Population dynamics of the long-snouted seahorse (Hippocampus guttulatus Cuvier, 1829) in the Mar Menor coastal lagoon.

A 10-year monitoring program was developed to quantify the population dynamics of the long-snouted seahorse population in the Mar Menor coastal lagoon. Based on 985 underwater visual censuses, we estimated the long-snouted seahorse (Hippocampus guttulatus Cuvier, 1829) population size in the Mar Menor lagoon and its reduction in size in the last decades, as well as the effect of eutrophication crises in 2016 and 2019 on the species. The annual recruitment for the 2013-2020 period was estimated by comparing the relative abundance of early seahorse life stages in the ichthyoplankton. The density ranged from 0.0458 specimens/m3 at the beginning of the sampling period to 0.0004 at the end, showing a statistically significant difference between the three analyzed periods (Hgl=2 = 14.0, p = 0.001). The long-snouted seahorse population from the Mar Menor lagoon exemplifies the impact of fishing activities and human pressure, especially euxinic episodes and habitat destruction. As a result of this, the Mar Menor population has decreased from several million specimens to a few thousand, in only three decades. This species showed considerable resilience, the seahorse population began to recover once fishing activity stopped. In contrast, the long-snouted seahorse showed high vulnerability to habitat loss and an episodic flooding event. Adult seahorses showed preferences for highly complex habitats, especially Caulerpa prolifera-Cymodocea nodosa mixed meadows and habitats of high complexity and anthropogenic origin, such as harbors, jetties, or breakwaters. In contrast, juvenile seahorses preferred monotonous seabeds with low complexity, such as the sandy beds that are characteristic of the Mar Menor lagoon littoral.

Gonioscopy in the dog: inter-examiner variability and the search for a grading scheme.

OBJECTIVES: To investigate inter-examiner variability in gonioscopic evaluation of pectinate ligament abnormality in dogs and to assess level of inter-examiner agreement for four different gonioscopy grading schemes. MATERIALS AND METHODS: Two examiners performed gonioscopy in 98 eyes of 49 Welsh springer spaniel dogs and estimated the percentage circumference of iridocorneal angle affected by pectinate ligament abnormality to the nearest 5%. Percentage scores assigned to each eye by the two examiners were compared. Inter-examiner agreement was assessed following assignment of the percentage scores to each of four grading schemes by Cohen's kappa statistic. RESULTS: There was a strong positive correlation between the results of the two examiners (R=0·91). In general, Examiner 1 scored individual eyes higher than Examiner 2, especially for eyes in which both examiners diagnosed pectinate ligament abnormality. A "good" level of agreement could only be achieved with a gonioscopy grading scheme of no more than three categories and with a relatively large intermediate bandwidth (κ=0·68). CLINICAL SIGNIFICANCE: A three-tiered grading scheme might represent an improvement on hereditary eye disease schemes which simply classify dogs to be either "affected" or "unaffected" for pectinate ligament abnormality. However, the large intermediate bandwidth of this scheme would only allow for the additional detection of those dogs with marked progression of pectinate ligament abnormality which would be considered most at risk of primary closed-angle glaucoma.

Prevalence and progression of pectinate ligament dysplasia in the Welsh springer spaniel.

OBJECTIVES: To determine the prevalence of pectinate ligament dysplasia in a large group of Welsh springer spaniels; to investigate associations between pectinate ligament dysplasia and age, sex and intraocular pressure and between intraocular pressure and age and sex; and to investigate progression of pectinate ligament dysplasia in individual dogs. METHODS: In a prospective study, gonioscopy was performed in both eyes of 227 Welsh springer spaniels and intraocular pressure measured by rebound tonometry. Eyes were classified as "unaffected" if 0% of the iridocorneal angle was affected with pectinate ligament dysplasia (grade 0), "mildly affected" if <20% was affected (grade 1), "moderately affected" if 20 to 90% was affected (grade 2) and "severely affected" if >90% was affected (grade 3). In a retrospective study, progression of pectinate ligament dysplasia over time was investigated for 65 dogs. RESULTS: One hundred and thirty-nine of 227 dogs (61·2%) were affected by pectinate ligament dysplasia (grades 1 to 3) and 82/227 (36·2%) were moderately or severely affected. There was a significant association between pectinate ligament dysplasia and age. There were no associations between pectinate ligament dysplasia and intraocular pressure or pectinate ligament dysplasia and sex. Thirty-five of 65 dogs (53·8%) demonstrated progression of pectinate ligament dysplasia. CLINICAL SIGNIFICANCE: Prevalence of pectinate ligament dysplasia was high despite widespread screening and selection against the condition. Our data indicate that gonioscopic features of pectinate ligament dysplasia can progress in the Welsh springer spaniel. Dogs deemed unaffected at an early age may subsequently be diagnosed with pectinate ligament dysplasia.

Integrated Microfluidic Aptasensor for Mass Spectrometric Detection of Vasopressin in Human Plasma Ultrafiltrate.

We present a microfluidic aptamer-based biosensor for detection of low-molecular-weight biomarkers in patient samples. Using a microfluidic device that integrates aptamer-based specific analyte extraction, isocratic elution, and detection by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, we demonstrate rapid, sensitive and label-free detection of arginine vasopressin (AVP) in human plasma ultrafiltrate. AVP molecules in complex matrices are specifically captured by an aptamer that is immobilized on microbeads via affinity binding in a microchamber. After the removal of unbound, contaminating molecules through washing, aptamer-AVP complexes are thermally disrupted via on-chip temperature control. Released AVP molecules are eluted with purified water and transferred to a separate microchamber, and deposited onto a single spot on a MALDI plate via repeated, piezoelectrically actuated ejection, which enriches AVP molecules over the spot area. This integrated on-chip sample processing enables the quantitative detection of low-abundance AVP by MALDI-TOF mass spectrometry in a rapid and label-free manner. Our experimental results show the detection of AVP in human plasma ultrafiltrate as low as physiologically relevant picomolar concentrations via aptamer-based selective preconcentration, demonstrating the potential of our approach as a rapid (~ 1hr), sensitive clinical AVP assay.

Survey of ophthalmic abnormalities in the labradoodle in the UK.

One-hundred and seventy-five labradoodles underwent slit-lamp biomicroscopy and direct and indirect ophthalmoscopy between January 2008 and December 2009. These examinations were performed at shows by the first author. In addition, labradoodle eye certificates from the 2008 and 2009 British Veterinary Association/Kennel Club/International Sheep Dog Society (BVA/KC/ISDS) Eye Scheme were analysed (n=260). The results of the examinations were reviewed, and all ophthalmic abnormalities were recorded. The prevalence of any abnormality was compared with that reported by the Eye Scheme and the KC during 2009 for the labrador retriever, miniature, toy and standard poodles. Multifocal retinal dysplasia (MRD) was identified in 20 labradoodles (4.6 per cent), and cataracts were identified in 16 labradoodles (3.7 per cent). The prevalence of MRD in labradoodles was significantly greater than in labrador retrievers (P<0.0001). There was no difference in the prevalence of cataract between labradoodles and labrador retrievers (P=0.4866). The results of this study suggest that MRD is a relatively common finding in the labradoodle population in the UK. Given such an apparent high prevalence of MRD, routine screening for hereditary eye disease before breeding is advised for this increasingly popular new crossbreed.

Expression of TopBP1 in canine mammary neoplasia in relation to histological type, Ki67, ERalpha and p53.

TopBP1 is aberrantly expressed in human and feline mammary carcinomas, but expression of this BRCA1-related protein has not been investigated in canine mammary carcinomas. In this study, 132 canine mammary tumours (46 benign, 86 carcinomas) were examined immunohistochemically for expression of TopBP1, oestrogen receptor alpha (ERalpha), Ki67 and p53. Positive staining for TopBP1 was evident in all canine mammary lesions, although five samples had <20% positive cells. The number of samples with high levels of staining increased in different categories from benign mixed tumour to adenoma to carcinoma. Most TopBP1 staining was nuclear, but both nuclear and cytoplasmic staining were observed as the degree of malignancy increased, similar to human and feline mammary carcinomas. Benign mixed tumours, however, had more cytoplasmic staining than adenomas. Expression of p53 and the proliferation marker Ki67 increased from benign mixed tumour to adenoma to carcinoma, but the differences between benign and malignant tumours were more distinct than for TopBP1 expression. ERalpha expression decreased from malignant to benign tumours, although over half of the benign mixed tumours were negative. TopBP1 was expressed in canine mammary tumours at higher levels than has been reported previously for cats, although the shift in cellular localisation with malignancy was similar.

Vasopressin administration facilitates fluid removal during hemodialysis.

Inadequate secretion of vasopressin during fluid removal by hemodialysis may contribute to the cardiovascular instability that complicates this therapy and administration of exogenous hormone, by supporting arterial pressure, may facilitate volume removal. To test this, we measured plasma vasopressin in patients with end-stage renal disease (ESRD) during hemodialysis and found that despite significant fluid removal, plasma vasopressin concentration did not increase. We further found that ESRD did not alter the endogenous removal rate of plasma vasopressin and that plasma hormone is not dialyzed. Finally, in a randomized, double-blinded, placebo-controlled trial in 22 hypertensive patients, we examined the effect of a constant infusion of a non-pressor dose of vasopressin on the arterial pressure response during a hemodialysis in which the target fluid loss was increased by 0.5 kg over the baseline prescription. We found that arterial pressure was more stable in the patients receiving vasopressin and that while only one patient (9%) in the vasopressin group had a symptomatic hypotensive episode, 64% of the patients receiving placebo had such an episode (P=0.024). Moreover, increased fluid removal was achieved only in the vasopressin group (520+/-90 ml vs 64+/-130 ml, P=0.01). Thus, administration of non-pressor doses of vasopressin to hypertensive subjects improves cardiovascular stability during hemodialysis and allows increased removal of excess extracellular fluid. Inadequate vasopressin secretion during hemodialysis-induced fluid removal is a likely contributor to the intradialytic hypotension that limits fluid removal.

Blood pressure instability during hemodialysis.

Most patients with end-stage renal disease (ESRD) maintained on hemodialysis have chronic hypertension. However, hypotension is a frequent complication of hemodialysis, probably because of impaired baroreflex function. Less frequently, increases in pressure can be a complication of hemodialysis. Detailed studies of patients with these abnormalities in arterial pressure during hemodialysis may yield insights into the regulation of arterial pressure during ESRD.

Receptor-mediated actions of renin and prorenin.

Renin can induce renal disease by generating angiotensin II and, thereby, increasing fibrosis. Huang et al describe a new mechanism of action whereby the renin-angiotensin system can also exert this effect. Direct activation of the renin/prorenin receptor in mesangial cells induced synthesis of TGF-beta and profibrotic proteins. Hence, like other proteases such as thrombin, renin and prorenin are capable of receptor-mediated cellular signaling.

Impact of procoagulant concentration on rate, peak and total thrombin generation in a model system.

Using a cell-based model system of coagulation, we performed a systematic examination of the effect of varying individual procoagulant proteins (over the range of 0-200% of pooled plasma levels) on the characteristics of thrombin generation. The results revealed a number of features unique to the different coagulation factors, as well as common features allowing them to be grouped according to the patterns observed. Variation of those factors contributing to formation of the tenase complex, factor (F)VIII, factor (F)IX and factor (F)XI, primarily affected the rate and peak of thrombin production, but had little to no effect on total thrombin production. The effect of decreased FXI was milder than seen with decreased FVIII or FIX, and more variable between platelet donors. In contrast, varying the concentration of factors that contribute to formation of the prothrombinase complex, prothrombin or factor (F)V (with FV-deficient platelets), significantly affected all three measures of thrombin production: rate, peak and total. Additionally, while no thrombin generation was observed with no factor X, only very small amounts (between 1% and < 10% of normal plasma levels) were required to normalize the measured parameters. Finally, our results with this cell-based system highlight differences in thrombin generation on cell surfaces (platelets) compared with phospholipids, and suggest that platelets contribute more than simply a surface for the generation of thrombin.

West Nile virus isolates from mosquitoes in New York and New Jersey, 1999.

An outbreak of encephalitis due to West Nile (WN) virus occurred in New York City and the surrounding areas during 1999. Mosquitoes were collected as part of a comprehensive surveillance program implemented to monitor the outbreak. More than 32,000 mosquitoes representing 24 species were tested, and 15 WN virus isolates were obtained. Molecular techniques were used to identify the species represented in the WN virus-positive mosquito pools. Most isolates were from pools containing Culex pipiens mosquitoes, but several pools contained two or more Culex species.

Mosquito surveillance and polymerase chain reaction detection of West Nile virus, New York State.

West Nile (WN) virus was detected in the metropolitan New York City (NYC) area during the summer and fall of 1999. Sixty-two human cases, 7 fatal, were documented. The New York State Department of Health initiated a departmental effort to implement a statewide mosquito and virus surveillance system. During the 2000 arbovirus surveillance season, we collected 317,676 mosquitoes, submitted 9,952 pools for virus testing, and detected 363 WN virus-positive pools by polymerase chain reaction (PCR). Eight species of mosquitoes were found infected. Our mosquito surveillance system complemented other surveillance systems in the state to identify relative risk for human exposure to WN virus. PCR WN virus-positive mosquitoes were detected in NYC and six counties in the lower Hudson River Valley and metropolitan NYC area. Collective surveillance activities suggest that WN virus can disperse throughout the state and may impact local health jurisdictions in the state in future years.

Cardiac involvement in autosomal-dominant polycystic kidney disease: a hypertensive heart disease.

BACKGROUND: There is little information regarding the occurrence and distribution of cardiovascular abnormalities during the course of autosomal-dominant polycystic kidney disease (ADPKD). We conducted a cross-sectional study in three different groups of ADPKD patients to determine the profile and prevalence of cardiac involvement in this population. METHODS: Doppler color echocardiography was performed in 130 ADPKD patients. Patients were divided into normotensive (Group I, n=60), hypertensive (Group II, n=32) and those undergoing hemodialysis (Group III, n=38). RESULTS: There was a progressive increase in left ventricular mass (LVM) index (88.6+/-19.7, 127.6+/-40.4 and 150.5+/-56.5 g/m2, p < 0.0001) and in the prevalence of left ventricular hypertrophy (LVH) (3%, 43%, 62%, p < 0.0001) in Groups I, II and III, respectively. E/A ratio < 1 was found in 2% of normotensives, 46% of hypertensives and 62% of hemodialysis patients (p < 0.0001). Prevalence ofmitral valve prolapse and aortic and/or mitral regurgitation was 4.3% and 8.6%, respectively, in non-dialysis patients. The majority of valvular abnormalities occurred in dialysis patients, and were generally related to annular mitral calcification (28%) or aortic valve calcification (38%). Age, sex, systolic blood pressure (BP) and hemoglobin were independent predictors of LVM index in the entire population, systolic BP and creatinine in non-dialysis patients and systolic BP in dialysis patients. Age, heart rate and diastolic BP in the entire group, and age, heart rate and LVM index in non-dialysis patients remained as independent predictors of abnormal diastolic function. CONCLUSIONS: Cardiac involvement in ADPKD patients is a continuous process that evolves during the course of this disease. It is characterized by a low prevalence of specific valvular abnormalities, a progressive increase in LVM, LVH, and diastolic dysfunction, which are greatest in the latter stages of the disease. This study confirms the major influence of BP on cardiovascular abnormalities of ADPKD patients.

LRP: a new adhesion molecule for endothelial and smooth muscle cells.

We recently generated a monoclonal antibody that disrupted the association of endothelial cells with their target location during kidney development. Here, we purified the antigen of this monoclonal antibody to homogeneity using rat mesangial cell cytosol. Sequence revealed that it is a previously identified protein, termed the "laminin receptor precursor" (LRP). We found that this protein is expressed in most tissues, but immunocytochemistry revealed that it is present largely or entirely in blood vessels where it is located underneath endothelial cells and in between smooth muscle cells of the vascular wall. Vascular smooth muscle cells such as mesangial cells produce and secrete LRP into their extracellular matrix where it is present in several molecular weight forms. Endothelial cells produce very little if any of the protein, but they bind avidly to LRP-coated dishes. Anti-LRP antibodies prevent the binding of smooth muscle cells to uncoated plates, implying that cells that secrete it use it for attachment. In an assay for heterologous cell-to-cell interaction, antibodies to LRP inhibited the binding of smooth muscle cells to endothelial cells. Maturation and differentiation of blood vessels require interaction between endothelial and smooth muscle cells. LRP is a new component of the mesangial matrix, and we propose that it is an adhesion molecule that mediates an interaction between smooth muscle cells and endothelia.

Sonographic pattern of recessive polycystic kidney disease in young adults. Differences from the dominant form.

BACKGROUND: To study the sonographic pattern of autosomal recessive polycystic kidney disease (ARPKD) in early adulthood in order to identify imaging criteria to diagnose this disease and to distinguish between recessive and autosomal dominant polycystic kidney disease (ADPKD) in that age group. METHODS: An abdominal ultrasound was performed on four ARPKD subjects (with a mean age of 20.2) and on 33 ADPKD subjects in early adulthood (29 without renal failure with a mean age of 20.5, and four with renal failure with a mean age of 26.5). Linkage studies with ADPKD and ARPKD markers were compatible with the clinical diagnosis in all cases. RESULTS: The renal sonographic features in ARPKD subjects included multiple small cysts in a normal-sized kidney, increased cortical echogenicity and loss of corticomedullary differentiation. In ADPKD subjects without renal failure, sonographic features included few or multiple cysts of different sizes, in normal-sized kidneys in 22 out of 29 patients (75.8%), normal cortical echogenicity and conserved corticomedullary differentiation, except in patients with nephromegaly. All ADPKD subjects with renal failure had nephromegaly and loss of corticomedullary differentiation. The hepatic sonographic features in ARPKD patients included portal fibrosis and in some cases Caroli's disease, while in ADPKD patients a normal hepatic echostructure was detected in all but one case, in addition to simple hepatic cysts in a few cases. CONCLUSIONS: The evaluation of the sonographic features of the kidneys and those of the liver may help in the differential diagnosis between ARPKD and ADPKD in early adulthood.

Left ventricular hypertrophy in hypertensive patients with autosomal dominant polycystic kidney disease: influence of blood pressure and humoral and neurohormonal factors.

Left ventricular hypertrophy (LVH) is a common finding in hypertensive autosomal dominant polycystic kidney disease (ADPKD) patients. There are few studies on the influence of blood pressure (BP) and nonhemodynamic factors on LVH in these patients. The aim of this study was to evaluate the relationship between BP, humoral and neurohormonal factors and left ventricular mass (LVM) in hypertensive ADPKD patients. In 20 hypertensive ADPKD patients, ambulatory BP was monitored for 24 h, left ventricular dimensions were estimated by echocardiography, and plasma renin activity (PRA), plasma noradrenaline (NA), angiotensin II (Ang II), aldosterone, atrial natriuretic peptide (ANP) and insulin-like growth factor I (IGF-I) were also determined. Twenty age- and sex-matched essential hypertensive subjects served as controls. Ambulatory BP and LVM index were similar in the two groups, although male ADPKD patients had higher LVM indices than their matched controls. Eight ADPKD patients (40%) and 6 essential hypertensives (30%) showed LVH. PRA, Ang II, aldosterone, ANP and IGF-I levels were similar in the two groups, but plasma NA levels were higher in ADPKD patients than in controls (281 +/- 158 vs. 160 +/- 62 pg/ml, p = 0.004). ADPKD patients with LVH did not differ from those without LVH with regard to humoral and neurohormonal parameters, but had higher ambulatory BP levels. In ADPKD patients, correlation analysis revealed a significant association between LVM index and 24-hour systolic and diastolic BP, but not with any of the hormonal factors evaluated. On multiple regression analysis, 24-hour diastolic BP was the only independent variable linked to LVM index. In conclusion, ambulatory BP is one of the most important determinants of LVM in hypertensive ADPKD patients. Further studies are warranted to elucidate the role of nonhemodynamic factors in the pathogenesis of LVH in this population.

Vasopressin in the treatment of milrinone-induced hypotension in severe heart failure.

The use of phosphodiesterase inhibitors such as milrinone in the treatment of severe heart failure is frequently restricted because they cause vasodilation and hypotension. In patients with decompensated heart failure with hypotension after treatment with milrinone, low doses of vasopressin restored blood pressure without inhibiting the inotropic effect of milrinone.

Vasopressin as an alternative to norepinephrine in the treatment of milrinone-induced hypotension.

OBJECTIVE: To determine whether vasopressin could be effective in treating the hypotension associated with phosphodiesterase III inhibition. Phosphodiesterase III inhibitors are cardiotonic agents that increase myocardial contractility and decrease vascular smooth muscle tone. The vasodilatory effect can be profound, and the resulting hypotension frequently requires the administration of catecholamine pressors. DESIGN: Retrospective analysis of existing data. SETTING: The medical or surgical intensive care unit of Columbia-Presbyterian Medical Center. PATIENTS: Three consecutive patients receiving milrinone and requiring catecholamine pressors to maintain systolic arterial pressure of > or =90 mm Hg. INTERVENTIONS: Vasopressin was administered to the three patients. MEASUREMENTS AND MAIN RESULTS: Vasopressin (0.03-0.07 units/min) increased systolic arterial pressure from 90+/-4.7 to 130+/-2.3 mm Hg while reducing the administration of catecholamine pressors. CONCLUSIONS: Vasopressin at very low doses appears to be an effective vasopressor for milrinone-induced hypotension.