Mistaken Endobronchial Placement of a Nasogastric Tube During Mandibular Fracture Surgery

A 64-year-old male had an awake right nasal fiber-optic intubation with an endotracheal tube for open reduction and internal fixation of bilateral displaced mandibular fractures. After induction of anesthesia, an 18 Fr nasogastric tube (NGT) was inserted through the left nostril and was secured. The patient required high flow rates to deliver adequate tidal volumes with the ventilator. A chest x-ray done in the postanesthesia care unit revealed a malpositioned NGT in the left lower lobe bronchus, which was immediately removed. The patient was extubated on postoperative day 2. Various traditional methods, such as aspiration of gastric contents, auscultation of gastric insufflations, and chest x-ray are in use to detect or prevent the misplacement of an NGT. These methods can be unreliable or impractical. Use of capnography to detect an improperly placed NGT should be considered in the operating room as a simple, cost-effective method with high sensitivity to prevent possibly serious sequelae of an NGT placed within the bronchial tree.Key words: Nasogastric tube, Misplacement, Oral surgeryPlacement of a nasogastric tube (NGT) preoperatively for decompression of the stomach is common practice to allow drainage of gastrointestinal contents in the case of bowel obstruction, or in other cases when the patient is at risk of aspiration for some other reason. This case report involves a patient who required aspiration precautions via NGT placement for mandibular surgery due to facial trauma; the NGT was later found to be misplaced in the left main stem bronchus as the misplacement was unrecognized intraoperatively. We discuss the necessity of preventing the possible intraoperative and postoperative complications of a misplaced NGT and simple measures to recognize misplacement in patients presenting for similar surgeries.     

Desmoplastic and non-desmoplastic ameloblastoma: a comparative clinicopathological analysis

OBJECTIVES: The aim of this study was to review a large series of ameloblastomas, accessioned during a period of 35 years in a single Oral Pathology Diagnostic Center, for the incidence of desmoplastic ameloblastoma (DA) and in order to analyze the clinical features of this unusual variant.
MATERIALS AND METHODS: All cases diagnosed as ameloblastoma were reviewed and 14 were rediagnosed as DA. These cases were analyzed in terms of gender, patient age, location, clinical diagnosis, radiographic features and recurrence following treatment. Data from DA and non-desmoplastic ameloblastoma (NDA) were compared.
RESULTS: The incidence of DA in this series was 8.8%. The mean age of NDA and DA were 39.1 and 38.8 years respectively, and a higher female prevalence was observed in the latter. The mandible was the most affected bone in both groups of tumors, but with a different regional distribution. Most NDA arose in the angle and ramus of the mandible, but the premolar/molar region was the preferential location for DA. The most common radiographic feature in DA was the osteolytic type, either monolocular or multilocular. Most of these cases were clinically diagnosed as ameloblastoma. According to follow-up data available, 21.4% of DA and 10.1% of NDA recurred.
CONCLUSIONS: The results of this study do not support the hypothesis that DA should be a separate clinicopathological entity. It seems most likely that DA is another his-tologic variant of ameloblastoma.     

Cortical Bone Porosity in Rabbit Models of Osteoporosis

Cortical bone porosity is intimately linked with remodeling, is of growing clinical interest, and is increasingly accessible by imaging. Thus, the potential of animal models of osteoporosis (OP) to provide a platform for studying how porosity develops and responds to interventions is tremendous. To date, rabbit models of OP have largely focused on trabecular microarchitecture or bone density; some such as ovariectomy (OVX) have uncertain efficacy and cortical porosity has not been extensively reported. Our primary objective was to characterize tibial cortical porosity in rabbit-based models of OP, including OVX, glucocorticoids (GC), and OVX + GC relative to controls (SHAM). We sought to: (i) test the hypothesis that intracortical remodeling is elevated in these models; (ii) contrast cortical remodeling and porosity in these models with that induced by parathyroid hormone (1–34; PTH); and (iii) contrast trabecular morphology in the proximal tibia across all groups. Evidence that an increase in cortical porosity occurred in all groups was observed, although this was the least robust for GC. Histomorphometric measures supported the hypothesis that remodeling rate was elevated in all groups and also revealed evidence of uncoupling of bone resorption and formation in the GC and OVX + GC groups. For trabecular bone, a pattern of loss was observed for OVX, GC, and OVX + GC groups, whereas the opposite was observed for PTH. Change in trabecular number best explained these patterns. Taken together, the findings indicated rabbit models provide a viable and varied platform for the study of OP and associated changes in cortical remodeling and porosity. Intriguingly, the evidence revealed differing effects on the cortical and trabecular envelopes for the PTH model. © 2020 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR)..     

Anti‐inflammatory effects of haptoglobin on LPS‐stimulated macrophages: Role of HMGB1 signaling and implications in chronic wound healing

Nonhealing wounds possess elevated numbers of pro‐inflammatory M1 macrophages, which fail to transition to anti‐inflammatory M2 phenotypes that promote healing. Hemoglobin (Hb) and haptoglobin (Hp) proteins, when complexed (Hb‐Hp), can elicit M2‐like macrophages through the heme oxygenase‐1 (HO‐1) pathway. Despite the fact that nonhealing wounds are chronically inflamed, previous studies have focused on non‐inflammatory systems, and do not thoroughly compare the effects of complexed vs individual proteins. We aimed to investigate the effect of Hb/Hp treatments on macrophage phenotype in an inflammatory, lipopolysaccharide (LPS)‐stimulated environment, similar to chronic wounds. Human M1 macrophages were cultured in vitro and stimulated with LPS. Concurrently, Hp, Hb, or Hb‐Hp complexes were delivered. The next day, 27 proteins related to inflammation were measured in the supernatants. Hp treatment decreased a majority of inflammatory factors, Hb increased many, and Hb‐Hp had intermediate trends, indicating that Hp attenuated overall inflammation to the greatest extent. From this data, Ingenuity Pathway Analysis software identified high motility group box 1 (HMGB1) as a key canonical pathway—strongly down‐regulated from Hp, strongly up‐regulated from Hb, and slightly activated from Hb‐Hp. HMGB1 measurements in macrophage supernatants confirmed this trend. In vivo results in diabetic mice with biopsy punch wounds demonstrated accelerated wound closure with Hp treatment, and delayed wound closure with Hb treatment. This work specifically studied Hb/Hp effects on macrophages in a highly inflammatory environment relevant to chronic wound healing. Results show that Hp—and not Hb‐Hp, which is known to be superior in noninflammatory conditions—reduces inflammation in LPS‐stimulated macrophages, and HMGB1 signaling is also implicated. Overall, Hp treatment on M1 macrophages in vitro reduced the inflammatory secretion profile, and also exhibited benefits in in silico and in vivo wound‐healing models.     

Treatment of normal individuals with granulocyte-colony-stimulating factor: donor experiences and the effects on peripheral blood CD34+ cell counts and on the collection of peripheral blood stem cells

BACKGROUND: Granulocyte-colony-stimulating factor (G-CSF) has been used in patients to increase the level of circulating hematopoietic progenitors. Although G-CSF has been administered to some healthy individuals, the kinetics of mobilization of peripheral blood stem cells (PBSCs), the optimum dose schedule and the incidence and nature of adverse reactions in normal individuals are not completely defined. STUDY DESIGN AND METHODS: Normal individuals (n = 102) who received G- CSF for 5 or 10 days at doses of 2, 5, 7.5, or 10 micrograms per kg per day were studied. The subjects were observed for symptoms and physical changes, and blood samples were obtained for a variety of laboratory tests. After 5 or 10 days of G-CSF treatment, PBSCs were collected by apheresis and analyzed. RESULTS: Overall, 89 percent of the individuals completed the 5-day treatment protocol and 88 percent completed the 10- day protocol without modification of the dose of G-CSF administered. Ninety percent of donors experienced some side effect of G-CSF. The most frequent effects noted were bone pain (83%), headache (39%), body aches (23%), fatigue (14%), and nausea and/or vomiting (12%). The dose of G-CSF administered directly affected the proportion of people with bone pain (p = 0.025) or body aches (p = 0.045) or who were feeling hot or having night sweats (p = 0.02) or taking analgesics (p = 0.01). With the 5-day dose schedule, several changes in serum chemistries occurred, including increases in alkaline phosphatase (p = 0.001), alanine aminotransferase (p = 0.0013), lactate dehydrogenase (p = 0.0001), and sodium (p = 0.0001). Decreases occurred in glucose (p = 0.045), potassium (p = 0.0004), bilirubin (p = 0.001), and blood urea nitrogen (p = 0.0017). In donors who received G-CSF for 5 days, the absolute neutrophil count was increased after one G-CSF dose, and it reached a maximum on Day 6, as did the number of CD34+ cells (64.6 +/? 55.9 × 10(6) cells/L). In those same donors, the platelet count after apheresis on Day 6 was 32 +/? 13 percent lower than pretreatment values (250 +/? 42 × 10(9) cells/L). In donors receiving G-CSF for 10 days, the neutrophil count reached a maximum on Day 8, but the number of CD34+ cells peaked on Day 6 (58.3 +/? 52.1 × 10(5) cells/L) and then declined. The platelet count decreased from pretreatment values by 28 +/? 12 percent prior to apheresis on Day 11. When individuals were treated for 5 days with G-CSF, the quantity of CD34+ cells collected was directly related to the G-CSF dose. When 5 micrograms per kg per day was given, 2.80 +/? 1.81 × 10(8) cells were collected, compared with collection of 4.67 +/? 3.11 × 10(8) cells when 10 micrograms per kg per day was given (p = 0.04). More important, PBSCs collected after 10 days of G-CSF administration (5 micrograms/kg/day) had significantly fewer CD34+ cells (0.82 +/? 0.37 × 10(8) cells, p = 0.01) than did PBSCs collected after 5 days of G-CSF (5 micrograms/kg/day). CONCLUSION: Most normal donors receiving G-CSF experience side effects, but these are mild to moderate in degree. Some alterations in blood chemistries occur, but none were clinically serious. Because of the symptoms associated with G-CSF, these individuals must be monitored closely. The treatment of normal donors with G-CSF for more than 5 days significantly decreased the number of circulating CD34+ cells and the quantity collected by apheresis.     

O等位基因引起ABO基因型与表现型定型差异

保证输血时血清学方面的安全,首要的是对受血者与献血者ABO血型定型,血清学检查通常分两个步骤.正定型通常使用鼠源单克隆抗体检测红细胞表面是否存在A或B抗原.互补的实验即反定型,利用当红细胞上缺乏A或B抗原时,人群可天然产生相对应的抗体的原理,检测血清中是否存在抗-A或者抗-B抗体.确定了受血者红细胞表面的ABO抗原以及血浆中的抗体,便能确定血型,为其提供相合的血液.     

汉语阅读障碍儿童在本顿视觉保持测验中的反应特征

目的:比较阅读障碍儿童与正常儿童在本顿视觉保持测验中的反应特征,探索阅读障碍儿童视觉空间记忆能力的特点。方法:①2005-07/2006-05在儿童发育行为门诊遴选阅读障碍儿童20名(平均年龄10.2岁),按1∶1配对原则,选择年龄、性别、年级和家庭状况等条件与阅读障碍组相似的20名正常阅读能力儿童为对照组(平均年龄10.1岁)。②应用国内修订版本顿视觉保持测验C式B法,D式C法和E式D法对两组儿童进行个别测试。C式图卡呈现5s后让被试默画(视觉记忆能力),D式图卡让被试临摹(视觉结构能力),E式图卡呈现10s后间隔15s再让被试默画(视觉延迟记忆能力)。③对两组儿童的视觉记忆保持能力、视觉结构能力和延迟记忆能力进行测试,分别记录两组儿童测验的正确分(每一图卡根据全或无的原则记1或0分,总分0～10)及错误次数(错误类型分为遗漏或增加、变形、持续、旋转、位置错误和大小错误6个范畴),进行配对t检验。结果:40名受试者均进入结果分析。①正确得分:在视觉记忆和视觉结构能力测验中阅读障碍组低于对照组(5.00±2.45,6.60±1.82,P=0.019;7.50±2.44,8.95±1.32,P=0.015),在视觉延迟记忆测试中,两组得分比较差异不显著(P=0.077)。②总错误分:在视觉记忆和视觉结构能力测验中阅读障碍组高于对照组(7.65±4.20,4.90±3.24,P=0.016;3.20±3.93,1.15±1.46,P=0.035),在视觉延迟记忆测试中,两组得分比较差异不显著(P=0.389)。③错误类型:阅读障碍组儿童在视觉记忆能力测试中变形和持续性错误次数均显著多于对照组(3.95±2.40,1.75±1.52;0.35±0.67,0;P均<0.05),在视觉结构能力测试中变形错误次数显著多于对照组(1.35±1.69,0.35±0.75,P<0.05)。结论:阅读障碍儿童的视觉空间短时记忆能力、视觉结构和视觉运动整合能力存在缺陷。     

Loss of high-affinity thrombin receptors during platelet concentrate storage impairs the reactivity of platelets to thrombin

BACKGROUND: The storage of platelet concentrates (PCs) induces a reduction in the platelet surface expression of glycoprotein (GP) Ib alpha. The location of the platelets' high-affinity binding site for thrombin has been postulated as being located on GPIb alpha. This study attempts to determine whether loss or alteration of GPIb alpha during storage of PCs is related to impairment in the reactivity of platelets to thrombin. STUDY DESIGN AND METHODS: In this study, platelet surface expression of GPIb alpha was monitored by means of flow cytometry, throughout standard storage of PCs for up to 10 days. Two thrombin- induced platelet responses, the binding of radiolabeled fibrinogen and the platelet surface expression of P-selectin, were evaluated. Thrombin- binding assays were also performed to assess the number of thrombin receptors in platelets. RESULTS: The surface expression of the GPIb/IX complex declines during storage of PCs. The thrombin-induced maximal binding of fibrinogen in platelets stored for 3, 7, and 10 days was 77 +/? 7 percent, 60 +/? 20 percent, and 34 +/? 25 percent, respectively, of that found in fresh platelets. Moreover, the concentration of thrombin needed for 50 percent of platelets to express the CD62 antigen P-selectin at the surface increased from 0.05 U per mL in fresh platelets to 0.11, 0.56, and 1.2 U per mL in platelets stored for 3, 7, and 10 days, respectively. Thrombin-binding experiments demonstrated a significant reduction in the number of high-affinity binding sites throughout storage of PCs (55 +/? 21 sites/platelet in 10-day-stored platelets vs. 73 +/? 25 in fresh platelets). A significant correlation was also observed between the number of high-affinity thrombin-binding sites and surface expression of GPIb alpha. Selective blockage of the thrombin-binding site on GPIb alpha with monoclonal antibody LJ-Ib10 also inhibited the response of fresh platelets to thrombin, up to a level equivalent to that found in 3-day-stored platelets. CONCLUSION: The loss of the GPIb alpha-located high-affinity thrombin-binding site may impair the ability of platelets to become activated by thrombin as storage time increases.     

O等位基因引起ABO基因型与表现型定型差异

保证输血时血清学方面的安全,首要的是对受血者与献血者ABO血型定型,血清学检查通常分两个步骤.正定型通常使用鼠源单克隆抗体检测红细胞表面是否存在A或B抗原.互补的实验即反定型,利用当红细胞上缺乏A或B抗原时,人群可天然产生相对应的抗体的原理,检测血清中是否存在抗-A或者抗-B抗体.确定了受血者红细胞表面的ABO抗原以及血浆中的抗体,便能确定血型,为其提供相合的血液.