Relationship of Schistonchus caprifici (Aphelenchoididae) with fig inflorescences, the fig pollinator Blastophaga psenes, and its cleptoparasite Philotrypesis caricae

L'association entre le nématode #Schistonchus caprifici, la guêpe pollinisatrice #Blastophaga psenes et le parasitoïde #Philotrypesis caricae a été étudiée en hiver, au printemps et en automne dans les inflorescences (sycones) du figuier (#Ficus carica var. #sylvestris) dans le sud de l'Italie. C'est la première fois qu'est signalée l'association d'un #Schistonchus sp. avec une guêpe parasitoïde. Tous les stades biologiques de #S. caprifici ont été trouvés dans l'hémocoele des femelles ailées de #B. psenes et de #P. caricae. Aucune association n'a été observée avec les mâles aptères des deux guêpes. Pour ces deux guêpes de la figue, le nombre de femelles ailées transportant des nématodes est plus élevé en juin qu'en mars. Cependant, le pourcentage de #P. caricae transportant #S. caprifici$est de 50$. Le nombre de nématodes transportés par chaque femelle ailée est de 1-3 et 1-23 pour #P. caricae et 1-14 et 1-116 pour #B. psenes en mars et juin, respectivement. Les mensurations de femelles associées aux insectes (provenant des deux guêpes) et, de celles phytoparasites, de #S. caprifici$ ne diffèrent pas. Les examens histopathologiques révèlent la présence des colonies de nématodes à l'intérieur et à l'extérieur des bouquets d'anthères et des filets. Le nématode provoque des nécroses de l'épiderme et du parenchyme cortical des filets et la formation dans les anthères de cellules épidermiques hypertrophiées, riches en cytoplasme à coloration foncée. (Résumé d'auteur

Familial gastrointestinal stromal tumors (GISTs)

Review on Familial gastrointestinal stromal tumors (GISTs), with data on clinics, and the genes involved

KITLG (KIT ligand)

Review on KITLG (KIT ligand), with data on DNA, on the protein encoded, and where the gene is implicated

Piebaldism

Review on Piebaldism, with data on clinics, and the genes involved

KIT (v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog)

Review on KIT (v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog), with data on DNA, on the protein encoded, and where the gene is implicated

PERLINDUNGAN KONSUMEN TERHADAP MAKANAN JAJANAN YANG MENGANDUNG FORMALIN DAN BORAKS(SUATU PENELITIAN DI KOTA BANDA ACEH)

ABSTRAKNANDA MAULINA SAFIRA,PERLINDUNGAN KONSUMEN TERHADAP 2014MAKANAN JAJANAN YANG MENGANDUNG FORMALIN DAN BORAKS (Studi Penelitian di Kota Banda Aceh)Fakultas Hukum Universitas Syiah Kuala(iv, 63) pp., tabl., bibl., appdx.( RISMAWATI, S.H., M.Hum. )Dalam Pasal 4 huruf a Undang-Undang Perlindungan Konsumen dijelaskan bahwa konsumen memiliki hak atas keselamatan dalam mengkonsumsi barang. Dalam Pasal 67 Undang-Undang Nomor 18 Tahun 2012 tentang Pangan dijelaskan bahwa ketentuan keamanan pangan diselenggarakan untuk menjaga pangan tetap aman dikonsumsi, sehingga terhindar dari kemungkinan cemaran biologis atau kimia yang dapat membahayakan kesehatan manusia. Dalam Peraturan Menteri Kesehatan Nomor 33 Tahun 2012 tentang Bahan Tambahan Pangan disebutkan bahwa bahan yang dilarang digunakan sebagai bahan tambahan pangan diantaranya adalah formalin dan boraks. Pada kenyataannya, di Kota Banda Aceh terdapat masalah dalam mewujudkan perlindungan konsumen terhadap makanan jajanan yang mengandung formalin dan boraks.Penulisan skripsi ini bertujuan untuk menjelaskan perlindungan konsumen terhadap makanan jajanan yang mengandung formalin dan boraks, faktor penyebab tidak berjalannya perlindungan konsumen terhadap makanan jajanan yang mengandung formalin dan boraks, dan upaya mengatasi hambatan perwujudan perlindungan konsumen terhadap makanan jajanan yang mengandung formalin dan boraks.Data yang diperlukan dalam tulisan ini adalah data sekunder dan data primer. Data sekunder diperoleh melalui penelitian kepustakaan dilakukan dengan cara membaca peraturan perundang-undangan, buku-buku, surat kabar dan bahan-bahan lain yang berkaitan dengan penelitian ini, dan data primer diperoleh dengan cara mewancarai responden dan informan.Hasil penelitian menunjukkan bahwa perlindungan konsumen terhadap makanan jajanan yang mengandung formalin dan boraks di Kota Banda Aceh, belum berjalan sebagaimana yang telah diatur dalam Undang-Undang Nomor 18 Tahun 2012 dan Peraturan Menteri Kesehatan Nomor 33 Tahun 2012. Faktor penyebab tidak berjalannya perlindungan konsumen terhadap makanan jajanan yang mengandung formalin dan boraks yaitu kurangnya sosialisasi peraturan perundang-undangan, kurangnya pengawasan, kurangnya ketegasan dalam penerapan sanksi dan kurangnya laporan dari pihak masyarakat.Upaya mengatasi hambatan perwujudan perlindungan konsumen terhadap makanan jajanan yang mengandung formalin dan boraks yaitu penyuluhan hukum, pengawasan, peringatan dan pembinaan.Disarankan kepada instansi pemerintahan seperti Dinas Kesehatan dan BBPOM untuk menambah jumlah petugas serta mengalokasikan dana dalam melakukan pemeriksaan dan pengujian makanan jajanan sehingga terselenggaranya perlindungan konsumen terhadap makanan jajanan yang mengandung formalin dan boraks.Banda Ace

The cooling of atomic and molecular gas in DR21

We present an overview of a high-mass star formation region through the major (sub-)mm, and far-infrared cooling lines to gain insight into the physical conditions and the energy budget of the molecular cloud. We used the KOSMA 3m telescope to map the core ($10'\times 14'$) of the Galactic star forming region DR 21/DR 21 (OH) in the Cygnus X region in the two fine structure lines of atomic carbon CI and four mid-$J$ transitions of CO and $^{13}$CO, and CS J=7\TO6. These observations have been combined with FCRAO J=1\TO0 observations of $^{13}$CO and C$^{18}$O. Five positions, including DR21, DR21 (OH), and DR21 FIR1, were observed with the ISO/LWS grating spectrometer in the \OI 63 and 145 $\mu$m lines, the \CII 158 $\mu$m line, and four high-$J$ CO lines. We discuss the intensities and line ratios at these positions and apply Local Thermal Equilibrium (LTE) and non-LTE analysis methods in order to derive physical parameters such as masses, densities and temperatures. The CO line emission has been modeled up to J=20. From non-LTE modeling of the low- to high-$J$ CO lines we identify two gas components, a cold one at temperatures of T_\RM{kin}\sim 30-40 K, and one with T_\RM{kin}\sim 80-150 K at a local clump density of about n(H$_2$)$\sim 10^4-10^6$ cm$^{-3}$. While the cold quiescent component is massive containing typically more than 94 % of the mass, the warm, dense, and turbulent gas is dominated by mid- and high-$J$ CO line emission and its large line widths. The medium must be clumpy with a volume-filling of a few percent. The CO lines are found to be important for the cooling of the cold molecular gas, e.g. at DR21 (OH). Near the outflow of the UV-heated source DR21, the gas cooling is dominated by line emission of atomic oxygen and of CO

Gender-based differences in the clustering of metabolic syndrome factors in children and adolescents

We depicted gender-differences in metabolic syndrome (MS) clustering before and after puberty in pediatrics, in order to develop gender specific preventive strategies for childhood obesity. We considered 1079 children and adolescents (529 females and 550 males; mean age 11.5 \ub1 2.8 year). According to body mass index (BMI) percentiles the subjects were classified as normal weight BMI <75th, overweight BMI 75-95th and with obesity BMI >95th. MS was diagnosed when three of the following criteria for age and sex percentiles were met: BMI >95th, triglycerides (TGs) level >95th, high-density lipoprotein-cholesterol (HDL-c) level <5th, blood pressure (blood pressure) >95th percentile, fasting blood glucose (FBG) >100 mg/dL and/or homeostatic model assessment-insulin resistance (HOMA-IR) >97.5th percentile. The prevalence of dismetabolic factors was similar in both genders, except for pathological BP, which was higher in males (p = 0.02). MS was detected only in patients with obesity, with a higher prevalence in pubertal than late/post-pubertal subjects (p < 0.001), without any significant difference between gender. In pre-puberty, the most common MS combination was obesity (HBMI) + hypertension (HBP) + hyperglycemia/insulin resistance (HGLY/IR) followed by HBMI + low HDL-levels (LHDL) + HGLY/IR versus HBMI + HBP + HGLY/IR followed by HBMI + HBP + LHDL, respectively, in females and males. In the early and late/post-pubertal periods, the most prevalent combination remained similar to pre-puberty, additionally in both sexes other combinations, such as HBMI + HTG + HBP + HGLY/IR, HBMI + HBP + LHDL + HGLY/IR, HBMI + HTG + LHDL + HGLY/IR and HBMI + HTG + LHDL + HBP + HGLY/IR were also detected, differently distributed in males and females. We confirm that MS is an important consequence related to obesity, particularly in the post-puberty stage. Some gender-based differences should be considered early in order to identify specific preventive and treatment strategies

9q34.3 microduplications lead to neurodevelopmental disorders through EHMT1 overexpression

Both copy number losses and gains occur within subtelomeric 9q34 region without common breakpoints. The microdeletions cause Kleefstra syndrome (KS), whose responsible gene is EHMT1. A 9q34 duplication syndrome (9q34 DS) had been reported in literature, but it has never been characterized by a detailed molecular analysis of the gene content and endpoints. To the best of our knowledge, we report on the first patient carrying the smallest 9q34.3 duplication containing EHMT1 as the only relevant gene. We compared him with 21 reported patients described here as carrying 9q34.3 duplications encompassing the entire gene and extending within ~\u20093 Mb. By surveying the available clinical and molecular cytogenetic data, we were able to discover that similar neurodevelopmental disorders (NDDs) were shared by patient carriers of even very differently sized duplications. Moreover, some facial features of the 9q34 DS were more represented than those of KS. However, an accurate in silico analysis of the genes mapped in all the duplications allowed us to support EHMT1 as being sufficient to cause a NDD phenotype. Wider patient cohorts are needed to ascertain whether the rearrangements have full causative role or simply confer the susceptibility to NDDs and possibly to identify the cognitive and behavioral profile associated with the increased dosage of EHMT1