139 research outputs found

    Differences in childhood stress between Neanderthals and early modern humans as reflected by dental enamel growth disruptions

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    Neanderthals’ lives were historically portrayed as highly stressful, shaped by constant pressures to survive in harsh ecological conditions, thus potentially contributing to their extinction. Recent work has challenged this interpretation, leaving the issue of stress among Paleolithic populations highly contested and warranting in-depth examination. Here, we analyze the frequency of dental enamel hypoplasia, a growth disruption indicator of early life stress, in the largest sample of Neanderthal and Upper Paleolithic dentitions investigated to date for these features. To track potential species-specific patterns in the ontogenetic distribution of childhood stress, we present the first comprehensive Bayesian modelling of the likelihood of occurrence of individual and matched enamel growth disruptions throughout ontogeny. Our findings support similar overall stress levels in both groups but reveal species-specific patterns in its ontogenetic distribution. While Neanderthal children faced increasing likelihoods of growth disruptions starting with the weaning process and culminating in intensity post-weaning, growth disruptions in Upper Paleolithic children were found to be limited around the period of weaning and substantially dropping after its expected completion. These results might, at least in part, reflect differences in childcare or other behavioral strategies between the two taxa, including those that were advantageous for modern humans’ long-term survival

    Occult hepatitis B virus infection in HIV-infected Lebanese patients with isolated antibodies to hepatitis B core antigen

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    The presence of hepatitis B virus (HBV) serological markers have been investigated in 101 Lebanese patients (69 men, 32 women; mean age 32.7 ± 1.7 years) infected with human immunodeficiency virus type 1 (HIV-1). Seven patients (6.9percent) were HBsAg carriers compared with 54 patients (53.5percent) who had no evidence of exposure to HBV infection. Twenty-four patients (23.8percent) had anti-HBc alone as a serological marker compared with four patients who were positive for anti-HBs alone and 12 patients (11.9percent) who were anti-HBc and anti-HBs-positive. Occult HBV infection (presence of HBV DNA in the absence of HBsAg) is found to be relatively high (28.7percent) in HIV-infected Lebanese patients and the overwhelming majority (83.3percent) of those who were positive for anti-HBc alone had a detectable HBV DNA in their serum. However, none of our HIV-positive patients with occult HBV infection had abnormal alanine aminotrasferase level, which also raises the question as to whether occult HBV plays a role in the aetiology of liver disease in HIV-infected patients. Further, studies on the association between HBV DNA levels and markers of liver function in addition to data on liver biopsy would help in answering this question.ALTER MJ, 1994, GASTROENTEROL CLIN N, V23, P437; Brechot C, 2001, HEPATOLOGY, V34, P194, DOI 10.1053-jhep.2001.25172; Burnett RJ, 2005, LIVER INT, V25, P201, DOI 10.1111-j.1478-3231.2005.01054.x; Cacciola I, 1999, NEW ENGL J MED, V341, P22, DOI 10.1056-NEJM199907013410104; Carman WF, 1997, J VIRAL HEPATITIS, V4, P11, DOI 10.1111-j.1365-2893.1997.tb00155.x; CHAN HLY, 1999, CLIN LIVER DIS, V3, P291, DOI 10.1016-S1089-3261(05)70069-6; Conjeevaram H, 2001, HEPATOLOGY, V34, P204, DOI 10.1053-jhep.2001.25225; Coursaget P, 1991, FEMS Microbiol Lett, V67, P35; El-Zaatari M, 2007, J HOSP INFECT, V66, P278, DOI 10.1016-j.jhin.2007.04.010; Fukuda R, 1999, J MED VIROL, V58, P201, DOI 10.1002-(SICI)1096-9071(199907)58:3201::AID-JMV33.0.CO;2-2; Gomes SA, 1996, ACTA VIROL, V40, P133; Grob P, 2000, J MED VIROL, V62, P450, DOI 10.1002-1096-9071(200012)62:4450::AID-JMV93.0.CO;2-Y; Hu KQ, 2002, J VIRAL HEPATITIS, V9, P243, DOI 10.1046-j.1365-2893.2002.00344.x; Lee WM, 1997, NEW ENGL J MED, V337, P1733, DOI 10.1056-NEJM199712113372406; Lindh M, 1997, J INFECT DIS, V175, P1285; LUO KX, 1991, J MED VIROL, V35, P55, DOI 10.1002-jmv.1890350112; Neau D, 2005, CLIN INFECT DIS, V40, P750, DOI 10.1086-427882; Nunez M, 2002, AIDS, V16, P2099, DOI 10.1097-00002030-200210180-00024; Osborn MK, 2007, HIV MED, V8, P271, DOI 10.1111-j.1468-1293.2007.00469.x; Palella FJ, 1998, NEW ENGL J MED, V338, P853, DOI 10.1056-NEJM199803263381301; Piroth L, 2002, J HEPATOL, V36, P681, DOI 10.1016-S0168-8278(02)00019-3; Raimondo G, 2005, LANCET, V365, P638; RAMIA S, 2007, EPIDEMIOL INFECT, V133, P695; RAMIA S, 2007, IN PRESS EUR J CLIN; Santos EA, 2003, EUR J CLIN MICROBIOL, V22, P92, DOI 10.1007-s10096-002-0868-0; Shire NJ, 2004, JAIDS-J ACQ IMM DEF, V36, P869, DOI 10.1097-00126334-200407010-00015; Wagner AA, 2004, AIDS, V18, P569, DOI 10.1097-01.aids.0000111449.61782.49; WANG JT, 1990, J MED VIROL, V32, P83, DOI 10.1002-jmv.1890320203; Weber B, 2001, J MED VIROL, V64, P312, DOI 10.1002-jmv.1052; Zuckerman AJ, 2000, LANCET, V355, P1382, DOI 10.1016-S0140-6736(00)02132-268

    The differential diagnosis of early gastric mucosa-associated lymphoma: polymerase chain reaction and paraffin section immunophenotyping.

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    The distinction between benign florid lymphoid hyperplasia and low-grade gastric mucosal-associated lymphoid tissue (MALT) lymphoma may be a challenge. The presence of monoclonal B cells in Helicobacter pylori-chronic active gastritis has suggested that polymerase chain reaction (PCR) data should be viewed with caution. We investigated the reliability of PCR versus immunophenotyping in diagnosing early gastric MALT lymphoma. We studied 1511 biopsies from eight patients with high-grade primary gastric lymphoma, 25 with low-grade MALT lymphoma, 32 with atypical lymphoid infiltrates, and 39 with Helicobacter pylori-chronic active gastritis. Paraffin sections from all cases were stained with antibodies to CD20, CD3, AE1/AE3, kappa and lambda. PCR was performed on paraffin sections using the primer set VH-FR3/J(H). Using histopathology as the gold standard in diagnosis, we confirmed monoclonality in 22 of 25 MALT lymphomas (88%); a clonal band was found in 38% (15 of 39) of patients with chronic active gastritis. An immunophenotype pattern with predominance of CD20-positive cells in lymphocytic infiltrates was associated with monoclonality in 92% of cases. The presence of an enlarged irregular mantle zone was found in both monoclonal and polyclonal areas. An equal prevalence of B and T cells in lymphocytic infiltrates was associated with a polyclonal pattern in 24 of 31 cases (77%). Immunostaining of sIg (kappa and lambda) was difficult in paraffin sections and convincing proof of monoclonality was not obtained. Lymphoepithelial lesions were infrequent in gastric biopsies and their presence was highlighted with keratin stains. Because monoclonal B cells are observed in Helicobacter pylori-associated gastritis, the correct interpretation of clonality by PCR remains unclear. Paraffin section IHC using CD20 and CD3 is especially useful to confirm the diagnosis of gastric MALT lymphoma

    Dietary reconstruction of the El Sidrón Neandertal familial group (Spain) in the context of other Neandertal and modern hunter-gatherer groups. A molar microwear texture analysis

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    Here, we present the analysis of occlusal molar microwear textures of eight individuals from the El Sidrón Neandertal group (Spain). The aims of the study were: 1) to document potential age-, sex-, and maternal lineage-related differences in diet within a Neandertal familial group, and 2) to place the diet of El Sidrón individuals in the context of those of other Neandertal groups. This study also offers an interpretation of the diet of the El Sidrón Neandertals by comparing their microwear signatures to those of recent hunter-gatherer populations with diverse but known diets. The intra-group examination of the microwear signatures are consistent with the females of the El Sidrón group having had more abrasive diets or having used their teeth in more para-masticatory activities than did the males. Aside from the potential sex-related differences in diet, no additional intra-group dietary separation, such as by age group or maternal lineage, was observed. In comparison to other Neandertals, El Sidrón individuals, as a group, have microwear signatures most similar to those of other Neandertals from wooded habitats and different from those that lived in more open habitats. This result is expected based on the available paleoenvironmental reconstructions from El Sidrón Cave. The diet of the El Sidrón Neandertals, just like their Neandertal counterparts from similar wooded habitats, is interpreted as having been mixed, consisting of both meat and vegetable foods.This research was funded by the local Government of the Principado de Asturias and by the Spanish Government (Project CGL2012-36682), and the European Community Research Infrastructure Action (SYNTHESYS Project; http://www.synthesys.info, to S. El Zaatari).Peer Reviewe

    Demonstration of unexpected antibiotic resistance of genotypically identicalHelicobacter pyloriisolates

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    With use of multiple- and single-colony expansion procedures, the results of susceptibility testing ofHelicobacter pyloriisolates from patients with duodenal ulcer were assessed by Etest. The H. pylori genotype was assessed by repetitive extragenic palindrome–based polymerase chain reaction (REP-PCR). There was a high degree of genotypic heterogeneity between different patients, but a single REP-PCR pattern was found for 92% of patients. In contrast, a high degree of phenotypic heterogeneity was shown among the isolated colonies. Antibiogram susceptibility patterns differed only with respect to metronidazole but not with respect to clarithromycin or amoxicillin. The 42% rate of resistance to metronidazole determined with use of the conventional multiple-strains expansion method was increased to 92% when the single-colony expansion method was used. Similarly, dual clarithromycin/metronidazole resistance was increased from 8% to 42% with single-colony expansion. Despite evidence of a single genotype in most patients, single-colony expansion shows that routine susceptibility testing may greatly underestimate the frequency of metronidazole resistance

    Prevalence of the genes encoding extended-spectrum β-lactamases, in Escherichia coli resistant to β-lactam and non-β-lactam antibiotics

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    The prevalences of extended-spectrum β-lactamases (ESBL) and their encoding bla genes, TEM, SHV and CTX_M, were investigated in isolates of Escherichia coli that were resistant to β-lactam and-or non-β-lactam antibiotics. Of the 250 E. coli isolates investigated, all of which came from patients in a major hospital in southern Lebanon, 61 (13.3percent) were found to have ESBL, their production of β-lactamase being confirmed by the ceftazidime and ceftazidime-clavulanic-acid disc methods. All 61 ESBL isolates were resistant to β-lactams and sensitive to imipenem, piperacillin-tazobactam and cefoxitime. Only 40percent were resistant to fluoroquinolones, 33percent were resistant to aminoglycosides, and 18percent were considered to have multi-drug resistance. The results of the PCR-based amplification of the bla gene in DNA samples from the 61 ESBL isolates indicated that 11 (18percent) of the isolates carried both the TEM and SHV genes, 37 (61percent) carried the TEM gene but not the SHV, and 13 (21percent) had the SHV gene but not the TEM. None of the isolates carried the CTX_M gene. Of the 37 TEM-positive-SHV-negative isolates, 43percent were resistant to fluoroquinolones and 37percent to aminoglycosides. Increased resistance to non-β-lactam antibiotics was observed in the isolates harbouring both the TEM and SHV genes, of which 54percent were resistant to all of the tested antibiotics except imipenem, 36percent were only resistant to fluoroquinolones, and 9.1percent only resistant to aminoglycosides. The possibility that the concomitant presence of TEM- and SHV-type β-lactamases is associated with resistance to non-β-lactam antibiotics requires further research. The prevalences of ESBL and their encoding genes in Gram-negative bacteria collected from various regions in Lebanon will now be investigated. © 2005 The Liverpool School of Tropical Medicine.Bonnet R, 2000, ANTIMICROB AGENTS CH, V44, P1936, DOI 10.1128-AAC.44.7.1936-1942.2000; Bradford PA, 2001, CLIN MICROBIOL REV, V14, P933, DOI 10.1128-CMR.14.4.933-951.2001; MATAR GM, 1999, BRIT MED J MIDDLE E, V7, P6; MEDEIROS AA, 1984, BRIT MED BULL, V40, P18; *NAT COMM CLIN LAB, 2004, 100S14 M NAT COMM CL; NUESCHINDERBINE.MT, 1997, ANTIMICROBIAL AGENTS, V41, P283; Paterson DL, 2000, CLIN INFECT DIS, V30, P473, DOI 10.1086-313719; Saurina G, 2000, J ANTIMICROB CHEMOTH, V45, P895, DOI 10.1093-jac-45.6.895; Tran JH, 2002, P NATL ACAD SCI USA, V99, P5638, DOI 10.1073-pnas.082092899; Tzouvelekis LS, 2000, INT J ANTIMICROB AG, V14, P137, DOI 10.1016-S0924-8579(99)00165-X78

    Occult hepatitis B virus infection in Lebanese patients with chronic hepatitis C liver disease

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    Occult hepatitis B virus (HBV) infection, characterised by the presence of HBV infection with undetectable hepatitis B surface antigen (HBsAg), was investigated in 98 Lebanese patients with chronic hepatitis C liver disease and 85 control subjects recruited from eight institutions in different parts of the country. The prevalence of occult HBV infection ranged from 11.9percent to 44.4percent in hepatitis C virus (HCV)-infected patients and it increased with increasing severity of the liver disease. The overall rate of HBV DNA in our 98 HCV-infected patients was 16.3percent. On the other hand, the rate of HBV DNA was 41.0percent in anti-HBc alone positive patients compared to only 7.1percent in healthy controls who were also anti-HBc alone positive (p 0.001). Moreover, the prevalence HBV DNA increased with increasing severity of the liver disease, but this increase was only marginally significant and, perhaps, could have been significant if more patients were involved in the study. Although Lebanon is an area of low endemicity for both HBV and HCV, occult HBV infection is common in HCV-infected patients. The presence of HBV DNA, therefore, presents a challenge for the effective laboratory diagnosis of hepatitis B, particularly if polymerase chain reaction (PCR)-based HBV detection methods are not used. © 2007 Springer-Verlag.ALBERTI A, 1995, J HEPATOL, V22, P38; Allain JP, 2004, TRANSFUS CLIN BIOL, V11, P18, DOI 10.1016-j.tracli.2003.11.007; Cacciola I, 1999, NEW ENGL J MED, V341, P22, DOI 10.1056-NEJM199907013410104; Drosten C, 2004, J CLIN VIROL, V29, P59, DOI 10.1016-S1386-6532(03)00090-8; El-Zaatari M, 2007, J HOSP INFECT, V66, P278, DOI 10.1016-j.jhin.2007.04.010; Fukuda R, 1999, J MED VIROL, V58, P201, DOI 10.1002-(SICI)1096-9071(199907)58:3201::AID-JMV33.0.CO;2-2; Gilbert N, 2002, J VIROL METHODS, V100, P37, DOI 10.1016-S0166-0934(01)00396-2; Huo TI, 1998, HEPATOLOGY, V28, P231, DOI 10.1002-hep.510280130; Kao JH, 2000, INFEC DIS S, P313; Kao JH, 1997, GASTROENTEROLOGY, V112, P1265, DOI 10.1016-S0016-5085(97)70139-2; Koike K, 1998, J MED VIROL, V54, P249, DOI 10.1002-(SICI)1096-9071(199804)54:4249::AID-JMV33.0.CO;2-4; KOO JH, 2002, J CLIN MICROBIOL, V40, P4068; Lindh M, 1997, J INFECT DIS, V175, P1285; Michalak TI, 1999, HEPATOLOGY, V29, P928, DOI 10.1002-hep.510290329; Nabulsi Mona M, 2003, J Med Liban, V51, P64; Pollicino T, 2004, GASTROENTEROLOGY, V126, P102, DOI 10.1053-j.gastro.2003.10.048; Ramia S, 2005, EPIDEMIOL INFECT, V133, P695, DOI 10.1017-S0950268805003948; Rehermann B, 1996, NAT MED, V2, P1104, DOI 10.1038-nm1096-1104; SATO S, 1994, J HEPATOL, V21, P159, DOI 10.1016-S0168-8278(05)80389-7; Sharara AI, 2007, EPIDEMIOL INFECT, V135, P427, DOI 10.1017-S0950268806006911; Sharara AI, 2004, EUR J CLIN MICROBIOL, V23, P861, DOI 10.1007-s10096-004-1222-5; Torbenson M, 2002, LANCET INFECT DIS, V2, P479, DOI 10.1016-S1473-3099(02)00345-6; Uchida T, 1997, J MED VIROL, V52, P399, DOI 10.1002-(SICI)1096-9071(199708)52:4399::AID-JMV103.0.CO;2-C; Weber B, 2005, EXPERT REV MOL DIAGN, V5, P75, DOI 10.1586-14737159.5.1.75; Yotsuyanagi H, 2000, J INFECT DIS, V181, P1920, DOI 10.1086-315512; Zarski JP, 1998, J HEPATOL, V28, P27, DOI 10.1016-S0168-8278(98)80198-0; ZHANG YY, 1993, HEPATOLOGY, V17, P538, DOI 10.1002-hep.1840170403; Zignego AL, 1997, J MED VIROL, V51, P31397
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