Small bowel obstruction (SBO) is an emergency that should be managed early to reduce the risk of bowel perforation, strangulation and subsequent life-threatening organ dysfunction caused by sepsis. A prompt diagnostic workup including imaging and lab studies is required to assess the severity of the obstruction and to establish if emergency surgery is required. We report the case of a 55-year-old male with a history of recurrent SBO, previous ventral hernia repair and indications of previous colonic tubular adenoma per colonoscopy findings. The patient underwent an exploratory laparotomy procedure and adhesiolysis to release the SBO. This case report emphasizes the safety and efficacy of Seprafilm placement intraoperatively in decreasing the occurrence of postoperative adhesions in abdominal laparotomy procedures.
Emphysematous cholecystitis (EC) is an acute infection caused by gas-forming organisms and is considered a surgical emergency. The presenting symptoms of EC are often difficult to distinguish from those of uncomplicated acute cholecystitis, necessitating the use of CT for diagnosis. EC is associated with higher rates of gangrene and perforation of the gallbladder compared to typical acute cholecystitis. It is also associated with significantly higher rates of mortality. In this report, we discuss the case of a 57-year-old African American female who presented to the emergency room with nausea, non-bloody vomiting, and abdominal pain for three days. Physical examination showed a soft but tender abdomen, especially in the right upper quadrant, and labs showed leukocytosis of 15.5/mm3. A CT of the abdomen and pelvis was ordered, which demonstrated air in the gallbladder lumen with extraluminal air adjacent indicating ruptured EC.
General surgeons frequently handle patients who present with an unknown neck mass. Due to the nature of diseases, medial neck soft tissue masses often manifest with variable etiologies and clinical signs and symptoms. Establishing a thorough evaluation of neck masses based on differential diagnoses is essential. The clinical evaluation of neck masses usually includes a thorough history and physical examination, advanced imaging techniques such as magnetic resonance imaging (MRI), ultrasonography, contrast-enhanced computed tomography (CT), and fine-needle aspiration biopsy. From a surgeon's standpoint, proper knowledge of tissue structure, anatomy, and pathology, and applying fundamental surgical principles ensure a successful management of such lesions. This case report intends to reveal the pathological and clinical nature of an unknown neck mass in a 60-year-old female, which was postoperatively diagnosed as an epidermal inclusion cyst (EIC). This report also intends to indicate the significance of surgical intervention to prevent EIC complications and improve patient's life quality.
Ehlers-Danlos syndrome (EDS) is a group of hereditary disorders characterized by fragility of connective tissue. Clinical manifestations of the disorder involve the skin, joints, blood vessels, and other internal organs. We report the case of a 29-year-old female suffering from EDS and mast cell activation syndrome (MCAS). Her history includes multiple orthopedic surgeries leading to the worsening of her symptoms. This was determined to be due to medical implants placed during her multiple procedures predisposing her to severe immunological reactions. This case report emphasizes the importance of meticulous surgical intervention when managing patients with EDS.
CAP1 ( C yclase A ssociated P rotein 1) is a conserved actin‐regulating protein that enhances actin filament dynamics and also regulates adhesion in mammalian cells. We previously found that phosphorylation at the Ser307/Ser309 tandem site controls its association with cofilin and actin, and is important for CAP1 to regulate the actin cytoskeleton. Here, we report that transient Ser307/Ser309 phosphorylation is required for both CAP1 functions in actin filament disassembly and cell adhesions. Both the phospho‐mimetic and non‐phosphorylatable CAP1 mutants, which resist transition between phosphorylated and dephosphorylated forms, had defects in rescuing the reduced rate of actin filament disassemblyin the CAP1‐knockdown HeLa cells. The phosphor mutants also had defects in alleviating the elevated FAK ( F ocal A dhesion K inase) activity and the enhanced focal adhesions in the knockdown cells. In dissecting further phosphor‐regulatory cell signals for CAP1, we found that CDK5 ( C yclin‐ D ependent K inase 5) phosphorylates both Ser307 and Ser309 residues, whereas cAMP signaling induces dephosphorylation at the tandem site, through its effectors PKA ( P rotein K inase A ) and Epac ( E xchange p roteins directly a ctivated by c AMP). No evidence supports involvement of activated protein phosphatase in executing the dephosphorylation downstream of cAMP, whereas preventing CAP1 access to its kinase CDK5 appears to underlie CAP1 dephosphorylation induced by cAMP. Therefore, this study provides direct cellular evidence that transient phosphorylation is required for both CAP1 functions in actin filament turnover and adhesion, and the novel mechanistic insights substantially extend our knowledge on the cell signals that function in concert to regulate CAP1 by facilitating its transient phosphorylation. Support or Funding Information This project was supported by an Institutional Development Award(IDeA) from the National Institute of General Medical Sciencesat the National Institutes of Health [Grant number: P20GM103429].
Cyclase-associated protein 1 (CAP1) is a conserved actin-regulating protein that enhances actin filament dynamics and also regulates adhesion in mammalian cells. We previously found that phosphorylation at the Ser307/Ser309 tandem site controls its association with cofilin and actin and is important for CAP1 to regulate the actin cytoskeleton. Here, we report that transient Ser307/Ser309 phosphorylation is required for CAP1 function in both actin filament disassembly and cell adhesion. Both the phosphomimetic and the nonphosphorylatable CAP1 mutant, which resist transition between phosphorylated and dephosphorylated forms, had defects in rescuing the reduced rate of actin filament disassembly in the CAP1 knockdown HeLa cells. The phosphorylation mutants also had defects in alleviating the elevated focal adhesion kinase (FAK) activity and the enhanced focal adhesions in the knockdown cells. In dissecting further phosphoregulatory cell signals for CAP1, we found that cyclin-dependent kinase 5 (CDK5) phosphorylates both Ser307 and Ser309 residues, whereas cAMP signaling induces dephosphorylation at the tandem site, through its effectors protein kinase A (PKA) and exchange proteins directly activated by cAMP (Epac). No evidence supports an involvement of activated protein phosphatase in executing the dephosphorylation downstream from cAMP, whereas preventing CAP1 from accessing its kinase CDK5 appears to underlie CAP1 dephosphorylation induced by cAMP. Therefore, this study provides direct cellular evidence that transient phosphorylation is required for CAP1 functions in both actin filament turnover and adhesion, and the novel mechanistic insights substantially extend our knowledge of the cell signals that function in concert to regulate CAP1 by facilitating its transient phosphorylation.
Mesenteric cysts are rare, usually benign, tumors that typically present asymptomatically and are found incidentally during evaluation for nonspecific abdominal symptoms. We present the case of a 41-year-old African American female who was found to have a mesenteric cyst in her jejunum during the evaluation of abdominal pain, nausea, and constipation that she had been experiencing for six weeks. Pre-operatively, an abdominal CT scan showed a 6x4x6 cm mesenteric cystic lesion in the right mid-abdomen, which was then successfully resected off the mesentery of the jejunum laparoscopically. Her postoperative course was uneventful and she was discharged home without complication a few hours after her procedure with appropriate follow-up.
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