Introduction: Ingrown toenails are one of the most common nail disorders, with complex and multifactorial causes, for all age groups, mostly young adults. The essence of disease is congenital or acquired distortion of the proportions between the size of the nail bed and the nail folds. Laser treatment consists of the vaporisation of the matrix and bed, i.e. the reproductive sphere of the nail, using a CO 2 laser. Aim of the research: Evaluation of the effectiveness of laser dissection using a CO 2 laser. Material and methods: The methodology was divided into two stages. The first stage consisted of a retrospective analysis of the medical documentation of 165 patients who had undergone laser CO 2 dissection, during the period from February 2011 to May 2015 in the Laser CO 2 Surgery Room, according to the developed scheme. The second stage was follow-up control of patients participating in the study, a week and then a month after surgery. In addition, in May 2015 90 patients were audited in terms of effectiveness and satisfaction of the treatment and recurrence of symptoms. The remaining 70 patients answered these questions by telephone. Results and conclusions: Laser dissection of the ingrown nail with matrixectomy is a very effective method, only in 4 (2%) patients was there a recurrence. Nearly 90% of patients expressed satisfaction with the outcome of the surgery. The cause of dissatisfaction was sometimes an anaesthetic appearance of the nail apparatus. Nearly 70% of patients were children and young adults aged up to 23 years. The most frequent cause of ingrown toenail was wearing inappropriate shoes and incorrect cutting of toenails.

Epidermal growth factor (EGF) stimulates the proliferation of many different types of cells and plays an important role in the formation and growth of tumours. The interaction of EGF with cells is possible by the EGF receptor (EGFR) anchored in the cell membrane. Excess EGFR expression is found in approximately 25-82% of colorectal cancer cases. Attachment of EGF to EGFR results in a conformational change in the receptor, an increase in affinity for neighbouring receptors, receptor dimerisation, and activation of tyrosine kinase in the intraplasmic domain. Activation of EGFR leads to the initiation of the signal transduction pathway to the cell nucleus, via a number of proteins with enzymatic activity-secondary messengers, including KRAS and BRAF proteins. The assessment of the presence of mutations in the KRAS gene has become a standard element in the qualification of patients with advanced colorectal cancer for therapy with the use of monoclonal antibodies. Streszczenie Naskórkowy czynnik wzrostu (EGF) stymuluje proliferację wielu różnych typów komórek i odgrywa ważną rolę w po wstawaniu i rozwoju nowotworów. Oddziaływanie EGF z komórkami jest możliwe dzięki receptorowi EGF (EGFR) zako twiczonemu w błonie komórkowej. Nadmierna ekspresja EGFR występuje w ok. 25-82% przypadków raka jelita grubego. Przyłączenie EGF do EGFR powoduje konformacyjną zmianę receptora, wzrost powinowactwa do sąsiednich receptorów, dimeryzację receptora i aktywację kinazy tyrozynowej w domenie wewnątrzplazmatycznej. Aktywacja EGFR prowadzi do inicjacji szlaku transdukcji sygnału do jądra komórkowego za pośrednictwem wielu białek o aktywności enzymatycz nej-wtórnych przekaźników, w tym białek KRAS i BRAF. Ocena obecności mutacji w genie KRAS stała się standardowym elementem kwalifikacji pacjentów z zaawansowanym rakiem jelita grubego do leczenia z zastosowaniem przeciwciał mono klonalnych.

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Cholecystolithiasis is among the most prevalent gastrointestinal disorders requiring surgical intervention, and iatrogenic damage to the bile tree is a severe complication. We aimed to present the frequency of bile duct injuries and how our facility handles these complications. We retrospectively analyzed bile duct injuries in patients undergoing surgery. We concentrated on factors such as sex, age, indications for surgery, type of surgery, primary procedure, bile tree injury, repair, and timing as well as early and late complications. There were 22 cases of bile duct injury in the studied material, primarily affecting women—15 individuals (68.2%). Eleven cases (45.7%) of acute cholecystitis were the primary reason for surgery, and an injury to the common bile duct that extended up to 2 cm from the common hepatic duct was the most common complication (European Association for Endoscopic Surgery grade 2). Roux-en-Y hepaticojejunostomy was the most common repair procedure in 14 cases (63.6%). Eleven patients (50%) experienced early complications following reconstruction surgery, whereas five patients (22.7%) experienced late complications. An annual mortality rate of 22.7% (five patients) was observed. Iatrogenic bile duct injury is a severe complication of surgical treatment for cholecystolithiasis. Reconstruction procedures are characterized by high complication rates and high mortality.

Colorectal cancer should be considered as a heterogeneous disease that leads to many different genetic changes, resulting in the existence of molecular subtypes that differ in response to the same treatment and have different prognosis. For this reason, research into new, sensitive, and specific molecular prognostic factors has been intensified. It is now clear that there are many pathways leading to tumour formation in this organ because only about 10% of intestinal tumours have mutations in three "classic" Fearon-Vogelstein genes: APC, KRAS, and P53. The study of the relationship between molecular changes and clinical and pathological features reflects the evolution of the disease. Effective care for the sick depends on appropriate pathological evaluation and the ability to perform effective research on disease mechanisms. StreszczenieRak jelita grubego powinien być uważany za chorobę heterogeniczną, do której powstania prowadzi wiele różnych zmian genetycznych, skutkiem czego jest istnienie podtypów molekularnych, odmiennie odpowiadających na taką samą terapię oraz mających różne rokowania. Z tego powodu intensyfikuje się badania nad poszukiwaniem nowych, czułych i swoistych molekularnych czynników prognostycznych. Obecnie wiadomo, że istnieje wiele szlaków prowadzących do powstania nowotworu w tym narządzie. Okazało się, że tylko ok. 10% nowotworów jelita ma mutacje w trzech "klasycznych" genach modelu Fearona-Vogelsteina: APC, KRAS i P53. Badanie związku między zmianami molekularnymi a cechami kliniczno-patologicznymi odzwierciedla ewolucję choroby. Od właściwej oceny patologicznej i trafnej kwalifikacji choroby zależy efektywna opieka nad chorym oraz możliwość przeprowadzenia skutecznych badań nad mechanizmami powstawania choroby.