hichews's picture
Uploaded biodex index folder
1bb2c64 verified
{
"config": {
"query_token_id": "[unused0]",
"doc_token_id": "[unused1]",
"query_token": "[Q]",
"doc_token": "[D]",
"ncells": null,
"centroid_score_threshold": null,
"ndocs": null,
"load_index_with_mmap": false,
"index_path": null,
"nbits": 2,
"kmeans_niters": 4,
"resume": false,
"similarity": "cosine",
"bsize": 64,
"accumsteps": 1,
"lr": 1e-5,
"maxsteps": 400000,
"save_every": null,
"warmup": 20000,
"warmup_bert": null,
"relu": false,
"nway": 64,
"use_ib_negatives": true,
"reranker": false,
"distillation_alpha": 1.0,
"ignore_scores": false,
"model_name": null,
"query_maxlen": 32,
"attend_to_mask_tokens": false,
"interaction": "colbert",
"dim": 128,
"doc_maxlen": 512,
"mask_punctuation": true,
"checkpoint": "colbert-ir\/colbertv2.0",
"triples": "\/future\/u\/okhattab\/root\/unit\/experiments\/2021.10\/downstream.distillation.round2.2_score\/round2.nway6.cosine.ib\/examples.64.json",
"collection": [
"list with 32235 elements starting with...",
[
"Kaposi sarcoma inflammatory cytokine syndrome (KICS) is a newly-described condition affecting individuals who are HIV-positive and are infected with human herpesvirus 8 (HHV-8). This is a syndrome that in some ways mimics severe sepsis with associated acute respiratory distress syndrome, possibly requiring a ventilator and vasopressor support. However, unlike severe sepsis, antibiotics provide no benefit. Management of KICS has not been fully elucidated because of its high mortality rate. However, the syndrome has been successfully treated in some cases with immunomodulatory therapy. It is crucial for oncologists to be able to recognize this syndrome and to institute the appropriate therapy. 2017;22:623-625.",
"Resistance to antimicrobial agents of pathogenic bacteria has become a major problem in routine medical practices. Carbapenem resistance has long been increasing. The production of carbapenem- hydrolysing \u03b2-lactamases (carbapenamases), which include NDM, KPC, OXA-48, IMP-1 and VIM is the most common mechanism.\n\n\n\nA 56\u2009years old male presented with fever and mental changes with progressively decreasing sensorium for the last 3 days. He was admitted to Intensive care unit (ICU) with a diagnosis of meningoencephalitis. On day seven, he developed ventilator associated pneumonia due Klebsiella pnemoniae and Acinetobacter baumannii. He was on meropenem, but the isolates were susceptible to colistin, tigecyclin and amikacin solely. Hence, amikacin was started with addition of intravenous and nebulized colistin. Subsequently, vital signs improved with resolution of fever. However, on day 18, he developed fever once again with a drop in blood pressure. Inotropic support was maintained, and echinocandins and tigecycline were added to the regimen.Repeat blood and urine culture grew Providencia species, which were resistant to most of the drugs on phenotypic Kirby-Bauer disk diffusion method and are intrinsically resistant to colistin and tigecycline. Phenotypic detection of ESBL (combined disk method), MBL, KPCs, AmpC and co-producer were tested according to updated CLSI guideline and all were negative. But the Modified Hodges test was found to be positive. Consequenty, OXA-48 drug resistance pattern was brought into action by blank disc method according to A Tsakris et al., which revealed indentation of growth toward both EDTA and EDTA\/PBA disk indicating production of OXA-48 carbapenamase. To confirm the resistance pattern we processed the isolated colonies for Xpert Carba-R (Cepheid) assay, which detected blaOXA-48 gene and confirmed the OXA-48 drug resistance pattern. Hence, the infecting organism was not susceptible to any of the antibiotics. The patient was kept under isolation and on 31th day of admission, he died of septic shock.\n\n\n\nCarbapenamase production along with intrinsic colistin resistance in infecting bacterial pathogens can cause fatal outcomes in the resource limited countries like Nepal where new antibiotic combinations ceftazidime+ Avibactam, or aztreonam +avibactam are not available. Drug resistance patterns including OXA 48 producer should be characterized in all cases by standard phenotypic methods or by Xpert Carba-R assay and larger studies are required to know the exact burden of OXA 48 producer in Nepal.",
"Here we report the case of a patient with psoriasis who developed ulcerative colitis most likely caused by adalimumab. After cessation of adalimumab, colitis improved significantly. However, as psoriasis worsened, the patient was switched to ustekinumab, which resulted in complete cessation of colitis. During the 2-year follow-up under ustekinumab therapy, no further gastrointestinal complaints occurred. Paradoxical psoriasis manifestations in inflammatory bowel disease (IBD) under tumour necrosis factor (TNF)-inhibitor therapy have been reported and paradoxical IBD occurred rarely (mostly Crohn disease) in patients with rheumatological conditions treated with infliximab or etanercept. Due to the highly probable association of adalimumab with the onset of colitis in this case, we would like to suggest the term 'paradoxical ulcerative colitis' (PUC) for this as yet extremely rarely reported phenomenon. To the best of our knowledge this is the first description of PUC in a patient with psoriasis and in adalimumab treatment. Our observation suggests that ustekinumab is an effective treatment option in patients with paradoxical anti-TNF-driven inflammatory reactions like psoriasis or IBD."
]
],
"queries": "\/future\/u\/okhattab\/data\/MSMARCO\/queries.train.tsv",
"index_name": "train",
"overwrite": false,
"root": "\/future\/u\/hichews\/home\/2024-win\/ColBERT\/experiments",
"experiment": "notebook",
"index_root": null,
"name": "2024-11\/06\/17.09.09",
"rank": 0,
"nranks": 1,
"amp": true,
"gpus": 4,
"avoid_fork_if_possible": false
},
"num_chunks": 2,
"num_partitions": 32768,
"num_embeddings": 7413601,
"avg_doclen": 229.98607104079417
}