Temperature dependent time resolved mid-IR photoacoustic spectroscopy of a nerve gas simulant DMMP.

The paper reports the temperature dependent pulsed photoacoustic spectroscopy of Dimethyl methylphosphonate (DMMP) a nerve gas simulant between 50 and 180 °C temperature range. The time domain PA spectra are recorded using two mid-IR wavelengths i.e. 3374 nm, 3495 nm of pulse duration 1.5 ns at 1 kHz repetition rate obtained from optical parametric oscillator. Two anti-symmetric stretching vibrational modes of (CH3P) and (CH3O) groups of DMMP molecules have very strong vibrational peaks at 2861.2 cm-1 (3495 nm) and 2963.8 cm-1 (3374 nm), respectively. In addition, we have also recorded the PA spectra of acetone at the vibrational frequency 3115.2 cm-1 (3210 nm), which is the strong vibrational mode of CH band. The comparison of two PA spectra of DMMP and acetone recorded using similar PA cavity help us to understand the effect of other functional groups with respect to different excitation wavelengths. The presence of additional acoustic modes in the PA spectra of DMMP (3374 nm) above the boiling point confirms the slow process of thermal decomposition. Finally, the low level detection limit of DMMP in air is of the of the order of 0.91 ppbV.

Laser induced fluorescence of biochemical for UV LIDAR application.

Laser induced fluorescence spectroscopy in the ultraviolet regime has been used for the detection of biochemical through a fiber coupled CCD detector from a distance of 2 m. The effect of concentration and laser excitation energy on the fluorescence spectra of nicotinamide adenine dinucleotide (NADH) has been investigated. The signature fluorescence peak of NADH was centred about 460 nm. At lower concentration Raman peak centred at 405 nm was also observed. The origin of this peak has been discussed. Detection limit with the proposed set up is found to be 1 ppm.

Mie lidar observations of lower tropospheric aerosols and clouds.

Mie lidar system is developed at Laser Science and Technology Centre, Delhi (28.38°N, 77.12°E) by using minimal number of commercially available off-the-shelf components. Neodymium Yttrium Aluminum Garnet (Nd:YAG) laser operating at 1064nm with variable pulse energies between 25 and 400 mJ with 10 Hz repetition rate and 7ns pulse duration is used as a transmitter and off-axis CASSEGRAIN telescope with 100mm diameter as a receiver. Silicon avalanche photodiode (Si-APD) module with built-in preamplifier and front-end optics is used as detector. This system has been developed for the studies of lower tropospheric aerosols and clouds. Some experiments have been conducted using this set up and preliminary results are discussed. The characteristics of backscattered signals for various transmitter pulse energies are also studied. Atmospheric aerosol extinction coefficient values are calculated using Klett lidar inversion algorithm. The extinction coefficient, in general, falls with range in the lower troposphere and the values lie typically in the range 7.5×10(-5) m(-1) to 1.12×10(-4) m(-1) in the absence of any cloud whereas this value shoots maximum up to 1.267×10(-3) m(-1) (peak extinction) in the presence of clouds.

Amenorrhea related to progestin excess in congenital adrenal hyperplasia.

Studies of the cause of amenorrhea in a patient with congenital adrenal hyperplasia (CAH) whose androgen levels were easily controlled suggested that inhibition of menses in CAH is more closely related to overproduction of progestins than to overproduction of androgens. Supporting this concept was the observation in another patient with CAH that menarche was associated with improved control of the plasma progesterone. Subsequent detailed investigation of the diurnal plasma steroid pattern of other treated CAH patients indicates that major intermittenet spisodic bursts of progestin secretion occur in many patients whose plasma androgen levels are well controlled. Estimation of 17-hydroxyprogesterone (17-P) production, by measurement of serum 17-P or urinary y pregnanetriol, provides the best index of biochemical control of the 21-hydroxylase deficiency form of CAH. In patients in whom poorly controlled progestins are possible contributers to abnormal menses, low-dose dexamethasone (about 0.25 mg/m2/day) in 1 or 2 divided doses seems to be the treatment of choice.

Gonadotropin-releasing hormone infusion test in the distinction of hypopituitary patients from normal subjects.

We undertook a pilot study to determine whether infusion of gonadotropin-releasing hormone (GnRH) might improve the distinction of hypogonadotropinism from the normal state and might permit gonadotropin deficiency to be diagnosed in the prepubertal child. Normal prepubertal and pubertal boys had a greater luteinizing hormone (LH) reaction (delta LH 54 +/- 15 [SD] ng/ml and 165 +/- 23 ng/ml, respectively) to a 4-hour infusion (100 microgram/hour) than to a 100-microgram bolus of GnRH (19 +/- 9 and 52 +/- 35 ng/ml). These augmented responses were observed in boys with delayed puberty, but not in apparently hypogonadotropic males greater than or equal to 12 years old. LH (delta LH 445 to 1602 ng/ml) and FSH (delta FSH 718 to 2112 ng/ml) surges were induced consistently by GnRH infusion only in normal, postmenarchial females. In all, of 13 hypopituitary cases classified as hypogonadotropic on the basis of a subnormal response to GnRH infusion, 31% had a normal response to the GnRH bolus (P = 0.05). Thus, GnRH infusion testing seems to improve the distinction of hypogonadotropic patients from normal individuals, including boys with delayed puberty.

Partial gonadotrophin-resistance in pseudohypoparathyroidism.

A patient with classical Albright's pseudohypoparathyroidism was investigated because of oligomenorrhoea. Hypo-oestrogenism was associated with elevated basal gonadotrophin values [mean basal serum LH and FSH were 272 +/- 84 (SD) ng/ml and 593 +/- 83 ng/ml, resplectively (normal less than or equal to 220 and less than or equal to 400, respectively)]. The response to gonadotrophin releasing hormone (Gn-RH) was exaggerated, with maximal LH and FSH increments of 1688 and 458 ng/ml, respectively. These results and the findings on ovarian biopsy were compatible with partial ovarian resistance to gonadotrophins. This resistance could be overcome by administration of human menopausal gonadotrophins. This is the first evidence for gonadotrophin resistance in pseudohypoparathyroidism. The plasma cyclic adenosine-3',5'-monophosphate response to glucagon administration by two different protocols was about 70% that of normal control subjects. Other endocrine glands whose responses to hormones are mediated via the adenylate cyclase system evidenced minor abnormalities of questionable significance. This indirect evidence is compatible with a more extensive defect in the adenylate cyclase system in pseudohypoparathyroidism than has hitherto been suspected.

Endocrinologic characteristics of partial ovarian failure.

Three young women with primary ovarian failure, secondary amenorrhea or oligo-ovulation, and normal gonadotropin levels are reported on here. Vaginal cytology and serum estradiol levels indicated the two women to be persistently hypoestrogenic. The third case, who had the Turner phenotype, was hypoestrogenic during anovulatory cycles but occasionally ovulated. Basal serum LH and FSH were normal. All were tested with synthetic LH-releasing hormone and had a brisk response, LH levels rising 51-198 ng/ml above baseline and FSH rising 278-536 ng/ml. Plasma levels of testosterone, dehydroepiandrosterone sulfate, and progesterone were normal. Gonadal dysgenesis was suggested in two on the basis of an abnormal karyotype, and isochromosome of the short arm of X in Case 2, and an isochromosome of the long arm of X in Case 3. The diagnosis of primary hypogonadism was established by laparoscopy and ovarian biopsy. The latter studies revealed small ovaries with a scarcity of primordial and primary follicles, yet with evidence of current or previous follicular activity. The observation that hypoestrogenism was so marked in two of our patients that elevated serum FSH would have been expected, suggests that the presence of a limited number of ovarian follicles suffices to prevent hypergonagotropism in hypoestrogenic women by a mechanism which does not involve elaboration of sex steroids.