Diabetic Gangrene of the Lower Extremities
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Efficacy of Texture and Color Enhancement Imaging In
www.nature.com/scientificreports OPEN Efcacy of Texture and Color Enhancement Imaging in visualizing gastric mucosal atrophy and gastric neoplasms Tsubasa Ishikawa1, Tomoaki Matsumura1*, Kenichiro Okimoto1, Ariki Nagashima1, Wataru Shiratori1, Tatsuya Kaneko1, Hirotaka Oura1, Mamoru Tokunaga1, Naoki Akizue1, Yuki Ohta1, Keiko Saito1, Makoto Arai1,2, Jun Kato1 & Naoya Kato1 In 2020, Olympus Medical Systems Corporation introduced the Texture and Color Enhancement Imaging (TXI) as a new image-enhanced endoscopy. This study aimed to evaluate the visibility of neoplasms and mucosal atrophy in the upper gastrointestinal tract through TXI. We evaluated 72 and 60 images of 12 gastric neoplasms and 20 gastric atrophic/nonatrophic mucosa, respectively. The visibility of gastric mucosal atrophy and gastric neoplasm was assessed by six endoscopists using a previously reported visibility scale (1 = poor to 4 = excellent). Color diferences between gastric mucosal atrophy and nonatrophic mucosa and between gastric neoplasm and adjacent areas were assessed using the International Commission on Illumination L*a*b* color space system. The visibility of mucosal atrophy and gastric neoplasm was signifcantly improved in TXI mode 1 compared with that in white-light imaging (WLI) (visibility score: 3.8 ± 0.5 vs. 2.8 ± 0.9, p < 0.01 for mucosal atrophy; visibility score: 2.8 ± 1.0 vs. 2.0 ± 0.9, p < 0.01 for gastric neoplasm). Regarding gastric atrophic and nonatrophic mucosae, TXI mode 1 had a signifcantly greater color diference than WLI (color diferences: 14.2 ± 8.0 vs. 8.7 ± 4.2, respectively, p < 0.01). TXI may be a useful observation modality in the endoscopic screening of the upper gastrointestinal tract. -
Gas Gangrene Infection of the Eyes and Orbits
Br J Ophthalmol: first published as 10.1136/bjo.69.2.143 on 1 February 1985. Downloaded from British Journal of Ophthalmology, 1985, 69, 143-148 Gas gangrene infection of the eyes and orbits GERARD W CROCK,' WILSON J HERIOT,' PATTABIRAMAN JANAKIRAMAN,' AND JOHN M WEINER2 From the 'Department of Ophthalmology, University ofMelbourne, and the2C H Greer Pathology Laboratory, the Royal Victorian Eye and Ear Hospital, East Melbourne, Australia SUMMARY The literature on Clostridium perfringens infections is reviewed up to 1983. An additional case is reported with bilateral clostridial infections of the eye and orbit. One eye followed the classical course of relentless panophthalmitis, amaurosis, and orbital cellulitis ending in enucleation. The second eye contained intracameral mud and gas bubbles that were removed by vitrectomy instrumentation. Subsequent removal of the toxic cataract resulted in a final aided visual acuity of 6/18, N8. This is the third report of a retained globe, and we believe the only known case where the patient was left with useful vision. Clostridium perfringens is a ubiquitous Gram- arms, chest, and abdomen. He was admitted to a positive bacillus found in soil and bowel flora. It is the general hospital, where he was examined under most common of four clostridia species identified in anaesthesia, and his injuries were attended to. copyright. cases of gas gangrene in man.' All species are obligate Ocular findings. The right cornea and anterior anaerobes and are usually saprophytic rather than chamber were intact. There was a scleral laceration pathogenic. Clostridium perfringens is a feared con- over the superonasal area of the pars plana with taminant of limb injuries and may result in death due vitreous prolapse. -
Spinal Muscular Atrophy Testing
Lab Management Guidelines v2.0.2019 Spinal Muscular Atrophy Testing MOL.TS.225.B v2.0.2019 Procedures addressed The inclusion of any procedure code in this table does not imply that the code is under management or requires prior authorization. Refer to the specific Health Plan's procedure code list for management requirements. Procedures addressed by this Procedure codes guideline SMN1 Gene Analysis; Dosage/Deletion 81329 Analysis (eg, carrier testing), includes SMN2 Analysis, if performed SMN1 Full Gene Sequencing 81336 SMN1 Known Familial Mutation Analysis 81337 What is spinal muscular atrophy Definition Spinal muscular atrophy (SMA) is a severe, autosomal recessive neuromuscular disease that affects 1 in 8000 to 1 in 10,000 people.1,2 SMA is caused by loss of lower motor neurons (anterior horn cells) in the spinal cord, resulting in progressive symmetrical muscle weakness and atrophy.1-3 SMA has historically been divided into three to five clinical subtypes based on age of onset and clinical course. While genetic testing has shown these clinical subtypes are not completely distinct, they are still widely used, and include:1-3 o Prenatal onset form (“Type 0” proposed) is characterized by polyhydramnios, decreased fetal movements, breech presentation, arthrogryposis multiplex congenita, respiratory failure at birth, and life span less than 6 months. o Type I (infantile or Werdnig-Hoffmann type) is the most common form (60-70% of cases). It presents before 6 months of age with death often before age 2 due to respiratory failure. Affected children have severe, generalized weakness and do not ever sit without support. -
Short Course 10 Metaplasia in The
0 3: 436-446 Rev Esp Patot 1999; Vol. 32, N © Prous Science, SA. © Sociedad Espajiola de Anatomia Patot6gica Short Course 10 © Sociedad Espafiola de Citologia Metaplasia in the gut Chairperson: NA. Wright, UK. Co-chairpersons: G. Coggi, Italy and C. Cuvelier, Belgium. Overview of gastrointestinal metaplasias only in esophagus but also in the duodenum, intestine, gallbladder and even in the pancreas. Well established is columnar metaplasia J. Stachura of esophageal squamous epithelium. Its association with increased risk of esophageal cancer is widely recognized. Recent develop- Dept. of Pathomorphology, Jagiellonian University ments have suggested, however, that only the intestinal type of Faculty of Medicine, Krakdw, Poland. metaplastic epithelium (classic Barrett’s esophagus) predisposes to cancer. Another field of studies is metaplasia in the short seg- ment at the esophago-cardiac junction, its association with Metaplasia is a reversible change in which one aduit cell type is Helicobacter pylon infection and/or reflux disease and intestinal replaced by another. It is always associated with some abnormal metaplasia in the cardiac and fundic areas. stimulation of tissue growth, tissue regeneration or excessive hor- Studies on gastric mucosa metaplasia could be divided into monal stimulation. Heterotopia, on the other hand, takes place dur- those concerned with pathogenesis and detailed structural/func- ing embryogenesis and is usually supposed not to be associated tional features and those concerned with clinical significance. with tissue damage. Pancreatic acinar cell clusters in pediatric gas- We know now that gastric mucosa may show not only complete tric mucosa form another example of aberrant cell differentiation. and incomplete intestinal metaplasia but also others such as ciliary Metaplasia is usually divided into epithelial and connective tis- and pancreatic metaplasia. -
Hyperplasia (Growth Factors
Adaptations Robbins Basic Pathology Robbins Basic Pathology Robbins Basic Pathology Coagulation Robbins Basic Pathology Robbins Basic Pathology Homeostasis • Maintenance of a steady state Adaptations • Reversible functional and structural responses to physiologic stress and some pathogenic stimuli • New altered “steady state” is achieved Adaptive responses • Hypertrophy • Altered demand (muscle . hyper = above, more activity) . trophe = nourishment, food • Altered stimulation • Hyperplasia (growth factors, . plastein = (v.) to form, to shape; hormones) (n.) growth, development • Altered nutrition • Dysplasia (including gas exchange) . dys = bad or disordered • Metaplasia . meta = change or beyond • Hypoplasia . hypo = below, less • Atrophy, Aplasia, Agenesis . a = without . nourishment, form, begining Robbins Basic Pathology Cell death, the end result of progressive cell injury, is one of the most crucial events in the evolution of disease in any tissue or organ. It results from diverse causes, including ischemia (reduced blood flow), infection, and toxins. Cell death is also a normal and essential process in embryogenesis, the development of organs, and the maintenance of homeostasis. Two principal pathways of cell death, necrosis and apoptosis. Nutrient deprivation triggers an adaptive cellular response called autophagy that may also culminate in cell death. Adaptations • Hypertrophy • Hyperplasia • Atrophy • Metaplasia HYPERTROPHY Hypertrophy refers to an increase in the size of cells, resulting in an increase in the size of the organ No new cells, just larger cells. The increased size of the cells is due to the synthesis of more structural components of the cells usually proteins. Cells capable of division may respond to stress by undergoing both hyperrtophy and hyperplasia Non-dividing cell increased tissue mass is due to hypertrophy. -
Ghasemi Gh. Comparison of Laparoscopic Ovarian Drilling
Archive of SID Original Article Comparison of Laparoscopic Ovarian Drilling Success between Two Standard and Dose-Adjusted Methods in Polycystic Ovary Syndrome: A Randomized Clinical Trial Leili Hafizi, M.D.1, Maliheh Amirian, M.D.2, Yasmin Davoudi, M.D.3, Mona Jaafari, M.D.1, Ghazal Ghasemi, M.D.1* 1. Department of Obstetrics and Gynaecology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran 2. Department of IVF and Infertility, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran 3. Department of Radiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran Abstract Background: One of the treatment methods for increasing the ovarian response to ovulation induction in polycystic ovary syndrome (PCOS) is laparoscopic ovarian drilling (LOD). The optimal amount of the electrosurgical energy discharged in the ovaries to achieve maximum treatment response with minimal follicle injury is unknown. This study was performed to compare the success level of LOD by means of standard and dose-adjusted treatment methods among infertile clomiphene-resistant PCOS women. Materials and Methods: This randomized clinical trial was conducted on infertile clomiphene citrate-resistant PCOS women in the Gynaecology Department of Imam Reza Hospital between 2016 and 2017. The patients were randomly di- vided into two groups based on the ovarian cautery method. The two groups were examined and compared regarding the antral follicles, the serum levels of anti-Müllerian hormone (AMH), androgens, and mid-luteal progesterone one month after surgery. The regularity of cycles, ovulation, and pregnancy were examined monthly up to six months after surgery. Results: In total, 60 women received bilateral LOD (n=30 per group). -
Cellular Adaptation
Cellular Adaptation Dr. Adeboye OO (MBBS, Cert. LMIH, FMCPath) Dept of Anatomic Pathology Bowen University Cellular adaptation • Cell death is not the only consequence of cellular injury or stress • Cells can respond to excessive physiologic or pathologic stimuli by undergoing both functional and morphologic change in which a new steady state is achieved that preserves the viability of the cell(Adaptation) . • The adaptive response include- • Adaptation of growth and differentiation • Intracellular accumulation • Pathologic calcification • Hyaline change • Cellular aging Adaptation of growth and differentiation • Adaptations are reversible changes in the size, number,phenotype, metabolic activity, or functions of cells in response to changes in their environment. Such adaptations may take several distinct forms : • 1. hyperplasia • 2. hypertrophy • 3. atrophy • 4. metaplasia hypertrophy • Increase in the size of cells that result in the increase in size of the affected organ. • No new cells just larger cells • May coexist with hyperplasia in cells capable of division( eg epithelial, hematopoesis etc), in non dividing cells (eg the nerve ,cardiac and skeletal muscle) increase tissue mass is due to hypertrophy • Can be physiologic or pathologic Physiologic hypertrophy • Caused by- (a) increased functional demand eg hypertrophy of striated muscle in muscle builder.(b) stimulation by hormones or growth factors eg physiologic hypertrophy of the uterus during pregnancy Hypertrophy of uterus during pregnancy Micrograph showing smooth muscle -
Brain-Derived Circulating Cell-Free DNA Defines the Brain Region and Cell Specific Origins Associated with Neuronal Atrophy
bioRxiv preprint doi: https://doi.org/10.1101/538827; this version posted February 2, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Brain-derived circulating cell-free DNA defines the brain region and cell specific origins associated with neuronal atrophy Chatterton. Zac1,2,4,6,9*, Mendelev. Natalia1,2,4,6, Chen. Sean1,2,4,6, Raj. Towfique1,2, Walker. Ruth1,2,6,7, Carr. Walter10,11, Kamimori. Gary10, Beeri. Michal8, Ge. Yongchao4, Dwork. Andrew5, Haghighi. Fatemeh1,2,4,6* *Corresponding author. Email: [email protected] & [email protected] 1Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, 2Department of Neuroscience, 3Department of Psychiatry, 4Department of Neurology, Icahn School of Medicine at Mount Sinai, 1425 Madison Avenue, New York, NY 10029. 5Department of Pathology and Cell Biology, Columbia University, New York, USA. 6Medical Epigenetics, James J. Peters VA Medical Center, Bronx, USA. 7Department of Neurology, James J. Peters VA Medical Center, Bronx, USA 8The Joseph Sagol Neuroscience Center, Sheba Medical Center, Ramat Gan, Israel 9Brain and Mind Centre, The University of Sydney, Camperdown, Australia 10Walter Reed Army Institute of Research, Silver Spring, MD, USA 11Oak Ridge Institute for Science and Education, Oak Ridge, TN, USA Liquid biopsies are revolutionizing the fields non-invasive prenatal testing (NIPT). The of prenatal non-invasive testing and cancer technological advancements in NGS have diagnosis by leveraging the genetic differences increased the limits of detection of these between mother and fetus, and, host and techniques [4] to ~0.02%, which hold the cancer. -
Sclerosing Lymphangitis of the Penis
Brit. J. vener. Dis. (1972) 48, 545 Br J Vener Dis: first published as 10.1136/sti.48.6.545 on 1 December 1972. Downloaded from Sclerosing lymphangitis of the penis A. LASSUS, K. M. NIEMI, S.-L. VALLE, AND U. KIISTALA From the Department of Dermatology and Venereology, University Central Hospital, Helsinki, Finland Non-venereal sclerosing lymphangitis of the penis of the lesion was perforated a clear yellowish fluid leaked (NSLP) has been considered a rare condition, and out and the lesion became softer and smaller. A biopsy only fourteen cases have been reported (Hoffmann, was taken from the wall of the lesion. After the operation, 1923, 1938; von Berde 1937; Nickel and Plumb, the lesion had clinically disappeared. 1962; Kandil and Al-Kashlan, 1970). The disorder was originally described by Hoffmann (1923), who referred to it as 'simulation of primary syphilis by gonorrhoeal lymphangitis (gonorrhoeal pseudo- chancre)'. In a later paper Hoffmann (1938) called the condition a 'non-venereal plastic lymphangitis of the coronary sulcus of the penis with circumscribed edema'. The aetiology of the disorder is not known, copyright. but its non-venereal nature has been stressed in subsequent reports (Nickel and Plumb, 1962; Kandil and Al-Kashlan, 1970). It has been suggested that it may be related to mechanical trauma, virus infection, irritation by menstrual blood, or tuber- culosis. NSLP appears suddenly as a firm, cordlike, encircle the translucent lesion, which may almost http://sti.bmj.com/ penis in the coronal sulcus. The histological findings suggest that it results from fibrotic thickening of a large lymph vessel. -
Stanford Emergency Department & Clinical
STANFORD EMERGENCY DEPARTMENT & CLINICAL DECISION UNIT EMPIRIC ANTIBIOTIC GUIDELINES FOR ACUTE BACTERIAL SKIN AND SKIN-STRUCTURE INFECTIONS PURULENT CELLULITIS (cutaneous abscess, carbuncle, furuncle) Common pathogen: Staphylococcus aureus Duration of Therapy: 5-10 days Condition/Severity Admit/CDU/Discharge Cultures? Antibiotic Recommendation Mild < 5 cm Discharge No I&D Only ± TMP-SMX DS 1-2 PO BID Mild > 5 cm Discharge Yes – I&D plus Antibiotics: wound TMP-SMX DS 1-2 PO BID Typical abscess +/- cellulitis with no I&D systemic signs of infection Alternative: Doxycycline 100 mg PO BID Moderate Discharge Yes – TMP-SMX DS 1-2 PO BID wound only one Purulent infection with I&D Alternative: Doxycycline 100 mg PO BID systemic sign of infection: CDU if any factors below1,2: EMPIRIC ANTIBIOTICS: temp>38°C - • Concern for poor adherence to therapy TMP-SMX DS 1-2 PO BID HR >90 bpm - • Exacerbation of comorbidities RR>24 bpm Alternative: - • Significant clinical concern Yes – abnormal WBC >12K or <400 • Doxycycline 100 mg PO BID - Note: cutaneous inflammation and systemic wound cells/mcg/L features often worsen after initiating therapy I&D Lymphangitis DEFINITIVE ANTIBIOTICS: - and failure to improve at 24 hours NOT MRSA: TMP-SMX DS 1-2 PO BID considered clinical failure MSSA: dicloxacillin 500mg PO QID or cephalexin 500mg PO QID Severe EMPIRIC ANTIBIOTICS: Vancomycin Per Pharmacy • Hypotension Alternatives: Consult pharmacy for restricted antibiotics • 2 or more systemic signs of Admission Yes - infection blood DEFINITIVE ANTIBIOTICS: - temp>38°C MRSA: Vancomycin - HR >90 bpm MSSA: Cefazolin 2g IV Q8H - RR>24 bpm - abnormal WBC >12K or <400 cells/mcg/L - Lymphangitis • Immunocompromised** CELLULITIS (NON-PURULENT) Common pathogens: Streptococcus spp (usually S. -
Lymphographic Studies in Acute Lymphogranuloma Venereum Infection
Brit. J7. vener. Dis. (1976) 52, 399 Br J Vener Dis: first published as 10.1136/sti.52.6.399 on 1 December 1976. Downloaded from Lymphographic studies in acute lymphogranuloma venereum infection A. 0. OSOBA AND C. A. BEETLESTONE From the Special Treatment Clinic and the Departments of Medical Microbology and Radiology, University of Ibadan, Nigeria Summary 1954) described a convenient method of cannulating Lymphography, a radiological method of demon- the lymph vessels and injecting water-soluble strating lymphatic channels and nodes, has been contrastmedium, the procedurehas become extensively used to investigate three cases of acute bubonic used. Lymphography has been used in a variety of lymphogranuloma venereum (LGV). There is conditions in which the pathological process origi- nates in or is associated with lymph nodes (Koehler, general agreement that LGV has a predilection for 1968a, b). In lymphomas, the lymphographic lymphatic channels and lymph nodes. However, appearance can be pathognomonic, hence much very little is known of the extent of lymph node excellent work has been done in this field (Abrams, involvement in the early bubonic stage and whether Takahashi, and Adams, 1968; Lee, 1968; Rosenberg, there is merely a lymphangitis or complete lymph- 1968). However, little work has been done on atic obstruction. inflammatory conditions such as tuberculosis, syphilis The present study was undertaken to determine and lymphogranuloma venereum (LGV), which copyright. the lymphographic appearance in acute bubonic produce lesions in lymph glands. Because lympho- LGV, the extent of lymphatic node involvement in graphy is the only direct method of visualizing the early LGV, and the usefulness of the procedure in lymphatics and lymph nodes, and since it can objectively evaluate the inaccessible pelvic and the management of LGV patients. -
Cellular Adaptation
ALTERATIONS IN CELLULAR AND TISSUE FUNCTION Lois E. Brenneman, MSN, APN, CELLULAR ADAPTATION Atrophy - decrease or shrinkage in cell size - Can (if sufficient numbers) result in shrinkage of entire organ Example: muscular atrophy after cast is removed Example: sports steroid abuse causes atrophy of penis - Physiologic atrophy - normal process Example: atrophy of thymus during childhood - Pathologic atrophy - disease process Example: Addison’s disease -> atrophy adrenal glands - Disuse Atrophy Example: Prolonged bed rest causes muscle atrophy Example: Casting limb causes atrophy Atrophic cells have fewer mitochondria and myofilaments Autophagic vacuoles occurs with malnutrition Lipofuscin - yellow-brown age pigment (may resist destruction) - Persists as membrane-bound residue bodies - Accumulates w age: liver, myocardial and atrophic cells - Results in “age spots” to skin “Age spots” Lipofuscin accumulation to skin © 2004 Lois E. Brenneman, MSN, CS, ANP, FNP all rights reserved - www.npceu.com 1 Hypertrophy - increase in cell size (vs cell number with hyperplasia) Results in increased size of organ Cardiac and kidney esp prone to hypertrophy Increased size -> increased cellular protein and not increased fluid Physiologic hypertrophy - normal process Example: muscle increase with exercise Example: genital size increase with hormones of puberty Pathologic hypertrophy - disease process Example - Left ventricular hypertrophy from hypertension -> congestive heart failure Triggers for hypertrophy Mechanical: stretch, exercise Trophic: growth factors, hormones, vasoactive agents CELLULAR HYPERTROPY Left: dependent edema in CHF Right: dilated cardiomyopathy Left ventricular hypertrophy (bottom) vs normal (top) © 2004 Lois E. Brenneman, MSN, CS, ANP, FNP all rights reserved - www.npceu.com 2 Hyperplasia - increase in number of cells (increased rate of cell division) - Can occur in response to injury esp with cell death - Can occur together with hypertrophy note: if organ with non-dividing cells (e.g.