A retrospective study was made of natural infections with Isospora suis in nursing piglets, recorded from April 1994 to May 1997, to determine the prevalence, microscopical lesions and other microorganisms associated with coccidiosis. One hundred and five (17.3 per cent) of the 605 nursing piglets submitted from 304 pig farms were diagnosed positive for coccidiosis. The affected piglets were from seven to 20 days old, with a mean age of 11.1 days. Coccidiosis occurred in each year but the incidence peaked in July (15 cases, 14.3 per cent), September (15 cases, 14.3 per cent), October (16 cases, 15.2 per cent) and November (18 cases, 17.1 per cent) and was lowest in May (no cases), August (two cases, 1.9 per cent) and June (four cases, 3.8 per cent). Histopathologically, villous atrophy resulting from the necrosis and sloughing of epithelial cells was a prominent feature of infection with I suis. In 49.5 per cent of the nursing piglets, other enteropathogens were identified, Escherichia coli (47.6 per cent) and transmissible gastroenteritis virus (3.8 per cent) being the most commonly diagnosed. Forty-five of 50 E coli isolates associated with coccidiosis tested negative by polymerase chain reaction for enterotoxigenic virulence factors, such as fimbriae and enterotoxins.
Premature fusion of the cranial suture and midface hypoplasia are common features of syndromic craniosynostosis caused by mutations in the FGFR2 gene. The only treatment for this condition involves a series of risky surgical procedures designed to correct defects in the craniofacial bones, which must be performed until brain growth has been completed. Several pharmacologic interventions directed at FGFR2 downstream signaling have been tested as potential treatments for premature coronal suture fusion in a mouse model of Apert syndrome. However, there are no published studies that have targeted for the pharmacologic treatment of midface hypoplasia. We used Fgfr2S252W/+ knock-in mice as a model of Apert syndrome and morphometric analyses to identify causal hypoplastic sites in the midface region. Three-dimensional geometric and linear analyses of Fgfr2S252W/+ mice at postnatal day 0 demonstrated distinct morphologic variance. The premature fusion of anterior facial bones, such as the maxilla, nasal, and frontal bones, rather than the cranium or cranial base, is the main contributing factor toward the anterior-posterior skull length shortening. The cranial base of the mouse model had a noticeable downward slant around the intersphenoid synchondrosis, which is related to distortion of the airway. Within a skull, the facial shape variance was highly correlated with the cranial base angle change along Fgfr2 S252W mutation–induced craniofacial anomalies. The inhibition of an FGFR2 downstream signaling enzyme, PIN1, via genetic knockdown or use of a PIN1 inhibitor, juglone, attenuated the aforementioned deformities in a mouse model of Apert syndrome. Overall, these results indicate that FGFR2 signaling is a key contributor toward abnormal anterior-posterior dimensional growth in the midface region. Our study suggests a novel therapeutic option for the prevention of craniofacial malformations induced by mutations in the FGFR2 gene.
Nail melanoma (NM) is an important differential diagnosis in patients with longitudinal melanonychia. However, diagnosis is often challenging as it is difficult to differentiate from other pigmented nail disorders. The main challenge for diagnosis is obtaining adequate nail matrix biopsy specimens for histopathological assessment. Furthermore, the histopathological changes in the early stages of NM are subtle and contribute to a delay in diagnosis and care. Therefore, the integration of clinical and histopathological analyses is essential. Clinical and dermoscopic features, such as a broadened width of asymmetric bands in an irregular pattern, with multicolour pigmentation, periungual pigmentation, and continuous growth, are features that support the diagnosis of NM. The essential histological features that must be assessed are cellular morphology, architectural features, melanocyte density, and inflammatory changes. The reported mutations in NMs were BRAF (0–43%), NRAS (0–31%), KIT (0–50%), NF1 (0–50%), and GNAQ (0–25%). Surgery is the primary treatment for NM. The recommended treatment for in situ or minimally invasive NM is functional surgery, but cases with suspected bone invasion should be treated with amputation. Targeted therapy and immunotherapy are indicated for advanced stages of NM. This review summarizes the updated guidelines for the diagnosis and treatment of NM.
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