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---
tags:
- sentence-transformers
- sentence-similarity
- feature-extraction
- generated_from_trainer
- dataset_size:34441
- loss:MultipleNegativesRankingLoss
base_model: ibm-granite/granite-embedding-107m-multilingual
widget:
- source_sentence: inhibitors as antifungal, and antibacterial agents. and in with
sulfonylureas, not combination insulin. During clinical tion in 0.4–0.9%. Adverse
an increased rate of infections (upper respiratory and tract), (when Tzd), hypoglycemia
(when a dose of insulin agogue lowered hypoglycemia. Linagliptin is the class
and appears have properties similar to and tin. It approved for and combination
with metformin, pioglitazone. COMBINATION THERAPY—ORAL ANTIDIABETIC & in 2 Diabetes
Mellitus Failure to maintain response over the owing a in mass, reduction physical
activity, mass, in remains disconcerting problem ment of type Multiple medications
may glycemic there a should initiated with biguanide. clinical failure monotherapy,
a agent or is be insulin dase inhibitor; sulfonylureas insulin because of adverse
safety concerns. Third-line multiple medications, or a injectable intensified
insulin
sentences:
- inhibitors such as antiviral, antifungal, and certain antibacterial agents. Saxagliptin
is approved as monotherapy and in combination with biguanides, sulfonylureas,
and Tzds. It has not been studied in combination with insulin. During clinical
trials, mono- and combination therapy with sitagliptin resulted in an HbA 1c reduc-
tion in the range of 0.4–0.9%. Adverse effects include an increased rate of infections
(upper respiratory tract and urinary tract), headaches, peripheral edema (when
combined with a Tzd), hypoglycemia (when combined with a sulfonylurea), and hypersensitivity
reactions (urticaria, facial edema). The dose of a concurrently administered insulin
secret- agogue or insulin may need to be lowered to prevent hypoglycemia. Linagliptin
is the most recently introduced drug in this class and appears to have properties
similar to sitagliptin and saxaglip- tin. It is approved for use as monotherapy
and in combination with metformin, glimepiride, and pioglitazone. COMBINATION
THERAPY—ORAL ANTIDIABETIC AGENTS & INJECTABLE MEDICATION Combination Therapy in
Type 2 Diabetes Mellitus Failure to maintain a good response to therapy over the
long term owing to a progressive decrease in beta-cell mass, reduction in physical
activity, decline in lean body mass, or increase in ectopic fat deposition remains
a disconcerting problem in the manage- ment of type 2 diabetes. Multiple medications
may be required to achieve glycemic control. Unless there is a contraindication,
medical therapy should be initiated with a biguanide. If clinical failure occurs
with metformin monotherapy, a second agent or insulin is added. The second-line
drug can be an insulin secret- agogue, Tzd, incretin-based therapy, amylin analog,
or a glucosi- dase inhibitor; preference is given to sulfonylureas or insulin
because of cost, adverse effects, and safety concerns. Third-line therapy can
include metformin, multiple other oral medications, or a noninsulin injectable
and metformin and intensified insulin
- '61. Glucocorticoids for gastrointestinal use: See Chapter 62. REFERENCES Alesci
S et al: Glucocorticoid-induced osteoporosis: From basic mechanisms to clinical
aspects. Neuroimmunomodulation 2005;12:1. Bamberger CM, Schulte HM, Chrousos GP:
Molecular determinants of gluco- corticoid receptor function and tissue sensitivity
to glucocorticoids. Endocr Rev 1996;17:245. Charmandari E, Kino T: Chrousos syndrome:
A seminal report, a phylogenetic enigma and the clinical implications of glucocorticoid
signaling changes. Eur J Clin Invest 2010;40:932. Charmandari E, Tsigos C, Chrousos
GP: Neuroendocrinology of stress. Ann Rev Physiol 2005;67:259. Chrousos GP: Stress
and disorders of the stress system. Nat Endocrinol Rev 2009;5:374. Chrousos GP,
Kino T: Glucocorticoid signaling in the cell: Expanding clinical implications
to complex human behavioral and somatic disorders. In: Glucocorticoids and mood:
Clinical manifestations, risk factors, and molecular mechanisms. Proc NY Acad
Sci 2009;1179:153. Elenkov IJ, Chrousos GP: Stress hormones, TH1/TH2 patterns,
pro/anti-in- flammatory cytokines and susceptibility to disease. Trends Endocrinol
Metab 1999;10:359. Elenkov IJ et al: Cytokine dysregulation, inflammation, and
wellbeing. Neuroimmunomodulation 2005;12:255. Franchimont D et al: Glucocorticoids
and inflammation revisited: The state of the art. Neuroimmunomodulation 2002–03;10:247.
Graber AL et al: Natural history of pituitary-adrenal recovery following long-term
suppression with corticosteroids. J Clin Endocrinol Metab 1965;25:11. Hochberg
Z, Pacak K, Chrousos GP: Endocrine withdrawal syndromes. Endocrine Rev 2003;24:523.
Kalantaridou S, Chrousos GP: Clinical review 148:'
- safely and effectively combined with 5-FU-, irinotecan-, and oxaliplatin-based
chemotherapy in the treatment of metastatic colorectal cancer. Bevacizumab is
FDA approved as a first-line treatment for metastatic colorectal cancer in combination
with any intravenous fluoropyrimidine-contain- ing regimen and is now also approved
in combination with che- motherapy for metastatic non-small lung cancer and breast
cancer. One potential advantage of this antibody is that it does not appear to
exacerbate the toxicities typically observed with cytotoxic che- motherapy. The
main safety concerns associated with bevacizumab include hypertension, an increased
incidence of arterial throm- boembolic events (transient ischemic attack, stroke,
angina, and myocardial infarction), wound healing complications, gastrointes-
tinal perforations, and proteinuria. Sorafenib is a small molecule that inhibits
multiple receptor tyrosine kinases (RTKs), especially VEGF-R2 and VEGF-R3, platelet-derived
growth factor-β (PDGFR-β), and raf kinase. It was initially approved for advanced
renal cell cancer and is also approved for advanced hepatocellular cancer. Sunitinib
is similar to sorafenib in that it inhibits multiple RTKs, although the specific
types are somewhat different. They include PDGFR-α and PDGFR-β, VEGF-R1, VEGF-R2,
VEGF-R3, and c-kit. It is approved for the treatment of advanced renal cell cancer
and for the treatment of gastrointestinal stromal tumors (GIST) after disease
progression on or with intolerance to imatinib. Pazopanib is a small molecule
that inhibits multiple RTKs, espe- cially VEGF-R2 and VEGF-R3, PDGFR-β, and raf
kinase. This oral agent is approved for the treatment of advanced renal cell cancer.
Sorafenib, sunitinib, and pazopanib are metabolized in the liver by the CYP3A4
system, and elimination is primarily hepatic with excretion in feces. Each of
these agents has potential interac-
- source_sentence: 774 VII that detected by parathyroid gland, increases in serum
phos- levels reduce the secretion. regulation is the net PTH serum calcium and
reduce serum at the amount increase the amount 24,25(OH) D produced. serum calcium
by reducing secretion. High phosphate by D calcium phosphate, has less effect,
such feedback is again appropriate. 1,25(OH) effect PTH patients chronic are loss
this 2 D-mediated loop intestinal absorption often leads secondary The D to PTH
being exploited with of absorption. Such useful the management of hyperparathy-
roidism chronic kidney be of 1,25(OH) also production This the loop in that FGF23
2 D promoting hypophosphatemia, turn inhibits and 2 production. HORMONAL OF
sentences:
- rier only when the meninges are inflamed. Concentrations in cerebrospinal fluid
are highly variable, ranging from 4% to 64% of serum levels in the setting of
meningeal inflammation. As with all antituberculous drugs, resistance to ethambutol
emerges rapidly when the drug is used alone. Therefore, ethambutol is always given
in combination with other antituberculous drugs. Ethambutol hydrochloride, 15–25
mg/kg, is usually given as a single daily dose in combination with isoniazid or
rifampin. The higher dose is recommended for treatment of tuberculous menin- gitis.
The dose of ethambutol is 50 mg/kg when a twice-weekly dosing schedule is used.
Adverse Reactions Hypersensitivity to ethambutol is rare. The most common serious
adverse event is retrobulbar neuritis, resulting in loss of visual acuity and
red-green color blindness. This dose-related adverse effect is more likely to
occur at dosages of 25 mg/kg/d continued for several months. At 15 mg/kg/d or
less, visual disturbances are very rare. Periodic visual acuity testing is desirable
if the 25 mg/kg/d dosage is used. Ethambutol is relatively contraindicated in
chil- dren too young to permit assessment of visual acuity and red- green color
discrimination. PYRAZINAMIDE Pyrazinamide (PZA) is a relative of nicotinamide.
It is stable and slightly soluble in water. It is inactive at neutral pH, but
at pH 5.5 it inhibits tubercle bacilli at concentrations of approximately 20 mcg/mL.
The drug is taken up by macrophages and exerts its activity against mycobacteria
residing within the acidic environ- ment of lysosomes. Pyrazinamide (PZA) N C
O NH2 N Mechanism of Action & Clinical Uses Pyrazinamide is converted to pyrazinoic
acid—the active form of the drug—by mycobacterial pyrazinamidase, which is encoded
by
- 774 SECTION VII Endocrine Drugs that is detected by the parathyroid gland, increases
in serum phos- phate levels reduce the ionized calcium, leading to enhanced PTH
secretion. Such feedback regulation is appropriate to the net effect of PTH to
raise serum calcium and reduce serum phosphate levels. Likewise, both calcium
and phosphate at high levels reduce the amount of 1,25(OH) 2 D produced by the
kidney and increase the amount of 24,25(OH) 2 D produced. High serum calcium works
directly and indirectly by reducing PTH secretion. High serum phosphate works
directly and indirectly by increasing FGF23 levels. Since 1,25(OH) 2 D raises
serum calcium and phosphate, whereas 24,25(OH) 2 D has less effect, such feedback
regulation is again appropriate. 1,25(OH) 2 D directly inhibits PTH secretion
(independent of its effect on serum calcium) by a direct inhibitory effect on
PTH gene transcription. This pro- vides yet another negative feedback loop. In
patients with chronic renal failure who frequently are deficient in producing
1,25(OH) 2 D, loss of this 1,25(OH) 2 D-mediated feedback loop coupled with impaired
phosphate excretion and intestinal calcium absorption often leads to secondary
hyperparathyroidism. The ability of 1,25(OH) 2 D to inhibit PTH secretion directly
is being exploited with calcitriol analogs that have less effect on serum calcium
because of their lesser effect on intestinal calcium absorption. Such drugs are
proving useful in the management of secondary hyperparathy- roidism accompanying
chronic kidney disease and may be useful in selected cases of primary hyperparathyroidism.
1,25(OH) 2 D also stimulates the production of FGF23. This completes the negative
feedback loop in that FGF23 inhibits 1,25(OH) 2 D production while promoting hypophosphatemia,
which in turn inhibits FGF23 production and stimulates 1,25(OH) 2 D production.
SECONDARY HORMONAL REGULATORS OF BONE MINERAL HOMEOST
- host disease after allogeneic stem cell trans- plantation. Cyclosporine has also
proved useful in a variety of autoimmune disorders, including uveitis, rheumatoid
arthritis, psoriasis, and asthma. Its combination with newer agents is show- ing
considerable efficacy in clinical and experimental settings where effective and
less toxic immunosuppression is needed. Newer for- mulations of cyclosporine have
been developed that are improving patient compliance (smaller, better tasting
pills) and increasing bioavailability. Tacrolimus Tacrolimus (FK 506) is an immunosuppressant
macrolide antibi- otic produced by Streptomyces tsukubaensis. It is not chemically
related to cyclosporine, but their mechanisms of action are similar. Both drugs
bind to cytoplasmic peptidylprolyl isomerases that are abundant in all tissues.
While cyclosporine binds to cyclophilin, tacrolimus binds to the immunophilin
FK-binding protein (FKBP). Both complexes inhibit calcineurin, which is necessary
for the activation of the T-cell-specific transcription factor NF-AT. On a weight
basis, tacrolimus is 10–100 times more potent than cyclosporine in inhibiting
immune responses. Tacrolimus is utilized for the same indications as cyclosporine,
particularly in organ and stem cell transplantation. Multicenter studies in the
USA and in Europe indicate that both graft and patient survival are similar for
the two drugs. Tacrolimus has proved to be effective therapy for preventing rejection
in solid-organ transplant patients even after failure of standard rejection therapy,
including anti-T- cell antibodies. It is now considered a standard prophylactic
agent (usually in combination with methotrexate or mycophenolate mofetil) for
graft-versus-host disease. Tacrolimus can be administered orally or intravenously.
The half-life of the intravenous form is approximately 9–12 hours. Like cyclosporine,
tacrolimus is metabolized primarily by P450 enzymes in the liver, and there is
potential for drug interactions. The dosage is determined by trough blood level
at
- source_sentence: Antiviral 865 TABLE Agents or (HSV) varicella-zoster virus (VZV)
Administration Recommended Dosage and Regimen Acyclovir1 Oral First treatment
mg tid mg 5 daily × Recurrent genital herpes mg 200 times daily 800 bid 3–5 tid
2 days Genital the host treatment Genital in host treatment 5 until healed Orolabial
treatment × days Varicella years) 800 mg qid days Zoster daily Intravenous HSV
5 in host mg/kg treatment 10–15 days Neonatal HSV infection 10–20 mg/kg × Varicella
the host treatment mg/kg q8h days (5% treatment lesion 4 Famciclovir1 episode
treatment mg × days genital 1000 day Genital in HIV-infected 500 5–10 days herpes
250 Genital in the HIV-infected 500 bid Orolabial or suppression 250-500 mg mg
days Oral herpes 1000 mg bid × 10 Recurrent mg Genital herpes HIV-infected 5–10
days herpes once suppression the
sentences:
- CHAPTER 49 Antiviral Agents 865 TABLE 49–1 Agents to treat or prevent herpes simplex
virus (HSV) and varicella-zoster virus (VZV) infections. Route of Administration
Use Recommended Adult Dosage and Regimen Acyclovir1 Oral First episode genital
herpes treatment 400 mg tid or 200 mg 5 times daily × 7–10 days Recurrent genital
herpes treatment 400 mg tid or 200 mg 5 times daily or 800 mg bid × 3–5 days or
800 mg tid × 2 days Genital herpes in the HIV-infected host treatment 400 mg 3–5
times daily × 5–10 days Genital herpes suppression in the HIV-infected host 400–800
mg bid–tid Herpes proctitis treatment 400 mg 5 times daily until healed Orolabial
herpes treatment 400 mg 5 times daily × 5 days Varicella treatment (age ≥ 2 years)
800 mg qid × 5 days Zoster treatment 800 mg 5 times daily × 7–10 days Intravenous
Severe HSV treatment 5 mg/kg q8h × 7–10 days Mucocutaneous herpes in the immunocompromised
host treatment 10 mg/kg q8h × 7–14 days Herpes encephalitis treatment 10–15 mg/kg
q8h × 14–21 days Neonatal HSV infection treatment 10–20 mg/kg q8h × 14–21 days
Varicella or zoster in the immunosuppressed host treatment 10 mg/kg q8h × 7 days
Topical (5% cream) Herpes labialis treatment Thin film covering lesion 5 times
daily × 4 days Famciclovir1 Oral First episode genital herpes treatment 500 mg
tid × 5–10 days Recurrent genital herpes treatment 1000 mg bid × 1 day Genital
herpes in the HIV-infected host treatment 500 mg bid × 5–10 days Genital herpes
suppression 250 mg bid Genital herpes suppression in the HIV-infected host 500
mg bid Orolabial herpes treatment 1500 mg once Orolabial or genital herpes suppression
250-500 mg bid Zoster 500 mg tid × 7 days Valacyclovir1 Oral First episode genital
herpes treatment 1000 mg bid × 10 days Recurrent genital herpes treatment 500
mg bid × 3 days Genital herpes in the HIV-infected host treatment 500–1000 mg
bid × 5–10 days Genital herpes suppression 500–1000 mg once daily Genital herpes
suppression in the HIV
- LA Human leukocyte antigen IFN Interferon IGIV Immune globulin intravenous IL
Interleukin LFA Leukocyte function-associated antigen MAB Monoclonal antibody
MHC Major histocompatibility complex NK cell Natural killer cell SCID Severe combined
immunodeficiency disease TCR T-cell receptor TGF-a Transforming growth factor-β
TH1, TH2 T helper cell types 1 and 2 TNF Tumor necrosis factor
- ', especially in adults with impaired renal function and prolonged elevation of
drug levels. The sudden absorption of postoperatively instilled kanamycin from
the peritoneal cavity (3–5 g) has resulted in curare-like neu- romuscular blockade
and respiratory arrest. Calcium gluconate and neostigmine can act as antidotes.
Although hypersensitivity is not common, prolonged applica- tion of neomycin-containing
ointments to skin and eyes has resulted in severe allergic reactions. ■ SPECTINOMYCIN
Spectinomycin is an aminocyclitol antibiotic that is structurally related to aminoglycosides.
It lacks amino sugars and glycosidic bonds. NH HN CH3 O O CH3 Spectinomycin O
CH3 HO O OH OH Spectinomycin is active in vitro against many gram-positive and
gram-negative organisms, but it is used almost solely as an alternative treatment
for drug-resistant gonorrhea or gonorrhea in penicillin-allergic patients. The
majority of gonococcal isolates are inhibited by 6 mcg/mL of spectinomycin. Strains
of gonococci may be resistant to spectinomycin, but there is no cross-resistance
with other drugs used in gonorrhea. Spectinomycin is rapidly absorbed after intramuscular
injection. A single dose of 40 mg/kg up to a maximum of 2 g is given. There is
pain at the injection site and, occasionally, fever and nausea. Nephrotoxicity
and anemia have been observed rarely. Spectinomycin is no longer available for
use in the United States but may be available elsewhere.'
- source_sentence: Against Gram-Positive Bacilli Aminoglycosides Carbapenems Carbapenems
Cephalosporins Chloramphenicol Tetracyclines Macrolides Penicillins Sulfonamides
Tetracyclines Tigecycline Trimethoprim TABLE Antimicrobial that require are in
with hepatic impairment. Dosage Needed in Contraindicated in Dosage Adjustment
Impairment amantadine, aminoglycosides, carbapenems, cycloserine, didanosine,
ethionamide, penicillins,3 pyrazinamide, stavudine, telavancin, telbivudine, telithromycin,
tenofovir, terbinafine, valacyclovir, zidovudine acid, (long-acting), tetracyclines2
Amprenavir, phenicol, indinavir, metronida- 2Except doxycycline and minocycline.
nafcillin and 4Except Alter Antimicrobi
sentences:
- Against Gram-Positive Cocci Against Gram-Negative Bacilli Aminoglycosides Aminoglycosides
Carbapenems Carbapenems Cephalosporins Chloramphenicol Chloramphenicol Quinolones
Clindamycin Rifampin Daptomycin Tetracyclines Glycopeptide antibiotics Tigecycline
Ketolides Macrolides Oxazolidinones Penicillins Quinolones Rifampin Streptogramins
Sulfonamides Tetracyclines Tigecycline Trimethoprim TABLE 51–5 Antimicrobial agents
that require dosage adjustment or are contraindicated in patients with renal or
hepatic impairment. Dosage Adjustment Needed in Renal Impairment Contraindicated
in Renal Impairment Dosage Adjustment Needed in Hepatic Impairment Acyclovir,
amantadine, aminoglycosides, aztreonam, carbapenems, cephalosporins,1 clarithromycin,
colistin, cycloserine, daptomycin, didanosine, emtricitabine, ethambutol, ethionamide,
famciclovir, fluconazole, flucytosine, foscarnet, ganciclovir, lamivudine, penicillins,3
pyrazinamide, quinolones, 4 rimantadine, stavudine, telavancin, telbivudine, telithromycin,
tenofovir, terbinafine, trimethoprim- sulfamethoxazole, valacyclovir, vancomycin,
zidovudine Cidofovir, methenamine, nalidixic acid, nitrofurantoin, sulfonamides
(long-acting), tetracyclines2 Amprenavir, atazanavir, chloram- phenicol, clindamycin,
erythromycin, fosamprenavir, indinavir, metronida- zole, rimantadine, tigecycline
1Except ceftriaxone. 2Except doxycycline and possibly minocycline. 3Except antistaphylococcal
penicillins (eg, nafcillin and dicloxacillin). 4Except moxifloxacin. Conditions
That Alter Antimicrobi
- 'of the integrity of membranes in cells and organelles. A. Nervous System The
developing central nervous system of the fetus and young child is the most sensitive
target organ for lead’s toxic effect. Epidemiologic studies suggest that blood
lead concentrations even less than 5 mcg/dL may result in subclinical deficits
in neurocog- nitive function in lead-exposed young children, with no demon- strable
threshold for a “no effect” level. The dose response between TABLE 57–1 Toxicology
of selected arsenic, lead, and mercury compounds. Form Entering Body Major Route
of Absorption Distribution Major Clinical Effects Key Aspects of Mechanism Metabolism
and Elimination Arsenic Inorganic arsenic salts Gastrointestinal, respiratory
(all mucosal surfaces) Predominantly soft tissues (highest in liver, kidney).
Avidly bound in skin, hair, nails Cardiovascular: shock, arrhythmias. CNS: encephalopathy,
peripheral neuropathy. Gastroenteritis; pan- cytopenia; cancer (many sites) Inhibits
enzymes; interferes with oxidative phosphorylation; alters cell signaling, gene
expression Methylation. Renal (major); sweat and feces (minor) Lead Inorganic
lead oxides and salts Gastrointestinal, respiratory Soft tissues; redistributed
to skeleton (> 90% of adult body burden) CNS deficits; peripheral neuropathy;
ane- mia; nephropathy; hypertension; reproductive toxicity Inhibits enzymes; interferes
with essential cations; alters membrane structure Renal (major); feces and breast
milk (minor) Organic (tetraethyl lead) Skin, gastrointesti- nal, respiratory Soft
tissues, especially liver, CNS Encephalopathy Hepatic dealkylation (fast) → trialkyme-
tabolites (slow) → dissociation to lead Urine and feces (major); sweat (minor)
Mercury Elemental mercury Respiratory tract Soft tissues, especially kidney, CNS
CNS: tremor, behavioral (erethism); gingivo'
- 708 SECTION VII Endocrine Drugs marked adverse effects because there is a recovery
period between each dose. The transition to an alternate-day schedule can be made
after the disease process is under control. It should be done gradu- ally and
with additional supportive measures between doses. When selecting a drug for use
in large doses, a medium- or intermediate-acting synthetic steroid with little
mineralocorticoid effect is advisable. If possible, it should be given as a single
morning dose. C. Special Dosage Forms Local therapy, such as topical preparations
for skin disease, oph- thalmic forms for eye disease, intra-articular injections
for joint disease, inhaled steroids for asthma, and hydrocortisone enemas for
ulcerative colitis, provides a means of delivering large amounts of steroid to
the diseased tissue with reduced systemic effects. Beclomethasone dipropionate,
and several other glucocorti- coids—primarily budesonide, flunisolide, and mometasone
furoate, administered as aerosols—have been found to be extremely useful in the
treatment of asthma (see Chapter 20 ). Beclomethasone dipropionate, triamcinolone
acetonide, budes- onide, flunisolide, and mometasone furoate are available as
nasal sprays for the topical treatment of allergic rhinitis. They are effec- tive
at doses (one or two sprays one, two, or three times daily) that in most patients
result in plasma levels that are too low to influ- ence adrenal function or have
any other systemic effects. Corticosteroids incorporated in ointments, creams,
lotions, and sprays are used extensively in dermatology. These preparations are
discussed in more detail in Chapter 61 . MINERALOCORTICOIDS (ALDOSTERONE, DEOXYCORTICOSTERONE,
FLUDROCORTISONE) The most important mineralocorticoid in humans is aldosterone.
However, small amounts of deoxycorticosterone (DOC) are also formed and released.
Although the amount is normally insignifi- cant, DOC was of some importance therapeut
- source_sentence: Antiprotozoal 923 MEFLOQUINE Mefloquine is effective therapy of
other Although toxicity is mefloquine one recommended for most regions with Chemistry
Mefloquine is 4-quinoline methanol is chemically quinine. can given because local
irritation with parenteral and hours. Mefloquine highly uted and treat- regimen.
elimination half-life about 20 allowing dosing chemoprophylaxis. With dos- drug
reached over number of interval can be shortened to 4 with daily doses 250 mg,
this is not and metabolites of in can be in the months completion therapy. Antimalarial
Action & strong P falciparum P is hepatic stages or gametocytes. The of unknown.
Sporadic mefloquine been from areas. At resistance appears to uncommon regions
Asia high rates border areas resis- tance quinine resistance to Clinical in
sentences:
- 938 SECTION VIII Chemotherapeutic Drugs Clinical Uses Albendazole is administered
on an empty stomach when used against intraluminal parasites but with a fatty
meal when used against tissue parasites. A. Ascariasis, Trichuriasis, and Hookworm
and Pinworm Infections For adults and children older than 2 years of age with
ascariasis and hookworm infections, the treatment is a single dose of 400 mg TABLE
53–1 Drugs for the treatment of helminthic infections. 1 Infecting Organism Drug
of Choice Alternative Drugs Roundworms (nematodes) Ascaris lumbricoides (roundworm)
Albendazole or pyrantel pamoate or mebendazole Ivermectin, piperazine Trichuris
trichiura (whipworm) Mebendazole or albendazole Ivermectin Necator americanus
(hookworm); Ancylostoma duodenale (hookworm) Albendazole or mebendazole or pyrantel
pamoate Strongyloides stercoralis (threadworm) Ivermectin Albendazole or thiabendazole
Enterobius vermicularis (pinworm) Mebendazole or pyrantel pamoate Albendazole
Trichinella spiralis (trichinosis) Mebendazole or albendazole; add corticosteroids
for severe infection Trichostrongylus species Pyrantel pamoate or mebendazole
Albendazole Cutaneous larva migrans (creeping eruption) Albendazole or ivermectin
Thiabendazole (topical) Visceral larva migrans Albendazole Mebendazole Angiostrongylus
cantonensis Albendazole or mebendazole Wuchereria bancrofti (filariasis); Brugia
malayi (filariasis); tropical eosinophilia; Loa loa (loiasis) Diethylcarbamazine
Ivermectin Onchocerca volvulus (onchocerciasis) Ivermectin Dracunculus medinensis
(guinea worm) Metronidazole Thiabendazole or mebendazole Capillaria philippinensis
(intestinal capillariasis) Albendazole Mebendazole Flukes (trematodes) Schistosoma
haematobium (bilharziasis)
- CHAPTER 52 Antiprotozoal Drugs 923 MEFLOQUINE Mefloquine is effective therapy
for many chloroquine-resistant strains of P falciparum and against other species.
Although toxicity is a concern, mefloquine is one of the recommended chemopro-
phylactic drugs for use in most malaria-endemic regions with chloroquine-resistant
strains. Chemistry & Pharmacokinetics Mefloquine hydrochloride is a synthetic
4-quinoline methanol that is chemically related to quinine. It can only be given
orally because severe local irritation occurs with parenteral use. It is well
absorbed, and peak plasma concentrations are reached in about 18 hours. Mefloquine
is highly protein-bound, extensively distrib- uted in tissues, and eliminated
slowly, allowing a single-dose treat- ment regimen. The terminal elimination half-life
is about 20 days, allowing weekly dosing for chemoprophylaxis. With weekly dos-
ing, steady-state drug levels are reached over a number of weeks; this interval
can be shortened to 4 days by beginning a course with three consecutive daily
doses of 250 mg, although this is not stan- dard practice. Mefloquine and acid
metabolites of the drug are slowly excreted, mainly in the feces. The drug can
be detected in the blood for months after the completion of therapy. Antimalarial
Action & Resistance Mefloquine has strong blood schizonticidal activity against
P falciparum and P vivax, but it is not active against hepatic stages or gametocytes.
The mechanism of action of mefloquine is unknown. Sporadic resistance to mefloquine
has been reported from many areas. At present, resistance appears to be uncommon
except in regions of Southeast Asia with high rates of multidrug resistance (especially
border areas of Thailand). Mefloquine resis- tance appears to be associated with
resistance to quinine and halofantrine but not with resistance to chloroquine.
Clinical Uses A. Chemoprophylaxis Mefloquine is effective in prophylaxis against
most strain
- the body to colonize various organs in the process called metastasis. Such tumor
stem cells thus can express clonogenic (colony-forming) capability, and they are
characterized by chromosome abnormalities reflecting their genetic instability,
which leads to progressive selection of subclones that can survive more readily
in the multicellular environment of the host. This genetic instability also allows
them to become resistant to chemotherapy and radiotherapy. The invasive and metastatic
processes as well as a series of metabolic abnormalities associated with the cancer
result in tumor-related symptoms and eventual death of the patient unless the
neoplasm can be eradicated with treatment. 54 CAUSES OF CANCER The incidence,
geographic distribution, and behavior of specific types of cancer are related
to multiple factors, including sex, age, race, genetic predisposition, and exposure
to environmental car- cinogens. Of these factors, environmental exposure is probably
most important. Exposure to ionizing radiation has been well documented as a significant
risk factor for a number of cancers, including acute leukemias, thyroid cancer,
breast cancer, lung cancer, soft tissue sarcoma, and basal cell and squamous cell
skin cancers. Chemical carcinogens (particularly those in tobacco smoke) as well
as azo dyes, aflatoxins, asbestos, benzene, and radon have all been well documented
as leading to a wide range of human cancers. Several viruses have been implicated
in the etiology of various human cancers. For example, hepatitis B and hepatitis
C are asso- ciated with the development of hepatocellular cancer; HIV is associated
with Hodgkin’s and non-Hodgkin’s lymphomas; human papillomavirus is associated
with cervical cancer and head and neck cancer; and Ebstein-Barr virus is associated
with nasopharyn- geal cancer. Expression of virus-induced neoplasia may also depend
on additional host and environmental factors that modu- late the transformation
process. Cellular genes are known that are homologous to the transforming genes
of the retroviruses, a family
pipeline_tag: sentence-similarity
library_name: sentence-transformers
---
# SentenceTransformer based on ibm-granite/granite-embedding-107m-multilingual
This is a [sentence-transformers](https://www.SBERT.net) model finetuned from [ibm-granite/granite-embedding-107m-multilingual](https://huggingface.co/ibm-granite/granite-embedding-107m-multilingual). It maps sentences & paragraphs to a 384-dimensional dense vector space and can be used for semantic textual similarity, semantic search, paraphrase mining, text classification, clustering, and more.
## Model Details
### Model Description
- **Model Type:** Sentence Transformer
- **Base model:** [ibm-granite/granite-embedding-107m-multilingual](https://huggingface.co/ibm-granite/granite-embedding-107m-multilingual) <!-- at revision 5c793ec061753b0d0816865e1af7db3f675d65af -->
- **Maximum Sequence Length:** 512 tokens
- **Output Dimensionality:** 384 dimensions
- **Similarity Function:** Cosine Similarity
<!-- - **Training Dataset:** Unknown -->
<!-- - **Language:** Unknown -->
<!-- - **License:** Unknown -->
### Model Sources
- **Documentation:** [Sentence Transformers Documentation](https://sbert.net)
- **Repository:** [Sentence Transformers on GitHub](https://github.com/UKPLab/sentence-transformers)
- **Hugging Face:** [Sentence Transformers on Hugging Face](https://huggingface.co/models?library=sentence-transformers)
### Full Model Architecture
```
SentenceTransformer(
(0): Transformer({'max_seq_length': 512, 'do_lower_case': False}) with Transformer model: XLMRobertaModel
(1): Pooling({'word_embedding_dimension': 384, 'pooling_mode_cls_token': True, 'pooling_mode_mean_tokens': False, 'pooling_mode_max_tokens': False, 'pooling_mode_mean_sqrt_len_tokens': False, 'pooling_mode_weightedmean_tokens': False, 'pooling_mode_lasttoken': False, 'include_prompt': True})
(2): Normalize()
)
```
## Usage
### Direct Usage (Sentence Transformers)
First install the Sentence Transformers library:
```bash
pip install -U sentence-transformers
```
Then you can load this model and run inference.
```python
from sentence_transformers import SentenceTransformer
# Download from the 🤗 Hub
model = SentenceTransformer("RikoteMaster/embedder-granite")
# Run inference
sentences = [
'Antiprotozoal 923 MEFLOQUINE Mefloquine is effective therapy of other Although toxicity is mefloquine one recommended for most regions with Chemistry Mefloquine is 4-quinoline methanol is chemically quinine. can given because local irritation with parenteral and hours. Mefloquine highly uted and treat- regimen. elimination half-life about 20 allowing dosing chemoprophylaxis. With dos- drug reached over number of interval can be shortened to 4 with daily doses 250 mg, this is not and metabolites of in can be in the months completion therapy. Antimalarial Action & strong P falciparum P is hepatic stages or gametocytes. The of unknown. Sporadic mefloquine been from areas. At resistance appears to uncommon regions Asia high rates border areas resis- tance quinine resistance to Clinical in',
'CHAPTER 52 Antiprotozoal Drugs 923 MEFLOQUINE Mefloquine is effective therapy for many chloroquine-resistant strains of P falciparum and against other species. Although toxicity is a concern, mefloquine is one of the recommended chemopro- phylactic drugs for use in most malaria-endemic regions with chloroquine-resistant strains. Chemistry & Pharmacokinetics Mefloquine hydrochloride is a synthetic 4-quinoline methanol that is chemically related to quinine. It can only be given orally because severe local irritation occurs with parenteral use. It is well absorbed, and peak plasma concentrations are reached in about 18 hours. Mefloquine is highly protein-bound, extensively distrib- uted in tissues, and eliminated slowly, allowing a single-dose treat- ment regimen. The terminal elimination half-life is about 20 days, allowing weekly dosing for chemoprophylaxis. With weekly dos- ing, steady-state drug levels are reached over a number of weeks; this interval can be shortened to 4 days by beginning a course with three consecutive daily doses of 250 mg, although this is not stan- dard practice. Mefloquine and acid metabolites of the drug are slowly excreted, mainly in the feces. The drug can be detected in the blood for months after the completion of therapy. Antimalarial Action & Resistance Mefloquine has strong blood schizonticidal activity against P falciparum and P vivax, but it is not active against hepatic stages or gametocytes. The mechanism of action of mefloquine is unknown. Sporadic resistance to mefloquine has been reported from many areas. At present, resistance appears to be uncommon except in regions of Southeast Asia with high rates of multidrug resistance (especially border areas of Thailand). Mefloquine resis- tance appears to be associated with resistance to quinine and halofantrine but not with resistance to chloroquine. Clinical Uses A. Chemoprophylaxis Mefloquine is effective in prophylaxis against most strain',
'the body to colonize various organs in the process called metastasis. Such tumor stem cells thus can express clonogenic (colony-forming) capability, and they are characterized by chromosome abnormalities reflecting their genetic instability, which leads to progressive selection of subclones that can survive more readily in the multicellular environment of the host. This genetic instability also allows them to become resistant to chemotherapy and radiotherapy. The invasive and metastatic processes as well as a series of metabolic abnormalities associated with the cancer result in tumor-related symptoms and eventual death of the patient unless the neoplasm can be eradicated with treatment. 54 CAUSES OF CANCER The incidence, geographic distribution, and behavior of specific types of cancer are related to multiple factors, including sex, age, race, genetic predisposition, and exposure to environmental car- cinogens. Of these factors, environmental exposure is probably most important. Exposure to ionizing radiation has been well documented as a significant risk factor for a number of cancers, including acute leukemias, thyroid cancer, breast cancer, lung cancer, soft tissue sarcoma, and basal cell and squamous cell skin cancers. Chemical carcinogens (particularly those in tobacco smoke) as well as azo dyes, aflatoxins, asbestos, benzene, and radon have all been well documented as leading to a wide range of human cancers. Several viruses have been implicated in the etiology of various human cancers. For example, hepatitis B and hepatitis C are asso- ciated with the development of hepatocellular cancer; HIV is associated with Hodgkin’s and non-Hodgkin’s lymphomas; human papillomavirus is associated with cervical cancer and head and neck cancer; and Ebstein-Barr virus is associated with nasopharyn- geal cancer. Expression of virus-induced neoplasia may also depend on additional host and environmental factors that modu- late the transformation process. Cellular genes are known that are homologous to the transforming genes of the retroviruses, a family',
]
embeddings = model.encode(sentences)
print(embeddings.shape)
# [3, 384]
# Get the similarity scores for the embeddings
similarities = model.similarity(embeddings, embeddings)
print(similarities.shape)
# [3, 3]
```
<!--
### Direct Usage (Transformers)
<details><summary>Click to see the direct usage in Transformers</summary>
</details>
-->
<!--
### Downstream Usage (Sentence Transformers)
You can finetune this model on your own dataset.
<details><summary>Click to expand</summary>
</details>
-->
<!--
### Out-of-Scope Use
*List how the model may foreseeably be misused and address what users ought not to do with the model.*
-->
<!--
## Bias, Risks and Limitations
*What are the known or foreseeable issues stemming from this model? You could also flag here known failure cases or weaknesses of the model.*
-->
<!--
### Recommendations
*What are recommendations with respect to the foreseeable issues? For example, filtering explicit content.*
-->
## Training Details
### Training Dataset
#### Unnamed Dataset
* Size: 34,441 training samples
* Columns: <code>anchor</code> and <code>positive</code>
* Approximate statistics based on the first 1000 samples:
| | anchor | positive |
|:--------|:-----------------------------------------------------------------------------------|:-------------------------------------------------------------------------------------|
| type | string | string |
| details | <ul><li>min: 3 tokens</li><li>mean: 99.93 tokens</li><li>max: 255 tokens</li></ul> | <ul><li>min: 14 tokens</li><li>mean: 245.16 tokens</li><li>max: 512 tokens</li></ul> |
* Samples:
| anchor | positive |
|:-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|:---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|
| <code>March Lecture Solving using by Svensson1 In this following: We describe Multiplicative Hedge) • We this method to solve is these lecture are on of “Lecture 11 of in 2015” written and Simon Rodriguez and on by Kaul that the lecture previous we to use the majority method order to fairly general with days N experts as For t . , gives advice: 2. advice the expert, of and the decides 4. observes suffers was majority parameterized by ε “learning rate”), now as follows: • each i weight initialized 1. are trustworthy the ning.) each t: • Predict based on w(t) After observing the vector, i expert the lecture we case = following any sequence of i of WM mistake</code> | <code>Advanced Algorithms March 22, 2022 Lecture 9: Solving LPs using Multiplicative Weights Notes by Ola Svensson1 In this lecture we do the following: • We describe the Multiplicative Weight Update (actually Hedge) method. • We then use this method to solve covering LPs. • This is a very fast and simple (i.e., very attractive) method for solving these LPs approximately. These lecture notes are partly based on an updated version of “Lecture 11 of Topics in TCS, 2015” that were written by Vincent Eggerling and Simon Rodriguez and on the lecture notes by Shiva Kaul that we used in the last lecture. 1 Recall last lecture In the previous lecture, we saw how to use the weighted majority method in order to fairly smartly follow the advice of experts. Recall that the general game-setting with T days and N experts was as follows: For t = 1, . . . , T: 1. Each expert i ∈[N] gives some advice: UP or DOWN 2. Aggregator (you) predicts, based on the advice of the expert, UP or DOWN. 3. Adversary, with k...</code> |
| <code>Last ε The same proof the For duration expert i ∈[N], of WM mistakes ε) · (# i’s mistakes) + O(log(N)/ε) 1Disclaimer: notes They not been and may typos,</code> | <code>Last lecture we analyzed the case when ε = 1/2. The same proof gives the following Theorem 1 For any sequence of outcomes, duration T, and expert i ∈[N], # of WM mistakes ≤2(1 + ε) · (# of i’s mistakes) + O(log(N)/ε) . 1Disclaimer: These notes were written as notes for the lecturer. They have not been peer-reviewed and may contain inconsistent notation, typos, and omit citations of relevant works. 1</code> |
| <code>[Sketch] The proof done by potential function: for each = 1, . , 1, Φ(t) = i We lower potential the mistakes of i. We it in of our mistakes. The weight of expert down by a −ε) i does. As weight is 1, Φ(T +1) = +1) ≥w(T +1) = (1 −ε)# of . Every the experts was (since majority weights are (1 −ε). that the factor every time Φ(T −ε/2)# mistakes = N −ε/2)# , equality used that = was initialized with a weight above bounds give us (1 mistakes ≤N · (1 of . sides, allowing for randomized strategies In the exercises, you proved that are instances for weighted This overcome this we allow random instead of always making prediction the to create A is often general is often good the of adversaries. Allowing randomized leads to following with T t . . ,</code> | <code>Proof [Sketch] The proof was done by defining a potential function: for each t = 1, . . . , T + 1, let Φ(t) = X i∈[N] w(t) i . We now lower bound the “final” potential Φ(T +1) using the number of mistakes of i. We then upper bound it in terms of our number of mistakes. Lower bound: The weight of expert i goes down by a factor (1 −ε) for each mistake i does. As the initial weight of i is 1, Φ(T +1) = X j∈[N] w(T +1) j ≥w(T +1) i = (1 −ε)# of i’s mistakes . Upper bound: Every time WM errs, at least half the weight of the experts was wrong (since weighted majority was wrong). These weights are then decreased by (1 −ε). It follows that the potential goes down by at least a factor (1 −ε/2) every time WM errs. And so Φ(T +1) ≤Φ(1) · (1 −ε/2)# of WM mistakes = N · (1 −ε/2)# of WM mistakes , where for the equality we used that Φ(1) = N since each expert was initialized with a weight of 1. The above bounds give us (1 −ε)# of i’s mistakes ≤Φ(T +1) ≤N · (1 −ε/2)# of WM mistakes . Taking logs on b...</code> |
* Loss: [<code>MultipleNegativesRankingLoss</code>](https://sbert.net/docs/package_reference/sentence_transformer/losses.html#multiplenegativesrankingloss) with these parameters:
```json
{
"scale": 20.0,
"similarity_fct": "cos_sim"
}
```
### Evaluation Dataset
#### Unnamed Dataset
* Size: 3,827 evaluation samples
* Columns: <code>anchor</code> and <code>positive</code>
* Approximate statistics based on the first 1000 samples:
| | anchor | positive |
|:--------|:-------------------------------------------------------------------------------------|:-------------------------------------------------------------------------------------|
| type | string | string |
| details | <ul><li>min: 15 tokens</li><li>mean: 174.64 tokens</li><li>max: 266 tokens</li></ul> | <ul><li>min: 55 tokens</li><li>mean: 432.79 tokens</li><li>max: 512 tokens</li></ul> |
* Samples:
| anchor | positive |
|:-------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|:---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------|
| <code>CHAPTER 39 Adrenocorticosteroids Adrenocortical Antagonists occurs. of /d of or in intermediate-, long-acting glucocorticoids greater growth-suppressing the steroid in larger than amounts, as cortisone hydrocortisone, which mineralocorticoid effects addition to glucocorticoid and fluid and loss of potassium. patients this a hypokalemic, and in blood pressure. hypoproteinemia, renal disease, liver disease, also occur. In patients with disease, small of may These by using non-salt-retaining and supplements. C. Suppression corticosteroids adrenal suppression occur. weeks the given appropriate at times dosage 24–48 hours) or stress ten-fold for or costeroid dosage be it slowly. If to reduction be slow levels. It take 2–12 to and cortisol may not to normal The suppression not treatment ACTH does time for normal function. the too receiving a certain disorder, the</code> | <code>CHAPTER 39 Adrenocorticosteroids & Adrenocortical Antagonists 707 hypertension also occurs. In dosages of 45 mg/m 2 /d or more of hydrocortisone or its equivalent, growth retardation occurs in children. Medium-, intermediate-, and long-acting glucocorticoids have greater growth-suppressing potency than the natural steroid at equivalent doses. When given in larger than physiologic amounts, steroids such as cortisone and hydrocortisone, which have mineralocorticoid effects in addition to glucocorticoid effects, cause some sodium and fluid retention and loss of potassium. In patients with normal cardiovas- cular and renal function, this leads to a hypokalemic, hypochloremic alkalosis and eventually to a rise in blood pressure. In patients with hypoproteinemia, renal disease, or liver disease, edema may also occur. In patients with heart disease, even small degrees of sodium retention may lead to heart failure. These effects can be minimized by using synthetic non-salt-retaining steroids, ...</code> |
| <code>is a treatment not reduce the return function. dosage rapidly a certain the symptoms the in patients an disorder patients Cushing’s disease) symptoms with rapid symptoms include anorexia, vomit- ing, weight loss, postural reflect true glucocorticoid deficiency, occur in the normal or even plasma levels, sug- gesting glucocorticoids must carefully the hyperglycemia, sodium with edema hypertension, hypokalemia, peptic osteopo- rosis, and and intermittent alternate-day) can on this Even patients may of stress, surgical are or or acci- occur. B. with with peptic hypertension with failure, cer- as varicella tuberculosis, psycho- ses, osteoporosis, Glucocorticoid differ respect relative anti- inflammatory and mineralocorticoid of available ( Table and these factors should be in drug to used. ACTH Adrenocortical Steroids patients normal</code> | <code>is not a pituitary problem, and treatment with ACTH does not reduce the time required for the return of normal function. If the dosage is reduced too rapidly in patients receiving gluco- corticoids for a certain disorder, the symptoms of the disorder may reappear or increase in intensity. However, patients without an underlying disorder (eg, patients cured surgically of Cushing’s disease) also develop symptoms with rapid reductions in cortico- steroid levels. These symptoms include anorexia, nausea or vomit- ing, weight loss, lethargy, headache, fever, joint or muscle pain, and postural hypotension. Although many of these symptoms may reflect true glucocorticoid deficiency, they may also occur in the presence of normal or even elevated plasma cortisol levels, sug- gesting glucocorticoid dependence. Contraindications & Cautions A. Special Precautions Patients receiving glucocorticoids must be monitored carefully for the development of hyperglycemia, glycosuria, sodium retention with ede...</code> |
| <code>( Table and these should be taken in be A. ACTH ACTH used past production to However, when is able, ACTH therapeutic agent has abandoned. which claimed be effective than were due of of were dosage Dosage the regimen physician consider the disease, amount likely to required the effect, therapy. required for the dose to obtain initial the for needed effect be until a small or symptoms is When it is continuously plasma levels to ACTH, paren- preparation oral doses frequent The situation with respect use of inflammatory allergic The same total quantity few be effective many smaller slowly absorbed autoimmune involving organs aggressively, is as treatment. complexes macrophages, of predni- divided doses dosage is serious dosage can gradually large required prolonged time, after control When used manner, large amounts</code> | <code>available ( Table 39–1 ), and these factors should be taken into account in selecting the drug to be used. A. ACTH versus Adrenocortical Steroids In patients with normal adrenals, ACTH was used in the past to induce the endogenous production of cortisol to obtain similar effects. However, except when an increase in androgens is desir- able, the use of ACTH as a therapeutic agent has been abandoned. Instances in which ACTH was claimed to be more effective than glucocorticoids were probably due to the administration of smaller amounts of corticosteroids than were produced by the dosage of ACTH. B. Dosage In determining the dosage regimen to be used, the physician must consider the seriousness of the disease, the amount of drug likely to be required to obtain the desired effect, and the duration of therapy. In some diseases, the amount required for maintenance of the desired therapeutic effect is less than the dose needed to obtain the initial effect, and the lowest possible dosage for th...</code> |
* Loss: [<code>MultipleNegativesRankingLoss</code>](https://sbert.net/docs/package_reference/sentence_transformer/losses.html#multiplenegativesrankingloss) with these parameters:
```json
{
"scale": 20.0,
"similarity_fct": "cos_sim"
}
```
### Training Hyperparameters
#### Non-Default Hyperparameters
- `eval_strategy`: steps
- `per_device_train_batch_size`: 128
- `per_device_eval_batch_size`: 128
- `learning_rate`: 2e-05
- `num_train_epochs`: 5
- `warmup_ratio`: 0.1
- `fp16`: True
- `dataloader_drop_last`: True
- `dataloader_num_workers`: 2
- `load_best_model_at_end`: True
- `push_to_hub`: True
- `hub_model_id`: RikoteMaster/embedder-granite
- `hub_strategy`: end
- `hub_private_repo`: True
#### All Hyperparameters
<details><summary>Click to expand</summary>
- `overwrite_output_dir`: False
- `do_predict`: False
- `eval_strategy`: steps
- `prediction_loss_only`: True
- `per_device_train_batch_size`: 128
- `per_device_eval_batch_size`: 128
- `per_gpu_train_batch_size`: None
- `per_gpu_eval_batch_size`: None
- `gradient_accumulation_steps`: 1
- `eval_accumulation_steps`: None
- `torch_empty_cache_steps`: None
- `learning_rate`: 2e-05
- `weight_decay`: 0.0
- `adam_beta1`: 0.9
- `adam_beta2`: 0.999
- `adam_epsilon`: 1e-08
- `max_grad_norm`: 1.0
- `num_train_epochs`: 5
- `max_steps`: -1
- `lr_scheduler_type`: linear
- `lr_scheduler_kwargs`: {}
- `warmup_ratio`: 0.1
- `warmup_steps`: 0
- `log_level`: passive
- `log_level_replica`: warning
- `log_on_each_node`: True
- `logging_nan_inf_filter`: True
- `save_safetensors`: True
- `save_on_each_node`: False
- `save_only_model`: False
- `restore_callback_states_from_checkpoint`: False
- `no_cuda`: False
- `use_cpu`: False
- `use_mps_device`: False
- `seed`: 42
- `data_seed`: None
- `jit_mode_eval`: False
- `use_ipex`: False
- `bf16`: False
- `fp16`: True
- `fp16_opt_level`: O1
- `half_precision_backend`: auto
- `bf16_full_eval`: False
- `fp16_full_eval`: False
- `tf32`: None
- `local_rank`: 0
- `ddp_backend`: None
- `tpu_num_cores`: None
- `tpu_metrics_debug`: False
- `debug`: []
- `dataloader_drop_last`: True
- `dataloader_num_workers`: 2
- `dataloader_prefetch_factor`: None
- `past_index`: -1
- `disable_tqdm`: False
- `remove_unused_columns`: True
- `label_names`: None
- `load_best_model_at_end`: True
- `ignore_data_skip`: False
- `fsdp`: []
- `fsdp_min_num_params`: 0
- `fsdp_config`: {'min_num_params': 0, 'xla': False, 'xla_fsdp_v2': False, 'xla_fsdp_grad_ckpt': False}
- `fsdp_transformer_layer_cls_to_wrap`: None
- `accelerator_config`: {'split_batches': False, 'dispatch_batches': None, 'even_batches': True, 'use_seedable_sampler': True, 'non_blocking': False, 'gradient_accumulation_kwargs': None}
- `deepspeed`: None
- `label_smoothing_factor`: 0.0
- `optim`: adamw_torch
- `optim_args`: None
- `adafactor`: False
- `group_by_length`: False
- `length_column_name`: length
- `ddp_find_unused_parameters`: None
- `ddp_bucket_cap_mb`: None
- `ddp_broadcast_buffers`: False
- `dataloader_pin_memory`: True
- `dataloader_persistent_workers`: False
- `skip_memory_metrics`: True
- `use_legacy_prediction_loop`: False
- `push_to_hub`: True
- `resume_from_checkpoint`: None
- `hub_model_id`: RikoteMaster/embedder-granite
- `hub_strategy`: end
- `hub_private_repo`: True
- `hub_always_push`: False
- `gradient_checkpointing`: False
- `gradient_checkpointing_kwargs`: None
- `include_inputs_for_metrics`: False
- `include_for_metrics`: []
- `eval_do_concat_batches`: True
- `fp16_backend`: auto
- `push_to_hub_model_id`: None
- `push_to_hub_organization`: None
- `mp_parameters`:
- `auto_find_batch_size`: False
- `full_determinism`: False
- `torchdynamo`: None
- `ray_scope`: last
- `ddp_timeout`: 1800
- `torch_compile`: False
- `torch_compile_backend`: None
- `torch_compile_mode`: None
- `include_tokens_per_second`: False
- `include_num_input_tokens_seen`: False
- `neftune_noise_alpha`: None
- `optim_target_modules`: None
- `batch_eval_metrics`: False
- `eval_on_start`: False
- `use_liger_kernel`: False
- `eval_use_gather_object`: False
- `average_tokens_across_devices`: False
- `prompts`: None
- `batch_sampler`: batch_sampler
- `multi_dataset_batch_sampler`: proportional
</details>
### Training Logs
| Epoch | Step | Training Loss | Validation Loss |
|:---------:|:--------:|:-------------:|:---------------:|
| 0.1859 | 50 | 0.3983 | - |
| 0.3717 | 100 | 0.193 | - |
| 0.5576 | 150 | 0.0828 | - |
| 0.7435 | 200 | 0.0409 | 0.0339 |
| 0.9294 | 250 | 0.0386 | - |
| 1.1152 | 300 | 0.0322 | - |
| 1.3011 | 350 | 0.0311 | - |
| 1.4870 | 400 | 0.0275 | 0.0167 |
| 1.6729 | 450 | 0.0252 | - |
| 1.8587 | 500 | 0.0254 | - |
| 2.0446 | 550 | 0.0254 | - |
| 2.2305 | 600 | 0.0227 | 0.0129 |
| 2.4164 | 650 | 0.0236 | - |
| 2.6022 | 700 | 0.0185 | - |
| 2.7881 | 750 | 0.0234 | - |
| 2.9740 | 800 | 0.0274 | 0.0118 |
| 3.1599 | 850 | 0.0208 | - |
| 3.3457 | 900 | 0.0245 | - |
| 3.5316 | 950 | 0.0242 | - |
| 3.7175 | 1000 | 0.0219 | 0.0112 |
| 3.9033 | 1050 | 0.0239 | - |
| 4.0892 | 1100 | 0.0223 | - |
| 4.2751 | 1150 | 0.0212 | - |
| **4.461** | **1200** | **0.0223** | **0.0107** |
| 4.6468 | 1250 | 0.0228 | - |
| 4.8327 | 1300 | 0.0196 | - |
* The bold row denotes the saved checkpoint.
### Framework Versions
- Python: 3.10.17
- Sentence Transformers: 4.1.0
- Transformers: 4.52.3
- PyTorch: 2.7.0+cu126
- Accelerate: 1.7.0
- Datasets: 3.6.0
- Tokenizers: 0.21.1
## Citation
### BibTeX
#### Sentence Transformers
```bibtex
@inproceedings{reimers-2019-sentence-bert,
title = "Sentence-BERT: Sentence Embeddings using Siamese BERT-Networks",
author = "Reimers, Nils and Gurevych, Iryna",
booktitle = "Proceedings of the 2019 Conference on Empirical Methods in Natural Language Processing",
month = "11",
year = "2019",
publisher = "Association for Computational Linguistics",
url = "https://arxiv.org/abs/1908.10084",
}
```
#### MultipleNegativesRankingLoss
```bibtex
@misc{henderson2017efficient,
title={Efficient Natural Language Response Suggestion for Smart Reply},
author={Matthew Henderson and Rami Al-Rfou and Brian Strope and Yun-hsuan Sung and Laszlo Lukacs and Ruiqi Guo and Sanjiv Kumar and Balint Miklos and Ray Kurzweil},
year={2017},
eprint={1705.00652},
archivePrefix={arXiv},
primaryClass={cs.CL}
}
```
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