Search

The aim of this paper was to study the occurrence of helminths in Mus musculus and Rattus rattus from urban, suburban and rural settlements in Yucatán, Mexico; and to analyse the host factors (e.g. sex) related to helminths’ distribution. Helminths in a total of 279 rodents were surveyed by visual examination of the liver for metacestodes and faecal examination for helminth eggs using the formalin-ethyl acetate sedimentation technique. The cestodes Hydatigera taeniaeformis (metacestodes detected in the liver) and Hymenolepis diminuta, and the nematodes Aspiculuris sp., Nippostrongylus brasiliensis, Syphacia muris, Syphacia obvelata, and Trichuris muris were identified. In M. musculus, the prevalence of infection with T. muris and H. taeniaeformis was higher in the rural village compared to those in the suburban neighbourhood. For R. rattus, a higher prevalence of infection with H. diminuta was found in the urban site compared to that in the suburban site. This study reports the occurrence of H. diminuta among rodents living in close proximity to humans, representing a potential public health risk. In addition, this survey increases our understanding of dynamic transmission among intestinal helminths recorded in Yucatán, Mexico.

Background: Thrombotic microangiopathy (TMA) is a complication of malignant hypertension (mHTN) attributed to high blood pressure (BP). However, no studies have investigated in patients with mHTN of different aetiologies whether the presence of TMA is associated with specific causes of mHTN., Methods: We investigated the presence of TMA (microangiopathic haemolytic anaemia and thrombocytopenia) in a large and well-characterized cohort of 199 patients with mHTN of different aetiologies [primary HTN 44%, glomerular diseases 16.6%, primary atypical haemolytic uraemic syndrome (aHUS) 13.1%, renovascular HTN 9.5%, drug-related HTN 7%, systemic diseases 5.5%, endocrine diseases 4.5%]. Outcomes of the study were kidney recovery and kidney failure., Results: Patients with TMA [40 cases (20.1%)] were younger, were more likely female and had lower BP levels and worse kidney function at presentation. Their underlying diseases were primary aHUS (60%), drug-related mHTN (15%), glomerular diseases [all of them immunoglobulin A nephropathy (IgAN); 10%], systemic diseases (10%) and primary HTN (5%). The presence of TMA was 92.3% in primary aHUS, 42.9% in drug-related HTN, 36.4% in systemic diseases, 12.1% in glomerular diseases and 2.3% in primary HTN. No patient with renovascular HTN or mHTN caused by endocrine diseases developed TMA, despite BP levels as high as patients with TMA. A higher proportion of TMA patients developed kidney failure as compared with patients without TMA (56.4% versus 38.9%, respectively)., Conclusions: The presence of TMA in patients with mHTN should guide the diagnosis towards primary aHUS, drug-related mHTN, some systemic diseases and IgAN, while it is exceptional in other causes of mHTN., (© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.)

The complement system is one of the first defense lines protecting from invading pathogens. However, it may turn offensive to the body's own cells and tissues when deregulated by the presence of rare genetic variants that impair physiological regulation and/or provoke abnormal activity of key enzymatic components. Factor B and complement C2 are examples of paralogs engaged in the alternative and classical/lectin complement pathway, respectively. Pathogenic mutations in the von Willebrand factor A domain (vWA) of FB have been known for years. Despite substantial homology between two proteins and the demonstration that certain substitutions in FB translated to C2 result in analogous phenotype, there was a limited number of reports on pathogenic C2 variants in patients. Recently, we studied a cohort of patients suffering from rare kidney diseases and confirmed the existence of two gain-of-function and three loss-of-function mutations within the C2 gene sequences coding for the vWA domain (amino acids 254-452) or nearly located unstructured region (243-253) of C2 protein. Herein, we report the functional consequences of amino acid substitution of glutamine at position 263. The p.Q263G variant resulted in the gain-of-function phenotype, similarly to a homologous mutation p.D279G in FB. Conversely, the p.Q263P variant found in a patient with C3 glomerulopathy resulted in the loss of C2 function. Our results confirm that the N-terminal part of the vWA domain is a hot spot crucial for the complement C2 function., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Kuźniewska, Thiel, Kowalska, Felberg-Miętka, Szynkowski, Ołdziej, Arjona, Jongerius, Rodriguez de Córdoba, Okrój and Urban.)

Atypical hemolytic uremic syndrome (aHUS) is a life-threatening thrombotic microangiopathy that can progress, when untreated, to end-stage renal disease. Most frequently, aHUS is caused by complement dysregulation due to pathogenic variants in genes that encode complement components and regulators. Among these genes, the factor H (FH) gene, CFH, presents with the highest frequency (15% to 20%) of variants and is associated with the poorest prognosis. Correct classification of CFH variants as pathogenic or benign is essential to clinical care but remains challenging owing to the dearth of functional studies. As a result, significant numbers of variants are reported as variants of uncertain significance. To address this knowledge gap, we expressed and functionally characterized 105 aHUS-associated FH variants. All FH variants were categorized as pathogenic or benign and, for each, we fully documented the nature of the pathogenicity. Twenty-six previously characterized FH variants were used as controls to validate and confirm the robustness of the functional assays used. Of the remaining 79 uncharacterized variants, only 29 (36.7%) alter FH expression or function in vitro and, therefore, are proposed to be pathogenic. We show that rarity in control databases is not informative for variant classification, and we identify important limitations in applying prediction algorithms to FH variants. Based on structural and functional data, we suggest ways to circumvent these difficulties and, thereby, improve variant classification. Our work highlights the need for functional assays to interpret FH variants accurately if clinical care of patients with aHUS is to be individualized and optimized., (© 2021 by The American Society of Hematology.)

The impairment of the alternative complement pathway contributes to rare kidney diseases such as atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy (C3G). We recently described an aHUS patient carrying an exceptional gain-of-function (GoF) mutation (S250C) in the classical complement pathway component C2 leading to the formation of hyperactive classical convertases. We now report the identification of the same mutation and another C2 GoF mutation R249C in two other patients with a glomerulopathy of uncertain etiology. Both mutations stabilize the classical C3 convertases by a similar mechanism. The presence of R249C and S250C variants in serum increases complement-dependent cytotoxicity (CDC) in antibody-sensitized human cells and elevates deposition of C3 on ELISA plates coated with C-reactive protein (CRP), as well as on the surface of glomerular endothelial cells. Our data justify the inclusion of classical pathway genes in the genetic analysis of patients suspected of complement-driven renal disorders. Also, we point out CRP as a potential antibody-independent trigger capable of driving excessive complement activation in carriers of the GoF mutations in complement C2., Competing Interests: SRC performed genetic analyses of aHUS patients for Alexion in the framework of contract and obtained honoraria for lectures/presentations. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Urban, Kowalska, Stasiłojć, Kuźniewska, Skrobińska, Arjona, Alonso, Fenollosa Segarra, Jongerius, Spaapen, Satchell, Thiel, Ołdziej, Rodriguez de Córdoba and Okrój.)

Complement overactivation has been reported in most patients with Barraquer-Simons syndrome (BSS), a rare form of acquired partial lipodystrophy. Complement Factor D (FD) is a serine protease with a crucial role in the activation of the alternative pathway of the complement system, which is mainly synthesized by adipose tissue. However, its role in the pathogenesis of BSS has not been addressed. In this study, plasma FD concentration was measured in 13 patients with BSS, 20 patients with acquired generalized lipodystrophy, 22 patients with C3 glomerulopathy (C3G), and 50 healthy controls. Gene expression and immunohistochemistry studies were assayed using atrophied adipose tissue from a patient with BSS. We found significantly elevated FD levels in BSS cases compared with the remaining cohorts ( p < 0.001). There were no significant differences in FD levels between sexes but FD was strongly and directly associated with age in BSS ( r = 0.7593, p = 0.0036). A positive correlation between FD and C3 was seen in patients with C3G, characterized by decreased FD levels due to chronic C3 consumption, but no correlation was detected for BSS. Following mRNA quantification in the patient's adipose tissue, we observed decreased C FD and C3 but elevated C5 transcript levels. In contrast, the increased FD staining detected in the atrophied areas reflects the effects of persistent tissue damage on the adipose tissue, thus providing information on the ongoing pathogenic process. Our results suggest that FD could be a reliable diagnostic biomarker involved in the pathophysiology of BSS by promoting unrestrained local complement system activation in the adipose tissue environment.

aHUS is a rare disease characterized by episodes of TMA that frequently progresses to CKD and often recurs after KT. The most frequent cause of aHUS is defective regulation of complement activation because of genetic anomalies. Eculizumab interrupts the process of TMA and improves renal function. We describe one female patient with aHUS who debuted in 2005 at 3-mo-old with extrarenal manifestations and progressed to end-stage kidney disease (ESKD) within a year. Her family history included several affected members with similar bad outcomes. Our patient carries a strong aHUS genetic predisposition consisting in a pathogenic gain-of-function mutation in complement factor B concurrent with the MCP aHUS risk haplotype MCPggaac. She received a kidney transplant in 2011 without eculizumab prophylaxis. The graft, which was negative for the MCPggaac risk haplotype, had an unexpected excellent evolution without aHUS recurrence. Different retrospective studies have shown that the risk of aHUS recurrence after KT correlates well with the genetic load of aHUS risk factors. Knowing important contribution of the MCPggaac risk haplotype to the risk of developing aHUS in Factor B mutations carriers, we speculate whether the absence of this polymorphism in the graft that our patient received may have decreased the risk of aHUS recurrence after KT., (© 2020 Wiley Periodicals LLC.)

Background: Kidney transplantation (KTx) is a strong trigger for the development of either recurrent or de novo atypical haemolytic uraemic syndrome (aHUS). According to previous studies, eculizumab (ECU) is effective for prophylaxis and for treatment of recurrence., Methods: We evaluated the experiences of Spanish patients with recurrent and de novo aHUS associated with KTx, treated or not treated with ECU. In the de novo group, we classified patients as having early de novo (during the first month) or late de novo aHUS (subsequent onset)., Results: We analysed 36 cases of aHUS associated with KTx. All of the 14 patients with pre-KTx diagnosis of aHUS were considered to have high or moderate risk of recurrence. Despite receiving grafts from suboptimal donors, prophylactic ECU was effective for avoiding recurrence. The drug was stopped only in two cases with low-moderate risk of recurrence and was maintained in high-risk patients with no single relapse. There were 22 de novo aHUS cases and 16 belonged to the early de novo group. The median time of onset in the late group was 3.4 years. The early group had a better response to ECU than the late group, probably due to earlier diagnosis and use of the drug. No genetic pathogenic variant was detected in de novo aHUS cases, suggesting a secondary profile of the disease. ECU was stopped in all de novo patients with no relapses. ECU was well tolerated in all cases., Conclusions: Both groups (pre-aHUS and de novo ) presented different clinical profiles, management approaches and outcomes. One should consider aHUS regardless of time after KTx. Genetic studies are crucial to stratify risks of relapse and to determine necessary lengths of treatment. We suggest short ECU treatment for de novo cases without pathogenic mutation and that ECU treatment be considered pre-emptively for patients with moderate or high risk of recurrence., (© The Author(s) 2020. Published by Oxford University Press on behalf of ERA-EDTA.)

Malignant hypertension is listed among the causes of secondary thrombotic microangiopathy, but pathogenic mutations in complement genes have been reported in patients with hypertension-induced thrombotic microangiopathy. Here we investigated the frequency and severity of hypertension in 55 patients with primary atypical hemolytic uremic syndrome (aHUS). A genetic analysis was performed in all patients, and funduscopic examination was performed in all the patients with Grades 2 and 3 hypertension. A cohort of 110 patients with malignant hypertension caused by diseases other than aHUS served as control. Thirty-six patients with aHUS presented Grade 2 or Grade 3 hypertension and funduscopic examination showed malignant hypertension in 19. Genetic abnormalities in complement were found in 19 patients (37% among patients with malignant hypertension). Plasmapheresis was performed in 46 patients and 26 received eculizumab. Renal and hematological responses were significantly lower after plasmapheresis (24%) than after eculizumab (81%). Renal survival was significantly higher in patients treated with eculizumab (85% at one, three and five years) compared to patients who did not receive this treatment (54%, 46% and 41%), respectively. Response to eculizumab was independent of hypertension severity and the presence of complement genetic abnormalities. Among patients with malignant hypertension caused by other diseases the prevalence of thrombotic microangiopathy was very low (5%). Thus, severe and malignant hypertension are common among patients with aHUS and eculizumab treatment leads to a higher renal survival when compared to plasmapheresis. However, thrombotic microangiopathy is uncommon among patients presenting with malignant hypertension caused by diseases other than aHUS., (Copyright © 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

The black rat Rattus rattus and the house mouse Mus musculus are two commensal rodent species that harbour and shed zoonotic pathogens, including helminths. The aim of this survey was to study the helminth community and the patterns of infections in R. rattus and M. musculus from two Mayan communities in Mexico. Gastrointestinal helminths were isolated from 322 M. musculus and 124 R. rattus, including Gongylonema neoplasticum, Hassalstrongylus aduncus, Hassalstrongylus musculi, Hydatigera taeniaeformis metacestode, Hymenolepis diminuta, Nippostrongylus brasiliensis, Oligacanthorhynchidae gen. sp., Syphacia muris, Syphacia obvelata, Rodentolepis microstoma and Trichuris muris. The overall richness of helminths was seven in R. rattus and six in M. musculus. The results of generalized linear models showed that juvenile rodents had lower probabilities of being infected with G. neoplasticum, H. taeniaeformis and H. musculi than adult rodents. A positive association between the prevalence of S. muris and rat abundance was found. The intensity of infection with S. muris was higher in the rainy season than in the dry season; the opposite result was found for H. musculi infection. Male R. rattus harboured more S. muris specimens. The intensity of infection with T. muris was inversely associated with mouse abundance. The presence of the zoonotic H. diminuta, as well as H. taeniaeformis and R. microstoma in rodent populations indicates that there is risk of transmission, and that their entire life cycle occurs in the study area.

Genetic analyses in atypical hemolytic uremic syndrome (aHUS) and C3-glomerulopathy (C3G) patients have provided an excellent understanding of the genetic component of the disease and informed genotype-phenotype correlations supporting an individualized approach to patient management and treatment. In this context, a correct categorization of the disease-associated gene variants is critical to avoid detrimental consequences for patients and their relatives. Here we describe a comprehensive procedure to measure levels and functional activity of complement regulator factor H (FH) encoded by CFH, the commonest genetic factor associated with aHUS and C3G, and present the results of the analysis of 28 uncharacterized, disease-associated, FH variants. Sixteen variants were not expressed in plasma and eight had significantly reduced functional activities that impact on complement regulation. In total, 24 of 28 CFH variants were unambiguously categorized as pathogenic and the nature of the pathogenicity fully documented for each. The data also reinforce the genotype-phenotype correlations that associate specific FH functional alterations with either aHUS or C3G and illustrate important drawbacks of the prediction algorithms dealing with variants located in FH functional regions. We also report that the novel aHUS-associated M823T variant is functionally impaired. This was unexpected and uncovered the important contribution of regions outside the N-terminal and C-terminal functional domains to FH regulatory activities on surfaces. Thus, our work significantly advances knowledge towards a complete functional understanding of the CFH genetic variability and highlights the importance of functional analysis of the disease-associated CFH variants., (Copyright © 2017 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Pregnancy-associated atypical hemolytic uremic syndrome (aHUS) refers to the thrombotic microangiopathy resulting from uncontrolled complement activation during pregnancy or the postpartum period. Pregnancy-associated aHUS is a devastating disease for which there is a limited clinical understanding and treatment experience. Here we report a retrospective study to analyze the clinical and prognostic data of 22 cases of pregnancy-associated aHUS from the Spanish aHUS Registry under different treatments. Sixteen patients presented during the first pregnancy and as many as nine patients required hemodialysis at diagnosis. Identification of inherited complement abnormalities explained nine of the 22 cases, with CFH mutations and CFH to CFHR1 gene conversion events being the most prevalent genetic alterations associated with this disorder (66%). In thirteen of the cases, pregnancy complications were sufficient to trigger a thrombotic microangiopathy in the absence of genetic or acquired complement alterations. The postpartum period was the time with highest risk to develop the disease and the group shows an association of cesarean section with pregnancy-associated aHUS. Seventeen patients underwent plasma treatments with a positive renal response in only three cases. In contrast, ten patients received eculizumab with an excellent renal response in all, independent of carrying or not inherited complement abnormalities. Although the cohort is relatively small, the data suggest that pregnancy-associated aHUS is not different from other types of aHUS and suggest the efficacy of eculizumab treatment over plasma therapies. This study may be useful to improve prognosis in this group of aHUS patients., (Copyright © 2017 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Atypical hemolytic uremic syndrome (aHUS), a rare form of thrombotic microangiopathy caused by complement pathogenic variants, mainly affects the kidney microvasculature. A retrospective genetic analysis in our aHUS cohort ( n =513) using multiple ligation probe amplification uncovered nine unrelated patients carrying a genetic abnormality in the complement factor H related 1 gene ( CFHR1 ) that originates by recurrent gene conversion events between the CFH and CFHR1 genes. The novel CFHR1 mutants encode an FHR-1 protein with two amino acid substitutions, L290S and A296V, converting the FHR-1 C terminus into that of factor H (FH). Next-generation massive-parallel DNA sequencing (NGS) analysis did not detect these genetic abnormalities. In addition to the CFHR1 mutant, six patients carried the previously uncharacterized CFH-411T variant. In functional analyses, the mutant FHR-1 protein strongly competed the binding of FH to cell surfaces, impairing complement regulation, whereas the CFH-411T polymorphism lacked functional consequences. Carriers of the CFHR1 mutation presented with severe aHUS during adulthood; 57% of affected women in this cohort presented during the postpartum period. Analyses in patients and unaffected carriers showed that FH plasma levels determined by the nonmutated chromosome modulate disease penetrance. Crucially, in the activated endothelial (HMEC-1) cell assay, reduced FH plasma levels produced by the nonmutated chromosome correlated inversely with impairment of complement regulation, measured as C5b-9 deposition. Our data advance understanding of the genetic complexities underlying aHUS, illustrate the importance of performing functional analysis, and support the use of complementary assays to disclose genetic abnormalities not revealed by current NGS analysis., (Copyright © 2018 by the American Society of Nephrology.)

Background: Atypical hemolytic uremic syndrome (aHUS) is a rare disease associated with congenital or acquired genetic abnormalities that result in uncontrolled complement activation, leading to thrombotic microangiopathy and kidney failure. Until recently, the only treatment was plasma exchange or plasma infusion (PE/PI), but 60% of patients died or had permanent kidney damage despite treatment. Eculizumab, a complement inhibitor, has shown promising results in aHUS. However, data are mainly extracted from case reports or studies of heterogeneous cohorts, and no direct comparison with PE/PI is available., Methods: An observational retrospective study of adult, dialysis-dependent aHUS patients with acute kidney injury (AKI) who were treated with either PE/PI alone or with second-line eculizumab in our center. We compared the effect of PE/PI and eculizumab on kidney function, hypertension, proteinuria, hematologic values, relapse, and death., Results: Thirty-one patients were included (females, 18; sporadic aHUS, 29; mean age, 46 ± 20 years). Twenty-six patients were treated with PE/PI alone, and 5 were deemed to be plasma-resistant and received eculizumab after stopping PE/PI. Among patients receiving eculizumab, 80% attained complete recovery of kidney function, 100% stopped dialysis, 20% had decreased proteinuria, and no patient relapsed (vs. 38.5, 50, 15.4, and 11.5%, respectively, of patients receiving only PE/PI). At 1-year of follow-up, no deaths had occurred in either group., Conclusion: Eculizumab shows greater efficacy than PE/PI alone for the treatment of adult aHUS patients with AKI. Prospective studies and meta-analyses are warranted to confirm our findings and set guidelines for treatment, monitoring, and maintenance., (© 2018 S. Karger AG, Basel.)

Background: Complement dysregulation occurs in thrombotic microangiopathies (TMAs) other than primary atypical haemolytic uraemic syndrome (aHUS). A few of these patients have been reported previously to be successfully treated with eculizumab., Methods: We identified 29 patients with so-called secondary aHUS who had received eculizumab at 11 Spanish nephrology centres. Primary outcome was TMA resolution, defined by a normalization of platelet count (>150 × 10 9 /L) and haemoglobin, disappearance of all the markers of microangiopathic haemolytic anaemia (MAHA), and improvement of renal function, with a ≥25% reduction of serum creatinine from the onset of eculizumab administration., Results: Twenty-nine patients with secondary aHUS (15 drug-induced, 8 associated with systemic diseases, 2 with postpartum, 2 with cancer-related, 1 associated with acute humoral rejection and 1 with intestinal lymphangiectasia) were included in this study. The reason to initiate eculizumab treatment was worsening of renal function and persistence of TMA despite treatment of the TMA cause and plasmapheresis. All patients showed severe MAHA and renal function impairment (14 requiring dialysis) prior to eculizumab treatment and 11 presented severe extrarenal manifestations. A rapid resolution of the TMA was observed in 20 patients (68%), 15 of them showing a ≥50% serum creatinine reduction at the last follow-up. Comprehensive genetic and molecular studies in 22 patients identified complement pathogenic variants in only 2 patients. With these two exceptions, eculizumab was discontinued, after a median of 8 weeks of treatment, without the occurrence of aHUS relapses., Conclusion: Short treatment with eculizumab can result in a rapid improvement of patients with secondary aHUS in whom TMA has persisted and renal function worsened despite treatment of the TMA-inducing condition., (© The Author 2017. Published by Oxford University Press on behalf of ERA-EDTA.)

Chagas disease is caused by the protozoan parasite Trypanosoma cruzi, and activation of CD8(+) T cells is crucial for a protective immune response. Therefore, the identification of antigens with major histocompatibility complex class I epitopes is a crucial step for vaccine development against T. cruzi. Our aim was to identify novel antigens and epitopes by immunoinformatics analysis of the parasite proteome (12 969 proteins) and to validate their immunotherapeutic potential in infected mice. We identified 172 predicted epitopes, using NetMHC and RANKPEP. The corresponding protein sequences were reanalyzed to generate a consensus prediction, and 26 epitopes were selected for in vivo validation. The interferon γ (IFN-γ) recall response of splenocytes from T. cruzi-infected mice confirmed that 10 of 26 epitopes (38%) induced IFN-γ production. The immunotherapeutic potential of a mixture of all 10 peptides was evaluated in infected mice. The therapeutic vaccine was able to control T. cruzi infection, as evidenced by reduced parasitemia, cardiac tissue inflammation, and parasite burden and increased survival. These findings illustrate the benefits of this approach for the rapid development of a vaccine against pathogens with large genomes. The identified peptides and the proteins from which they are derived are excellent candidates for the development of a vaccine against T. cruzi., (© The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Objective: The objective of this work was to understand how the baseball bat is a silent weapon. The baseball bat has been utilized illegally in different areas of the world. In the past, several case reports are known for their lethal effect. In this paper, we analyse the outcome of the utilization of baseball bat for illegal purposes as well as review the principal injury and the utilization of baseball bat as explained by an engineer., Material and Method: The medical and radiographic records of patients admitted to Sinai-Grace and Detroit Receiving Hospitals in Detroit, MI, USA, from June 1997 to June 2000, were reviewed. Ninety patients presented with documented baseball bat injury by history. Clinical data were obtained from the patients charts. Detailed descriptions of those body parts affected by baseball bat injury were registered and classified by anatomical regions., Results: A total of 39 cranial fractures were observed, mainly on the skull base and orbital wall., Discussion: Baseball bat-related injury is an endemic problem in Detroit. This urban use of the baseball bat as a weapon is getting severe. A team approach to this type of injury is recommended.

Child abuse is both socially and medically troublesome and many times produces permanent consequences. A review of the literature is done from a neurosurgical standpoint, and the lesions produced at the Central Nervous System are evaluated in detail, including their physiopathology, neurological sequels and implications for rehabilitation treatment and the child's future life.

Endovascular reconstruction of basilar artery (BA) apex aneurysms has been augmented by adjunctive techniques such as balloon and stent assistance. We present three cases of a wide-necked BA apex aneurysm involving the bilateral P1 segments of both posterior cerebral arteries (PCAs) treated by placement of BA to PCA stents bilaterally in a 'Y' configuration to reconstruct the BA apex for effective coil embolization. Three patients (aged 70, 65 and 37 years) with wide-necked basilar artery aneurysms presented for endovascular treatment. All aneurysms had necks that involved the bilateral P1 segments. Each patient was deemed an appropriate candidate for endovascular reconstruction. Patients were pretreated with clopidogrel (75 mg) and aspirin (325 mg) each day for 3 days prior to the procedure. Following induction of general anesthesia, access to the right femoral artery was obtained by placement of a 6F sheath. Intravenous heparin was administered to achieve an activated coagulation time (ACT) of approximately 300 seconds. A 6F guide catheter was placed within the left vertebral artery (VA) in two patients, the right VA in a third. Utilizing over-the-wire (OTW) technique, a microcatheter was advanced into the left P2-P3 junction of the PCA. A 300-cm 0.014-inch microwire was passed through the microcatheter into the distal PCA and the microcatheter was removed. In each case, two neuroform stents were prepared (SMART Therapeutics Inc., San Leandro, CA) and advanced OTW into the PCA with the most acute angle relative to the BA. The initial stent placed was 20 mm in length and was deployed from the P1 segment into the BA. The microwire was pulled retrograde into the BA apex, then advanced though the stent struts and into the right PCA. A second stent, 15 mm in length, was advanced OTW through the struts of the previously placed stent. It was then deployed from the P1 into the BA where it overlapped the first stent, resulting in a stent-in-stent 'Y' configuration at the BA apex. A microcatheter was advanced OTW into the BA apex aneurysm and coil embolization proceeded in the usual fashion. Following the procedure, each patient was maintained in the neurosurgical intensive care unit (NICU). All remained neurologically intact. The two elderly patients were discharged to home the morning following the procedure. The third patient suffered an upper GI bleed and was treated an additional 3 days in hospital. Oral clopidogrel (75 mg by mouth) and aspirin (325 mg by mouth) were continued daily for 4 weeks. The 'Y' stent configuration for reconstruction of the BA apex is a safe effective technique in patients with wide-necked BA aneurysms.

The omentum has been utilized in Neurosurgery since the late 1960s. Its overwhelming effects on fibroblast and peripheral nerve growths were soon noticed. However, there was no direct evidence of production of any of the growth factors by the omentum, although substances were shown to be present in the omentum. Three animals were used in the study. After removal of the omentum in one, the tissue was submitted to PCR for BDNF, NT3/4 and NT5. Water was the negative control utilized. There was marked expression of all neurotrophins in the omentum, indicating local production of all those substances. The omentum has, for the first time, demonstrated to produce and not only accumulate neurotrophins. Utilization of this concept may permit transplant or transposition of parts of the omentum into the central nervous system for the management of multiple diseases, including vascular dementia, strokes, Alzheimer's disease or Moya-Moya disease.

This paper reviews the literature of the brain retraction injury during the last century. The review focused on the instrument characteristic as well as the physiopathological and histopathological damage of the brain induced by brain retraction. It was found that lesions were induced by cerebral ischemia. We conclude that a better monitoring system needs to be developed to avoid brain injury.

We present material to define and understand the concept of Stereolithography (STL) and its potential benefits to the field of neurosurgery and other medical specialties. A historical and scientific review of the literature on stereolithography, its evolution and uses in neurosurgery, forensic medicine, and other medical specialties are described. Considerations regarding different techniques used to obtain STL are discussed. The reproduction of cranial and vascular structures using this technique is evaluated. Data acquisition and model fabrication are the two basic steps required for stereolithography to create custom models for multiple applications in cranio-facial surgery, vascular studies, orthopedic surgery, urology and forensic medicine, among others. Stereolithography is a relatively new technique which continues to grow in many medical fields. Pre-operative education of patients, better understanding of patient anatomy, and the creation of custom-made prostheses are proven benefits of this technique.

Objective: The object of this study was to increase our understanding of the social, clinical, radiographic and psychological consequences of child abuse after the initial insult and to describe the role of neurosurgery and other specialties in this context., Methods: A review of the literature on child abuse (using scientific journals, textbooks, and internet reports) was conducted, with special attention given to child abuse in infants. The biomechanical patterns of injury, the long-term neurological, psychological, and social outcomes and methods of rehabilitation are reviewed., Conclusions: Head injury associated with physical abuse carries a significantly worse clinical outcome than accidental trauma. Late findings in CT scans and MRI show evidence of cerebral atrophy in 100% and cerebral ischemia in 50% of physical abuse cases. Abuse and neglect have a strong impact in developing children, producing emotional, cognitive, and social problems that may persist throughout the rest of their lives. Outcome cannot be improved without an integrated rehabilitation strategy encompassing early field management, hospital therapy, precise targeting of educational and cognitive needs, and finally return to the community. New ancillary tests have emerged that are aimed at improving rehabilitation and illuminating the long-term physiological and functional impact of abuse.

The problem of child abuse and the central nervous system implications are reviewed from a multidimensional approach. Statistics regarding prevalence, risk factors, epidemiological considerations, and physiological aspects are studied. The incidence is reviewed in the United States and in other countries where incidence and social services are also described. Implications for prevention efforts are considered.