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

Glutamatergic Reinnervation and Assembly of Glutamatergic Synapses in Adult Rat Skeletal Muscle Occurs at Cholinergic Endplates

After denervation of adult rat abdominal muscles, the postsynaptic apparatus of neuromuscular junctions (NMJs) retains its original architecture and clustering of acetylcholine receptors (AChRs). When descending fibers of the spinal cord are surgically diverted to this muscle by a nerve grafting procedure, supraspinal glutamatergic neurons can innervate muscle fibers and restore motor function; the newly formed NMJs switch from a cholinergic to a glutamatergic-type synapse. We show here that regenerating nerve endings contact the fibers in an area occupied by cholinergic endplates. These NMJs are morphologically indistinguishable from those in controls, but they differ in the subunit composition of AChRs. Moreover, by immunofluorescence and immunoelectron microscopy, new NMJs express glutamatergic synapse markers. The \u3b1-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluR1 partially colocalizes with AChRs, and vesicular glutamate transporter 2 is localized in the presynaptic compartment. Immunoprecipitation analysis of membranes from reinnervated muscle showed that AMPA receptor subunits GluR1 and GluR2 coimmunoprecipitate with rapsyn, the AChR-anchoring protein at the NMJ. Taken together, these results indicate that cholinergic endplates can be targeted by new glutamatergic projections and that the clustering of AMPA receptors occurs there

Adult Autism Subthreshold Spectrum (AdAS Spectrum): Validation of a questionnaire investigating subthreshold autism spectrum.

Aim Increasing literature has shown the usefulness of a dimensional approach to autism. The present study aimed to determine the psychometric properties of the Adult Autism Subthreshold Spectrum (AdAS Spectrum), a new questionnaire specifically tailored to assess subthreshold forms of autism spectrum disorder (ASD) in adulthood. Methods 102 adults endorsing at least one DSM-5 symptom criterion for ASD (ASDc), 143 adults diagnosed with a feeding and eating disorder (FED), and 160 subjects with no mental disorders (CTL), were recruited from 7 Italian University Departments of Psychiatry and administered the following: SCID-5, Autism-Spectrum Quotient (AQ), Ritvo Autism and Asperger Diagnostic Scale 14-item version (RAADS-14), and AdAS Spectrum. Results The AdAS Spectrum demonstrated excellent internal consistency for the total score (Kuder–Richardson's coefficient=.964) as well as for five out of seven domains (all coefficients>.80) and sound test–retest reliability (ICC=.976). The total and domain AdAS Spectrum scores showed a moderate to strong (>.50) positive correlation with one another and with the AQ and RAADS-14 total scores. ASDc subjects reported significantly higher AdAS Spectrum total scores than both FED (p<.001) and CTL (p<.001), and significantly higher scores on the Childhood/adolescence, Verbal communication, Empathy, Inflexibility and adherence to routine, and Restricted interests and rumination domains (all p<.001) than FED, while on all domains compared to CTL. CTL displayed significantly lower total and domain scores than FED (all p<.001). A significant effect of gender emerged for the Hyper– and hyporeactivity to sensory input domain, with women showing higher scores than men (p=.003). A Diagnosis Gender interaction was also found for the Verbal communication (p=.019) and Empathy (p=.023) domains. When splitting the ASDc in subjects with one symptom criterion (ASD1) and those with a ASD, and the FED in subjects with no ASD symptom criteria (FED0) and those with one ASD symptom criterion (FED1) a gradient of severity in AdAS Spectrum scores from CTL subjects to ASD patients, across FED0, ASD1, FED1 was shown. Conclusions The AdAS Spectrum showed excellent internal consistency and test–retest reliability and strong convergent validity with alternative dimensional measures of ASD. The questionnaire performed differently among the three diagnostic groups and enlightened some significant effects of gender in the expression of autistic traits

New Copy Number Variations in Schizophrenia

Genome-wide screenings for copy number variations (CNVs) in patients with schizophrenia have demonstrated the presence of several CNVs that increase the risk of developing the disease and a growing number of large rare CNVs; the contribution of these rare CNVs to schizophrenia remains unknown. Using Affymetrix 6.0 arrays, we undertook a systematic search for CNVs in 172 patients with schizophrenia and 160 healthy controls, all of Italian origin, with the aim of confirming previously identified loci and identifying novel schizophrenia susceptibility genes. We found five patients with a CNV occurring in one of the regions most convincingly implicated as risk factors for schizophrenia: NRXN1 and the 16p13.1 regions were found to be deleted in single patients and 15q11.2 in 2 patients, whereas the 15q13.3 region was duplicated in one patient. Furthermore, we found three distinct patients with CNVs in 2q12.2, 3q29 and 17p12 loci, respectively. These loci were previously reported to be deleted or duplicated in patients with schizophrenia but were never formally associated with the disease. We found 5 large CNVs (>900 kb) in 4q32, 5q14.3, 8q23.3, 11q25 and 17q12 in five different patients that could include some new candidate schizophrenia susceptibility genes. In conclusion, the identification of previously reported CNVs and of new, rare, large CNVs further supports a model of schizophrenia that includes the effect of multiple, rare, highly penetrant variants

High depression symptomatology and mental pain characterize suicidal psychiatric patients

Background: Symptoms of depression are transdiagnostic heterogenous features frequently assessed in psychiatric disorders, that impact the response to first-line treatment and are associated with higher suicide risk. This study assessed whether severe mental pain could characterize a specific phenotype of severely depressed high-risk psychiatric patients. We also aimed to analyze differences in treatments administered. Methods: 2,297 adult patients (1,404 females and 893 males; mean age = 43.25 years, SD = 15.15) treated in several Italian psychiatric departments. Patients were assessed for psychiatric diagnoses, mental pain, symptoms of depression, hopelessness, and suicide risk. Results: More than 23% of the patients reported high depression symptomatology and high mental pain (HI DEP/HI PAIN). Compared to patients with lower symptoms of depression, HI DEP/HI PAIN is more frequent among females admitted to an inpatient department and is associated with higher hopelessness and suicide risk. In addition, HI DEP/HI PAIN (compared to both patients with lower symptoms of depression and patients with higher symptoms of depression but lower mental pain) were more frequently diagnosed in patients with personality disorders and had different treatments. Conclusions: Patients reporting severe symptoms of depression and high mental pain presented a mixture of particular dangerousness (high trait hopelessness and the presence of suicide ideation with more frequency and less controllability and previous suicide behaviors). The presence of severe mental pain may act synergically in expressing a clinical phenotype that is likewise treated with a more complex therapeutic regime than that administered to those experiencing symptoms of depression without mental pain

Altered mRNA Editing and Expression of Ionotropic Glutamate Receptors after Kainic Acid Exposure in Cyclooxygenase-2 Deficient Mice

Kainic acid (KA) binds to the AMPA/KA receptors and induces seizures that result in inflammation, oxidative damage and neuronal death. We previously showed that cyclooxygenase-2 deficient (COX-2−/−) mice are more vulnerable to KA-induced excitotoxicity. Here, we investigated whether the increased susceptibility of COX-2−/− mice to KA is associated with altered mRNA expression and editing of glutamate receptors. The expression of AMPA GluR2, GluR3 and KA GluR6 was increased in vehicle-injected COX-2−/− mice compared to wild type (WT) mice in hippocampus and cortex, whereas gene expression of NMDA receptors was decreased. KA treatment decreased the expression of AMPA, KA and NMDA receptors in the hippocampus, with a significant effect in COX-2−/− mice. Furthermore, we analyzed RNA editing levels and found that the level of GluR3 R/G editing site was selectively increased in the hippocampus and decreased in the cortex in COX-2−/− compared with WT mice. After KA, GluR4 R/G editing site, flip form, was increased in the hippocampus of COX-2−/− mice. Treatment of WT mice with the COX-2 inhibitor celecoxib for two weeks decreased the expression of AMPA/KA and NMDAR subunits after KA, as observed in COX-2−/− mice. After KA exposure, COX-2−/− mice showed increased mRNA expression of markers of inflammation and oxidative stress, such as cytokines (TNF-α, IL-1β and IL-6), inducible nitric oxide synthase (iNOS), microglia (CD11b) and astrocyte (GFAP). Thus, COX-2 gene deletion can exacerbate the inflammatory response to KA. We suggest that COX-2 plays a role in attenuating glutamate excitotoxicity by modulating RNA editing of AMPA/KA and mRNA expression of all ionotropic glutamate receptor subunits and, in turn, neuronal excitability. These changes may contribute to the increased vulnerability of COX-2−/− mice to KA. The overstimulation of glutamate receptors as a consequence of COX-2 gene deletion suggests a functional coupling between COX-2 and the glutamatergic system