shown that brown adipocytes can promote endochondral ossification in an HO mouse model by regulating oxygen availability and inducing a hypoxic microenvironment [18] and [19].

Despite the recent decrease in total catch compared with 10 years ago, fish exports have increased constantly; this

increase seems to occur at the expense of local consumption and has caused significant increases in fish prices in local markets [44]. Artisanal fishing accounts for well over 90% of the total production [27]. The key fisheries resources, shown in Table 1, include pelagic fishery for tuna and tuna-like species and demersal fishery for fish, cuttlefish, shrimp, and lobster. Tuna and tuna-like species and cuttlefish are prevalent in the Gulf of Aden and the Arabian Sea, whereas demersal fish are more abundant in the Red Sea. Key pelagic species include yellowfin tuna, longtail tuna, little tuna, narrow-barred Spanish mackerel, Indian mackerel, anchovy, and sharks; key demersal fish species include emperors, groupers, snappers, and jacks [27] and [32]. Despite selleck screening library the lack of comprehensive AZD2281 stock assessment studies and reliable catch statistics, it is believed that most fish stocks, except small pelagic species for which there is no market demand, are either fully exploited or overexploited [37]; interviews with fishermen and

different stakeholders confirm these beliefs. Cuttlefish (Sepia pharaonis) has been harvested since 1967 by industrial fleets in the Gulf of Aden and the Arabian Sea region. The intensive trawling on their spawning aggregations has led to overfishing and a major decline of the fishery by 1982–1983 with reported annual landings falling from around 9000 to 1500 t. Landings of the rock lobster (Panulirus homarus) virtually collapsed to near zero in the late 1990s from peaks of around 400 t in the early part of the decade. This collapse was attributed to the widespread use of nets rather than traps to capture lobsters [37]. Large-scale harvest of sea cucumbers started in 2003 with the advent of air compressors, which facilitated diving; this process

led, a few years later, to the collapse of the fishery [45]. Many important demersal fish stocks and some pelagic species, such as Indian PLEKHM2 mackerel [41], narrow-barred Spanish mackerel, and sharks [40] and [46], have experienced severe overfishing and their production levels have been beyond the maximum sustainable yields. The lack of FMPs, widespread IUU fishing, uncontrolled growth of fishing effort, and weak compliance and enforcement arrangements have led to significant economic losses associated with the suboptimal use of the resources, which has in turn resulted from weak and ineffective governance and subsequent overfishing. Small-scale fishermen typically use two types of fishing boats: small fiberglass boats called huris, 7–16 m long, with outboard engines and 2–6 crew members, and larger wooden boats called sambuks, 10–20 m long, with inboard or outboard engines and with a crew from 10 up to 25 or more [4] and [27]. Huris were traditionally used for single day trips in inshore waters, within 40 km of the shore [4].