Abstract: The present invention relates to 3-(benzylamino)-4-(cyclohexylamino)-N-(2-(piperazin-1-yl)ethyl)benzenesulfonamide derivatives and related ferrostatin-1 (Fer-1) analogues as cell death inhibitors by inhibition of ferroptosis and/or oxytosis for the treatment of stroke, myocardial infarction, diabetes, sepsis, the prevention of transplant rejection, neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, Huntington's disease, dementia with Lewy bodies and Friedreich's ataxia. The present invention further relates to pharmaceutical compositions of these compounds and discloses methods for making the compounds and the corresponding intermediate.

Abstract: The present invention relates to 3-(benzylamino)-4-(cyclohexylamino)-N-(2-(piperazin-1-yl)ethyl)benzenesulfonamide derivatives and related ferrostatin-1 (Fer-1) analogues as cell death inhibitors by inhibition of ferroptosis and/or oxytosis for the treatment of stroke, myocardial infarction, diabetes, sepsis, the prevention of transplant rejection, neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, Huntington's disease, dementia with Lewy bodies and Friedreich's ataxia. The present invention further relates to pharmaceutical compositions of these compounds and discloses methods for making the compounds and the corresponding intermediate.

Abstract: The present invention relates to the inactivation of interleukin-1 and interleukin-18 signaling in treatment of inflammation and septic shock. More specifically, it relates to a sequential or simultaneous application of both an interleukin-1 receptor antagonist and an interleukin-18 antibody. In one preferred embodiment, a combination treatment of an IL-1 receptor antagonist and an IL-18 antibody is used.

Abstract: This disclosure relates to a novel class of compounds having the structure of formula I as defined herein and pharmaceutical compositions comprising a compound of formula I or a pharmaceutically acceptable salt thereof. This disclosure also comprises methods of treating a subject by administering a therapeutically effective amount of a compound of formula I or a pharmaceutically acceptable salt thereof to the subject. These compounds are useful for the conditions disclosed herein. This disclosure further comprises methods for making the compounds of formula I and corresponding intermediates.

Abstract: This disclosure relates to a novel class of compounds having the structure of formula I as defined herein and pharmaceutical compositions comprising a compound of formula I or a pharmaceutically acceptable salt thereof. This disclosure also comprises methods of treating a subject by administering a therapeutically effective amount of a compound of formula I or a pharmaceutically acceptable salt thereof to the subject. These compounds are useful for the conditions disclosed herein. This disclosure further comprises methods for making the compounds of formula I and corresponding intermediates.

Abstract: The present invention relates to the inactivation of interleukin-1 and interleukin-18 signaling in treatment of inflammation and septic shock. More specifically, it relates to a sequential or simultaneous application of both an interleukin-1 receptor antagonist and an interleukin-18 antibody. In one preferred embodiment, a combination treatment of an IL-1 receptor antagonist and an IL-18 antibody is used.

Abstract: The present invention relates to a novel member of the card protein family. More specifically, it relates to a novel human card-only protein. The invention relates further to the use of this protein to inhibit pro-interleukin-1? maturation, preferably without inducing NF-?B activity or apoptosis.

Abstract: The present invention comprises a method of protecting organs or tissue susceptible to reperfusion-induced dysfunction after ischemia. The method comprises parenterally administering to a patient a therapeutical composition containing natural alpha-1 acid glycoprotein, natural alpha-1 antitrypsin or a mixture thereof. Alternatively, organ or tissue transplants can be contacted with natural alpha-1 acid glycoprotein, natural alpha-1 antitrypsin or mixtures by perfusing or flushing them with a solution containing natural alpha-1 acid glycoprotein, natural alpha-1 antitrypsin or mixtures thereof in a concentration of 0.1 to 5 g/l.

Abstract: The present invention comprises a method of protecting organs or tissue susceptible to reperfusion-induced dysfunction after ischemia. The method comprises parenterally administering to a patient a therapeutical composition containing natural alpha-1 acid glycoprotein, natural alpha-1 antitrypsin or a mixture thereof. Alternatively, organ or tissue transplants can be contacted with natural alpha-1 acid glycoprotein, natural alpha-antitrypsin or mixtures by perfusing or flushing them with a solution containing natural alpha-1 acid glycoprotein, natural alpha-1 antitrypsin or mixtures thereof in a concentration of 0.1 to 5 g/l.

Abstract: Caspases are cysteinyl aspartate-specific proteinases, many of which play a central role in apoptosis. This invention relates to the identification of a new murine caspase and its human homologue. The new molecules are most related to human/murine caspase-2 and human caspase-9 and possesses all the typical amino acid residues of the caspases involved in catalysis, including the QACRG box, and contains no or only a very short prodomain. Northern blot analysis revealed that mRNA expression of the new caspase is predominant in skin.

Abstract: The method is used in a telecommunication network wherein a central station (CS) is coupled to a plurality of residences (R1,R2,R3). One of the residences (R3) includes a termination unit (TU) which is coupled to the central station (CS) via a first port (P1). The residence (R3) also includes subscriber terminals, e.g. a personal computer (PC), a telephone set (TEL), a television set (TV) and a set-top box (STB) which are coupled to the termination unit (TU) via a second port (P2). The method includes amplifying an upstream signal (US) applied to the second port (P2) with an upstream gain value (UG) by means of an upstream signal amplifier (U-AMP3) which is included in the termination unit (TU). Thereby, an amplified upstream signal (AUS) is generated and provided to the first port (P1).

Abstract: The present invention comprises a method of protecting organs or tissue susceptible to reperfusion-induced dysfunction after ischemia. The method comprises parenterally administering to a patient a therapeutical composition containing natural alpha-1 acid glycoprotein, natural alpha-1 antitrypsin or a mixture thereof. Alternatively, organ or tissue transplants can be contacted with natural alpha-1 acid glycoprotein, natural alpha-antitrypsin or mixtures by perfusing or flushing them with a solution containing natural alpha-1 acid glycoprotein, natural alpha-1 antitrypsin or mixtures thereof in a concentration of 0.1 to 5 g/l.

Abstract: Caspases are cysteinyl aspartate-specific proteinases, many of which play a central role in apoptosis. This invention relates to the identification of a new murine caspase and its human homologue. The new molecules are most related to human/murine caspase-2 and human caspase-9 and possesses all the typical amino acid residues of the caspases involved in catalysis, including the QACRG box, and contains no or only a very short prodomain. Northern blot analysis revealed that mRNA expression of the new caspase is predominant in skin.

Abstract: To allocate time slots to terminal stations (T1 . . . Ti . . . Tn) for transmission of upstream burst (UB) in a network system wherein a central station (CS) is coupled to a plurality of terminal stations (T1 . . . Ti . . . Tn), the central station (CS) downstream transmits access grant information (AGI) which forms part of downstream frames (DE). Each terminal station (Ti) is equipped with a cyclic local grant counter (LGC) which generates a local grant counter value between zero and a predetermined limit, and which is synchronized with a cyclic master grant counter (MGC) included in the central station (CS). The upstream time slots are bounded by two zero crossings of the cyclic local grant counter (LGC) and a terminal station (Ti) is allowed to transfer an upstream burst (UB) in such a time slot provided that this time slot is allocated to the terminal station (Ti) via previously received access grant information (AGI).

Abstract: The radiation generated by at least one radiation source is controlled so as to generate a constant radiation intensity, thereby to cause the object to be heated, and the radiation intensity from the object at a first wavelength is sensed until it is equal to the present radiation intensity generated by the at least one radiation source, whereby the temperature of the object has a predetermined value. From that time on, the development of the actual temperature of the object is controlled accurately according to a predetermined program merely by sensing the radiation intensity from the object at a second wavelength larger than the first wavelength, and using the measuring signal representative of the sensed radiation intensity to continuously control the radiation intensity generated by the at least one radiation source.