Suppression of canine antral gastrin secretion by urine

Distention of the gastric antrum with an alkaline fluid normally results in the secretion of gastrin. Following gastrocystoplasty in humans, however, hypergastrinemia has not been observed. We explored the possibility that a component of urine may suppress antral gastrin activity in the dog. Partial cystectomy and antral transposition to the bladder (ATB) was performed in five animals and antral transposition to the colon (ATC) was performed in five other dogs to serve as a hypergastrinemic controls. At four and eight weeks after surgery the mean serum gastrin levels in the ATC dogs were significantly greater than the mean preoperative levels (p less than 0.05). In contrast, at four and eight weeks after surgery the mean serum gastrin levels in the ATB animals were significantly less than the mean preoperative levels (p less than 0.05). The antral G-cell density as determined by immunohistochemical study at eight weeks after surgery was greater than normal in the ATC dogs but less than normal in the ATB dogs; but the differences did not achieve statistical significance. In another series of experiments using four other dogs a 4% aqueous peptone solution and a 4% peptone solution in concentrated dog urine were instilled into exteriorized antral pouches. The mean serum gastrin levels at 60 and 90 minutes after instillation of the former were significantly increased (p less than 0.05), but there was little or no change after instillation of the latter. Urine, or a component of urine, appears to suppress canine antral gastrin secretion and may explain the absence of hypergastrinemia following gastrocystoplasty in humans.     

Potential biosoluble carriers: biocompatibility and biodegradability of oxidized cellulose

The biocompatibility and biodegradability of periodate oxidized cellulose is assessed in vivo. Morophological and histopathological studies over a period of six months indicate that oxidized cellulose degrades slowly without producing excessive tissue reaction. Preliminary investigations on the kinetics of degradation of oxidized cellulose in vitro, immobilization of alpha-chymotrypsin on it and the rate of the enzyme release in a solution of pH 7.4 are also briefly reported.     

Estimation accuracy of surgically induced astigmatism on the cornea when neglecting the posterior corneal surface measurement

Purpose: To evaluate the accuracy of corneal surgically induced astigmatism (SIA) estimation when neglecting the posterior corneal surface measurement. Methods: Fifty right eyes undergoing phacoemulsification were measured with a rotating Scheimpflug camera (Pentacam; Oculus Inc., Wetzlar, Germany) both before and after surgery. Clear corneal incisions with one suture were used in the phacoemulsification surgery. The keratometric corneal SIA (KSIA) was derived using the anterior corneal surface measurement and the keratometric index (1.3375) while neglecting the posterior corneal surface measurement. The Pentacam‐derived total corneal SIA (PSIA) was derived by vergence tracing and polar value analysis [KP(135) and KP(180)] of the measurements on both corneal surfaces. Results: The mean arithmetic estimation errors of the KSIA for the PSIA were 0.16 ± 0.32 (?0.52 to 1.14) D for the KP(135), and ?0.02 ± 0.30 (?0.75 to 1.29) D for the KP(180). There was a significant difference between the KP(135) components of the KSIA and PSIA. Bivariate analysis revealed a statistically significant difference between the combined means of the KSIA and PSIA. Overall, 24% had either a KP(135) component of the KSIA that differed by > 0.50 D from that of the PSIA or a KP(180) component of the KSIA that differed by > 0.50 D from that of the PSIA. The blurring strength caused by neglecting the posterior corneal measurement was > 0.50 D in 24% of eyes. Conclusion: Neglecting the posterior corneal surface measurement may lead to significant deviation in the corneal SIA estimation after phacoemulsification in a proportion of eyes.     

Contribution of genotyping for fetal sex determination in maternal serum for preimplantation genetic diagnosis of X-linked diseases

OBJECTIVE: Couples with a risk of transmitting X-linked diseases included in a preimplantation genetic diagnosis (PGD) center need early and rapid fetal sex determination during pregnancy in two situations. The first situation corresponds to control of embryo sexing after PGD, the second one being that of couples in PGD program having a spontaneous pregnancy. Determination of fetal sex can be achieved by karyotyping using invasive procedures such as chorionic villus sampling (CVS), amniocentesis or cordocentesis and by non-invasive procedures such as ultrasound (US) examination. CVS is the earliest invasive procedure for fetal sex determination and molecular analysis of X-linked genetic disorders during the first trimester but it is associated with a risk of fetal loss. US allows reliable fetal sex determination only during the second trimester. Recently, reliable non-invasive fetal sex determination was realized by using SRY gene amplification in maternal serum. PATIENTS AND METHODS: We report the prospective use of fetal sex determination in maternal serum in our PGD center. Management of pregnancies was performed using this non-invasive procedure in four cases of embryo sexing control and nine cases of spontaneous pregnancies in couples included in PGD program for X-linked diseases. RESULTS: Fetal sex results using SRY gene amplification on maternal serum were in complete concordance with fetal sex observed by cytogenetic analysis or US examination, as well as at birth. DISCUSSION AND CONCLUSION: This new strategy allowed rapid sex determination during the first trimester and permitted to avoid performing invasive procedures in nine pregnancies.     

A new mutation identified in <Emphasis Type="Italic">SPATA16</Emphasis> in two globozoospermic patients

Purpose

The aim of this study is to identify potential genes involved in human globozoopsermia.

Methods

Nineteen globozoospermic patients (previously screened for DPY19L2 mutations with no causative mutation) were recruited in this study and screened for mutations in genes implicated in human globozoospermia SPATA16 and PICK1. Using the candidate gene approach and the determination of Spata16 partners by Glutathione S-transferase (GST) pull-down four genes were also selected and screened for mutations.

Results

We identified a novel mutation of SPATA16: deletion of 22.6 Kb encompassing the first coding exon in two unrelated Tunisian patients who presented the same deletion breakpoints. The two patients shared the same haplotype, suggesting a possible ancestral founder effect for this new deletion. Four genes were selected using the candidate gene approach and the GST pull-down (GOPC, PICK1, AGFG1 and IRGC) and were screened for mutation, but no variation was identified.

Conclusions

The present study confirms the pathogenicity of the SPATA16 mutations. The fact that no variation was detected in the coding sequence of AFGF1, GOPC, PICK1 and IRGC does not mean that they are not involved in human globozoospermia. A larger globozoospermic cohort must be studied in order to accelerate the process of identifying new genes involved in such phenotypes. Until sufficient numbers of patients have been screened, AFGF1, GOPC, PICK1 and IRGC should still be considered as candidate genes.