on 08-May-2021 (Sat)

The documentation does not tell anything about video frames,

Эксперты — они потому и эксперты, что узкая специализация.
Чем больше времени потрачено на что-то одно, тем меньше его на всё остальное.

For this exploration, I just saved the logs to text files and did some grep/sed wrangling to coerce the data I wanted into CSV and JSON files. Then, I loaded them into a notebook with some more Python data torturing tricks.

Inference speeds close to native Android Apps built using the Java API.

In the past, IE was classified as acute or subacute. This distinction was based on the usual progression of the untreated disease and is mainly of historical interest.

he acute form follows a fulminant course, usually with high fever, systemic toxicity, and leukocytosis; death occurs in several days to less than 6 weeks. It classically is associated with infection caused by Staphylococcus aureus, Streptococcus pyogenes, Streptococcus pneumoniae, or Neisseria gonorrhoeae

The subacute form (death occurring in 6 weeks to 3 months) and the chronic form (death occurring later than 3 months) usually are considered together. They commonly occur in the setting of prior valvular disease and are characterized by a slow, indolent course with low-grade fever, night sweats, weight loss, and vague systemic complaints. These two forms of IE classically are caused by the viridans streptococci

Although useful conceptually, this classification ignores the nonbacte- rial forms of IE and the frequent overlap in manifestations of infection by specific organisms, such as the enterococci. A classification based on the etiologic agent responsible is preferable because it has implications for the course usually followed, the likelihood of preexisting heart disease, and the appropriate antimicrobial agents to use.

The incidence of IE is difficult to determine, because the criteria for diagnosis and the methods of reporting vary with different series. 3,4 An analysis based on strict case definitions often reveals that only a small proportion (approximately 20%) of clinically diagnosed cases are categorized as definite.

n a systematic review of IE epidemiology studies from 1980 to 2008, crude incidence of IE ranged between 1.5 and 11.6 cases per 100,000 people.

The mean age of patients with IE has increased gradually in the antibiotic era. In 1926, the median age was younger than 30 years 8 ; by 1943, it was 39 years, and currently more than half of patients are older than 50 years. 7,9,10

In ICE-PCS, among more than 2700 patients from 58 centers in 25 countries with definite IE according to the modified Duke criteria, the median age was 57.9 years. 7

The emerging importance of health care–associated IE in industrialized nations has also influenced the microbiology of IE, with an increasing prevalence of S. aureus and decreasing prevalence of viridans streptococci in much of the industrialized world.

Involvement of the aortic valve alone is increasing in frequency and correlates with the increase in acute cases; the incidence was 5% in 1938 and increased to 38% by 2000

Rheumatic heart disease was the underlying lesion in 37% to 76% of infections in the past, and the mitral valve is involved in more than 85% of cases related to rheumatic heart disease. 13 If the mitral valve alone is involved, women outnumber men by 2 to 1. The aortic valve is affected in approximately 50% of these cases; if it alone is involved, men outnumber women by 4 to 1. Right-sided endocarditis is rare (except in injection drug users and patients with indwelling transvenous pacemakers) and accounts for fewer than 10% of all cases occurring in patients with rheumatic heart disease

Although it is not classically recognized as a condition leading to bacterial endocarditis, up to 5% of patients with idiopathic hypertrophic subaortic stenosis develop IE. 34

New murmurs develop in 36% of patients with idiopathic hypertrophic subaortic stenosis complicated by IE, and this new physical finding correlates with a higher mortality rate. 34

Mitral valve prolapse should be suspected in patients who have midsystolic clicks with or without a late systolic murmur. The condition is common and has been recognized in 0.5% to 20% of otherwise healthy people, especially young women. It has become apparent that mitral valve prolapse is only one component of a developmental syndrome. This lesion often is associated with a distinct habitus in women, 36 with von Willebrand disease, or with ophthalmoplegia

It seems that when IE develops in people with mitral valve prolapse, the symptoms and signs are more subtle and the mortality rate is less than in left-sided IE of other types.

In vitro observations and studies in experimental animals have shown that development of IE probably requires the simultaneous occurrence of several independent events, each of which may be influenced by a cadre of distinct factors.

These alterations result in the deposition of platelets, fibronectin, fibrin, and other matrix ligands in the formation of so-called sterile vegetation—the lesions of nonbacterial thrombotic endocarditis (NBTE). Bacteria then must reach this site and adhere to and invade the involved tissue to produce coloniza- tion and persistence.

It is important to point out that, at least for left-sided IE, neutrophils play little role in the pathogenesis of or defense against evolution of IE

It now is clear that the initial colonization occurs on the damaged endothelial surface of the valve. In experimental animals, it is almost impossible to produce IE with intravenous injections of bacteria unless the valvular surface is first perturbed

Scanning electron micrographs of the damaged valvular surface confirm the adhesion of microorganisms to these areas of fibrin-platelet deposition early in the disease course. 52 The organisms are covered rapidly by fibrin. 53

Opossums and pigs are the only animals known to develop spontane- ous IE readily (i.e., without experimentally induced valvular altera- tion). 44,54 The stress of captivity is apparently sufficient in these animals to produce subtle valvular changes that lead to spontaneous endocarditis and a markedly increased susceptibility to the disease after intravenous injection of bacteria. In other animals and probably in humans, alteration of the valve surface is a prerequisite for bacterial colonization

Many forms of exogenous stress produce these lesions experimentally, including infection, hypersensitivity states, cold exposure, simulated high altitude, high cardiac output states, cardiac lymphatic obstruction, and hormonal manipulations. 44 These procedures all increase the susceptibility of the animals to IE.

NBTE has been found in patients with malignancy (particularly pancreatic, gastric, or lung adenocarcinoma) and other chronic wasting diseases, rheumatic and congenital heart disease, 47 uremia, and connective tissue diseases such as systemic lupus erythematosus (SLE) and rheu- matoid arthritis; after the placement of intracardiac catheters (e.g., Swan-Ganz); and after a self-limited acute illness.

NBTE generally reflects one of two pathogenic mechanisms: hypercoagulability (especially related to secondary antiphospholipid syndromes) or endothelial damage

Valvular lesions were most common among patients with carcinoma of the pancreas or lung or lymphoma.

NBTE is most common on the low-pressure side of the cardiac valves along the line of closure, precisely the site most often involved in IE. Whether this lesion is always essential for the development of IE in humans is unknown. Secondary hypercoagulable states (e.g., as seen in secondary antiphospholipid syndromes in SLE) may contribute to the development and propagation of the NBTE lesion. 57

The degree of mechanical stress exerted on the valve also affects the location of the IE. 59 In 1024 autopsy cases of IE reviewed through 1952, the incidence of valvular lesions was as follows: mitral, 86%; aortic, 55%; tricuspid, 19.6%; and pulmonic, 1.1%. This incidence correlates with the pressure resting on the closed valve: 116, 72, 24, and 5 mm Hg, respectively.

When associated with valvular insufficiency, IE characteristically occurs on the atrial surface of the mitral valve and the ventricular surface of the aortic valve. Rodbard 58 showed that this localization is related to a decrease in lateral pressure (presumably with decreased perfusion of the intima) immediately downstream from the regurgitant flow. Lesions with high degrees of turbulence (e.g., small ventricular septal defect with a jet lesion, valvular stenosis resulting from insufficient valves) readily create conditions that lead to bacterial colonization, whereas defects with a large surface area (large ventricular septal defect), low flow (ostium secundum atrial septal defect), or attenuation of turbulence (chronic congestive heart failure [CHF] with atrial fibrillation) rarely are implicated in IE

Cures of IE achieved with ligation of an arteriovenous fistula or patent ductus arteriosus without further treatment also highlight the importance of hemodynamic factors.

In the setting of preexistent NBTE, transient bacteremia may result in colonization of these lesions and may lead to the development of IE. 60

The degree of bacteremia is proportional to the trauma produced by the procedure and to the number of organisms inhabiting the surface; the organisms isolated reflect the resident microbial flora. The bacteremia usually is low grade (≤10 colony-forming units [CFUs]/mL) and transient; the bloodstream usually is sterile in less than 15 to 30 minutes.

Frequent episodes of silent bacteremia also are suggested by the identification of circulating humoral antibodies to the resident oral flora and by the noted increase in sensitized peripheral T cells to the flora of dental plaque.

Another crucial factor during the transient bacteremia stage is susceptibility of the potential pathogen to complement-mediated bactericidal activity. Only “serum-resistant,” gram-negative aerobic bacilli (e.g., Escherichia coli, Pseudomonas aeruginosa, Serratia marcescens) reliably produce experimental IE in rabbits, 65,66 and this property is found in all isolates from human cases of IE

Gould and associates 67 showed that organisms commonly associated with IE (enterococci, viridans strep- tococci, S. aureus, S. epidermidis, P. aeruginosa) adhered more avidly to normal canine aortic leaflets in vitro than did organisms uncommon in IE (Klebsiella pneumoniae, E. coli).

Differences in the propensity to cause IE are apparent even within a single species. For example, specific clones of S. aureus, including clonal complexes 30 69,70 and 22, 71 have been reported to be associated with an increased risk for IE.

The adherence of oral streptococci to NBTE may depend on the production of a complex extracellular polysaccharide, dextran. This polymer plays an essential role in the pathogenesis of dental caries by Streptococcus mutans. 80 Dextran allows the organism to adhere tightly to the surface of dental enamel

Ratios of endocarditis to nonendocarditis bacteremia caused by particular organisms have been derived (Table 80 .2 ), allowing prediction of the relative propensity for a particular organism to cause IE. The ratios range from 14.2 : 1 for S. mutans to a reversed ratio of 1 : 32 for S. pyogenes. Only the first four organisms listed in Ta bl e 80 .2 (all with ratios > 3 : 1) produce extracellular dextran.

xtran formation (or, more properly, exopolysaccharide or glycocalyx production) by oral streptococci may be a virulence factor for the production of IE by these organisms. 85

Measurement of cell- adherent glycocalyx with a quantitative spectrophotometric tryptophan assay among viridans streptococci isolated from blood cultures has potential value as an independent predictor of the likelihood of IE. 88

FimA, a surface adhesin expressed by viridans streptococci, has been shown to mediate the attachment of such organisms to platelet-fibrin matrices in vitro and to experimental NBTE lesions in the animal model of IE. 91

In addition, animals either passively immunized with anti-FimA antibody or actively immunized with a FimA vaccine were significantly less susceptible to experimental IE than nonimmunized controls. 92

The viridans-group streptococci interact with human platelets through several mechanisms that may contribute to the pathogenesis of IE. A locus of Streptococcus gordonii, important for binding to human platelets, 93 encodes a large, serine-rich repeat (SRR) cell wall–anchored glycoprotein adhesin (GspB), which comprises four proteins mediating the glyco- sylation of the adhesion, 94–96 and a specialized, multicomponent transporter (the accessory Sec system) that mediates the export of the adhesin to the bacterial surface

This is a remarkable system, because it is perhaps the first example of a phage-encoded bacterial surface structure and adhesin, and because it suggests a coadaptation or coevolution of the bacterium and the phage, wherein the bacterium is essential for phage replication and the phage gives the bacterium a selective advantage by providing it with a critical adhesin to colonize cognate ligands on platelets

A similar important role of adhesion to NBTE in the pathogenesis of IE has been shown for yeasts. Candida albicans adheres to NBTE in vitro and produces IE in rabbits more readily than does Candida krusei, a nonadherent yeast rarely implicated in IE in humans. 113

Other organisms may bind directly to, or become ingested by, endothelial cells as the initial event. 121–124 This sequence appears to be important in the initiation of IE by S. aureus on “normal” cardiac valves or on native endothelial surfaces adjacent to damaged endothelial sites.

Recently, the expression, structure, and binding activity of the two major S. aureus fibronectin-binding proteins (FnBPA, FnBPB) were determined in clinical isolates from patients with persistent bacteremia (frequently IE) or resolving bacteremia. 134

These complementary sequence and binding data suggest that differences in fnbA and fnbB, particularly polymorphisms and duplications in FnBPA, give S. aureus two distinct advantages in human endovascular infections: (1) FnBPs similar to that of CC5 enhance ligand binding and foster initiation of disease, and (2) CC45-like FnBPs promote cell invasion, a key attribute in persistent endovascular infections.

Infective Endocarditis The importance of adherence characteristics in the development of IE also has been examined through the use of preincubation of organisms with antibiotics. Many classes of drugs, after incubation even at subinhibi- tory concentrations, decrease the adhesion of streptococcal species to fibrin-platelet matrices and damaged canine valves in vitro. 135

Antibiotics may prevent IE by at least two mechanisms: bacterial killing and inhibition of adhesion to NBTE- involved tissue. 139

Agent The performer of a verbal action: in an ACTIVE sentence, the agent is typically the SUBJECT of the sentence; in a PASSIVE sentence, the agent (the subject of the corresponding active sentence) is usually introduced by ‘by’ in English and by por in Portuguese.