The surgical treatment of groin hernias continues to undergo technical modifications. The introduction of minimally invasive surgery had added a possible new dimension, replacing an inguinal approach by laparoscopy. Conceived some 15 years ago, the thesis was subjected to a clinical trial where coincidental abdominal hernial openings were closed at laparotomy. This study was followed by an experimental study at which time the openings were closed laparoscopically. The satisfactory results led to the development of a stapling instrument that could be passed through a cannula at laparoscopy and used to close the abdominal hernial opening. The clinical trial of treating hernias by laparoscopy was originally directed to the management of indirect inguinal hernias, but its use has since been expanded to include treatment of direct, femoral, obturator, incarcerated, recurrent, and bilateral hernias. The laparoscopic anatomy of the inguinal hernia, different from that seen by an inguinal approach, is briefly reviewed. The details of the operative technique are presented, as are the bases of other laparoscopic techniques that have evolved. Thirty-one hernial orifices have been closed and followed over 18 months. The results appear to be satisfactory in 27 instances. There were early technical failures in 2: One patient developed a recurrence after 5 months, later shown to be due to a sliding hernia; and symptoms of meralgia paresthetica of indeterminate origin appeared in one case. The advantages over the traditional approach are described; the disadvantages of the laparoscopic approach are those of laparoscopy itself and the absence of a long-term follow-up.

Adolescent↗

PubMedDate not supplied

Phenotypic expression of histocompatibility antigens in human primary tumours and metastases.

HLA class I and II expression was studied on 244 (177 primary and 67 metastatic) solid human tumours of different origin. Alkaline immunophosphatase (APAAP) and immunoperoxidase were used on cryostatic sections to stain MHC antigens. Monomorphic MoAbs were used against class I heavy chain, beta 2-microglobulin, DR, DQ and DP molecules. Class I expression was homogeneous on colon, melanoma and epidermoidal primitive tumours. Loss of HLA class I antigens was more frequent on basal cell carcinomas and sarcomas and was related to tumour differentiation on larynx carcinoma. Class I expression was heterogeneous on breast, larynx and stomach primitive neoplasias. Class I negative tumours were more frequent on metastatic than on primitive melanomas. Divergence of class I between primary tumours and autologous metastases was observed on melanomas, larynx and colorectal carcinomas. Class II expression was heterogeneous on all tumours and in a large number of cases was associated with high intensity of leukocytic infiltrate. HLA-DR expression was higher than HLA-DP and HLA-DQ (DR greater than DP greater than DQ) and was related to tumour progression. Four human tumour cell lines were modulated with recombinant interferon-gamma for HLA class I and II antigens. Different HLA profiles were obtained: increased class I and II expression, increased class II or a low response. Finally, class I genes from 22 tumours were compared with autologous normal cells by Southern blot analysis: 12 tumours were class I positive and 10 negative. No clear differences in RFLP were observed that could be associated with class I rearrangement. The results are discussed in relation to the role that histocompatibility antigens may play in tumour progression and invasiveness.

Genes, MHC Class I↗

PubMedDate not supplied

Repression of class I H-2K, H-2D antigens on GR9 methylcholanthrene-induced tumour cell clones is related to the level of DNA methylation.

The correlation between gene expression and DNA methylation is well established. In the present study we examined DNA methylation as a potential regulatory mechanism of class I histocompatibility antigen expression. We selected for study two cell clones from the same mouse tumour (GR9). One of them is H-2 class I-positive (A7) and the other negative (B9). Using five enzymes and three different probes, no rearrangement or deletion was detected in the MHC class I genes of the negative clone compared with the positive one. These results do not provide an explanation for the differences observed in the expression of class I antigens in A7 (Kd, Dd positive) and B9 (Kd, Dd negative). We then studied the DNA methylation status in both clones by Southern blot analysis. Clear differences between the Kd, Dd positive and negative clones were detected. Furthermore, both Kd and Dd were clearly expressed after culturing the H-2 class I negative clone with the demethylating agent 5-azacytidine. These results suggest that the methylation of certain MHC cytosines is a regulatory mechanism of H-2 class I gene expression.

Animals↗