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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
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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
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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:
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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-
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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
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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
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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
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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
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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
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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
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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
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, 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.
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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
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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
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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
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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
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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
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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)
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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
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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 model finetuned from 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
- Maximum Sequence Length: 512 tokens
- Output Dimensionality: 384 dimensions
- Similarity Function: Cosine Similarity
Model Sources
- Documentation: Sentence Transformers Documentation
- Repository: Sentence Transformers on GitHub
- Hugging Face: Sentence Transformers on Hugging Face
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:
pip install -U sentence-transformers
Then you can load this model and run inference.
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]
Training Details
Training Dataset
Unnamed Dataset
- Size: 34,441 training samples
- Columns:
anchorandpositive - Approximate statistics based on the first 1000 samples:
anchor positive type string string details - min: 3 tokens
- mean: 99.93 tokens
- max: 255 tokens
- min: 14 tokens
- mean: 245.16 tokens
- max: 512 tokens
- Samples:
anchor positive 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 mistakeAdvanced 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...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,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[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 . . ,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... - Loss:
MultipleNegativesRankingLosswith these parameters:{ "scale": 20.0, "similarity_fct": "cos_sim" }
Evaluation Dataset
Unnamed Dataset
- Size: 3,827 evaluation samples
- Columns:
anchorandpositive - Approximate statistics based on the first 1000 samples:
anchor positive type string string details - min: 15 tokens
- mean: 174.64 tokens
- max: 266 tokens
- min: 55 tokens
- mean: 432.79 tokens
- max: 512 tokens
- Samples:
anchor positive 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, theCHAPTER 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, ...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 normalis 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...( 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 amountsavailable ( 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... - Loss:
MultipleNegativesRankingLosswith these parameters:{ "scale": 20.0, "similarity_fct": "cos_sim" }
Training Hyperparameters
Non-Default Hyperparameters
eval_strategy: stepsper_device_train_batch_size: 128per_device_eval_batch_size: 128learning_rate: 2e-05num_train_epochs: 5warmup_ratio: 0.1fp16: Truedataloader_drop_last: Truedataloader_num_workers: 2load_best_model_at_end: Truepush_to_hub: Truehub_model_id: RikoteMaster/embedder-granitehub_strategy: endhub_private_repo: True
All Hyperparameters
Click to expand
overwrite_output_dir: Falsedo_predict: Falseeval_strategy: stepsprediction_loss_only: Trueper_device_train_batch_size: 128per_device_eval_batch_size: 128per_gpu_train_batch_size: Noneper_gpu_eval_batch_size: Nonegradient_accumulation_steps: 1eval_accumulation_steps: Nonetorch_empty_cache_steps: Nonelearning_rate: 2e-05weight_decay: 0.0adam_beta1: 0.9adam_beta2: 0.999adam_epsilon: 1e-08max_grad_norm: 1.0num_train_epochs: 5max_steps: -1lr_scheduler_type: linearlr_scheduler_kwargs: {}warmup_ratio: 0.1warmup_steps: 0log_level: passivelog_level_replica: warninglog_on_each_node: Truelogging_nan_inf_filter: Truesave_safetensors: Truesave_on_each_node: Falsesave_only_model: Falserestore_callback_states_from_checkpoint: Falseno_cuda: Falseuse_cpu: Falseuse_mps_device: Falseseed: 42data_seed: Nonejit_mode_eval: Falseuse_ipex: Falsebf16: Falsefp16: Truefp16_opt_level: O1half_precision_backend: autobf16_full_eval: Falsefp16_full_eval: Falsetf32: Nonelocal_rank: 0ddp_backend: Nonetpu_num_cores: Nonetpu_metrics_debug: Falsedebug: []dataloader_drop_last: Truedataloader_num_workers: 2dataloader_prefetch_factor: Nonepast_index: -1disable_tqdm: Falseremove_unused_columns: Truelabel_names: Noneload_best_model_at_end: Trueignore_data_skip: Falsefsdp: []fsdp_min_num_params: 0fsdp_config: {'min_num_params': 0, 'xla': False, 'xla_fsdp_v2': False, 'xla_fsdp_grad_ckpt': False}fsdp_transformer_layer_cls_to_wrap: Noneaccelerator_config: {'split_batches': False, 'dispatch_batches': None, 'even_batches': True, 'use_seedable_sampler': True, 'non_blocking': False, 'gradient_accumulation_kwargs': None}deepspeed: Nonelabel_smoothing_factor: 0.0optim: adamw_torchoptim_args: Noneadafactor: Falsegroup_by_length: Falselength_column_name: lengthddp_find_unused_parameters: Noneddp_bucket_cap_mb: Noneddp_broadcast_buffers: Falsedataloader_pin_memory: Truedataloader_persistent_workers: Falseskip_memory_metrics: Trueuse_legacy_prediction_loop: Falsepush_to_hub: Trueresume_from_checkpoint: Nonehub_model_id: RikoteMaster/embedder-granitehub_strategy: endhub_private_repo: Truehub_always_push: Falsegradient_checkpointing: Falsegradient_checkpointing_kwargs: Noneinclude_inputs_for_metrics: Falseinclude_for_metrics: []eval_do_concat_batches: Truefp16_backend: autopush_to_hub_model_id: Nonepush_to_hub_organization: Nonemp_parameters:auto_find_batch_size: Falsefull_determinism: Falsetorchdynamo: Noneray_scope: lastddp_timeout: 1800torch_compile: Falsetorch_compile_backend: Nonetorch_compile_mode: Noneinclude_tokens_per_second: Falseinclude_num_input_tokens_seen: Falseneftune_noise_alpha: Noneoptim_target_modules: Nonebatch_eval_metrics: Falseeval_on_start: Falseuse_liger_kernel: Falseeval_use_gather_object: Falseaverage_tokens_across_devices: Falseprompts: Nonebatch_sampler: batch_samplermulti_dataset_batch_sampler: proportional
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
@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
@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}
}