Burden Of Proof 3rd Edition Crosman 1377

Recently shown off at the IWA tradeshow over in Germany, BRNO Defense has introduced their 7.5 FK BRNE Combat Field Pistol. Built around a proprietary caliber, the handgun is designed for military, law enforcement, and government personnel. Externally, the handgun bears a striking resemblance to the CZ series of handguns. Cocking serrations are both forward and to the rear with the sights mounted to the slide. Controls are biased to right-hand shooters with magazine release behind the trigger guard, slide release above and a 1911/CZ safety mounted at the top rear of the frame. Its a decided fail to extended handgun size using a 6 inch barrel and coming in 45 ounces, nearly 3 lbs!

Width is an inch (impressively thin), but over all length is 9 inches so it will have a long draw stroke for a combat pistol. The 7.5 FK is a unique round. BRNO Defense lists it at 2000 FPS and 880 ft/lbs of energy at the muzzle with the ability to roughly replicate the.44 Magnum in terms of route energy. Accuracy is touted as a 1.5 inches at 100 meters (an interesting mix of units, eh?). The round is rated to pierce Class IIIA ballistic protection (typical combat soft armor is IIIA) at 100 meters as well. The sights are likewise unique. The front sight is lined up not just between, but inside the rear sight aperture to create the sight picture.

Its a novel approach, as it will allow a shooter to see how far the blade is off when the pistol has a downward declination. No word yet on final specs or availability/price. We’ll keep our eyes peeled for further details. Specs per BRNO Defense. A 360p video for a promo from an arms manufacturer in 2016 that’s weird. The video did not really show much. They just said, “The weight of a.45, the recoil of a.40, and the power of a.44 Magnum” as if that is enough for everyone to drop their current handguns and buy this niche piece.

MDRL Marauder BullPup Kit: AirForce Airguns Crosman Air Rifles Benjamin Air guns . Crosman 1377c American Classic Old Version 0.177 caliber Pellets, Grips Plastic Pump Bolt Action Air. 'Life Is Precious' Survival Kit by Fort Standard; This is a piece of art, so let's call it 'highbrow' packaging. Welcome to the October edition of. Victorian Pistol News. Coaching happening. Will Crossman, who was a level 1 coach. State Record 570 Lucas Finken (2010). 25m Centrefire. State Record 585 Bruce Quick (1996). Standard Pistol. State Record 580 Bruce Quick (1999). 25 Metre Pistol Women.

I like to see new and different things, but this isn’t enough for me to see the true practical application in civilian, hunting, police, or military use. And I kind of chuckled when they mentioned competition use. Very few people want a competition gun that has recoil similar to a.40 S&W. Some may, but most do not. And being such a niche gun, there is likely not going to be a whole lot of aftermarket support for it. I don’t see this gun catching on any time soon.

Well at this point it’s a mixture of “getting ready to fight the last war” combined with technical limitations. Current handgun selection is trending towards 9mm/.45 handguns using newly approved JHP ammunition for the MHS program. This is based on the assumption that adversaries in the future will be much like the ones we face today – unarmored militants and 3rd world armies. If climate change leads to widespread upheaval, mass migration, water wars, and other nastiness that requires “urban pacification missions” around the South, then this is likely the correct call. However if the next war is against any type of modern adversary, using level III or IV armor, then the 5.7, 7.5. 7.62×25 will all be as ineffective as 9mm against hard armor (although possibly effective against helmets.) To meet the challenges of that level of protection, it’s going to require saboted tungsten ammunition similar to 6.5CBJ.

And once your there, it really doesn’t even make sense to use a handgun when micro-PDW’s like the B&T MP9 are only 12″ long and weigh 3lbs, given the forward grip, integral red dot, and folding stock that this slightly larger platform offers. Hey that just gave me an idea – what would a kriss vector optimized for 7.5FK BRNO in full auto be like as compared to an akm? Would the extra barrel length over the pistol get comparable velocity to a 10″ ak pattern rifle?

Would having a full auto smg that shares ammo with your pistol be useful now that they are chambered in a powerful armor defeating pdw cartridge? And what would a 30rd magazine of lehigh defense controlled chaos projectile in 7.5FK look like ripping up a gel block in full auto? I have recently installed the 460 Rowland in one of my 1911 45acp pistols, I have not tried it at long distances yet but power wise it looks to be in the same ballpark as the 7.5 or 44 magnum power range. The advantage with the 460 is being able to reload for it as the 460 Rowland brass is readily available and being a straight walled case and common bullet size means projectiles are easily obtained as well. Also if you want to swap back to the 45acp, all you have to do is change out the components and you have the 45acp pistol in it`s original form. That is versatility.

A 10mm magnum necked down to 30 caliber producing 2000 fps out of a six inch barrel with a 100 grain bullet is nothing to sneeze. Those are 30 carbine rifle ballistics out of a pistol.

10mm magnum Brass is available from Starline, the 10mm magnum case is 1.242 – 1.248 O.A.L while a standard 10mm auto case is only.990 OAL and the 40 S&W is.850 I like this gun a lot. As far as the sights, I’d actually have to try the gun out before I made a judgment call, but sights are easy enough to change on any handgun and I notice the rear sight is dovetailed, •. Lack of stopping power relative to the standards set by rifles of the time.

That is,.30-06. It’s a very wimpy RIFLE round. Comparing it to -pistol- rounds is something entirely different. That said, I wonder about the terminal ballistics at ranges under 100 meters. I notice that that is not discussed in the video. Sure, muzzle energy is super high, but how much of that is actually delivered to the target?

Is it actually tumbling/fragmenting the way a high-velocity, low diameter round needs to in order to deliver serious damage, or at 5-25 meters are we going to get the same sort of inconsistent terminal performance and overpenetration that led the US military to spend lots of time and money reworking our 5.56 ammo? The uninformed think this round does not equal the power of the 44 mag, but the 44 mag loses velocity in the air like pulling a sailboat. This round is small diameter and long so it does not lose velocity as fast. They also seem to forget that this round is larger in diameter than a 7mm Rem Mag, no one would doubt it’s ability to take down a large brown bear.

I would sure like to have one of these pistols. I have a 44 mag revolver and will keep it.

But a 44 mag will not penetrate body armor at point blank range, this pistol will do the job at 100 yards.

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Original Article Brief Report Actionable Diagnosis of Neuroleptospirosis by Next-Generation Sequencing Michael R. Wilson, M.D., Samia N.

Naccache, Ph.D., Erik Samayoa, B.S., C.L.S., Mark Biagtan, M.D., Hiba Bashir, M.D., Guixia Yu, B.S., Shahriar M. Salamat, M.D., Ph.D., Sneha Somasekar, B.S., Scot Federman, B.A., Steve Miller, M.D., Ph.D., Robert Sokolic, M.D., Elizabeth Garabedian, R.N., M.S.L.S., Fabio Candotti, M.D., Rebecca H. Buckley, M.D., Kurt D. Reed, M.D., Teresa L. Meyer, R.N., M.S., Christine M.

Seroogy, M.D., Renee Galloway, M.P.H., Sheryl L. Henderson, M.D., Ph.D., James E.

Gern, M.D., Joseph L. DeRisi, Ph.D., and Charles Y.

Chiu, M.D., Ph.D. N Engl J Med 2014; 370:2408-2417 DOI: 10.1056/NEJMoa1401268. A 14-year-old boy with severe combined immunodeficiency presented three times to a medical facility over a period of 4 months with fever and headache that progressed to hydrocephalus and status epilepticus necessitating a medically induced coma. Diagnostic workup including brain biopsy was unrevealing. Unbiased next-generation sequencing of the cerebrospinal fluid identified 475 of 3,063,784 sequence reads (0.016%) corresponding to leptospira infection.

Clinical assays for leptospirosis were negative. Targeted antimicrobial agents were administered, and the patient was discharged home 32 days later with a status close to his premorbid condition. Polymerase-chain-reaction (PCR) and serologic testing at the Centers for Disease Control and Prevention (CDC) subsequently confirmed evidence of Leptospira santarosai infection. Figure 1 Clinical Course of the 14-Year-Old Patient with Fulminant Meningoencephalitis. Panel A shows a timeline beginning with the patient's trip to Puerto Rico in August 2012 and ending after his recovery in October 2013. Major events during the course of the patient's illness are indicated by arrows.

Panel B shows laboratory values obtained and pertinent medications administered during the patient's third hospitalization. The upper graph shows the body-temperature curve (red line) and peripheral-blood leukocyte counts (purple bars). The lower graph shows the leukocyte count and differential (bars) and the glucose (dashed line) and protein (solid line) levels in serially collected cerebrospinal fluid samples. Online Library Management System Template Free Download there. The horizontal thick gray lines show the medications administered. The asterisk denotes the first course of cefuroxime (CFX) given to the patient, which did not result in clinical improvement. CFPM denotes cefepime, EVD extraventricular drain, MEP methylprednisolone, MRI magnetic resonance imaging, PCN G penicillin G, PEG-ADA polyethylene glycol–modified adenosine deaminase, and VANC vancomycin.

Figure 2 Neuroradiologic MRI and Brain-Biopsy Findings. The images shown in Panels A, B, and C were acquired on day 13 of the patient's third hospitalization, whereas the image shown in Panel D was acquired on day 55, after the patient had completed a 7-day course of intravenous penicillin G. An axial T 2-weighted image of the head revealed persistent hyperintensities in the basal ganglia and deep frontal white matter (Panel A, arrows). Sagittal and axial T 2-weighted fluid-attenuated inversion recovery (FLAIR) images (Panels B and C, respectively) showed thickening in and around the basilar meninges (arrows). An axial T 2-weighted FLAIR image (Panel D) depicts near resolution of the previously seen (Panels B and C) basilar meningitis. Results of a biopsy of the right frontal lobe performed 2 weeks after the third hospital admission showed infiltration by lymphocytes and epithelioid histiocytes in the subarachnoid space with a perivascular predilection (Panel E, hematoxylin and eosin). T lymphocytes were visualized by means of immunolabeling with anti-CD3 antibody (Panel F).

Various stains also showed the absence of mycobacteria (Panel G, acid-fast), fungi (Panel H, Gomori methenamine silver), and leptospira or other spirochetes (Panel I, Warthin–Starry silver). Electron microscopy revealed the presence of an inflammatory infiltrate and the absence of inclusion bodies, viral particles, or other evidence of microorganisms (Panel J). More than half the cases of meningoencephalitis remain undiagnosed, despite extensive clinical laboratory testing. Because more than 100 different infectious agents can cause encephalitis, establishing a diagnosis with the use of cultures, serologic tests, and pathogen-specific PCR assays can be difficult. Unbiased next-generation sequencing has the potential to revolutionize our ability to discover emerging pathogens, especially newly identified viruses. However, the usefulness of next-generation sequencing for the diagnosis of infectious diseases in a clinically relevant timeframe is largely unexplored. We used unbiased next-generation sequencing to identify a treatable, albeit rare, bacterial cause of meningoencephalitis.

In this case, the results of next-generation sequencing contributed directly to a dramatic effect on the patient's care, resulting ultimately in a favorable outcome. Case Report A 14-year-old boy with severe combined immunodeficiency (SCID) caused by adenosine deaminase deficiency and partial immune reconstitution after he had undergone two haploidentical bone marrow transplantations initially presented to the emergency department in early April 2013 after having had headache and fevers, with temperatures up to 39.4°C, for 6 days ( Figure 1 Clinical Course of the 14-Year-Old Patient with Fulminant Meningoencephalitis. Panel A shows a timeline beginning with the patient's trip to Puerto Rico in August 2012 and ending after his recovery in October 2013. Major events during the course of the patient's illness are indicated by arrows.

Panel B shows laboratory values obtained and pertinent medications administered during the patient's third hospitalization. The upper graph shows the body-temperature curve (red line) and peripheral-blood leukocyte counts (purple bars). The lower graph shows the leukocyte count and differential (bars) and the glucose (dashed line) and protein (solid line) levels in serially collected cerebrospinal fluid samples. The horizontal thick gray lines show the medications administered. The asterisk denotes the first course of cefuroxime (CFX) given to the patient, which did not result in clinical improvement.

CFPM denotes cefepime, EVD extraventricular drain, MEP methylprednisolone, MRI magnetic resonance imaging, PCN G penicillin G, PEG-ADA polyethylene glycol–modified adenosine deaminase, and VANC vancomycin. He was admitted to the hospital and discharged 1 day later after resolution of his fever and headache. The patient's outpatient medications included monthly infusions of intravenous immune globulin for hypogammaglobulinemia and trimethoprim–sulfamethoxazole or atovaquone for prophylaxis against Pneumocystis jirovecii pneumonia. He had no known sick contacts but did have three pet cats. He had gone on a missionary trip to Puerto Rico during the first 2 weeks of August 2012 ( ), where he swam in a river and the ocean.

Notably, a 17-year-old fellow traveler had been hospitalized for 4 days with fever and hematuria. The patient had also vacationed in Florida in March 2013, where he swam in a pool at a resort where there were a number of feral cats. In September 2012, the patient had presented to his primary care physician with fever, headache, and bilateral conjunctivitis that resolved spontaneously in 10 days ( ). At the end of October 2012, he had had photophobia and pain with movement of his left eye. His ophthalmologist had prescribed eyedrops consisting of a combination of a glucocorticoid, a vasoconstrictor, and an antibiotic (ciprofloxacin) for uveitis.

One week later, uveitis had developed in the contralateral eye and was treated in a similar manner. The ophthalmologic symptoms had resolved by December 2012. Thrombocytopenia had also developed in October 2012, and the patient was treated with rituximab for presumed immune thrombocytopenic purpura, with subsequent normalization of his platelet counts.

After the brief hospitalization in early April 2013, the patient was readmitted to the hospital at the end of April 2013 with fever, photophobia, and daily frontotemporal headaches ( ). In addition, he reported increasing fatigue, abdominal pain, and a weight loss of 2.3 kg. On admission, he had normal vital signs, and the physical examination was unremarkable. The peripheral-blood leukocyte count was 3800 per cubic millimeter with 78% neutrophils. The erythrocyte sedimentation rate was 39 mm per hour (normal range, 0 to 20 mm per hour).

The deoxyadenosine nucleotide percentage in the red cells, a measure of control of adenosine deaminase deficiency, was 5.9% (target range. Methods Analysis of the patient's clinical samples for the identification of potential pathogens was approved by the institutional review board at the University of Wisconsin and at the University of California, San Francisco (UCSF). Amplified DNA libraries for next-generation sequencing were constructed from extracted nucleic acid derived from clinical samples as previously described, followed by library validation and sequencing on an Illumina MiSeq instrument. Reads were analyzed with the use of sequence-based ultra-rapid pathogen identification (SURPI), a bioinformatics pipeline developed at UCSF to rapidly classify next-generation sequencing reads according to their origin.

The SURPI pipeline first identifies and subtracts human host sequences, followed by alignment of reads to reference sequences in National Center for Biotechnology Information (NCBI) databases, including all of GenBank, for the comprehensive identification of bacteria, viruses, fungi, and parasites. Full details regarding sample processing, next-generation sequencing analysis, PCR confirmation, and phylogenetic analysis are provided in the. Rapid Identification of Leptospira Sequences in CSF CSF and serum samples were processed in a clinical laboratory with the use of an unbiased next-generation sequencing assay protocol with a sample-to-answer turnaround time of 48 hours ( ). Approximately half the total CSF volume (750 μl) was pretreated with DNase before nucleic acid extraction to enrich the sample for viral sequencing; the remaining half was not pretreated (i.e., untreated CSF), and the nucleic acid was directly extracted for the detection of bacteria, fungi, and parasites. The next-generation sequencing run of four individually indexed samples, including a serum sample from an unrelated patient that served as a negative control, yielded 10,196,620 raw reads. A total of 8,187,737 reads were derived from the patient's serum, untreated CSF, and DNase-treated CSF, and the remaining 2,008,883 reads corresponded to the negative control sample. The full data set of 10,196,620 raw single-end reads was analyzed in approximately 100 minutes with the use of SURPI.

In the untreated CSF, the majority of bacterial reads (475 of 589 reads; 80.6%) corresponded to the Leptospiraceae family (, and Table S2 in the ), with the mapped reads spanning the closest matched full leptospira genome deposited in the NCBI nucleotide reference database at the time, L. Borgpetersenii, at 3.7% and 2.2% coverage for chromosomes 1 and 2, respectively. No convincing hits to other bacteria or viruses were found in the next-generation sequencing data (Tables S3 and S4 in the ), and no reads corresponding to leptospira, either single-end or paired-end, were detected in serum samples from the patient or the negative control (Table S3 in the ). Confirmatory Testing for Leptospirosis Primers targeting the genes ompA and secY were designed directly from the mapped next-generation sequencing reads, and the identification of leptospira was confirmed 5 days after the next-generation sequencing analysis with the use of PCR analysis and Sanger sequencing (, and Fig. S1 and Table S5 in the ). This approach was also used to sequence the partial-length gene lipL32 and the full-length genes lipL41, rpoB, and secY. Employee Absence Template 2010 Nfl. Phylogenetic analysis revealed that the CSF sample harbored L.

Santarosai (, and Fig. S2 in the ), a pathogenic species whose genome has been sequenced but was not deposited in the NCBI nucleotide reference database as of August 2013 and thus was not identified by the SURPI pipeline. The CSF titer, calculated from a sample collected 1 day before the initiation of vancomycin and cefepime (Fig. S3 in the ), was 958 genome copies per milliliter. Clinical diagnostic tests of CSF and serum samples obtained during the acute and convalescent periods were negative for leptospirosis; testing included IgM and IgG antibody testing by means of dot-blot enzyme-linked immunosorbent assay, direct culture, and a Clinical Laboratory Improvement Amendments–validated PCR assay targeting the gene lipL32 ( ). These results suggest that the diagnosis could not have been made routinely with the use of available clinically validated assays for leptospirosis. The CDC eventually detected leptospira in the CSF 5 months after the next-generation sequencing analysis by repeating the PCR assay targeting lipL32 with the use of a different amplification mix (cycle threshold of approximately 35; Fig.

This yielded an amplicon that was shown by means of direct Sanger sequencing to correspond to L. Separate confirmation of leptospira infection from a serum sample drawn in October 2013 (during the convalescent period) was also obtained with the use of a qualitative IgM latex agglutination assay targeting pathogenic leptospira that had been newly approved by the Food and Drug Administration. Discussion Leptospirosis is a worldwide zoonotic disease caused by a spirochete. Bacteria are shed in urine from reservoir animals and transmitted to humans by means of mucosal exposure or breaks in the skin.

The disease phenotype varies from subclinical infection to severe illness with multiorgan involvement. The acute stage of the disease is characterized by fever, myalgias, headache, and conjunctivitis. The chronic stage of the disease can include meningitis, encephalitis, or both (predominantly in male patients), nephritis, cholecystitis, uveitis, and thrombocytopenia. The standard diagnostic assay for leptospirosis detects the host's serologic response. The degree of immunosuppression resulting from SCID and rituximab therapy in the case patient made it unlikely that he would have had a detectable antibody response even if the diagnosis had been considered a priori. Furthermore, his treatment with intravenous immune globulin may have clouded the interpretation of a positive result.

Leptospires, like other spirochetes, are typically not detected by means of routine microscopy and cannot be cultured with the use of standard media. PCR-based testing is available but has limited sensitivity given the wide diversity of leptospira species and the lack of standardization among assays. We suspect that the patient most likely contracted leptospirosis during his trip to Puerto Rico in August 2012, during which he swam in freshwater and during which fever and hematuria suggestive of leptospira-associated nephritis developed in a fellow traveler. The diagnosis of L. Santarosai infection is also consistent with the geographic distribution of this bacterial species, which includes Latin America, the Caribbean, and Taiwan.

The patient's fever, headache, thrombocytopenia, uveitis, and conjunctivitis within 3 months after visiting Puerto Rico were, in hindsight, probable clinical manifestations of leptospirosis. Although the neurotropism and persistence of leptospira in the brains of animal reservoir hosts are well described, this case is a rare instance of chronic neuroleptospirosis in a human lasting for months after the acute presentation. The decision to treat this patient before confirmatory tests could be completed was the result of a 2-hour multidisciplinary discussion during which the risk that the leptospirosis result was a spurious finding was weighed against the potential benefit of treatment and the low toxicity of penicillin G. The concern that the finding was spurious was considered to be negligible given that a large number of reads spanning the leptospira genome were detected in the patient's CSF ( ), leptospira reads were absent in the patient's serum and in a control sample from an unrelated patient processed concomitantly (Tables S2, S3, and S4 in the ), and leptospira sequences have hitherto never been detected in the next-generation sequencing laboratory. In addition, the patient's travel history, clinical presentation, and CSF values were all consistent with a diagnosis of neuroleptospirosis, and no other pathogens associated with the clinical syndrome were identified in the next-generation sequencing data or by means of conventional microbiologic testing. In summary, unbiased next-generation sequencing coupled with a rapid bioinformatics pipeline provided a clinically actionable diagnosis of a specific infectious disease from an uncommon pathogen that eluded conventional testing for months after the initial presentation.

This approach thus facilitated the use of targeted and efficacious antimicrobial therapy. Supported by the American Brain Foundation Clinical Research Training Fellowship (to Dr. Wilson), a National Human Genome Research Institute Intramural Research Program appointment (to Dr. Garabedian, and Dr. Candotti), a Howard Hughes Medical Institute appointment (to Dr. DeRisi), a grant from the National Institutes of Health (R01-HL105704, to Dr.

Chiu), a University of California Discovery Grant (to Dr. Chiu), an Amazon Web Services in Education Research Grant (to Dr. Chiu), and an Abbott Viral Discovery Award (to Dr. Provided by the authors are available with the full text of this article at NEJM.org. This article was published on June 4, 2014, at NEJM.org. We thank Nicholas Marinelli, M.D., in the Department of Radiology at the University of Wisconsin, for providing the magnetic resonance images and associated text; and Jerome LeGoff for editorial comments on an earlier version of the manuscript. References • 1 Glaser CA, Gilliam S, Schnurr D, et al.

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