原位肝移植术后急性肺损伤的相关因素的临床分析

目的:探讨肝移植后急性肺损伤(ALI)的相关因素,为肝移植术后ALI的预防和治疗提供参考。方法:回顾性分析了2005年1月~2010年10月在我院行肝移植术的98例患者的临床资料,对术后并发ALI的相关因素进行分析。结果:98例行肝移植术后发生ALI12例,发生率为12.24%。单因素分析显示年龄、术前血清TBIL、术中失血量、术中尿量和术后血BUN对ALI的发生有显著影响(P<0.05)。多因素Logistic回归法分析表明,术中失血量、术前TBIL、年龄为术后并发ALI的危险因素。结论:术中失血量、术前TBIL、年龄为术后并发ALI的危险因素,对上述因素加以重点评估和合理控制,可以控制肝移植术后ALI的发生。     

原位肝移植术后急性肺损伤的相关因素的临床分析

目的：探讨肝移植后急性肺损伤（ALI）的相关因素,为肝移植术后ALI的预防和治疗提供参考。方法：回顾性分析了2005年1月-2010年10月在我院行肝移植术的98例患者的临床资料,对术后并发ALI的相关因素进行分析。结果：98例行肝移植术后发生ALI12例,发生率为12．24％。单因素分析显示年龄、术前血清TBIL、术中失血量、术中尿量和术后血BUN对ALI的发生有显著影响（P〈0．05）。多因素Logistic回归法分析表明,术中失血量、术前TBIL、年龄为术后并发ALI的危险因素。结论：术中失血量、术前TBIL、年龄为术后并发ALI的危险因素,对上述因素加以重点评估和合理控制,可以控制肝移植术后ALI的发生。     

Gene flow, historical population dynamics and genetic diversity within French Guianan populations of a rainforest tree species, Vouacapoua americana

Both gene flow and historical events influence the genetic diversity of natural populations. One way to understand their respective impact is to analyze population genetic structure at large spatial scales. We studied the distribution of genetic diversity of 17 populations of Vouacapoua americana (Caesalpiniaceae) in French Guiana, using nine microsatellite loci. Low genetic diversity was observed within populations, with a mean allelic richness and gene diversity of 4.1 and 0.506, respectively, which could be due to low effective population size and/or past bottlenecks. Using the regression between Fst/(1-Fst), estimated between pairs of populations, and the logarithm of the geographical distance, the spatial genetic structure can partly be explained by isolation-by-distance and limited gene flow among populations. This result is in agreement with the species' biology, including seed and pollen dispersal by rodents and insects, respectively. In contrast, no clear genetic signal of historical events was found when examining genetic differentiation among populations in relation to biogeographical hypotheses or by testing for bottlenecks within populations. Our conclusion is that nuclear spatial genetic structure of V. americana, at the geographic scale of French Guiana, is better explained by gene flow rather than by historical events.     

Lung Transplantation in a Patient with Fibrosing Alveolitis

The transplantation of the right lung into a man aged 40 who was suffering from cryptogenic fibrosing alveolitis is described. Before transplantation he had been dependent on oxygen, even at rest, for 24 hours a day for almost two years. The donor was a boy of 16 years who had had a fatal cerebral haemorrhage. The transplanted lung functioned perfectly from the time of operation until the patient''s sudden death two months later from an overwhelming haemoptysis apparently from a small peribronchial abscess rupturing into the pulmonary artery. By the third postoperative week the patient had been able to walk unaided and without distress outdoors. The problem of differentiating infection from incipient rejection is discussed. We conclude that clinically successful lung transplantation can be achieved, but only if the problems of lung function, infection, and immunosuppression can all be overcome.     

肝移植术后急性肾功能衰竭的相关因素的临床分析

目的:探讨肝移植术后并发急性肾功能衰竭(ARF)的相关因素,为肝移植术后ARF的预防和治疗提供参考。方法:回顾性分析了2005年1月~2010年10月在我院行肝移植术的98例患者的临床资料,对术后并发ARF的相关因素进行分析。结果:98例行肝移植术后发生ARF 13例,发生率为13.27%。单因素分析显示术前血尿素氮(BUN)、术前血清肌酐(Scr)、术前血清白蛋白(Alb)、手术时间、失血量与ARF的发生有关(P<0.05)。多因素Logistic回归法分析表明,术前Scr和BUN是肝移植术后并发ARF的危险因素。结论:术前血BUN、血清Scr、血清Alb、手术时间和失血量是肝移植术后并发ARF主要因素,而术前Scr和BUN水平升高是肝移植术后并发ARF的危险因素。对上述因素加以重点评估和合理控制,可以控制肝移植术后ARF的发生。     

肝移植术后急性肾功能衰竭的相关因素的临床分析

目的：探讨肝移植术后并发急性肾功能衰竭（ARF）的相关因素,为肝移植术后ARF的预防和治疗提供参考。方法：回顾性分析了2005年1月-2010年10月在我院行肝移植术的98例患者的临床资料,对术后并发ARF的相关因素进行分析。结果：98例行肝移植术后发生ARF13例,发生率为13．27％。单因素分析显示术前血尿素氮CBUN）、术前血清肌酐（Scr）、术前血清白蛋白（Alb）、手术时间、失血量与ARF的发生有关（P〈0．05）。多因素Logistic回归法分析表明,术前Ser和BUN是肝移植术后并发ARF的危险因素。结论：术前血BUN、血清Scr、血清Alb、手术时间和失血量是肝移植术后并发ARF主要因素,而术前Scr和BUN水平升高是肝移植术后并发ARF的危险因素。对上述因素加以重点评估和合理控制,可以控制肝移植术后ARF的发生。     

The Novel Cytokine Interleukin-33 Activates Acinar Cell Proinflammatory Pathways and Induces Acute Pancreatic Inflammation in Mice

Background

Acute pancreatitis is potentially fatal but treatment options are limited as disease pathogenesis is poorly understood. IL-33, a novel IL-1 cytokine family member, plays a role in various inflammatory conditions but its role in acute pancreatitis is not well understood. Specifically, whether pancreatic acinar cells produce IL-33 when stressed or respond to IL-33 stimulation, and whether IL-33 exacerbates acute pancreatic inflammation is unknown.

Methods/Results

In duct ligation-induced acute pancreatitis in mice and rats, we found that (a) IL-33 concentration was increased in the pancreas; (b) mast cells, which secrete and also respond to IL-33, showed degranulation in the pancreas and lung; (c) plasma histamine and pancreatic substance P concentrations were increased; and (d) pancreatic and pulmonary proinflammatory cytokine concentrations were increased. In isolated mouse pancreatic acinar cells, TNF-α stimulation increased IL-33 release while IL-33 stimulation increased proinflammatory cytokine release, both involving the ERK MAP kinase pathway; the flavonoid luteolin inhibited IL-33-stimulated IL-6 and CCL2/MCP-1 release. In mice without duct ligation, exogenous IL-33 administration induced pancreatic inflammation without mast cell degranulation or jejunal inflammation; pancreatic changes included multifocal edema and perivascular infiltration by neutrophils and some macrophages. ERK MAP kinase (but not p38 or JNK) and NF-kB subunit p65 were activated in the pancreas of mice receiving exogenous IL-33, and acinar cells isolated from the pancreas of these mice showed increased spontaneous cytokine release (IL-6, CXCL2/MIP-2α). Also, IL-33 activated ERK in human pancreatic tissue.

Significance

As exogenous IL-33 does not induce jejunal inflammation in the same mice in which it induces pancreatic inflammation, we have discovered a potential role for an IL-33/acinar cell axis in the recruitment of neutrophils and macrophages and the exacerbation of acute pancreatic inflammation.

Conclusion

IL-33 is induced in acute pancreatitis, activates acinar cell proinflammatory pathways and exacerbates acute pancreatic inflammation.     

Studies in a Patient with Acute Leukaemia after Lysergide Treatment

The second case of acute leukaemia developing after administration of lysergide is reported. The unusual bone-marrow chromosome pattern and the presence of large cells containing multiple micronucleoli suggest that this association may be causal.     

Taenia saginata Infection Misdiagnosed as Acute Cholecystitis in a Tibetan Patient,in China

The present study reports a rare case of Taenia saginata infection, which was initially diagnosed as acute cholecystitis in a Tibetan patient at the Qinghai-Tibetan Plateau pastoral area, China. A 45-year-old female was initially diagnosed with acute cholecystitis at a hospital in China. She had a slight fever, weight loss and constipation and complained of pain in the upper abdomen and left back areas. Increase of monocyte, eosinophil and basophil levels were shown. Taenia sp. eggs were detected in a fecal examination. An adult tapeworm approximately 146 cm in length, whitish-yellow color, was collected from the patient after treatment with traditional Chinese medicine. The adult tapeworm had a scolex and proglottids with genital pores. The scolex was rectangular shape with 4 suckers and rostellum without hooklet. The cox1 gene sequence shared 99.5–99.8% homology with that of T. saginata from other regions in China. The patient was diagnosed finally infected with T. saginata by morphological and molecular charateristics.     

Involvements of a novel protein, DIA2, in cAMP signaling and spore differentiation during Dictyostelium development

Abstract The novel gene dia2 (differentiation-associated gene 2) was originally isolated as a gene expressed specifically in response to initial differentiation of Dictyostelium discoideum Ax-2 cells. Using dia2^AS cells in which the dia2 expression was inactivated by the antisense RNA method, DIA2 protein was found to be required for cAMP signaling during cell aggregation. During late development, the DIA2 protein changed its location from the endoplasmic reticulum (ER) to prespore-specific vacuoles (PSVs) that are specifically present in prespore cells of the slug. In differentiating prestalk cells, however, DIA2 was found to be nearly lost from the cells. Importantly, exocytosis of PSVs from prespore cells and the subsequent spore differentiation were almost completely impaired in dia2^AS cells. In addition, spore induction by externally applied 8-bromo cAMP was significantly suppressed in dia2^AS cells. Taken together, these results strongly suggested that DIA2 might be closely involved in cAMP signaling and spore differentiation as well as in the initiation of differentiation during Dictyostelium development.     

A Novel Deletion Mutation in the Men1 Gene in a Patient with Prolactinoma and a Family History of Pancreatic Tumors

ObjectiveMultiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant tumor syndrome caused by mutations in the MEN1 gene. Mutations in this tumor suppressor gene are often associated with neuroendocrine tumors. Here we describe a novel deletion mutation at codon 304 in the MEN1 gene of a patient with a prolactinoma and strong family history of pancreatic tumors.MethodsWe describe the patient’s clinical course and mutational analysis and review the relevant literature. Results: A 30-year-old pregnant female was referred to our institution’s psychological department for treatment of depression. She had developed a prolactinoma at age 17 and was being treated with 1 mg/week of cabergoline. A medical interview revealed a family history of pancreatic islet cell and other tumors; her mother died of pancreatic cancer, her brother is living with gastrinoma, and her sister died of leiomyosarcoma. Extensive examinations performed after delivery, including laboratory tests and computed tomography (CT) scans, did not reveal any other tumors. Mutational analysis of the MEN1 gene identified a heterozygous deletion mutation (c911_914delAGGT) at codon 304. This mutation produces a frameshift at p.304Lys and might disturb the splicing of intron 6 due to the lack of a donor site. The predicted menin protein from the mutated allele is truncated at amino acid 328.ConclusionWe report a novel deletion mutation (c911_914delAGGT) in the MEN1 gene that was likely associated with the patient’s prolactinoma and her strong family history of pancreatic tumors. (Endocr Pract. 2014; 20:e162-e165)     

Circulating microRNAs and Outcome in Patients with Acute Heart Failure

Background

The biomarker value of circulating microRNAs (miRNAs) has been extensively addressed in patients with acute coronary syndrome. However, prognostic performances of miRNAs in patients with acute heart failure (AHF) has received less attention.

Methods

A test cohort of 294 patients with acute dyspnea (236 AHF and 58 non-AHF) and 44 patients with stable chronic heart failure (CHF), and an independent validation cohort of 711 AHF patients, were used. Admission levels of miR-1/-21/-23/-126/-423-5p were assessed in plasma samples.

Results

In the test cohort, admission levels of miR-1 were lower in AHF and stable CHF patients compared to non-AHF patients (p = 0.0016). Levels of miR-126 and miR-423-5p were lower in AHF and in non-AHF patients compared to stable CHF patients (both p<0.001). Interestingly, admission levels of miR-423-5p were lower in patients who were re-admitted to the hospital in the year following the index hospitalization compared to patients who were not (p = 0.0001). Adjusted odds ratio [95% confidence interval] for one-year readmission was 0.70 [0.53–0.93] for miR-423-5p (p = 0.01). In the validation cohort, admission levels of miR-423-5p predicted 1-year mortality with an adjusted odds ratio [95% confidence interval] of 0.54 [0.36–0.82], p = 0.004. Patients within the lowest quartile of miR-423-5p were at high risk of long-term mortality (p = 0.02).

Conclusions

In AHF patients, low circulating levels of miR-423-5p at presentation are associated with a poor long-term outcome. This study supports the value of miR-423-5p as a prognostic biomarker of AHF.     

Acute Myocardial Infarction Attributable to Adrenergic Crises in a Patient with Pheochromocytoma and Neurofibromatosis 1

ObjectiveTo describe a rare case of acute myocardial infarction in a patient with neurofibromatosis 1 and pheochromocytoma and to review the literature on the coexistence of these 2 diseases, the causes of myocardial injury in patients with pheochromocytoma, and the utility of genetic testing and pheochromocytoma screening for those patients and their families.MethodsWe present a case report, including the detailed clinical, laboratory, and radiographic data, results of adrenal mass pathology, and results of coronary angiography. We also survey other relevant reports available in the literature.ResultsA 43-year-old woman with a history of longstanding hypertension, neurofibromatosis 1, headaches, sweating, and palpitations presented to the hospital with chest pain and shortness of breath. She was found to have an acute myocardial infarction and pulmonary edema, as well as a right adrenal mass. A pheochromocytoma was suspected, and phenoxybenzamine was added to her treatment regimen. Cardiac catheterization showed nonobstructive coronary disease. The levels of plasma catecholamine metabolites were extremely high. The patient underwent uncomplicated laparoscopic right adrenalectomy 2 weeks after this admission. Surgical pathology confirmed the diagnosis of pheochromocytoma.ConclusionAdrenergic crisis attributable to pheochromocytoma can result in acute myocardial infarction even in the absence of obstructive coronary disease. Inclusion of pheochromocytoma in the differential diagnosis of hypertension in patients with neurofibromatosis is very important and helps avoid mistakes in the management of such patients. (Endocr Pract. 2007;13:269-273)     

Host Platelets and,in Part,Neutrophils Mediate Lung Accumulation of Transfused UVB-Irradiated Human Platelets in a Mouse Model of Acute Lung Injury

We previously reported that ultraviolet light B (UVB)-treated human platelets (hPLTs) can cause acute lung injury (ALI) in a two-event SCID mouse model in which the predisposing event was Lipopolysaccharide (LPS) injection and the second event was infusion of UVB-treated hPLTs. To delineate contributions of host mouse platelets (mPLTs) and neutrophils in the pathogenesis of ALI in this mouse model, we depleted mPLTs or neutrophils and measured hPLT accumulation in the lung. We also assessed lung injury by protein content in bronchoalveolar lavage fluid (BALF). LPS injection followed by infusion of UVB-treated hPLTs resulted in sequestration of both mPLTs and hPLTs in the lungs of SCID mice, although the numbers of neutrophils in the lung were not significantly different from the control group. Depletion of mouse neutrophils caused only a mild reduction in UVB-hPLTs accumulation in the lungs and a mild reduction in protein content in BALF. In comparison, depletion of mPLTs almost completely abolished hPLTs accumulation in the lung and significantly reduced protein content in BALF. UVB-treated hPLTs bound to host mPLTs, but did not bind to neutrophils in the lung. Aspirin treatment of hPLTs in vitro abolished hPLT accumulation in the lung and protected mice from lung injury. Our data indicate that host mPLTs accumulated in the lungs in response to an inflammatory challenge and subsequently mediated the attachment of transfused UVB-hPLTs. Neutrophils also recruited a small percentage of platelets to the lung. These findings may help develop therapeutic strategies for ALI which could potentially result from transfusion of UV illuminated platelets.     

Age-Related Changes in Aldehyde Dehydrogenase Activity of Rat Brain, Liver, and Heart

Abstract: Aldehyde dehydrogenase (ALDH) activity was measured in brains, livers, and hearts of 23–26-month-old and 3-month-old rats. A significant increase of ALDH activity was found in whole brain of old rats with both acetaldehyde (39%) and propionylaldehyde (15%) used as substrates. In different brain areas of old rats, with acetaldehyde used as substrate, a significant increase of ALDH activity was found in striatum (30–50%) and cerebral cortex (37%). However, no significant difference in ALDH activity was found in livers and hearts of young and old rats. Preliminary experiments showed a significant increase of aldehyde reductase activity (52%) with p -nitrobenzaldehyde used as substrate in whole brain of old rats compared with young rats. The present work indicates that an increase of ALDH activity in brain of old rats may be an adaptive phenomenon.     

急性心力衰竭患者就诊时血压心率及血浆BNP水平与心功能的关系分析

目的:探讨急性心力衰竭(AHF)患者就诊时血压心率及血浆脑钠肽(BNP)水平与心功能的关系。方法:选取2013年4月-2014年12月于本院治疗的AHF患者134例,于就诊时测量患者血压、心率、BNP及心脏超声相关指标,分析血压心率及血浆BNP水平与心功能的关系。结果:就诊时SBP水平与左心室舒张末期直径及每搏输出量呈现正相关性(r=0.134、0.238,均P0.05);心率与每搏输出量、左室缩短率以及射血分数呈现负相关性(r=-0.177,-0.231,-0.197,均P0.05);BNP水平与左心室舒张末直径成正相关性,与左室缩短率以及射血分数呈负相关性(r=0.150、-0.247、-0.271,均P0.05)。结论:血压、心率以及BNP是临床诊断、评估AHF的重要指标。     

Extensive Deep Dermatophytosis Cause by Trichophyton rubrum in a Patient with Liver Cirrhosis and Chronic Renal Failure

Dermatophytes are the main pathogen of superficial skin fungal infections. On rare occasions, they can cause deep and extensive infections, especially in immunocompromised hosts. We reported a 48-year-old patient with liver cirrhosis and chronic renal failure who developed an extensive deep dermatophytosis with possible hematogenous dissemination. Skin histopathology showed extensive involvement of hair follicles and dermis by fungal elements. The pathogen was cultured from both skin biopsy specimen and central venous line. It was identified as Trichophyton rubrum by morphology and further conformed by sequencing of internal transcribed spacers of ribosomal DNA. The patient died quickly before the identification was available.