Transcutaneous oximetry values in chronic ulcer patients during Hyperbaric treatment at 1.4 ATA compared to 2 ATA.

Chronic wounds have a significant impact on a patient's quality of life. Different pathologies, such as poor blood supply and tissue breakdown, may lead to inadequate oxygenation of the wound. Hyperbaric oxygen (HBO2) is a widely used treatment for an increasing number of medical practices. A new so-called "hyperbaric treatment" trend has emerged. The use of low-pressure, soft-sided, or inflatable chambers represents a growing trend in hyperbaric medicine. Used in professional settings as well as directly marketed to individuals for home use, they are promoted as equivalent to clinical hyperbaric treatments provided in medical centers. However, these chambers are pressurized to 1.3 atmospheres absolute (ATA) on either air or with an oxygen concentrator, both generate oxygen partial pressures well below those used in approved hyperbaric centers for UHMS-approved indications. A total of 130 consecutive patients with chronic ulcers where tested. TcPO2 was measured near the ulcer area while the patient was breathing 100% O2 at 1.4 ATA for five and 10 minutes. The average TcPO2 at 1.4 ATA after 10 minutes of O2 breathing was 161 mmHg (1-601 mmHg, standard deviation 137.91), compared to 333 mmHg in 2 ATA (1-914±232.56), p < 0.001. Each electrode tested was also statistically significant, both after five minutes of O2 breathing and after 10 minutes. We have not found evidence supporting the claim that 1.4 ATA treatment can benefit a chronic ulcer patient. The field of HBO2 is constantly evolving. We have discovered new ways to treat previously incurable ailments. Nevertheless, it is important to note that new horizons must be examined scientifically, supported by evidence-based data. The actual effect of 1.4 ATA on many ailments is yet to be determined.

Lower core body temperature and attenuated nicotine-induced hypothermic response in mice lacking the beta4 neuronal nicotinic acetylcholine receptor subunit.

Diverse physiological and pathological effects of nicotine, including the alteration of body temperature, are presumably mediated by neuronal nicotinic acetylcholine receptors (nAChR). Previous studies have suggested the involvement of distinct nAChR subunits in nicotine-induced thermoregulation. We studied genetically manipulated knockout mice lacking the alpha7, alpha5 or beta4 subunit genes, in order to assess the effects of subunit deficiency on temperature regulation. Using a telemetry system, core body temperature was monitored continuously prior to and following nicotine administration in mutant mice and in wild-type littermates. Mice lacking in the beta4 nAChR subunit gene had significantly lower baseline core body temperature than all other mouse strains studied. beta4 null mice also demonstrated a reduced nicotine-induced hypothermic response and impaired desensitization following repeat nicotine exposure. These findings suggest the involvement of the beta4 nAChR subunit in both core body temperature homeostasis and nicotine-elicited thermo-alterations in mice.

Increased sensitivity to nicotine-induced seizures in mice heterozygous for the L250T mutation in the alpha7 nicotinic acetylcholine receptor.

alpha7 Nicotinic acetylcholine receptors (nAChRs) are sparsely distributed throughout the peripheral and central nervous systems. Several studies have suggested that central alpha7 nicotinic receptors may influence sensitivity to nicotine-induced seizures in mice. In order to investigate the effect of alpha7 nAChRs on seizure sensitivity, we tested heterozygous mice with a threonine for leucine substitution at position 250 (L250T) within the channel domain, which is known to increase current amplitude and decreases desensitization of the channel. We show that administration of low doses of nicotine to these mutant mice increased the sensitivity to nicotine-induced seizures and the mortality rate. EEG recordings showed high amplitude rhythmic activity during tonic-clonic seizures. Pretreatment with the alpha7 nicotinic receptor antagonist methyllycaconitine inhibited the seizures induced by nicotine. These findings further suggest an important role for alpha7 nAChRs in the nicotine-induced seizures model of epilepsy.